Show of the Month November 2014
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Silver nanoparticle applications and human health
Purslane weed (Portulaca oleracea): a prospective plant source of nutrition, omega-3 fatty acid, and antioxidant attributes.
Could copper prevent spread of Ebola
Tea, citrus products could lower ovarian cancer risk, new research finds
Date:October 28, 2014 –Source-University of East Anglia
Tea and citrus fruits and juices are associated with a lower risk of developing ovarian cancer, according to new research from the University of East Anglia (UEA).--The research reveals that women who consume foods containing flavonols and flavanones (both subclasses of dietary flavonoids) significantly decrease their risk of developing epithelial ovarian cancer, the fifth-leading cause of cancer death among women.--The research team studied the dietary habits of 171,940 women aged between 25 and 55 for more than three decades.--The team found that those who consumed food and drinks high in flavonols (found in tea, red wine, apples and grapes) and flavanones (found in citrus fruit and juices) were less likely to develop the disease.--Ovarian cancer affects more than 6,500 women in the UK each year. In the United States, about 20,000 women are diagnosed with ovarian cancer each year.--Prof Aedin Cassidy, from the Department of Nutrition at UEA's Norwich Medical School, led the study. She said: "This is the first large-scale study looking into whether habitual intake of different flavonoids can reduce the risk of epithelial ovarian cancer.--"We found that women who consume foods high in two sub-groups of powerful substances called flavonoids -- flavonols and flavanones -- had a significantly lower risk of developing epithelial ovarian cancer.--"The main sources of these compounds include tea and citrus fruits and juices, which are readily incorporated into the diet, suggesting that simple changes in food intake could have an impact on reducing ovarian cancer risk.--"In particular, just a couple of cups of black tea every day was associated with a 31 per cent reduction in risk."--The research was the first to comprehensively examine the six major flavonoid subclasses present in the normal diet with ovarian cancer risk, and the first to investigate the impact of polymers and anthocyanins.--The study was led by Prof Cassidy and Prof Shelley Tworoger, from the Brigham and Women's Hospital and Harvard Medical School. Data was derived from the Nurses' Health Study.--Story Source-The above story is based on materials provided by University of East Anglia. Note: Materials may be edited for content and length.--Journal Reference--A. Cassidy, T. Huang, M. S. Rice, E. B. Rimm, S. S. Tworoger. Intake of dietary flavonoids and risk of epithelial ovarian cancer. American Journal of Clinical Nutrition, 2014; 100 (5): 1344 DOI: 10.3945/%u200Bajcn.114.088708
SaskPower CEO resigns after smart meter report
SaskPower CEO Robert Watson speaks at the official opening of a carbon capture and storage facility at the Boundary Dam Power Station in Estevan, Sask. on Thursday, October 2, 2014. (THE CANADIAN PRESS/Michael Bell)-- The head of Saskatchewan's Crown power company resigned Monday following a report into smart-meter fires that said customer safety wasn't enough of a priority.--Economy Minister Bill Boyd said SaskPower CEO Robert Watson "took responsibility for the problems experienced with this project."--"(He) felt it was time that there was new leadership at SaskPower," said Boyd, who added that Mike Marsh, vice-president of operations, will step into the job for the interim.
Smart meters are seen in this photo taken July 31, 2014 in Regina.-Last summer, the province ordered SaskPower to remove more than 100,000 smart meters that had already been installed in homes after at least eight of the devices caught fire in June and July.-Boyd said it was evident for some time that there were problems with the meters.-"There was not enough consideration given to customer safety, the program was rushed and there (were) warning signs that were overlooked. It was clear that there was no one that was in overall charge of the program," the minister said.-Watson won't be receiving severance pay, Boyd said.-Saskatchewan's Crown Investment Corp. was directed to do a review after the fires. The investigation results released Monday found that rain water and contaminants getting into the meters appeared to contribute to them failing.-"In various parts of the province, eight meters failed catastrophically, melting or burning and in some cases damaging the sides of houses," the report[F1] said. The failures were not related to "hot sockets" or installation issues, it said.-The report also said SaskPower failed to look at the possibility that the meters could short out and catch fire.-It said that the utility looked at 359 returns and found that 18 smart meters were burned and no longer operational. Three more had high temperature errors, while 107 had display problems and 67 showed error codes.-"The (Return Material Authorization) process involves meters that have had issues in the field, and includes the eight meters involved in the destructive failures," the review said. "The causes of these issues range from broken displays, over-voltage, communication issues, or simply the meters were dropped and no longer function properly."-Boyd said the government is taking the review's findings seriously and the Crown corporation will be directed to follow its recommendations. They include replacing all the meters that were provided by U.S. manufacturer Sensus. SaskPower is planning to have removal completed by March 15.--Watson announced in September that Sensus was refunding $24 million for all the smart meters the province purchased. That covered all devices that were installed and had to be removed, as well as those that hadn't been put in yet.-Watson said Sensus was also giving SaskPower $18 million in credit for new meters, and another $5 million was to go toward developing a device suited to the Saskatchewan climate.--The NDP Opposition is asking for an independent investigation by the provincial auditor. New Democrat finance critic Trent Wotherspoon said the report is "damning."-"This government simply didn't have the consideration of the safety of Saskatchewan people, which is appalling in and of itself," said Wotherspoon, who added that the problems with the meters were "concealed."-"They rejected looking into the examples in other jurisdictions -- Alabama and Philadelphia -- where there was meter failure going on with the very meters that this government was putting taxpayers on the hook to pay."-Wotherspoon said while the government claims to have recouped costs from the program, "millions of dollars (have been) wasted."-The problems in Saskatchewan prompted officials in Medicine Hat, Alta., to suspend installation of electricity smart meters in August. A spokesman for the city said there had been no reported problems.-In Ontario, smart meters have been linked to 23 reports to Ontario's fire marshal between 2011 and 2013, including 13 small fires. Karen Cormier, a spokeswoman for the Ontario Energy Board, has said that 36 of 77 utilities in Ontario use smart meters from Sensus, but none of them are the model used in Saskatchewan.-A smart meter records consumption of energy in small intervals and can relay the information electronically to a utilities company. It eliminates the need to estimate bills when a meter reader can't do an on-site check.
CIC SMART METER REVIEW MAKES RECOMMENDATIONS TO IMPROVE CROWN PROCUREMENT
Released on October 27, 2014
Review Finds Customer Safety Was Not Given Enough Priority
An investigation into the causes of fires and the procurement practices surrounding SaskPower’s smart meter program has concluded that customer safety was not given a high enough priority by SaskPower. This and other findings have led to a series of recommendations aimed at preventing such problems in the future.-“Customer safety does not appear to have been a consideration until after reports of smart meter fires involving Philadelphia Electric Company (PECO) arose,” independent experts at the law firm Robertston Stromberg found. “It did not become a matter of central importance until June of 2014.”-During June and July of 2014, there were eight different cases where smart meters caught fire, prompting the suspension of the installation program and a later cabinet order to remove the meters.-Crown Investments Corporation (CIC) was directed to conduct a review and commissioned a number of independent experts to examine different aspects of the issue. -PwC was asked to review procurement and contract management. Consulting engineers Ritenburg and Associates of Regina was asked to examine the technical and safety issues and the law firm Robertson Stromberg was commissioned to look at legal and product liability issues.-An initial study of the causes of the fires shows that rainwater and contaminants getting into the meters appear to be a major contributing factor in the failures, not issues related to their installation.[F2] That portion of the CIC review, conducted by Regina’s Ritenburg and Associates, shows that some of the Sensus meters used in Saskatchewan have a tendency to leak. The eight meters in question were completely destroyed and impossible to analyze.[F3] However, others that quit because of other problems and were removed have shown signs of moisture and conductive contaminants getting in.-This will have to be confirmed by other testing now underway by consultants for SaskPower, but Ritenburg found no evidence that the failures were related to “hot sockets” or installation problems[F4] . -The review also identified a number of problems in the procurement and project management processes.--Overall, the company’s risk management process was found to be lacking. While SaskPower did identify a number of risks, the possibility the meters could actually short out and catch fire was not considered until similar fires at the PECO became public.-- While contractor and employee safety were considered, customer safety was not given enough priority, the review found.--SaskPower had also received advice that it should buy small batches of smart meters through a “stepped procurement” process, install them gradually and watch for problems. The company did not do that. After some smaller initial purchases, it went on to buy more than 100,000 meters in a three week period and initiated a full-scale installation program. This was done because they had the budget available for it in 2013.-Both PwC and Robertson Stromberg found that there was no single point of control overseeing the smart meter project, making it easier for warning signals to go unheeded.
There were several such warnings:
- A suit filed in Alabama in May of 2010 alleged Sensus meters were catching fire;
- After losing the SaskPower contract to Sensus in December of 2011, a meter manufacturer warned SaskPower of past problems with Sensus; and
- Fires in Philadelphia forced the PECO to remove Sensus meters in October of 2012.
While SaskPower did respond to the PECO fires with changes to the smart meter program, the review questions whether enough was done.-SaskPower did increase its efforts to detect faulty sockets, enabling an extra temperature sensor and seeking assurances from Sensus that the meters were safe. -However, the remote reading function never did work properly and there were so many false alarms for overheating, SaskPower could not investigate them all[F5] . Even after 100,000 installations, SaskPower had to read all of the smart meters manually.-
Ritenburg made several recommendations including:
- Given the potential fire hazard, all of the existing Sensus meters should be removed before next spring and potentially rainy weather;
- Those meters should be examined for arcing or other problems when they come out, to establish more information;
- When installing meters, more site photos should be taken in case the scene has to be analyzed after any future failures; and
- All meter incidents should be reported and a data base created.
[F6] PwC made the following recommendations:
- SaskPower should have specific guidelines on identifying and operating high-risk procurement projects;
- SaskPower needs a more formal “process safety management” program to ensure customer safety is paramount;
- There should be a single “contract owner” for such important, complex projects with a specific risk management process built in; and
- Clearly identify the roles and responsibilities for the management of enterprise risks relevant to procurement.
Robertson Stromberg also concluded that in large scale procurements of this kind, the vendor should consider buying product liability insurance to cover the buyer, in case of problems.--CIC Minister Don McMorris said the provincial cabinet has reviewed a summary of the findings and the government has directed CIC to:
- Ensure that SaskPower removes all Sensus meters by March 15, 2015 at the latest;
- Ensure that SaskPower implements all of the consultants’ recommendations; and
- Work with all the Crowns to ensure they are applying the lessons from this incident across the Crown sector.
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Silver nanoparticle applications and human health.
Ahamed M1, Alsalhi MS, Siddiqui MK.
Nanotechnology is rapidly growing with nanoparticles produced and utilized in a wide range of commercial products throughout the world. For example, silver nanoparticles (Ag NP) are used in electronics, bio-sensing, clothing, food industry, paints, sunscreens, cosmetics and medical devices. These broad applications, however, increase human exposure and thus the potential risk related to their short- and long-term toxicity. A large number of in vitro studies indicate that Ag NPs are toxic to the mammalian cells derived from skin, liver, lung, brain, vascular system and reproductive organs. Interestingly, some studies have shown that this particle has the potential to induce genes associated with cell cycle progression, DNA damage and apoptosis in human cells at non-cytotoxic doses. Furthermore, in vivo bio-distribution and toxicity studies in rats and mice have demonstrated that Ag NP administered by inhalation, ingestion or intra-peritoneal injection were subsequently detected in blood and caused toxicity in several organs including brain. Moreover, Ag NP exerted developmental and structural malformations in non-mammalian model organisms typically used to elucidate human disease and developmental abnormalities. The mechanisms for Ag NP induced toxicity include the effects of this particle on cell membranes, mitochondria and genetic material. This paper summarizes and critically assesses the current studies focusing on adverse effects of Ag NPs on human health.- Copyright © 2010 Elsevier B.V. All rights reserved.
Purslane weed (Portulaca oleracea): a prospective plant source of nutrition, omega-3 fatty acid, and antioxidant attributes.
Authors: Uddin MK, Juraimi AS, Hossain MS, Nahar MA, Ali ME, Rahman MM
Purslane (Portulaca oleracea L.) is an important plant naturally found as a weed in field crops and lawns. Purslane is widely distributed around the globe and is popular as a potherb in many areas of Europe, Asia, and the Mediterranean region. This plant possesses mucilaginous substances which are of medicinal importance. It is a rich source of potassium (494 mg/100 g) followed by magnesium (68 mg/100 g) and calcium (65 mg/100 g) and possesses the potential to be used as vegetable source of omega-3 fatty acid. It is very good source of alpha-linolenic acid (ALA) and gamma-linolenic acid (LNA, 18 : 3 w3) (4 mg/g fresh weight) of any green leafy vegetable. It contained the highest amount (22.2 mg and 130 mg per 100 g of fresh and dry weight, resp.) of alpha-tocopherol and ascorbic acid (26.6 mg and 506 mg per 100 g of fresh and dry weight, resp.). The oxalate content of purslane leaves was reported as 671-869 mg/100 g fresh weight. The antioxidant content and nutritional value of purslane are important for human consumption. It revealed tremendous nutritional potential and has indicated the potential use of this herb for the future.-PMID: 24683365 [PubMed - indexed for MEDLINE]
PSA test should be abandoned as screen for prostate cancer, task force says
The blood test mostly commonly used to screen men for prostate cancer should be dropped, because it can result in more harm than good, says a Canadian task force. The prostate-specific antigen, or PSA, test measures inflammation that can be elevated for many reasons other than cancer, such as normal enlargement of the prostate with age or an infection. Researchers said over-diagnosis occurs when cancer is detected correctly but would not cause symptoms or death. The main problems are false-positive results and over-diagnosis, the review indicated. A positive PSA test result often leads to more tests such as a biopsy, which carries risks of bleeding, infection, and urinary incontinence. In most men with prostate cancer, the tumour grows slowly, and they’re likely to die of another cause before the prostate tumour causes any symptoms. Prostate cancer is the most commonly diagnosed non-skin cancer in men. The prognosis for most prostate cancers is good, with a 10-year survival rate of 95 per cent.
Screening aims to find cancer before symptoms appear and reduce the chance of dying from cancer with early treatment. In Monday’s issue of the Canadian Medical Association Journal, the Canadian Task Force on Preventive Health Care reviewed the latest evidence and international best practice to weigh the benefits and harms of PSA screening with or without digital rectal exams. "Available evidence does not conclusively show that PSA screening will reduce prostate cancer mortality, but it clearly shows an elevated risk of harm. The task force recommends that the PSA test should not be used to screen for prostate cancer," Dr. Neil Bell, chair of the prostate cancer guideline working group member, and his team concluded. The guideline is aimed at physicians and other health-care professionals and policymakers. It updates the task force’s recommendation from 1994 on screening with the PSA test.
The new recommendations include:
- For men under age 55 and over age 70, the task force recommends not using the PSA test to screen for prostate cancer. This strong recommendation is based on the lack of clear evidence that screening with the PSA test reduces mortality and on the evidence of increased risk of harm.
- For men aged 55–69 years, the task force also recommends not screening, although it recognizes that some men may place high value on the small potential reduction in the risk of death and suggests that physicians should discuss the benefits and harms with these patients.
- These recommendations apply to men considered high risk — black men and those with a family history of prostate cancer — because the evidence does not indicate that the benefits and harms of screening are different for this group.
The key evidence was from a well-done European study. It showed inconsistent results, with a small potential positive effect over a long period of time, which the reviewers balanced against the clear evidence of harm, said Dr. James Dickinson, a member of the prostate cancer guideline working group and a professor of family medicine at the University of Calgary. "Fundamentally this is not a good enough test to be worth using," Dickinson said in an interview. "Let's hope that better things come in the future, but right now it's not worth using. It's more likely to cause harm than benefit."
Watchful waiting advocated
A Canadian specialist, however, takes issue with the recommendation. The task force’s guidelines are flawed for Canada, said Dr. Neil Fleshner, who studies and treats prostate cancer at Princess Margaret Cancer Centre in Toronto. "By using the PSA test, we can absolutely find lethal cancers early and by intervening in those men, we can save their lives. Therefore, these recommendations ndoubtedly will lead to more prostate cancer deaths," Fleshner said. [F7] --The task force's Bell said almost one in five men aged 55 to 69 have at least one false-positive PSA test, and about 17 per cent end up with unnecessary biopsies.--"If you screen men [aged 55 to 69] based on the protocol in those trials, every two to four years for 13 years, five out of 1,000 will die from prostate cancer. If you don't screen, six out of 1,000 men will die from prostate cancer," Bell said. "So the reduction in prostate cancer mortality is one in 1,000 or about 0.1 per cent."--"To get the benefit, you're diagnosing about 27 or 28 men with prostate cancer who would never benefit from the treatment related to prostate cancer because they would never suffer any difficulty from it."--Bell added that more than half of detected prostate cancers are over-diagnosed. The task force said that separating screening from treatment through watchful waiting or active surveillance, could change the ratio of risks to benefits of PSA screening, but the hypothesis needs to be tested. Dr. Murray Krahn of Toronto's University Health Network wrote a journal commentary on prostate cancer screening. Krahn said the task force guideline provides a good summary, but he would like to see more emphasis on patient preference, such as whether the harms are important, and shared decision-making.. With files from CBC's Kas Roussy and The Canadian Press
Could copper prevent spread of Ebola?
October 30, 2014
University of Southampton
"Based on our research on viruses of similar genetic structure, we expect copper surfaces to inactivate Ebola, and to help control the spread of this virus if employed for publicly-used touch surfaces," explains Professor Keevil, pictured here.--Research from the University of Southampton has indicated that copper could help to prevent the spread of Ebola.--Hand washing, disinfectants and quarantine procedures alone have been found to be insufficient to contain the spread of the virus. Research by Professor Bill Keevil at the University of Southampton has offered promising evidence that antimicrobial copper -- engineering materials with intrinsic hygiene benefits -- could be a valuable addition to these existing measures.--The US Centers for Disease Control and Prevention (CDC) note the Ebola virus is transmitted through direct contact with the bodily fluids of an infected person, or through exposure to contaminated objects. Viruses similar to Ebola are susceptible to a broad range of surface disinfectants, however testing against Ebola itself cannot currently be conducted due to limited access to laboratories with the required safety clearances. The CDC has therefore instructed hospitals to use disinfectants with proven efficacy against resistant viruses such as norovirus, adenovirus and poliovirus1.--Peer-reviewed and published data from laboratory studies conducted by Professor Bill Keevil, Chair of Environmental Healthcare at the University of Southampton, demonstrates copper's ability to rapidly and completely inactivate norovirus2. Recent work in Germany has also explored its effectiveness against other viral biothreat agents3. Clinical trials conducted in the UK, US and Chile have shown surfaces made from solid copper or copper alloys -- collectively termed 'antimicrobial copper' -- continuously reduce surface contamination by greater than 80 per cent. These results indicate a potential role for antimicrobial copper touch surfaces in preventing the spread of Ebola.--"Based on our research on viruses of similar genetic structure, we expect copper surfaces to inactivate Ebola, and to help control the spread of this virus if employed for publicly-used touch surfaces," explains Professor Keevil.-Antimicrobial copper surfaces have been described as a 'no touch' solution, meaning that no special measures or human intervention are required for it to continuously kill pathogens, in between regular cleans. Replacing frequently-touched surfaces, such as door handles, taps and light switches, with solid copper or copper alloy equivalents will provide a more hygienic environment, with fewer bacteria and viruses available to spread infections. With this in mind, the use of antimicrobial copper surfaces could offer an additional method of controlling the current spread of Ebola.--Interim Guidance for Environmental Infection Control in Hospitals for Ebola Virus, Centers for Disease Control and Prevention: http://www.cdc.gov/vhf/ebola/hcp/environmental-infection-control-in-hospitals.html----Story Source-The above story is based on materials provided by University of Southampton. Note: Materials may be edited for content and length.-Journal Reference-Sarah L. Warnes, C. William Keevil. Inactivation of Norovirus on Dry Copper Alloy Surfaces. PLoS ONE, 9(5): e98333 DOI: 10.1371/journal.pone.0098333
[F1]Reports can be altered to offset and litigation that the company or province or electric company may have to pay out---imagine the electric company installing these things and a house—for a ˝ a mill breaks down and burns as a result of this anal technology---that can add up---this was the situation in Vancouver Island when a 250,000 home caught fire and the electrical company went into deniability because of the cost to replace that home would have doubled
[F2]This is such BS and a real uncreative report to show that it was an environmental issue rather then a technical one or even inadequate installation procedures –would be as well curious to see if the backing plates were also removed or replaced—the one on Vancouve island was left on and not repaced and the technician forced the meter on the plate causing a over heating of the plate—technical error down by the installer which would have made the company liable
[F3]As I said BS –these were convienantly destroyed beyond examination—and based on the others –they made a conclusion based on a guess—this is really interesting to make such a claim without a real dissection of the unit and a real examination---chances are the unit was working and it was not compliant to the current tech in the home
[F4]And I wonder how they came to that conclusion since the devixces were convienantly destroyed beyond there capability to examine---would indicate a huge surge or a Hot Socket to me
[F5]This is incredibly alarming they had so many issues before the fires occurred that they should have seen the red flags on this and yanked them right then and there ---to have so many problems on going and not being able to maintain or repair the issues would have been a clear sign to pull them off the house
[F6]I love how this is showing incompetence ---these things were probably already being implemented—this is normal procedures when something goes wrong –photos—reports and follow through so this is basically a smoke screen to again alleviate responsibilty and litigation
[F7]Here is a Money making Doctor –as you can see he is making hhis dollars by sticking his finger up someone’s arse –and then possibly billing the gov’t for a surgical procedure ---yet with all the men who do reach 80+ and have prostate issues---it never kills them---something else usually does ---so is the test necessary at all…from the research ---only if there is a need to investigate and the procedure itself could cause death to examine the person
Show of the Month November 8 2014
Alzheimer's Disease and Parkinson's Disease. A Dietary Connection
Niacin and Schizophrenia-- History and Opportunity
by Nick Fortino, PhD Candidate
(OMNS Oct 27, 2014) Schizophrenia is usually treated with prescription antipsychotic drugs, many of which produce severe adverse effects (1-6); are linked to an incentive for monetary profit benefiting pharmaceutical corporations (7-13); lack sufficient evidence for safety and efficacy (9, 14); and have been grossly misused (15-20). Orthomolecular (nutritional) medicine provides another approach to treating schizophrenia, which involves the optimal doses of vitamin B3-also known as niacin, niacinamide, nicotinamide, or nicotinic acid-in conjunction with an individualized protocol of multiple vitamins. The orthomolecular approach involves treating "mental disease by the provision of the optimum molecular environment for the mind, especially the optimum concentrations of substances normally present in the human body" (21).
Evidence for the Niacin Treatment of Schizophrenia
Vitamin B3 as a treatment for schizophrenia is typically overlooked, which is disconcerting considering that historical evidence suggests it effectively reduces symptoms of schizophrenia, and has the added advantage, in contrast to pharmaceuticals, of mild to no adverse effects (22-35). After successful preliminary trials treating schizophrenia patients with niacin, pilot trials of larger samples commenced in 1952-reported in 1957 by Hoffer, Osmond, Callbeck, and Kahan. Dr. Abram Hoffer began an experiment involving 30 patients who had been diagnosed with acute schizophrenia. Participants were given a series of physiological and psychological tests to measure baseline status and were subsequently assigned randomly to treatment groups. Nine subjects received a placebo, 10 received nicotinic acid, and 11 received nicotinamide (the latter two are forms of vitamin B3). All participants received treatment for 42 days, were in the same hospital, and received psychotherapy from the same group of clinicians. The two experimental groups were administered three grams of vitamin B3 per day. Each of the three treatment groups improved, but the two vitamin B3 groups improved more than the placebo group as compared to baseline measures. At one year follow up, 33% of patients in the placebo group remained well, and 88% of patients in the B3 groups remained well. These results inspired many subsequent trials, and those that replicated the original method produced similarly positive results.
That schizophrenia may be caused or aggravated by a deficiency of essential nutrients appears to have eluded the majority of the health care providers serving the schizophrenic population, as evidenced by the fact that "antipsychotic medications represent the cornerstone of pharmacological treatment for patients with schizophrenia" (36). Waves of different antipsychotic drugs have been developed throughout the last 60 years, which have not decreased the prevalence of schizophrenia; in fact it has increased (15, 37).--Although dangerous when taken in high doses and for a long period of time, the value of antipsychotics appears to be that in the short term they can help to bring some control to schizophrenic symptoms, not by curing the condition but by inducing a neurological effect that is qualitatively different from the schizophrenic state. Dr. Hoffer acknowledged their value and in his private practice he would introduce antipsychotics and vitamins simultaneously because antipsychotics work rapidly and vitamins work more slowly, so a person could benefit from the short term relief from symptoms that antipsychotics provide while the vitamins slowly, but surely, healed the deficiency causing the schizophrenic symptoms. This also allowed for a much easier process of tapering from the drugs.
"For schizophrenia, the recovery rate with drug therapy is under 15%. With nutritional therapy, the recovery rate is 80%." - Abram Hoffer, MD, PhD
More Research Needed
Further research into the orthomolecular treatment of schizophrenia is imperative. Saha, Chant, and McGrath (38) found that mortality rates in schizophrenia have increased in recent decades and warned, "in light of the potential for second-generation antipsychotic medications to further adversely influence mortality rates in the decades to come, optimizing the general health of people with schizophrenia warrants urgent attention." The orthomolecular approach may be, at least, an integral part of a treatment program that optimizes general health and leads to a life free from schizophrenic symptoms.--Questions abound regarding individuals' experiences while on these different treatments. Particularly the psychological and relational, or, intrapersonal and interpersonal experience while on antipsychotics versus an orthomolecular treatment must be more thoroughly documented because it is in this domain that a person ascertains his/her quality of life. And only the person who has these experiences can provide such an account; no psychiatrist peering in from outside a one-way mirror on a person hearing voices, nor any brain image, nor any valid and reliable measure can ever reflect the person's living qualitative experience as accurately as the person can[F1] . This is why I have designed a multiple case study to explore in depth the experiences of individuals successfully treating their schizophrenia using orthomolecular medicine. The central research question is: What is the experience of individuals with schizophrenia who switched from using antipsychotics to orthomolecular medicine to treat their condition?
A Call for Participants
Inclusion criteria for this study are: over age 18, diagnosed as having schizophrenia, treated for a period of time primarily with antipsychotics, and are currently treated by or were cured by an orthomolecular protocol. Participation will consist of three interviews with the researcher (in person or online video conference), each of which will focus on a distinct period: symptomatic but unmedicated, primarily using antipsychotic drugs, and primarily using orthomolecular medicine. The researcher will also request one interview with the orthomolecular practitioner if possible, the diagnosing psychiatrist if possible, and at least two close friends and/or family members about their experiences of relating with the primary participant during these different periods. Anonymity is guaranteed if requested.--I am a Psychology Ph.D. student and this is my dissertation study. I never had the privilege of meeting Dr. Hoffer, but his spirit, conviction, and massive production of great work have inspired my writing this dissertation. Toward that latter part of his career, he commented on the nature of schizophrenia treatment research:
Case histories have disappeared from journal articles, as if living patients no longer existed or counted for very much. Instead, authors describe their methods, describe what criteria they used in selecting their groups of patients which were used in their prospective double blind controlled studies, and provide ample charts and statistics. I have read many papers where it is impossible to get any feeling for a single patient. (29)[F2]
This dissertation attempts to address this deficit of qualitative data. The narrative accounts that multiple case studies yield are invaluable, and can be accessible and relatable for people in a position of gathering information about schizophrenia treatments for themselves or a loved one. This dissertation is not an attempt to prove the legitimacy of the orthomolecular treatment; Dr. Hoffer and others have dedicated their professional lives to that endeavor. This is meant to explore the experience of the treatment, especially as it compares to the experience of the antipsychotic treatment. I am recruiting from a very small population of people, so I ask you to consider participating if you fit the criteria, or pass this invitation along to someone you know who fits the criteria. I can be reached by phone (408) 840-1253 or email (email@example.com) to answer questions and/or to begin the research process.
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6. Woods, S. W., Morgenstern, H., Saksa, J. R., Walsh, B. C., Sullivan, M. C., Money, R., Hawkins, K. A., Gueorguieva, R. V., & Glazer, W. M. (2010). Incidence of tardive dyskinesia with atypical and conventional antipsychotic medications: Prospective cohort study. The Journal of Clinical Psychiatry, 71(4), 463-475. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3109728/
7. Angell, M. (2004). The truth about the drug companies: How they deceive us and what to do about it. New York, N.Y.: Random House LLC.
8. Berenson, A. (2007, January 05). Lilly settles with 18,000 over zyprexa. The New York Times, pp. 1-2. Retrieved from http://www.nytimes.com/2007/01/05/business/05drug.html?_r=0
9. Kendall, T. (2011). The rise and fall of atypical antipsychotics. The British Journal of Psychiatry, 199(4), 266-268. doi:10.1192/bjp.bp.110.083766 http://www.ncbi.nlm.nih.gov/pubmed/22187726
10. Moynihan, R., & Alan, C. (2005). Selling sickness: How the world's biggest pharmaceutical companies are turning us all into patients. New York, N.Y.: Nation Books.
11. Moynihan, R., Heath, I., & Henry, D. (2002). Selling sickness: the pharmaceutical industry and disease mongering. British Medical Journal, 324(7342), 886. http://www.ncbi.nlm.nih.gov/pubmed/11950740
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14. Lieberman, J. A., Stroup, T. S., McEvoy, J. P., Swartz, M. S., Rosenback, R. A., Perkins, D. O., Keefe, R. S. E., Davis, S. M., Davis, C. E., Lebowitz, B. D., Severe, J., Hsiao, J. K. (2005). Effectiveness of antipsychotic drugs in patients with chronic schizophrenia. The New England Journal of Medicine, 353(12), 1209-1223. http://www.ncbi.nlm.nih.gov/pubmed/17335312
15. Whitaker, R. (2010). Anatomy of an epidemic: Magic bullets, psychiatric drugs, and the astonishing rise of mental illness in America. New York, N.Y.: Crown Publishers.
16. Kuehn, B. M. (2010). Questionable antipsychotic prescribing remains common, despite serious risks. Journal of the American Medical Association, 303(16), 1582-1584. http://www.ncbi.nlm.nih.gov/pubmed/20424239
17. Moran, M. (2011). Misuse of antipsychotics widespread in nursing homes. Psychiatric News, 46(11), 2. http://psychnews.psychiatryonline.org/newsarticle.aspx?articleid=108671
18. Ray, W. A., Federspiel, C. F., & Schaffner, W. (1980). A study of antipsychotic drug use in nursing homes: Epidemiologic evidence suggesting misuse. American Journal of Public Health, 70(5), 485-491. http://www.ncbi.nlm.nih.gov/pubmed/6103676
19. Stevenson, D. G., Decker, S. L., Dwyer, L. L., Huskamp, H. A., Grabowski, D. C., Metzger, E. D., & Mitchell, S. L. (2010). Antipsychotic and benzodiazepine use among nursing home residents: Findings from the 2004 National Nursing Home Survey. The American journal of Geriatric Psychiatry: Official Journal of the American Association for Geriatric Psychiatry, 18(12), 1078-1092. http://www.ncbi.nlm.nih.gov/pubmed/20808119
20. Szaz, T. (1974). The myth of mental illness: Foundations of a theory of personal conduct. New York, N.Y.: Harper Perennial.
21. Pauling, L. (1968). Orthomolecular psychiatry. Varying the concentrations of substances normally present in the human body may control mental disease. Orthomolecular psychiatry. Science, 160, 265-271. http://www.ncbi.nlm.nih.gov/pubmed/5641253
22. Cleckley, H. M., Sydenstricker, V. P., & Geeslin, L. E. (1939). Nicotinic acid in the treatment of atypical psychotic states. The Journal of the American Medical Association, 112(21), 2107-2110. http://jama.jamanetwork.com/article.aspx?articleid=288714
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29. Hoffer, A. (1996). Inside schizophrenia: Before and after treatment. Journal of Orthomolecular Medicine, 11(1), 45-48. http://orthomolecular.org/library/jom/1996/pdf/1996-v11n01-p045.pdf
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31. Hoffer, A., & Osmond, H. (1964). Treatment of schizophrenia with nicotinic acid: A ten year follow up. Acta Psychiatrica Scandinavica, 40, 171-189. doi:10.1111/j.1600-0447.1964.tb05744.x http://www.ncbi.nlm.nih.gov/pubmed/14235254.
32. Hoffer, A., & Osmond, H. (1980). Schizophrenia: Another long term follow-up in Canada. Orthomolecular Psychiatry, 9(2), 107-113. http://psycnet.apa.org/psycinfo/1981-13316-001
33. Hoffer, A., Osmond, H., Callbeck, M. J., & Kahan, I. (1957). Treatment of schizophrenia with nicotinic acid and nicotinamide. Journal of Clinical and Experimental Psychopathology, 18(2), 131-157. http://www.ncbi.nlm.nih.gov/pubmed/13439009
34. Tung-Yep, T. (1981). The use of orthomolecular therapy in the control of schizophrenia-a study preview. The Australian Journal of Clinical Hypnotherapy, 2(2), 111-116. http://schizophreniabulletin.oxfordjournals.org/content/12/1/141.full.pdf
35. Verzosa, P. L. (1976). A report on a twelve-month period of treating metabolic diseases using mainly vitamins and minerals on the schizophrenias. Orthomolecular Psychiatry, 5(4), 253-260. http://www.orthomolecular.org/library/jom/1976/pdf/1976-v05n04-p253.pdf
36. Gilmer, T. P., Dolder, C. R., Lacro, J. P., Folsom, D. P., Lindamer, L., Garcia, P., & Jeste, D. V. (2004). Adherence to treatment with antipsychotic medication and health care costs among Medicaid beneficiaries with schizophrenia. American Journal of Psychiatry, 161(4), 692-699. http://www.ncbi.nlm.nih.gov/pubmed/15056516
37. McGrath, J., Saha, S., Chant, D., & Welham, J. (2008). Schizophrenia: A concise overview of incidence, prevalence, and mortality. Epidemiologic Reviews, 30, 67-76. http://www.ncbi.nlm.nih.gov/pubmed/18480098.
38. Saha, S., Chant, D., & McGrath, J. (2007). A systematic review of mortality in schizophrenia. Archives of General Psychiatry, 64(10), 1123-1131. http://www.ncbi.nlm.nih.gov/pubmed/17909124
Healing the Kidneys with Sodium Bicarbonate (Baking Soda)
Posted by on November 11, 2009 | Filed under Medicine, Sodium Bicarbonate (Baking Soda)
Sodium bicarbonate is not only an excellent agent for natural chemotherapy, bringing as it does higher O2 levels through increased alkalinity to the cells, it is also one of the most basic medicines we have for kidney disease. New research by British scientists at the Royal London Hospital shows that sodium bicarbonate can dramatically slow the progress of chronic kidney disease. We don’t need a thousand years of tests to understand something as simple as water and it is quite the same with bicarbonate, which is always present in the best drinking waters. Bicarbonate acts to stimulate the ATPase by acting directly on it. -The simple household product used for baking, cleaning, bee stings, treating asthma, cancer and acid indigestion is so effective in treating kidney disease that it prevents patients from having to be put on kidney machines. The findings have been published in the Journal of the American Society of Nephrology. Bicarbonate is a truly strong universal concentrated nutritional medicine that works effectively in many clinical situations that we would not normally think of. It is a prime emergency room and intensive care medicine that can save a person’s life in a heartbeat and it is also a supermarket item that you can take right off the shelf and use for more things than one can imagine – including diaper rash. -Dr. SK Hariachar, a nephrologist who oversees the Renal Hypertension Unit in Tampa Florida stated, upon seeing the research on bicarbonate and kidney disease, ”I am glad to see confirmation of what we have known for so long. I have been treating my patients with bicarbonate for many years in attempts to delay the need for dialysis, and now we finally have a legitimate study to back us up. Not only that, we have the added information that some people already on dialysis can reverse their condition with the use of sodium bicarbonate”. -John, a dialysis technician at the same center as Dr. Hariachar, who used to be on dialysis himself for 2 years as a result of kidney failure, had his kidneys miraculously start functioning to the point where dialysis was no longer needed. He states that he was prescribed oral doses of sodium bicarbonate throughout his treatment, and still takes it daily to prevent recurrences of kidney failure. Dr. Hariachar maintains though, that not everyone will be helped by taking bicarbonate. He says that those patients who have difficulty excreting acids, even with dialysis using a bicarbonate dialysate bath, that, “oral bicarbonate makes all the difference.”
Kidneys Produce Bicarbonate
The exocrine section of the pancreas has been greatly ignored in the treatment of diabetes even though its impairment is a well documented condition. The pancreas is primarily responsible for the production of enzymes and bicarbonate necessary for normal digestion of food. Bicarbonate is so important for protecting the kidneys that even the kidneys get into the act of producing bicarbonate and now we know the common denominator between diabetes and kidney disease. When the body is hit with reductions in bicarbonate output by these two organs,’ acid conditions build and then entire body physiology begins to go south. Likewise when acid buildup outstrips these organs normal bicarbonate capacity cellular deterioration begins.-The kidneys alone produce about two hundred and fifty grams (about half a pound) of bicarbonate per day in an attempt to neutralize acid in the body. -The kidneys monitor and control the acidity or “acid-base” (pH) balance of the blood. If the blood is too acidic, the kidney makes bicarbonate to restore the bloods pH balance. If the blood is too alkaline, then the kidney excretes bicarbonate into the urine to restore the balance. Acid-base balance is the net result of two processes, first, the removal of bicarbonate subsequent to hydrogen ion production from the metabolism of dietary constituents; second, the synthesis of “new” bicarbonate by the kidney. -It is considered that normal adults eating ordinary Western diets have chronic, low-grade acidosis which increases with age. This excess acid, or acidosis, is considered to contribute to many diseases and to contribute to the aging process. Acidosis occurs often when the body cannot produce enough bicarbonate ions (or other alkaline compounds) to neutralize the acids in the body formed from metabolism and drinking highly acid drinks like Coke, Pepsi and we are even seeing reports on bottled mineral water being way too acidic.-Acid-buffering by means of base supplementation is one of the major roles of dialysis. Bicarbonate concentration in the dialysate (solution containing water and chemicals (electrolytes) that passes through the artificial kidney to remove excess fluids and wastes from the blood, also called “bath.”) should be personalized in order to reach a midweek pre-dialysis serum bicarbonate concentration of 22 mmol/l. Use of sodium bicarbonate in dialysate has been shown in studies to better control some metabolic aspects and to improve both treatment tolerance and patients’ life quality. Bicarbonate dialysis, unlike acetate-free biofiltration, triggers mediators of inflammation and apoptosis.-One of the main reasons we become acid is from over-consumption of protein. Eating meat and dairy products may increase the risk of prostate cancer, research suggests. We would find the same for breast and other cancers as well. Conversely mineral deficiencies are another reason and when you combine high protein intake with decreasing intake of minerals you have a disease in the making through lowering of pH into highly acidic conditions. When protein breaks down in our bodies they break into strong acids.-Unless a treatment actually removes acid toxins from the body and increases oxygen, water, and nutrients most medical interventions come to naught.-These acids must be excreted by the kidneys because they contain sulfur, phosphorus or nitrogen which cannot break down into water and carbon dioxide to be eliminated as the weak acids are. In their passage through the kidneys these strong acids must take a basic mineral with them because in this way they are converted into their neutral salts and don’t burn the kidneys on their way out. This would happen if these acids were excreted in their free acid form.-Substituting a sodium bicarbonate solution for saline infusion prior to administration of radiocontrast material seems to reduce the incidence of nephropathy. - Dr. Thomas P. Kennedy
American Medical Association
Bicarbonate ions neutralize the acid conditions required for chronic inflammatory reactions. Hence, sodium bicarbonate is of benefit in the treatment of a range of chronic inflammatory and autoimmune diseases. Sodium bicarbonate is a well studied and used medicine with known effects. Sodium bicarbonate is effective in treating poisonings or overdoses from many chemicals and pharmaceutical drugs by negating their cardiotoxic and neurotoxic effects. It is the main reason it is used by orthodox oncology – to mitigate the highly toxic effects of chemotherapy.-Sodium bicarbonate possesses the property of absorbing heavy metals, dioxins and furans. Comparison of cancer tissue with healthy tissue from the same person shows that the cancer tissue has a much higher concentration of toxic chemicals, pesticides, etc.-Sodium bicarbonate injection is indicated in the treatment of metabolic acidosis, which may occur in severe renal disease, uncontrolled diabetes, and circulatory insufficiency due to shock or severe dehydration, extracorporeal circulation of blood, cardiac arrest and severe primary lactic acidosis. The acid/alkaline balance is one of the most overlooked aspects of medicine. In general, the American public is heavily acid, excepting vegetarians, and even their bodies have to face increasing levels of toxic exposure, which help turn the body to acidic pH conditions.-For more detailed information feel free to consult my book Sodium Bicarbonate E-Book that’s with a reasonable price, or for a more personal approach check my Consultations page.
 Origin of the Bicarbonate Stimulation of Torpedo Electric Organ Synaptic Vesicle ATPase. Joan E. Rothlein 1 Stanley M. Parsons. Department of Chemistry and the Marine Science Institute, University of California, Santa Barbara, Santa Barbara, California, U.S.A.
 Levine DZ, Jacobson HR: The regulation of renal acid secretion: New observations from studies of distal nephron segments. Kidney Int 29:1099–1109, 1986
 JAMA 2004;291:2328-2334,2376-2377.
 These include, Benzotropines (valium) cyclic antidepressants (amytriptayine), organophosphates, methanol (Methyl alcohol is a cheap and potent adulterant of illicit liquors) Diphenhydramine (Benedryl), Beta blockers (propanalol) Barbiturates, and Salicylates (Aspirin). Poisoning by drugs that block voltage-gated sodium channels produces intraventricular conduction defects, myocardial depression, bradycardia, and ventricular arrhythmias. Human and animal reports suggest that hypertonic sodium bicarbonate may be effective therapy for numerous agents possessing sodium channel blocking properties, including cocaine, quinidine, procainamide, flecainide, mexiletine, bupivacaine, and others.
Effects of poor eating habits persist even after diet is improved
Date-November 3, 2014
Source-Federation of American Societies for Experimental Biology
Almost everyone knows that improving your eating habits will most likely improve your health. What most people may not know, however, is that the effects of poor eating habits persist long after dietary habits are improved. In a new report appearing in the November 2014 issue of the Journal of Leukocyte Biology, scientists use mice to show that even after successful treatment of atherosclerosis (including lowering of blood cholesterol and a change in dietary habits) the effects of an unhealthy lifestyle still affect the way the immune system functions. This change in function occurs largely because poor eating habits alter the way genes express themselves, including genes related to immunity. This change in gene expression (epigenetics) ultimately keeps the risk of cardiovascular disorders higher than it would be had there been no exposure to unhealthy foods in the first place.--"I hope that this study demonstrates the importance of diet-induced changes in the epigenome and encourages further research into the interaction between dietary patterns, DNA methylation and disease," said Erik van Kampen, a researcher involved in the work from the Division of Biopharmaceutics at the Leiden Academic Centre for Drug Research at Leiden University in Leiden, The Netherlands.--To make their discovery, scientists used two groups of mice that had an altered gene making them more susceptible to developing high blood cholesterol and atherosclerosis. These mice were either fed a high-fat, high-cholesterol diet (Western-type diet, WTD) or a normal diet (chow). After a long period of feeding, bone marrow was isolated from the mice and transplanted into mice with a similar genetic background that had their own bone marrow destroyed. The recipient mice were left on chow diet for several months, after which the development of atherosclerosis in the heart was measured. The number and status of immune cells throughout the body and epigenetic markings on the DNA in the bone marrow also were examined. They found that DNA methylation, an epigenetic signature, in the bone marrow was different in mice that received bone marrow from the WTD-fed donors compared to the mice receiving bone marrow from chow-fed donors. Furthermore, these mice had large differences in their immune system and increased atherosclerosis.--"We've long known that lifestyle and nutrition could affect immune system function," said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology. "The ability of nutritional history to have durable affects on immune cells demonstrated in this new report could have profound implications for treatment of diseases with immune underpinnings. The length of such effects will be critical to determine and it will be interesting to examine the effects of drugs that can modify epigenetics."--Story Source-The above story is based on materials provided by Federation of American Societies for Experimental Biology. Note: Materials may be edited for content and length.---Journal Reference-E. van Kampen, A. Jaminon, T. J. C. van Berkel, M. Van Eck. Diet-induced (epigenetic) changes in bone marrow augment atherosclerosis. Journal of Leukocyte Biology, 2014; 96 (5): 833 DOI: 10.1189/jlb.1A0114-017R
Alzheimer's Disease and Parkinson's Disease. A Dietary Connection
By Fred Kummerow, Ph.D.
For the past 70 years I have been researching lipids (fats) and their relationship to heart disease. I found that patients who ate an overabundance of deep fat fried foods and too much polyunsaturated fatty acids (PUFAs) produced a chemical change in the composition of their arteries. --When I analyzed the blood of these patients I found that their arteries had an increase of calcification. If these patients continue to eat these oxidized fats, the calcification will completely block their arteries. Heart disease can be prevented if these foods are not consumed. ----The oils generally used in deep fat frying, like soybean oil (and other vegetable oils) are readily oxidized because they contain linoleic and linolenic acids. These acids are easily oxidized. Prolonged exposure to air causes them to pick up oxygen and become oxidized. Repeated use just creates more oxidation.---In my laboratory we have fed weanling rats oils that had been heated at various temperatures. The rats that were fed the high temperature fats (365°F / 180°C) had lower growth rates than the rats that were fed lower temperature fats. Any foods that have been deep fried should be avoided, including potato chips and fried food from fast-food restaurants. Oils that are high in linoleic acid and linolenic acid should be avoided. ----The current research is on Alzheimer's disease (AD) and Parkinson's disease (PD.---AD is the most common cause of dementia. During the course of the disease, the chemistry and structure of the brain changes, leading to the death of brain cells. The challenges in AD research today include discovering methods to diagnose patients in an earlier stage and to find new treatments to prevent or cure the disease.--The brain is 81% lipids and over half of these lipids are phospholipids (fatlike, phosphorus-containing substances). PUFAs, which are easily oxidized (combined with oxygen), attach to the phospholipid molecule creating oxidative stress. The damaging consequences of oxidative stress have been implicated in a variety of very different human disorders including arteriosclerosis and diseases of the nervous system. Oxidative stress is an important pathogenic factor in AD. --I believe, just like heart disease patients, people with AD are eating too many polyunsaturated fatty acids (PUFAs) and deep fried foods. The American Heart Association and the National Institute of Health have recommended increasing PUFA consumption and decreasing saturated fat intake. Doing this increases free radicals when it is not offset with enough antioxidant rich fruits and vegetables. ---Free radical damage accumulates with age. They may cause cells to function poorly or even die. When free radicals overwhelm the body's ability to regulate them, oxidative stress occurs. An excess of oxidative stress can lead to the oxidation of lipids and proteins.
The research on preventing heart disease can also be used to prevent brain diseases. Tissue from the brain of someone who had AD is receptive to dyes that do not stain normal tissue suggesting that a chemical change occurred. --I suspect this chemical change occurs during oxidation of PUFAs. Discoverying that PUFAs are easily oxidized in the arterial cells and this could also be a factor in brain cells. The fact that AD is steadily increasing is alerting to the fact that --there is something wrong in the diet of these patients. –The Idea that AD and PD can be alleviated by monitoring the diets of patients with these diseases. A recent study at UCLA has shown that cognitive decline can be reversed by controlling the diet.--Patients eliminated simple carbohydrates and processed food from their diets. They increased their consumption of vegetables and fruits and limited their consumption of fish to non-farmed. The patients increased their sleep to almost 8 hours nightly, exercised 4-5 times per week and reduced their stress with meditation and relaxation.[F3] These patients also fasted three hours between meals and 12 hours between dinner and breakfast[F4] . The personalized therapeutic program was used based on the underlying pathogenesis of AD. Nine out of ten showed improvement and improvements have been sustained after two and one half years. This shows that more extensive therapeutic trials are needed. --The aim of my research is to find a way to prevent AD by analyzing the lipid plasma for two oxysterols. These two oxysterols were present in the plasma of the patients who needed bypass operations and are present in the food supply as frying fats and powdered egg yolk. My hypothesis is based on my studies of preventing calcification of the coronary arteries. I want to show that these two components are in the blood of patients with AD. --- Controlling the amount of oxidation and consuming a healthy balanced diet the body can rid itself of the oxidized polyunsaturated fat. If this is the cause of Alzheimer's disease, proper nutrition will end this terrible disease.[F5] --The diet plan that I would suggest would be to eat three balanced meals a day. Including 3 serving of protein, 5 -8 servings of fruits and vegetables, 3 servings of whole dairy products, at least one egg daily and eliminating simple carbohydrates and processed foods. Adequate amounts of sleep and exercise would also be encouraged. I then hope to continue this research with Parkinson's disease patients. --.
Fred A. Kummerow, Ph.D.
Adjunct professor in biochemistry at the University of Illinois
Biological fat with a sugar attached essential to maintaining brain's supply of stem cells
Date-November 3, 2014
Source-Medical College of Georgia at Georgia Regents University
Dr. Robert Yu, MCG neuroscientist and corresponding author of the study in The Journal of Neuroscience and Dr. Jing Wang, MCG postdoctoral fellow and the study's first author.
Fat and sugar aren't usually considered healthy staples, but scientists have found that a biological fat with a sugar attached is essential for maintaining the brain's store of stem cells.--Neural stem cells help the brain develop initially, then repopulate brain cells lost to usual cell turnover as well as to a trauma or malady, such as a head injury or stroke.--While the cell population and activity decrease as a natural part of aging, scientists at the Medical College of Georgia at Georgia Regents University are studying how neural stem cells are normally maintained with the long-term goal of helping the supply stay robust despite aging as well as infirmity.--They have discovered that in mice missing the sugar containing lipid ganglioside GD3, neural stem cells have a dramatically impaired ability to self-renew, said Dr. Robert K. Yu, MCG neuroscientist and corresponding author of the study in The Journal of Neuroscience.--The scientists focused on brain areas with typically the largest supply of neural stem cells: an area just below several midbrain cavities filled with cerebrospinal fluid, called the subventricular zone, as well as the hippocampus, a major center for learning and memory.--Mice missing ganglioside GD3 on the membranes of neural stem cells had much smaller supplies of the cells in these key areas throughout life and expressed signs of lost hope with behaviors such as not actively seeking dry land when placed in water, Yu said. Additionally, the mice had impaired maintenance of the area of the brain involved in the sense of smell as well as the portion of the hippocampus that enables formation of new memories.--The changes, which correlate with aging or illness, were corrected when GD3 was restored.--"If GD3 is missing, we found these neural stem cells cannot be maintained throughout life; they are reduced by a big percentage even in a one-month-old mouse," said Dr. Jing Wang, MCG postdoctoral fellow and the study's first author. In fact, by one month of life, there was about a 60 percent reduction in the supply and by six months, which is considered aged in a mouse, there were only a handful of neural stem cells remaining, Wang said.--The scientists note that in healthy young mice, GD3 is abundant but seems to naturally decrease with age.--A Yu and Wang paper published in the journal PNAS in 2013 showed that GD3 is the predominant ganglioside in mouse neural stem cells where it interacts with epidermal growth factor receptors, also found on the cell surface. GD3 plays an important role in growth factor signaling, which, in turn, tells neural stem cells to proliferate or die.--"In a normal situation, that growth factor enables the neural stem cells to reproduce more stem cells," Wang said. "This gives us a better idea about how our neural stem cell population is maintained over our life. Our long-term goal is to use endogenous neural stem cells for repair of brain or spinal cord damage, so we need to learn how they proliferate, how to keep them inside the brain."--The two are optimistic that one day manipulating levels of growth factors and sugar-containing lipids will enable a more steadfast supply of neural stem cells throughout life, although getting the substances into the brain is a challenge. It's already known that, at least in rats, exercise can also help.--Neural stem cells are able to self-renew, in theory at least, forever. Their ability to maintain a steady supply of themselves and to differentiate into different types of brain cells are their most important properties, Yu said.--Next steps include examining the role of other growth factors and gangliosides.--Yu is the Georgia Research Alliance Eminent Scholar Chair in Molecular and Cellular Neurobiology. The studies were funded by the National Institutes of Health and the Veterans Administration.-Story Source-The above story is based on materials provided by Medical College of Georgia at Georgia Regents University. Note: Materials may be edited for content and length.--Journal Reference-J. Wang, A. Cheng, C. Wakade, R. K. Yu. Ganglioside GD3 Is Required for Neurogenesis and Long-Term Maintenance of Neural Stem Cells in the Postnatal Mouse Brain. Journal of Neuroscience, 2014; 34 (41): 13790 DOI: 10.1523/JNEUROSCI.2275-14.2014
Suggestions to consider—MCT Oils- Glycerol—Octacosanol—ATP—Ribose—Saturated Fats—these are components that activate the body on several fronts and support immune functions—regeneration—immune protecting---
Show of the Month November 15 2014
Ignoring This will cost You
This Drug Has Sickened Thousands of Animals – Will It Be At Your Holiday Feast?
I have been to countless holiday meals when I had no control over the ingredients. Of course, I ate what was offered and was polite but knowing what I know now about what’s really in food – it’s hard for me to just shut up and take it. The more we shut up and take it, the more disgusting things like what I am about to share with you continue to happen. That’s why I am sharing these important facts about how to avoid drugged up turkeys this holiday season.
I know it’s tempting this time of year when you get coupons from the grocery store offering a whole turkey for FREE in exchange for shopping in their store. These “FREE” store-brand turkeys generally aren’t free of antibiotics and are raised on a diet of GMOs. Most conventionally raised (non-organic) turkeys are pumped full of antibiotics, and this overuse of antibiotics is creating a major human health issue.. There is another drug that is permitted to be fed to turkeys in the U.S. that is banned in dozens of countries due to health issues. You won’t find it on the label, it’s been shown to leave residues in the meat, and the meat companies are not required to tell you whether they use it.-----I’m talking about Topmax (otherwise known as Ractopamine).-Ractopamine is a growth enhancing drug that’s fed to some turkeys to increase their muscle mass. Basically, it’s used to make big turkeys look perfect for a big Holiday feast. We’ve been conditioned to think that “bigger is better” - but when it comes to turkey, its not! This drug has been shown to cause horrible health problems (and even the death of) animals, as can be witnessed by it’s rampant use on pigs during the last decade. As reported by NBC News, “Since it was introduced, ractopamine had sickened or killed more than 218,000 pigs as of March 2011, more than any other animal drug on the market, a review of FDA veterinary records shows. Pigs suffered from hyperactivity, trembling, broken limbs, inability to walk and death, according to FDA reports released under a Freedom of Information Act request.”--It’s fed to some conventional turkeys, and we might be eating it too.-Residues of ractopamine have been found in meat samples tested by the USDA and Consumer Reports. This is because there’s no mandatory withdrawal period for the drug, which can be fed to turkeys right up until the day they are slaughtered. The FDA established some “safe maximum residue limits” (MRLs) for ractopamine residue, so they are allowing some of this residue to remain in the meat sold at the store. Most meat is never tested for ractopamine residues, so it’s anyone’s guess how much we are really eating. That’s frightening, considering that ractopamine carries a bold warning label that states:
“NOT FOR HUMAN USE”
Why is this permitted?
The FDA has allowed widespread use of ractopamine in turkey feed since its approval in 2008. This led the Animal Legal Defense Fund and the Center For Food Safety to file a legal petition with FDA demanding that they conduct comprehensive scientific studies that document the risks of ractopamine to human and animal health – because clearly more needed to be done before it gained FDA approval. The FDA approved ractopamine based on safety studies submitted by the company that makes it (Elanco), which is standard for most food and drugs on the market, and have reportedly refused to share their records. To date, ractopamine is still allowed to be fed to turkeys, cows, and pigs (up to 80% of pigs eat ractopamine-laced feed).
Other countries don’t take the use of ractopamine so lightly. For instance, China and Taiwan prohibit any traces of ractopamine residue in meat, and have rejected some U.S. exports. Also any meat exported to the European Union needs to be certified as ractopamine-free or it will be rejected.
Jennie-O’s customer service agent told us that it’s not routinely used and only used on a limited basis if necessary — whatever that means, because ractopamine is not a “necessary” drug used to treat disease. Jennie-O indicated that there would be no way of knowing at the store if their turkeys were fed ractopamine because it’s not labeled or otherwise indicated.
According to Safeway Grocery Stores – “Ractopamine is a growth promotant that can be feed to turkeys so our Safeway Farms turkey may or may not have the promotant in their feed. To guarantee that growth promotant was not part of the diet, please choose our Open Nature or O Organics brands which do not allow growth promotants.”
As these companies aren’t required to disclose whether ractopamine is used, and their claims are not third-party certified, it’s difficult to confirm its use. Even turkeys that are labeled “No Hormones Added” or “Raised Without Hormones” may have still been fed ractopamine to promote growth (because it is not a hormone), so don’t be fooled by this label. Growth hormones aren’t allowed to be used in raising poultry, so this label is meaningless and used as a marketing trick when labeled on turkeys (such as Butterball).
BREAKING NEWS UPDATE!
I just found out that two lawsuits were filed against the FDA yesterday (11/6/14), as reported in the Wall Street Journal, “In two different lawsuits filed on Thursday…groups including the Center for Food Safety, the Humane Society of the United States and United Farm Workers of America argue that in approving drugs like Topmax, a medicated feed additive used to produce lean muscle instead of fat, the FDA failed to adequately consider the drugs’ collective effects on animal welfare, worker safety, wildlife and U.S. waterways”. Both of these lawsuits are asking the Court to set aside FDA’s unlawful approval of these drugs until the FDA issues a more thorough environmental analyses. You can read these Complaints here and here.
From Humane Society, et al:
“FDA approved Ractopamine for use in pigs in 1999 under the brand name Paylean, and subsequently approved Ractopamine for cattle and turkeys under the brand names Optaflexx and Topmax, respectively. Since its initial approval as Paylean, Ractopamine use has increased significantly in the pork, beef, and turkey industries”--“Today, Ractopamine is fed to approximately 60% to 80% of pigs, cattle, and turkeys raised in the United States”--“The FDA also apparently failed to provide for any public or expert comment on its NEPA analysis for Topmax”.
From The Center for Food Safety, et al:
“FDA does not require any withdrawal period for ractopamine before slaughter. A 2006 scientific study concluded “there is a possibility that adulteration of feed with ractopamine could result in residues in animal tissues and lead to human poisoning.” A 2013 Consumer Reports test of 240 U.S. pork products found that about one in five tested positive for ractopamine residues”
Startling decline in European birds- Majority of losses from most common species
November 2, 2014 Source:University of Exeter
Around 90 percent of these losses were from the 36 most common and widespread species, including house sparrows, skylarks, grey partridges and starlings.--Bird populations across Europe have experienced sharp declines over the past 30 years, with the majority of losses from the most common species, say the University of Exeter, the RSPB and the Pan-European Common Bird Monitoring Scheme (PECBMS) in a new study. However numbers of some less common birds have risen.-The study, published today in the journal Ecology Letters, reveals a decrease of 421 million individual birds over 30 years. Around 90 percent of these losses were from the 36 most common and widespread species, including house sparrows, skylarks, grey partridges and starlings, highlighting the need for greater efforts to halt the continent-wide declines of our most familiar countryside birds.--Richard Inger from the University of Exeter said: "It is very worrying that the most common species of bird are declining rapidly because it is this group of birds that people benefit from the most."--"It is becoming increasingly clear that interaction with the natural world and wildlife is central to human wellbeing and significant loss of common birds could be quite detrimental to human society."--Birds provide multiple benefits to society. They help to control agricultural pests, are important dispersers of seeds, and scavenging species play a key role in the removal of carcasses from the environment. In addition, for many people birds are the primary way in which they interact with wildlife, through listening to bird song, enjoying the sight of birds in their local environment, feeding garden birds and through the hobby of bird watching.--The majority of the declines can be attributed to considerable losses from relatively few common birds, but not all common species are declining. Numbers of great tits, robins, blue tits and blackbirds were all shown to be increasing. Populations of rarer species, including marsh harriers, ravens, buzzards and stone curlews have also shown increases in recent years: this is likely to be the result of direct conservation action and legal protection in Europe.--Head of Species Monitoring and Research at the RSPB's Centre for Conservation Science Richard Gregory said: "The rarer birds in this study, whose populations are increasing, have benefited from protection across Europe. For example, white storks and marsh harriers receive among the highest level of protection in the EU -- this is why their numbers have increased. The conservation and legal protection of all birds and their habitats in tandem are essential to reverse declines.--"This is a warning from birds throughout Europe. It is clear that the way we are managing the environment is unsustainable for many of our most familiar species."--Petr Vorisek from the PECBMS said: "The study brings a very important message to conservation practice in Europe. This would not have been possible without thousands of skilled volunteer fieldworkers who count birds according to high scientific standards and contribute their data to the national monitoring schemes."--Conservation efforts tend to be focused on rarer species but the research suggests that conservationists should also address issues affecting common birds, for example those traditionally associated with farmland. The decline in bird populations can be linked to modern farming methods, deterioration of the quality of the environment and habitat fragmentation, although the relative importance of these pressures remains unclear.--The study brought together data on 144 species of European bird from many thousands of individual surveys in 25 different countries, highlighting the value of the different national monitoring schemes increasingly working together. The researchers suggest that greater conservation funding and effort should be directed to wider scale environmental improvement programmes. These could include urban green space projects, and effective agri-environment schemes, which, informed by lessons learned from past schemes, should aim to deliver real outcomes for declining bird species whether they are rare or common.--Story Source-The above story is based on materials provided by University of Exeter.-Journal Reference-Richard Inger, Richard Gregory, James P. Duffy, Iain Stott, Petr Voříšek, Kevin J. Gaston. Common European birds are declining rapidly while less abundant species' numbers are rising. Ecology Letters, 2014; DOI: 10.1111/ele.12387
Ignoring This will cost You
37 Million Bees Found Dead In Ontario, Canada After Planting Large GMO Corn Field
Millions of bees dropped dead after GMO corn was planted few weeks ago in Ontario, Canada. The local bee keeper, Dave Schuit who produces honey in Elmwood lost about 37 million bees which are about 600 hives.--“Once the corn started to get planted our bees died by the millions,” Schuit said. While many bee keepers blame neonicotinoids, or “neonics.” for colony collapse of bees and many countries in EU have banned neonicotinoid class of pesticides, the US Department of Agriculture fails to ban insecticides known as neonicotinoids, manufactured by Bayer CropScience Inc.--Two of Bayer’s best-selling pesticides, Imidacloprid and Clothianidin, are known to get into pollen and nectar, and can damage beneficial insects such as bees. The marketing of these drugs also coincided with the occurrence of large-scale bee deaths in many European countries and the United States.--Nathan Carey another local farmer says that this spring he noticed that there were not enough bees on his farm and he believes that there is a strong correlation between the disappearance of bees and insecticide use.--In the past, many scientists have struggled to find the exact cause of the massive die-offs, a phenomenon they refer to as “colony collapse disorder” (CCD). In the United States, for seven consecutive years, honeybees are in terminal decline.--US scientists have found 121 different pesticides in samples of bees, wax and pollen, lending credence to the notion that pesticides are a key problem. “We believe that some subtle interactions between nutrition, pesticide exposure and other stressors are converging to kill colonies,” said Jeffery Pettis, of the ARS’s bee research laboratory.-The collapse in the global honeybee population is a major threat to crops. It is estimated that a third of everything we eat depends upon honeybee pollination, which means that bees contribute over 30 billion to the global economy.--A new study published in the Journal Proceedings of the National Academy of Sciences revealed that neonicotinoid pesticides kill honeybees by damaging their immune system and making them unable to fight diseases and bacteria.--After reporting large losses of bees after exposure to Imidacloprid, banned it for use on corn and sunflowers, despite protests by Bayer. In another smart move, France also rejected Bayer’s application for Clothianidin, and other countries, such as Italy, have banned certain neonicotinoids as well.--After record-breaking honeybee deaths in the UK, the European Union has banned multiple pesticides, including neonicotinoid pesticides.
Glyphosate-based herbicides are toxic and endocrine disruptors in human cell lines
Glyphosate-based herbicides are the most widely used across the world; they are commercialized in different formulations. Their residues are frequent pollutants in the environment. In addition, these herbicides are spread on most eaten transgenic plants, modified to tolerate high levels of these compounds in their cells. Up to 400 ppm of their residues are accepted in some feed. We exposed human liver HepG2 cells, a well-known model to study xenobiotic toxicity, to four different formulations and to glyphosate, which is usually tested alone in chronic in vivo regulatory studies. We measured cytotoxicity with three assays (Alamar Blue®, MTT, ToxiLight®), plus genotoxicity (comet assay), anti-estrogenic (on ERα, ERβ) and anti-androgenic effects (on AR) using gene reporter tests. We also checked androgen to estrogen conversion by aromatase activity and mRNA. All parameters were disrupted at sub-agricultural doses with all formulations within 24 h. These effects were more dependent on the formulation than on the glyphosate concentration. First, we observed a human cell endocrine disruption from 0.5 ppm on the androgen receptor [F6] in MDA-MB453-kb2 cells for the most active formulation (R400), then from 2 ppm the transcriptional activities on both estrogen receptors were also inhibited on HepG2[F7] . Aromatase transcription and activity were disrupted from 10 ppm. Cytotoxic effects started at 10 ppm with Alamar Blue assay (the most sensitive), and DNA damages at 5 ppm. A real cell impact of glyphosate-based herbicides residues in food, feed or in the environment has thus to be considered, and their classifications as carcinogens/mutagens/reprotoxics is discussed.
Glyphosate-based herbicides toxicity
Roundup (R) was highly toxic on human cells, from 10-20 ppm, far below agricultural dilutions. This occurred on hepatic (HepG2, Hep3B and embryonic (HEK293) as well on placental (JEG3) cell lines, but also on human placental extracts, primary umbilical cord cells (HUVEC) and freshly isolated testicular cells (Richard et al. 2005; Benachour et al. 2007; Benachour & Seralini 2009; Gasnier et al. 2010; Clair et al. 2012). All formulations cause total cell death within 24 h, through an inhibition of the mitochondrial succinate dehydrogenase activity, and necrosis, through the release of cytosolic adenylate kinase measuring membrane damage. They also induced apoptosis through the activation of enzymatic caspases 3 / 7 activities. Most importantly, the R commercialized formulation is always more toxic than the active principle alone, the glyphosate (G). These effects were more dependent on the formulation and thus adjuvants content than on the G concentration. We recently measured compositions and effects of 9 Gbased formulations and identified ethoxylated adjuvants (commonly called POEA) asthe active principle of cytotoxicity (Messnage et al. 2012a). However, these are considered as inert diluents in international regulations and are not taken into account for chronic effects which are insufficiently tested, and only with G in pre-commercial testing. We previously underlined this loophole (Mesnage 2010). Long term feeding and reproductive trials with pesticides are the only tests long enough to reveal a potential endocrine disruption which was consequently never studied for R until recently (Seralini et al. 2012), however it was for G by itself. We investigated it by measuring androgen to estrogen conversion by aromatase activity and mRNA on placental human cells and showed that G interacts with the active site of the purifed enzyme (Richard et al. 2005). Both parameters were disrupted at subagricultural doses within 24 h. We also observed a human cell endocrine disruption from 0.5 ppm on the androgen receptor in transfected cells, and then from 2 ppm the transcriptional activities on both estrogen receptors which were also inhibited (Gasnier et al. 2009). Aromatase transcription and activity were disrupted from 10 ppm on
HepG2. On freshly isolated rat testicular cells, low non-toxic concentrations of R and G (1 ppm) induced a testosterone decrease by 35 % (Clair et al. 2012). This is expected to occur in human cells which are fitted with the same steroidogenic equipment. G-based formulations are claimed to have been extensively studied by industry and regulatory agencies and are considered as one of the safest pesticides (Williams et al.2000). This allowed the establishment of high maximum residue limits (MRL) for GM food / feed (up to 400 ppm). For instance, 20 ppm of G are authorized in GM soy and this MRL is in the range of concentrations typically found in a GM soy harvest. In the light of our results, the safety of these thresholds is clearly challenged.
Time- and dose-dependent effects of roundup on human embryonic and placental cells.
Benachour N1, Sipahutar H, Moslemi S, Gasnier C, Travert C, Séralini GE.
Roundup is the major herbicide used worldwide, in particular on genetically modified plants that have been designed to tolerate it. We have tested the toxicity and endocrine disruption potential of Roundup (Bioforce on human embryonic 293 and placental-derived JEG3 cells, but also on normal human placenta and equine testis. The cell lines have proven to be suitable to estimate hormonal activity and toxicity of pollutants. The median lethal dose (LD(50)) of Roundup with embryonic cells is 0.3% within 1 h in serum-free medium, and it decreases to reach 0.06% (containing among other compounds 1.27 mM glyphosate) after 72 h in the presence of serum. In these conditions, the embryonic cells appear to be 2-4 times more sensitive than the placental ones. In all instances, Roundup (generally used in agriculture at 1-2%, i.e., with 21-42 mM glyphosate) is more efficient than its active ingredient, glyphosate, suggesting a synergistic effect provoked by the adjuvants present in Roundup. We demonstrated that serum-free cultures, even on a short-term basis (1 h), reveal the xenobiotic impacts that are visible 1-2 days later in serum. We also document at lower non-overtly toxic doses, from 0.01% (with 210 microM glyphosate) in 24 h, that Roundup is an aromatase disruptor. The direct inhibition is temperature-dependent and is confirmed in different tissues and species (cell lines from placenta or embryonic kidney, equine testicular, or human fresh placental extracts). Furthermore, glyphosate acts directly as a partial inactivator on microsomal aromatase, independently of its acidity, and in a dose-dependent manner. The cytotoxic, and potentially endocrine-disrupting effects of Roundup are thus amplified with time. Taken together, these data suggest that Roundup exposure may affect human reproduction and fetal development in case of contamination. Chemical mixtures in formulations appear to be underestimated regarding their toxic or hormonal impact.
Glyphosate inhibits beneficial gut bacteria
Tuesday, Jan. 8, 2013 - A new study published in the journal Current Microbiology describes the harmful effect of glyphosate on intestinal bacteria in poultry. The evidence is that glyphosate is toxic to beneficial bacteria such as Enterococcus faecalis, Enterococcus faecium, Bacillus badius, Bifidobacterium adolescentis and Lactobacillus spp, while pathogenic bacteria such as Salmonella Entritidis, Salmonella Gallinarum, Salmonella Typhimurium, Clostridium perfringens and Clostridium botulinum are highly resistant to glyphosate.--A reduction of beneficial bacteria in the gastrointestinal tract disturbs the normal gut bacterial community and allows salmonella and clostridia species to grow unchecked thus increasing the incidence of these two diseases.--The researchers pointed out that glyphosate also has the potential to induce genetic mutations within bacteria, making it possible for a new level of pathogenicity to emerge following chronic exposure to this chemical.- Oral bioavailability of glyphosate: studies using two intestinal cell lines.
Vasiluk L1, Pinto LJ, Moore MM.--Author information --Abstract
Glyphosate is a commonly used nonselective herbicide that inhibits plant growth through interference with the production of essential aromatic amino acids. In vivo studies in mammals with radiolabeled glyphosate have shown that 34% of radioactivity was associated with intestinal tissue 2 h after oral administration. The aim of our research was to investigate the transport, binding, and toxicity of glyphosate to the cultured human intestinal epithelial cell line, Caco-2, and the rat small intestinal crypt-derived cell line, ileum epithelial cells-18 (IEC-18). An in vitro analysis of the transport kinetics of [14C]-glyphosate showed that 4 h after exposure, approximately 8% of radiolabeled glyphosate moved through the Caco-2 monolayer in a dose-dependent manner. Binding of glyphosate to cells was saturable and approximately 4 x 10(11) binding sites/cell were estimated from bound [14C]. Exposure of Caco-2 cells to > or =10 mg/ml glyphosate reduced transmembrane electrical resistance (TEER) by 82 to 96% and increased permeability to [3H]-mannitol, indicating that paracellular permeability increased in glyphosate-treated cells. At 10-mg/ml glyphosate, both IEC-18 and Caco-2 cells showed disruption in the actin cytoskeleton. In Caco-2 cells, significant lactate dehydrogenase leakage was observed when cells were exposed to 15 mg/ml of glyphosate. These data indicate that at doses >10 mg/ml, glyphosate significantly disrupts the barrier properties of cultured intestinal cells
HOW WELL DO FLU VACCINES WORK? FALL CAMPAIGN IS IN FULLSWING
One easily gets the impression that the answer is very well indeed. Get your shot and you will be protected. Flu vaccination has become mandatory in many health care institutions. No shot and either wear a mask or quit. One would expect that most would be protected. The efficacy (relative risk reduction in controlled trials) is typically 50-60 % and can go higher, especially for children. Vaccine Manufacturers and promoters would of course like it close to 100% which would justify the claim if one gets their shot, they won’t get the flu. If one took an exit poll was taken from a vaccination clinic at a local mall, probably a surprising number would say just that. Thus it is of interest to look at two recent meta-analyses and examine the other side of the coin, the absolute benefits, a taboo subject in this field. International Health News November 2014 Page 7 --Recently, Ossterholm et al16 examined the efficacy of influenza vaccination as indicated by studies that were randomized, placebo controlled and where the cases were laboratory verified as viral influenza. It was required that vaccine efficacy be reported for all circulating influenza strains. Meta analyses of qualifying trials were conducted separately for adults and children or just adults A second recent study by Tricco et al17 compared the efficacy of influenza vaccines depending on whether or not they were matched to at least one of the strains circulating that year. Both matched and unmatched randomized controlled trials involving either trivalent inactivated vaccine (TIV) or nasal spray containing live attenuated influenza vaccine (LAIV) were analyzed. All the meta analyses had a mixture of studies involving children and adults in varying proportions, but more than half of the studies using LAIV involved children. The results of these two studies are given in the table below. Both papers provided enough information to calculate absolute results, actually by two methods which gave very close to identical results. The published papers ignored absolute results.
VACCINE EFFICACY IN RECENT META -ANALYSES
Study STUDIES Age NNT RRR No Benefit Vaccine
Osterholm16 8 18-64 64 60% 98.4% TIV
Osterholm 16 7 0.5-7 8 84% 87.3% LAIV
Trico17 12 A&C 93 62% 98.9% TIV-Matched
Tricco17 11 A&C 204 51% 99.5% TIV-Mismatched
Tricco17 15 A&C 18 77% 94.4% LAIV-Matched
Tricco17 15 A&C 48 60% 97.9% LAIV-Mismatched
TIV—Trivalent inactivated vaccine. LAIV—Live attenuated influenza vaccine.
NNT—Number needed to treat. RRR—Relative risk reduction. A&C—adults and children. Note that most of the relative risk reductions (RRR) are impressive. Those who do not understand relative risk reduction will assume that for example, a RRR of 60% means that 60% of those vaccinated will not get the flu. However, only 1.6% will actually benefit whereas 98.4 will not. The magnitude of the relativemrisk reduction is related to the absolute risk reduction divided by the absolute risk in the control group, and thus can be very large for small absolute benefits in the case of disorders or diseases that have a low population incidence, which is the case with the flu in adults. Children have a higher untreated population risk, but it is still only generally only a few percentage points. Risk reductions are generally adjusted for confounding, and but these can be used to calculate the adjusted absolute risk reduction and number needed to treat. Note also that the RRR correlate rather poorly with the NNT, something at the very heart of the problem of using the RRR. The above table suggests that independent of the type of the vaccine or how well it matches the strains during a given year, most vaccinated individuals do not benefit but must simply hope they are lucky. For TIV, a very common vaccine, mismatching does not seem to make much difference. However, the benefit for children from the LAIV is quite strong, as seen in the analysis involving LAIV by Osterholm et al and in the two by Tricco et al involving both LAIV which had heavy representation of children in the studies included, since it is the popular vaccine type for children. While numbers needed to treat of 8 are not common in clinical trials or their pooled analyses, it is unfortunately still true, as shown in the table, that even with such a low number, most do not benefit. There is very little data for those over 65 of age. The analysis by Osterholm et al prompted a number of comments in the literature. It is interesting in these comments that the focus was universally on relative risk reduction, never on the percentage treated that do or do not benefit, i.e. the absolute results. This appears to be a taboo point of view. Commentators worried that the “modest” relative risk reductions in the 50% range would be used by critics to discourage vaccination, but if this is the case, the more realistic view based on absolute benefit would rightly terrify proponents of this popular public health intervention and the related desire to develop herd immunity. Furthermore, there is always the worrisome problem that adverse effects have been suppressed by the industry, certainly far from an unheard of approach to doing business; therefore one cannot do a risk/benefit analysis.-The above results are a nice example of how a given set of trial results can be presented in different ways (another term is spin) that either accentuate the positive or provide a more realistic view. For those who find this hard to believe, an appendix at the end of this issue is included which gives a sample calculation. The potential for creating unrealistic expectations is obviously great and an almost universally used approach. It seems worth mentioning in passing that pregnant women, if they decide to get a flu shots, should demand the mercury free one which generally comes in a single dose vial not a septum capped little bottle. Live attenuated influenza vaccine which is delivered as a nasal spray, in generally mercury free. However, given that the vaccine preparation may have other dangers to the fetus aside from mercury toxicity which may be unknown or suppressed, perhaps the dismal percentage of adults benefiting should be given considerable weight by this special group. What should one do? There do not appear to be studies that have provided strong evidence concerning actions found to dramatically reduce the risk of the flu. Mainstream medicine regards the problem solved with vaccination. While maintaining a vitamin D status that is sufficient or more than just sufficient can be justified from a number of studies and is easy and inexpensive to accomplish and justified for a large number of other reasons, definitive studies have yet to appear. The subject of maintaining a high level of immune response will have to wait for a future issue of IHN.
CDC REPORTS INFLUENZA OUTBREAK IN A VACCINATED POPULATION
On October 24, 2014 the Centers for Disease Cont rol in its Morbidity and Mortality Report described a flu outbreak among the crew of a navy ship moored in San Diego. In February of 2014, 25 cases of influenza, of which 20 were influenza A, occurred over a short period among a crew of 102. Ninety-nine percent of the crew had been vaccinated with a vaccine very well matched with the flu viruses circulating in 2013-14. The fact that it was influenza was documented by laboratory tests. The headline in the New England Journal of Medicine’s daily online Journal Watch of October 24 read as follows: Flu Outbreak Aboard Navy Ship Highlights Possibility of Illness in Vaccinated Populations. The interesting word is “possibility.” Reference to the above table indicates that 94.4% to 98.9% of vaccinated populations are not protected with a matched vaccine, depending on the type of vaccine, and the 94.4% is due in part to heavy weighting from children. These results apply to large pooled populations and studies covered a number of years. Of the 25 flu cases, 16 received the TIV form, 8 the LAIV and one was unvaccinated. Using the term “possibly” seems rather an understatement. According to the CDC report, Tamiflu was given to the crew to “reduce the impact and spread of the disease.” This is the same antiviral that has been discredited and found virtually useless after huge amounts of government funds throughout the world were spend stockpiling it. See the February 2013 issue of IHN for the full story of the shocking Tamiflu saga.
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Pooled data from 8 studies, adults 18-64 years of age, given trivalent inactivated influenza vaccine compared to unvaccinated controls. Cases laboratory -validated as viral influenza. Taken from Figure 2.16
THE RAW DATA
Cases of flu 221 357
Total in group 18,797 13,095
Flu Case %: (221/18,797) X 100 = 1.118%, No Flu % (357/13,095) X 100 = 2.730%,
Percentage who benefited: 2.730% -- 1.118% = 1.55% or 1.55 per 100
Percentage with no benefit: 100% – 1.55% = 98.4%
The absolute risk reduction produced by vaccination was the percentage that benefited, 1.55% is the difference between the flu rates in the two groups, expressed as a percentage rather than probability, i.e. 0.0155. If 1.55/100 had benefit, how many must be vaccinated for one to benefit? It is calculated from 1.55/100 = 1/x and thus x = 64. This number needed to treat for one individual to benefit, i.e. not get the viral flu, and is the NNT. Put another way, it is the reciprocal of the absolute risk reduction expresses as a probability (range 1.0 to 0), not a percentage, i.e. NNT = 1/0.0155. The time interval is approximately the flu season. The unadjusted risk ratio 0.4 is obtained from the ratio 1.118/ 2.730 = 0.4 and the relative risk reduction (RRR) was 1 -- 0.4 = 0.60 or as a percentage 60%. Why is this true? Details. Risk ratio = (case % in treated group)/(case % in untreated group) = T/U. But 1 = (T/U) = (U – T)/U = RRR, the relative risk reduction obtained comparing the % of cases prevented to the case % in the untreated (control) group. The same calculation can be done without expressing the numbers as percentages, since the 100 cancels out. Thus the four numbers, i.e. the cases and size of the groups, constitute the input data that produce these various final results used to express how well the treatment works. The 60% RRR looks great, the number who do not benefit looks terrible. Same data, just different presentations, both correct. Some think that by getting the vaccination they will not get the flu, some think that their risk is reduced by 60%, but interpret this by thinking that if a group of 100 are vaccinated, 60 will not get the flu. In fact, if 100 are vaccinated, between 1 and 2 individuals will be protected and 98% to 99% will not be protected. This is what the critics of the use of relative risk reductions are talking about, but no one is listening. Why spoil a nice picture based on a perfectly valid calculation. It is also noteworthy that when a disease or disorder has a very small population prevalence reflected by the percentage of cases in the control group, this forces the NNT and the percentage that do not benefit into the range seen in this example. This is the consequence of treating a group where the vast majority will not become cases, treatment or no treatment. One can argue that treatment is still desirable, but one must not have unrealistic expectations, and now the risk of adverse side effects becomes a major issue. Small absolute benefits and large NNT should stimulate research to find something better. Instead the RRR becomes a powerful marketing and public health tool.
Show of the Month November 22 2014
Repeated Oral AdministrationHistopathological and ultra structural effects of nanoparticles on rat testis following 90 days
Synthetic biology-- 'Telomerator' reshapes synthetic yeast chromosome into more flexible, realistic form, redefining what geneticists can build
November 3, 2014
NYU Langone Medical Center / New York University School of Medicine
The telomerator can reformat the “clockface” of a synthetic yeast chromosome into 12 unique linear “timelines,” or chromosomes of equal length.
Credit: Courtesy of NYU Langone.--NYU Langone yeast geneticists report they have developed a novel tool -- dubbed "the telomerator" -- that could redefine the limits of synthetic biology and advance how successfully living things can be engineered or constructed in the laboratory based on an organism's genetic, chemical base-pair structure.--Synthetic biologists aim to use such "designer" microorganisms to produce novel medicines, nutrients, and biofuels[F8] .--In a report in the Proceedings of the National Academy of Sciences online Nov. 3, NYU Langone scientists say the telomerator should also improve study of yeast genetics, the model microorganism for human genetics, and help researchers determine how genes, as well as the chromosomes housing them, interact with each other.--The research team, led by Jef Boeke, PhD, a professor and director of NYU Langone's Institute for Systems Genetics, built the telomerator to convert circular chromosomes into linear ones. Boeke says this better resembles the natural structure of more complex organisms, including humans. Comprising about 1,500 chemical base pairs linked together, the human-made piece of telomerator code can be inserted as a single unit at any position on circular DNA and almost anywhere among a chromosome's other genes, whose base pairs can number into the hundreds of thousands.---"Our new telomerator resolves a serious and practical issue facing biologists everywhere by helping us experiment with synthetic genes in ways that are more realistic and more closely aligned to the biology of higher organisms, such as humans," says Boeke. "Until now, we've relied on synthesizing functional and stable yeast chromosomes in a circular format -- with their telomeres cut off -- so they can be uniformly reproduced for easy experimentation within bacteria, whose chromosomes are circular in shape," he says.--What makes the telomerator particularly effective, researchers say, is its precise capacity to add buffering chromosome endings, or telomeres, to newly linearized yeast chromosomes.--Moreover, the telomerator, which took Boeke and lead study investigator Leslie Mitchell, PhD, two years to construct and test, allows researchers to study how a gene's position or placement on a chromosome affects the gene's function.--The key components of the telomerator are its telomere seed sequences, which are exposed when the telomerator "cassette" -- its packaged components -- is activated.--To test the device, Mitchell inserted a telomerator cassette at 54 different locations on a circular synthetic yeast chromosome of about 90,000 base pairs and tested whether the chromosome could be segmented and straightened at each position. Researchers compared the process to a clock dial, in which they could insert the telomerator at any "hour" on the clock face to break the circle and yield 12 different timelines, but all of equal length. Colonies grew for 51 of the linear yeast chromosomes, failing only in chromosomes where essential genes were placed too close to the telomere ends.--Additional testing confirmed that the modified yeast chromosomes were in a linear format and of the precise length predicted by researchers.--Boeke's research is part of an international effort to manufacture all the yeast chromosomes, threadlike structures that carry genes in the nucleus of all plant and animal cells, and move genetic research one step closer to constructing the organism's entire functioning genome. Earlier this year, Boeke's team reported building the first of the 16 yeast chromosomes, which they call synIII, and successfully incorporating it into brewer's yeast, known scientifically as Saccharomyces cerevisiae.--Story Source-The above story is based on materials provided by NYU Langone Medical Center / New York University School of Medicine. Note: Materials may be edited for content and length.[F9]
First functional 'designer' chromosome in yeast synthesized by scientists
Date-March 27, 2014 Source-NYU Langone Medical Center
Researchers have synthesized the first functional chromosome in yeast, an important step in the emerging field of synthetic biology, designing microorganisms to produce novel medicines, raw materials for food, and biofuels.--An international team of scientists led by Jef Boeke, PhD, director of NYU Langone Medical Center's Institute for Systems Genetics, has synthesized the first functional chromosome in yeast, an important step in the emerging field of synthetic biology, designing microorganisms to produce novel medicines, raw materials for food, and biofuels.--Over the last five years, scientists have built bacterial chromosomes and viral DNA, but this is the first report of an entire eukaryotic chromosome, the threadlike structure that carries genes in the nucleus of all plant and animal cells, built from scratch. Researchers say their team's global effort also marks one of the most significant advances in yeast genetics since 1996, when scientists initially mapped out yeast's entire DNA code, or genetic blueprint.--"Our research moves the needle in synthetic biology from theory to reality," says Dr. Boeke, a pioneer in synthetic biology who recently joined NYU Langone from Johns Hopkins University.--"This work represents the biggest step yet in an international effort to construct the full genome of synthetic yeast," says Dr. Boeke. "It is the most extensively altered chromosome ever built. But the milestone that really counts is integrating it into a living yeast cell. We have shown that yeast cells carrying this synthetic chromosome are remarkably normal[F10] . They behave almost identically to wild yeast cells, only they now possess new capabilities and can do things that wild yeast cannot."-In this week's issue of Science online March 27, the team reports how, using computer-aided design, they built a fully functioning chromosome, which they call synIII, and successfully incorporated it into brewer's yeast, known scientifically as Saccharomyces cerevisiae.--The seven-year effort to construct synIII tied together some 273, 871 base pairs of DNA, shorter than its native yeast counterpart, which has 316,667 base pairs. Dr. Boeke and his team made more than 500 alterations to its genetic base, removing repeating sections of some 47,841 DNA base pairs, deemed unnecessary to chromosome reproduction and growth. Also removed was what is popularly termed junk DNA, including base pairs known not to encode for any particular proteins, and "jumping gene" segments known to randomly move around and introduce mutations. Other sets of base pairs were added or altered to enable researchers to tag DNA as synthetic or native, and to delete or move genes on synIII.--"When you change the genome you're gambling. One wrong change can kill the cell," says Dr. Boeke. "We have made over 50,000 changes to the DNA code in the chromosome and our yeast still live. That is remarkable. It shows that our synthetic chromosome is hardy, and it endows the yeast with new properties[F11] ."--The Herculean effort was aided by some 60 undergraduate students enrolled in the "Build a Genome" project, founded by Dr. Boeke at Johns Hopkins. The students pieced together short snippets of the synthetic DNA into stretches of 750 to 1,000 base pairs or more, an effort led by Srinivasan Chandrasegaran, PhD, a professor at Johns Hopkins. Chandrasegaran is also the senior investigator of the team's studies on synIII.--Student participation kicked off what has become an international effort, called Sc2.0 for short, in which several academic researchers have partnered to reconstruct the entire yeast genome, including collaborators at universities in China, Australia, Singapore, the United Kingdom, and elsewhere in the U.S.-Yeast chromosome III was selected for synthesis because it is among the smallest of the 16 yeast chromosomes and controls how yeast cells mate and undergo genetic change. DNA comprises four letter-designated base macromolecules strung together in matching sets, or base pairs, in a pattern of repeating letters. "A" stands for adenine, paired with "T" for thymine; and "C" represents cysteine, paired with "G" for guanine. When stacked, these base pairs form a helical structure of DNA resembling a twisted ladder.--Yeast shares roughly a third of its 6,000 genes -- functional units of chromosomal DNA for encoding proteins -- with humans. The team was able to manipulate large sections of yeast DNA without compromising chromosomal viability and function using a so-called scrambling technique that allowed the scientists to shuffle genes like a deck of cards, where each gene is a card. "We can pull together any group of cards, shuffle the order and make millions and millions of different decks, all in one small tube of yeast," Dr. Boeke says. "Now that we can shuffle the genomic deck, it will allow us to ask, can we make a deck of cards with a better hand for making yeast survive under any of a multitude of conditions, such as tolerating higher alcohol levels."--Using the scrambling technique, researchers say they will be able to more quickly develop synthetic strains of yeast that could be used in the manufacture of rare medicines, such as artemisinin for malaria, or in the production of certain vaccines, including the vaccine for hepatitis B, which is derived from yeast. Synthetic yeast, they say, could also be used to bolster development of more efficient biofuels, such as alcohol, butanol, and biodiesel[F12] .--The study will also likely spur laboratory investigations into specific gene function and interactions between genes, adds Dr. Boeke, in an effort to understand how whole networks of genes specify individual biological behaviors.--Their initial success rebuilding a functioning chromosome will likely lead to the construction of other yeast chromosomes (yeast has a total of 16 chromosomes, compared to humans' 23 pairs), and move genetic research one step closer to constructing the organism's entire functioning genome, says Dr. Boeke.--Dr. Boeke says the international team's next steps involve synthesizing larger yeast chromosomes, faster and cheaper. His team, with further support from Build a Genome students, is already working on assembling base pairs in chunks of more than 10,000 base pairs. They also plan studies of synIII where they scramble the chromosome, removing, duplicating, or changing gene order.--Detailing the Landmark Research Process--Before testing the scrambling technique, researchers first assessed synIII's reproductive fitness, comparing its growth and viability in its unscrambled from -- from a single cell to a colony of many cells -- with that of native yeast III. Yeast proliferation was gauged under 19 different environmental conditions, including changes in temperature, acidity, and hydrogen peroxide, a DNA-damaging chemical. Growth rates remained the same for all but one condition.--Further tests of unscrambled synIII, involving some 30 different colonies after 125 cell divisions, showed that its genetic structure remained intact as it reproduced. According to Dr. Boeke, individual chromosome loss of one in a million cell divisions is normal as cells divide. Chromosome loss rates for synIII were only marginally higher than for native yeast III.--To test the scrambling technique, researchers successfully converted a non-mating cell with synIII to a cell that could mate by eliminating the gene that prevented it from mating.--Story Source-The above story is based on materials provided by NYU Langone Medical Center. Note: Materials may be edited for content and length.-Journal Reference-N. Annaluru, H. Muller, L. A. Mitchell, S. Ramalingam, G. Stracquadanio, S. M. Richardson, J. S. Dymond, Z. Kuang, L. Z. Scheifele, E. M. Cooper, Y. Cai, K. Zeller, N. Agmon, J. S. Han, M. Hadjithomas, J. Tullman, K. Caravelli, K. Cirelli, Z. Guo, V. London, A. Yeluru, S. Murugan, K. Kandavelou, N. Agier, G. Fischer, K. Yang, J. A. Martin, M. Bilgel, P. Bohutski, K. M. Boulier, B. J. Capaldo, J. Chang, K. Charoen, W. J. Choi, P. Deng, J. E. DiCarlo, J. Doong, J. Dunn, J. I. Feinberg, C. Fernandez, C. E. Floria, D. Gladowski, P. Hadidi, I. Ishizuka, J. Jabbari, C. Y. L. Lau, P. A. Lee, S. Li, D. Lin, M. E. Linder, J. Ling, J. Liu, J. Liu, M. London, H. Ma, J. Mao, J. E. McDade, A. McMillan, A. M. Moore, W. C. Oh, Y. Ouyang, R. Patel, M. Paul, L. C. Paulsen, J. Qiu, A. Rhee, M. G. Rubashkin, I. Y. Soh, N. E. Sotuyo, V. Srinivas, A. Suarez, A. Wong, R. Wong, W. R. Xie, Y. Xu, A. T. Yu, R. Koszul, J. S. Bader, J. D. Boeke, S. Chandrasegaran. Total Synthesis of a Functional Designer Eukaryotic Chromosome. Science, 2014; DOI: 10.1126/science.1249252
Scientists 'boot up' a bacterial cell with a synthetic genome
Date-May 20, 2010-Source-American Association for the Advancement of Science
Scanning electron micrographs of M. mycoides JCVI-syn1. Samples were post-fixed in osmium tetroxide, dehydrated and critical point dried with CO2 , then visualized using a Hitachi SU6600 scanning electron microscope at 2.0 keV.
Credit: Electron micrographs were provided by Tom Deerinck and Mark Ellisman of the National Center for Microscopy and Imaging Research at the University of California at San Diego--Scientists have developed the first cell controlled by a synthetic genome. They now hope to use this method to probe the basic machinery of life and to engineer bacteria specially designed to solve environmental or energy problems[F13] .--The study will be published online by the journal Science, at the Science Express website, on May 20.--The research team, led by Craig Venter of the J. Craig Venter Institute, has already chemically synthesized a bacterial genome, and it has transplanted the genome of one bacterium to another.[F14] Now, the scientists have put both methods together, to create what they call a "synthetic cell," although only its genome is synthetic.--"This is the first synthetic cell that's been made, and we call it synthetic because the cell is totally derived from a synthetic chromosome, made with four bottles of chemicals on a chemical synthesizer, starting with information in a computer," said Venter.--"This becomes a very powerful tool for trying to design what we want biology to do. We have a wide range of applications [in mind]," he said.--For example, the researchers are planning to design algae that can capture carbon dioxide and make new hydrocarbons that could go into refineries. They are also working on ways to speed up vaccine production. [F15] Making new chemicals or food ingredients and cleaning up water are other possible benefits, according to Venter.--In the Science study, the researchers synthesized the genome of the bacterium M. mycoides and added DNA sequences that "watermark" the genome to distinguish it from a natural one.--Because current machines can only assemble relatively short strings of DNA letters at a time, the researchers inserted the shorter sequences into yeast, whose DNA-repair enzymes linked the strings together. They then transferred the medium-sized strings into E. coli and back into yeast. After three rounds of assembly, the researchers had produced a genome over a million base pairs long.--The scientists then transplanted the synthetic M. mycoides genome into another type of bacteria, Mycoplasm capricolum.[F16] The new genome "booted up" the recipient cells. Although fourteen genes were deleted or disrupted in the transplant bacteria, they still looked like normal [F17] M. mycoides bacteria and produced only M. mycoides proteins, the authors report.--"This is an important step we think, both scientifically and philosophically. It's certainly changed my views of the definitions of life and how life works," Venter said.--Acknowledging the ethical discussion about synthetic biology research, Venter explained that his team asked for a bioethical review in the late 1990s and has participated in variety of discussions on the topic.--"I think this is the first incidence in science where the extensive bioethical review took place before the experiments were done. It's part of an ongoing process that we've been driving, trying to make sure that the science proceeds in an ethical fashion, that we're being thoughtful about what we do and looking forward to the implications to the future," he said.--This research was funded by Synthetic Genomics, Inc. Three of the authors and the J. Craig Venter Institute hold Synthetic Genomics, Inc. stock. The J. Craig Venter Institute has filed patent applications on some of the techniques described in this paper.--More information can be found on the J. Craig Venter Institute web site at: http://www.jcvi.org/cms/research/projects/first-self-replicating-synthetic-bacterial-cell/---Story Source--The above story is based on materials provided by American Association for the Advancement of Science. Note: Materials may be edited for content and length.--Journal Reference--Daniel G. Gibson, John I. Glass, Carole Lartigue, Vladimir N. Noskov, Ray-Yuan Chuang, Mikkel A. Algire, Gwynedd A. Benders, Michael G. Montague, Li Ma, Monzia M. Moodie, Chuck Merryman, Sanjay Vashee, Radha Krishnakumar, Nacyra Assad-Garcia, Cynthia Andrews-Pfannkoch, Evgeniya A. Denisova, Lei Young, Zhi-Qing Qi, Thomas H. Segall-Shapiro, Christopher H. Calvey, Prashanth P. Parmar, Clyde A. Hutchison III, Hamilton O. Smith, and J. Craig Venter. Creation of a Bacterial Cell Controlled by a Chemically Synthesized Genome. Science, May 20, 2010 DOI: 10.1126/science.1190719
Repeated Oral AdministrationHistopathological and ultra structural effects of nanoparticles on rat testis following 90 days (Chronic study)
Mansee Thakur, Himanshu Gupta, Dipty Singh, Ipseeta R Mohanty, Ujjwala Maheswari, Geeta Vangae, Arvind Joshi
ABSTRACT: Background Nanoparticles (Ag NPs)[F18] have recently received much attention for their possible applications in biotechnology and biomedical. However, little is known about the toxicity in reproductive organs of animal model following exposure to Nanoparticles.Objective This study therefore, tried to examine the effects of Nanoparticles with a mean diameter of 5-20 nm range on the histology of the testis of wistar rats and correlate it with Transmission Electron Microscopy results.Materials and methods Sixteen wistar rats were randomly divided into two groups of 8 rats each. Each group received the following via gavage technique for 90 days: Control Group (Group-1)-tap water; Experimental group (Group 2) - Nanoparticles (20ug/kg/day). After ninety days (chronic study), rats were sacrificed and testis tissues was processed for histology and transmission electron microscopic study. There was significant difference between the observations of group-1 and group 2. The changes observed in the testis were disarray of the spermatogenic cells and disorientation of the testis. These changes were observed to have been disappearing from normal histological features. Detailed structural damages were observed with TEM analysis, such as depletion of germ cells, germinal cells necrosis, especially in spermatogonia and Leydig cells had an abnormal fibroblast-like appearance, abnormal space between neighboring sertoli cells, mitochondria, lost cristae and vacuolated (none energized) with those animals exposed to nanoparticles.Conclusion It seems that nanoparticles have acute and significant effects on spermatogenesis and number of spermatogenic cells. More experimental investigations are necessary to elucidate better conclusion regarding the safety of nanoparticles on male reproduction system.
Journal of nanobiotechnology. 10/2014; 12(1):42.
High-fat diet postpones brain aging in mice
November 5, 2014
University of Copenhagen – The Faculty of Health and Medical Sciences
Coconut oil and fresh coconut The researchers see a particular positive effect when the mice are given the so-called medium chain fatty acids -- e.g., from coconut oil.---New Danish-led research suggests that signs of brain aging can be postponed in mice if placed on a high-fat diet. In the long term, this opens the possibility of treatment of children suffering from premature aging and patients with Alzheimer's and Parkinson's disease. The research project is headed by the Center for Healthy Aging, University of Copenhagen and the National Institute of Health.--When we get older, defects begin to develop in our nervous system, our brain loses some of its intellectual capacity, and the risk of developing diseases such as Parkinson's and Alzheimer's increases. Alzheimer's disease is currently the fastest-growing age-related disease.--Throughout our lives, it is important that our cells -- to the extent possible -- keep our DNA undamaged, and, therefore, the cells have a system that repairs the damage that occurs all the time. Humans age when the repair system ceases to function. In diseases such as Alzheimer's, the researchers also see damage to the DNA--A new research project headed by the Center for Healthy Aging, University of Copenhagen and the National Institute of Health has studied mice having a defect in their DNA repair system. In humans, this defect causes the disorder Cockayne syndrome, where patients prematurely age as children and die at an age of 10-12 years. The study shows that placing a mouse model of Cockayne syndrome on a high-fat diet will postpone aging processes such as impaired hearing and weight loss.
Fat putting a stop to premature aging--"The study is good news for children with Cockayne syndrome, because we do not currently have an effective treatment. Our study suggests that a high-fat diet can postpone aging processes. A diet high in fat also seems to postpone the aging of the brain. The findings therefore potentially imply that patients with Alzheimer's and Parkinson's disease in the long term may benefit from the new knowledge," says Professor Vilhelm Bohr from the Center for Healthy Aging, University of Copenhagen and the National Institute of Health, who has headed the study.--Our brain has a constant need for fuel in the form of either sugar or so-called ketones. Ketones are the brain's fuel reserve, and, in particular, play an important role in periods of low blood sugar levels, e.g. if you are fasting[F19] . This is because the body breaks down fat if it needs sugar, and during this process it produces ketones. The researchers see a particular positive effect when the mice are given the so-called medium chain fatty acids -- e.g. from coconut oil.[F20]
Brain cells need extra fuel
"In cells from children with Cockayne syndrome, we have previously demonstrated that aging is a result of the cell repair mechanism being constantly active. It eats into the resources and causes the cell to age very quickly. We therefore hope that a diet with a high content of coconut oil or similar fats will have a beneficial effect, because the brain cells are given extra fuel and thus the strength to repair the damage," says postdoc Morten Scheibye-Knudsen from the National Institute of Health.--The study has just been published in the scientific journal Cell Metabolism.--Story Source-The above story is based on materials provided by University of Copenhagen – The Faculty of Health and Medical Sciences. Note: Materials may be edited for content and length.--Journal Reference-Morten Scheibye-Knudsen, Sarah J. Mitchell, Evandro F. Fang, Teruaki Iyama, Theresa Ward, James Wang, Christopher A. Dunn, Nagendra Singh, Sebastian Veith, Md Mahdi Hasan-Olive, Aswin Mangerich, Mark A. Wilson, Mark P. Mattson, Linda H. Bergersen, Victoria C. Cogger, Alessandra Warren, David G. Le Couteur, Ruin Moaddel, David M. Wilson, Deborah L. Croteau, Rafael de Cabo, Vilhelm A. Bohr. A High-Fat Diet and NAD Activate Sirt1 to Rescue Premature Aging in Cockayne Syndrome. Cell Metabolism, 2014; 20 (5): 840 DOI: 10.1016/j.cmet.2014.10.005
[F1]In other words the results will be reflective back the individual who is using the methods---proof is in the results
[F2]In other words ---the glory was in the practice rather then the results
[F3]A process to alleviate and reverse the decline require habits and chemistry
[F4]Key point here ---allowing the body to utilize and rest –so not to overload and over consume
[F5]At this point it is theoretical but anyone who makes the right changes to what they consume and eliminate things that cause organ or tissue failure or eliminate cellular damage will slow down or reverse negative implication causing health to become dysfunctional or debilitated
[F8]This is utilizing things on a nanoscale—we are dealing here with creation with no restrictions---and with nanogenetics there is a real danger and a significant concern on what these things will assimilate with---what they can alter—disrupt or incorporate into there matrix or be incorporated—and it’s effect on NORMAL biological life and if once incorporated can it be removed and the original DNA or GENE be restored to it’s original design
[F9]This is a form of weaponizing the genes as a bionano weapon ---which may have been already releases through chemtrails and other bioagents in the water supply and food chain—with this technology you could insert this sequence target a specific gene or gene type and activate or deactivate the signals or program that the gene des ---disrupting any biology in the system ---anything from heart rate to sugar regulation to immune response or non response—this is the real implication to this ---another form of weaponizing ones own body against itself through genetic manipulation
[F10]Normal!!!--- only they now possess new capabilities and can do things that wild yeast cannot—and this is called NORMAL
[F11]Now the question remains what are those new properties---what do they do ---how do they work---what function do they fulfil
[F12]Will never happen unless the oil industry controls this technology---whenthey mention the benfits they forget to mention who will have this technology to produce these wonderful developments as well—when you are talking progress and development things like this are utilized more for war and control then benefit
[F13]That could be classified as anything---from human populations to environmental
[F15]Bio Manipulation and incorporating this with a nano delivery method---you will have genetic alterations with this in anything you inject this into--
[F16]Disease Creation??—pestilence—even an accidental release of this could wipe out –populations and set back people in evolution
[F17]But the alterations caused a different effect---what was that effect
[F18]Silver Nano Particles
From a nutritional standpoint, saturated triglycerides with a medium (6 to 12) carbon chain length (MCT) have traditionally been regarded as biologically inert substances, merely serving as a source of fuel calories that is relatively easily accessible for metabolic breakdown compared with long chain triglycerides (LCT). This quality of MCT has been shown to offer both benefits and risks depending on the clinical situation, with potential positive effects on protein metabolism in some studies on one side, and an increased risk for ketogenesis and metabolic acidosis on the other. At another level, studies regarding lipid effects of MCT on the immune system, as with LCT, so far have yielded equivocal results, although there is a recent experimental evidence to suggest that MCT posses immune modulating properties and should in fact be regarded as bioactive mediators. Most of this information comes from studies where effects of MCT have been compared with those of LCT in lipid emulsions, as part of parenteral (intravenous) nutrition formulations. Unfortunately, the relevance of these observations for clinical practice remains largely unclear because adequately powered trials that clearly point out the position of MCT in relation to structurally different lipids have not been performed. In the present paper we review the experimental and clinical evidence for cellular and physiological effects of nutritional MCT. In addition, studies describing possible mechanisms behind the observed effects
Show of the Month November 29 2014
Improved neuroprotective effects by combining Bacopa monnieri and Rosmarinus officinalis supercritical CO2 extracts
Industrial pollution turning Canadian lakes into ‘jelly’
Published time: November 20, 2014 01:03
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Canada, Ecology, Science
The Canadian lakes are slowly but steadily turning into jelly since the industrial pollution has given jelly-clad organisms an edge over their calcium-protected competitors, researchers say, warning about potential impact on drinking water systems.---A battle between competing planktons in the delicate Ontario Lakes ecosystems is being won by “jelly-clad organism” called Holopedium that’s got an advantage over the planktonic Daphnia – all thanks to industrial pollution and acid rain – says new research by Cambridge University scientists published in Proceedings of the Royal Society B[F1] . The population of Holopedium – which has a “jelly” coat that gives them more protection from water predators – have doubled since the 1980s in many of the lakes, scientists behind the study say. [F2] — Eric Cai (@chemstateric) November 19, 2014 ---------The dramatic decline in the water calcium levels has left Daphnia without crucial component to develop their exoskeleton defending them from predators. Thus Daphnia populations are declining, leaving more algae for other organisms to feed on, such as jelly-protected Holopedium. [F3] -“Lakes across eastern Canada have seen Holopedium populations explode in the last thirty years; particularly in lakes in the province of Ontario that have seen a recent Eurasian invasion of the spiny water flea – which also favours hunting Daphnia, affording Holopedium even more room in these ecosystems to expand,” Cambridge said in a press release. --Scientists warn that the “jellification” of Canada’s lakes will further prevent vital nutrients in the food chain flow and may eventually clog filtration and drinking water systems, as in Ontario, some 20 percent of drinking water comes from lakes with depleted calcium concentrations. [F4] --“As calcium declines, the increasing concentrations of jelly in the middle of these lakes will reduce energy and nutrient transport right across the food chain, and will likely impede the withdrawal of lake water for residential, municipal and industrial uses,” said study co-author Dr Andrew Tanentzap, from the University of Cambridge’s Department of Plant Sciences. [F5]
'Daphnia Family' by Karl Gaff, winner 2014 UCD Images of Research Competition @UCD_Research @ucdscience @UCDSciEx pic.twitter.com/4zhaGSSZnu ---— UCD Innovation (@UCDinnovation) September 26, 2014 --Tanentzap says that industrialization in northern hemisphere deposited a lot of acid that displaced calcium from soil that feed these lakes. ----“Pollution control may have stopped acid deposits in the landscape, but it’s only now that we are discovering the damage wasn’t entirely reversed,” he says. --Besides Calcium loss, scientists also suggest that climate change is causing depletion of oxygen in the lakes that could lead to increasing populations of “larval midges – the main predator of Daphnia.” --“It may take thousands of years to return to historic lake water calcium concentrations solely from natural weathering of surrounding watersheds,” Tanentzap warned. “In the meanwhile, while we’ve stopped acid rain and improved the pH of many of these lakes, we cannot claim complete recovery from acidification. Instead, we many have pushed these lakes into an entirely new ecological state.” --
Improved neuroprotective effects by combining Bacopa monnieri and Rosmarinus officinalis supercritical CO2 extracts.
J Evid Based Complementary Altern Med. 2014 Apr;19(2):119-27
Authors: Ramachandran C, Quirin KW, Escalon E, Melnick SJ
Ethnobotanical evidence suggests that herbs such as brahmi (Bacopa monnieri) and rosemary (Rosmarinus officinalis) may possess antioxidant and neuroprotective properties. We compared the antioxidant and neuroprotective effects of supercritical extract of Bacopa monnieri and rosemary antioxidant extract obtained from Rosmarinus officinalis as well as their combination to examine the effects on human glial (U-87 MG) and embryonic mouse hypothalamus cells. Bacopa monnieri extract, rosemary antioxidant extract, and their combination (1:1) are not cytotoxic in both glial and embryonic mouse hypothalamus cell lines up to 200 μg/mL concentration. The combination of extracts of Bacopa monnieri + rosemary antioxidant has better antioxidant potential and antilipid peroxidation activity than either agent alone[F6] . Although the extract of Bacopa monnieri + rosemary antioxidant showed almost similar inhibition of phospho tau expression as Bacopa monnieri or rosemary antioxidant extract alone, the combination has better inhibitory effect on amyloid precursor protein synthesis and higher brain-derived neurotrophic factor production in hypothalamus cells than single agents. These results suggest that the extract of Bacopa monnieri + rosemary antioxidant is more neuroprotective than Bacopa monnieri or rosemary antioxidant extract. --PMID: 24647092 [PubMed - indexed for MEDLINE]
Recipe---make either a tea or extract of these and make them separate as extracts---then when done---combine ---as a tea take equal portions of each Boil together and drink as a tea---may see other benefits as well other then brain support ---may see analgesic effects as well as heart –eye—and liver support
If you have powdered rosemary and bacopa then sprinkle on eggs and othee fats to increase protection of lipid issues and use as a brain tonic since all foods here mentioned are brain support
Derivative of vitamin B3 prevents liver cancer in mice
Date-November 20, 2014--Source-Centro Nacional de Investigaciones Oncologicas (CNIO)
Liver cancer is one of the most frequent cancers in the world, and with the worst prognosis; according to the World Health Organisation (WHO), in 2012, 745,000 deaths were registered worldwide due to this cause, a figure only surpassed by lung cancer. The most aggressive and frequent form of liver cancer is hepato-cellular carcinoma (HCC); little is known about it and there are relatively few treatment options.--Researchers from the Spanish National Cancer Research Centre (CNIO), have produced the first mouse model that faithfully reproduces the steps of human HCC development, from the appearance of the first lesions in the liver to the development of metastasis. The results, published in the journal Cancer Cell, indicate that diets rich in nicotinamide riboside, a derivative of vitamin B3, protect these mice from developing HCC in its most initial stage, when genotoxic stress is damaging cellular DNA. [F7] They also show a curative effect of the diet in those mice that had previously developed the disease.
A MOUSE MODEL FOR HUMAN HEPATIC CANCER
One obstacle to the study of human HCC is the absence of mouse models that replicate the disease, which could be used to investigate molecular pathways or new therapies. Given that human HCC is associated to alterations in hepatocytes survival, and that the URI oncogene plays a role in this process, the researchers genetically engineered mice that contained high levels of URI only in the liver, in a controlled manner over time.At 30 weeks, the mice with high levels of URI generated sporadic tumours in the liver and even metastasis when the induction lasted longer. The study details how deficiency in nicotinamide adenine dinucleotide (NAD+), a universal compound found in living organisms that is needed to burn calories via cell metabolism, orchestrates the development of the disease.[F8] --"An increase in URI reduces cellular NAD+ and as a consequence produces genotoxic stress and DNA damage," says Nabil Djouder, leader of the study and Head of the Growth Factors, Nutrients and Cancer Group in the BBVA Foundation-CNIO Cancer Cell Biology Programme. "It is still not totally clear, however, why the deficit in NAD+ causes these lesions," he adds.
ENERGY METABOLISM AND CANCER
The appearance of DNA damage is the first link in the chain of events that activate the carcinogenic process in the liver, even before apoptosis or cell death, as has been described in the literature. "We normally say that oncogenes induce DNA damage. Now we may be able to say, more appropriately, that oncogenes induce NAD+ depletion [or deficits in NAD+] which causes DNA damage," says Djouder--The inverse relationship between NAD+ and cancer awakened the curiosity of the researchers: could an increase in NAD+ have beneficial effects on the disease? When the scientists supplemented the diet in genetically modified mice with nicotinamide riboside, a derivative of vitamin B3 that increases intracellular levels of NAD+, they did not observe tumour development. Surprisingly, when they gave this diet to mice that had already developed the disease, the size of the tumours was reduced and they eventually disappeared.--The results have been reproduced in other types of cancer such as pancreatic cancer. "We observed the same results in mice with pancreatic adenocarcinoma with regards to DNA damage[F9] , so we could conclude that this treatment is effective on tumours caused by oncogene[F10] -induced DNA damage and thus, deficit in NAD+," says Krishna Tummala, first author of the study.--In addition to working with the mouse model, the authors have collated the results of nearly a hundred human samples. "Those from patients with HCC contain URI levels that double those of healthy samples," according to the article. The data, which also associates URI with a worse prognosis or evolution of the illness, suggests that the gene could be a possible new HCC marker, and nicotinamide riboside boosting NAD+ levels may have a human relevance.
FUTURE RESEARCH--------Several epidemiological studies coincide in associating diets low in tryptophan [a NAD+ precursor] with an increased incidence of certain types of cancer[F11] . It has also been observed that daily supplements of vitamin B3 in populations with chronic nutritional deficiencies, reduces the incidence of some cancers including esophageal cancer.--Despite the results, the researchers underline that the efficiency of NAD+ enhancing nutritional supplements to protect healthy cells from chemotoxic stress as a combined therapy in oncology still needs to be demonstrated. Djouder's team is collaborating with the CNIO Clinical Research Programme, lead by the oncologist Manuel Hidalgo to broaden these studies in mice and evaluate the possibility of carrying out clinical trials in humans in the future.
Story Source--The above story is based on materials provided by Centro Nacional de Investigaciones Oncologicas (CNIO). Note: Materials may be edited for content and length.--Journal Reference-Krishna S. Tummala, Ana L. Gomes, Mahmut Yilmaz, Osvaldo Graña, Latifa Bakiri, Isabel Ruppen, Pilar Ximénez-Embún, Vinayata Sheshappanavar, Manuel Rodriguez- Justo, David G. Pisano, Erwin F. Wagner & Nabil Djouder. Inhibition of De Novo NAD Synthesis by Oncogenic URI Causes Liver Tumorigenesis through DNA Damage. Cancer Cell, November 2014 DOI: 10.1016/j.ccell.2014.10.002
Energizing sick mitochondria with vitamin B3- Effective treatment for mitochondrial disease
Date-April 7, 2014
Source-Helsingin yliopisto (University of Helsinki)
The researchers of the University of Helsinki, Finland, and École Polytechnique Fédérale de Lausanne, Switzerland, have shown that vitamin B3 form nicotinamide riboside can slow down the progression of mitochondrial disease, suggesting its potential as a novel therapy approach to adult-onset mitochondrial muscle diseases.-Vitamins B have recently been turned out to be potent modifiers of energy metabolism, especially the function of mitochondria. Vitamin B3, (niacin) has been found to delay the signs of aging in animal models.--An international collaboration between the University of Helsinki and École Polytechnique Fédérale de Lausanne reported today in the journal Embo Molecular Medicine that vitamin B3 form, nicotinamide riboside, can slow down the progression of mitochondrial disease, suggesting its potential as a novel therapy approach to adult-onset mitochondrial muscle diseases.--Mitochondria power up all cells in our bodies, by generating fuel, ATP, for all cellular functions. Dysfunction of these cellular engines can cause mitochondrial disorders, which are the most common cause of inherited metabolic diseases in adults and children. Mitochondrial myopathy is the most frequent form of adult mitochondrial disorder. The typical symptoms in the patients are muscle weakness, pain and cramps. Despite the progressive nature of these diseases, no curative treatment is available.--In their current publication, Dr Nahid Khan in Prof Anu Suomalainen Wartiovaara's group showed that feeding mice with food supplemented with B3 form, nicotinamide riboside, delayed their mitochondrial myopathy[F12] . The treatment increased mitochondrial mass and function, and cured the structural abnormalities. These results clearly showed the potential of this vitamin B form, a natural constituent of milk, to activate dysfunctional mitochondrial metabolism.--"These results are a breakthrough for understanding the mechanisms of human mitochondrial muscle diseases and for exploring the efficient treatment options for these progressive disorders of adults. They also highlight the potent role of niacin in guiding mitochondrial energy metabolism," Professor Anu Suomalainen Wartiovaara states.-Story Source-The above story is based on materials provided by Helsingin yliopisto (University of Helsinki). Note: Materials may be edited for content and length.-Journal Reference-Nahid A Khan, Mari Auranen, Ilse Paetau, Eija Pirinen, Liliya Euro, Saara Forsström, Lotta Pasila, Vidya Velagapudi, Christopher J Carroll, Johan Auwerx and Anu Suomalainen. Effective treatment of mitochondrial myopathy by nicotinamide riboside, a vitamin B3. EMBO Molecular Medicine, April 2014 DOI: 10.1002/emmm.201403943
Copper on the brain at rest
Date:November 26, 2014
Source:DOE/Lawrence Berkeley National Laboratory
Two-photon imaging of CF3 shows that the addition of acute BCS dosages also reduces labile copper pools in retinal neurons.
In recent years it has been established that copper plays an essential role in the health of the human brain. Improper copper oxidation has been linked to several neurological disorders including Alzheimer's, Parkinson's, Menkes' and Wilson's. Copper has also been identified as a critical ingredient in the enzymes that activate the brain's neurotransmitters in response to stimuli. Now a new study by researchers with the U.S. Department of Energy (DOE)'s Lawrence Berkeley National Laboratory (Berkeley Lab) has shown that proper copper levels are also essential to the health of the brain at rest.-"Using new molecular imaging techniques, we've identified copper as a dynamic modulator of spontaneous activity of developing neural circuits, which is the baseline activity of neurons without active stimuli, kind of like when you sleep or daydream, that allows circuits to rest and adapt," says Chris Chang, a faculty chemist with Berkeley Lab's Chemical Sciences Division who led this study. "Traditionally, copper has been regarded as a static metabolic cofactor that must be buried within enzymes to protect against the generation of reactive oxygen species and subsequent free radical damage. We've shown that dynamic and loosely bound pools of copper can also modulate neural activity and are essential for the normal development of synapses and circuits."--Chang , who also holds appointments with the University of California (UC) Berkeley's Chemistry Department and the Howard Hughes Medical Institute (HHMI), is the corresponding author of a paper that describes this study in the Proceedings of the National Academy of Sciences (PNAS). The paper is titled "Copper is an endogenous modulator of neural circuit spontaneous activity." Co-authors are Sheel Dodani, Alana Firl, Jefferson Chan, Christine Nam, Allegra Aron, Carl Onak, Karla Ramos-Torres, Jaeho Paek, Corey Webster and Marla Feller.--Although the human brain accounts for only two-percent of total body mass, it consumes 20-percent of the oxygen taken in through respiration. This high demand for oxygen and oxidative metabolism has resulted in the brain harboring the body's highest levels of copper, as well as iron and zinc. Over the past few years, Chang and his research group at UC Berkeley have developed a series of fluorescent probes for molecular imaging of copper in the brain.--"A lack of methods for monitoring dynamic changes in copper in whole living organisms has made it difficult to determine the complex relationships between copper status and various stages of health and disease," Chang said. "We've been designing fluorescent probes that can map the movement of copper in live cells, tissue or even model organisms, such as mice and zebra fish."
For this latest study, Chang and his group developed a fluorescent probe called Copper Fluor-3 (CF3) that can be used for one- and two-photon imaging of copper ions. This new probe allowed them to explore the potential contributions to cell signaling of loosely bound forms of copper in hippocampal neurons and retinal tissue.--"CF3 is a more hydrophilic probe compared to others we have made, so it gives more even staining and is suitable for both cells and tissue," Chang says. "It allows us to utilize both confocal and two-photon imaging methods when we use it along with a matching control dye (Ctrl-CF3) that lacks sensitivity to copper."--With the combination of CF3 and Ctrl-CF3, Chang and his group showed that neurons and neural tissue maintain stores of loosely bound copper that can be attenuated by chelation to create what is called a "labile copper pool." Targeted disruption of these labile copper pools by acute chelation or genetic knockdown of the copper ion channel known as CTR1 (for copper transporter 1) alters spontaneous neural activity in developing hippocampal and retinal circuits.[F13] - "We demonstrated that the addition of the copper chelator bathocuproine disulfonate (BCS) modulates copper signaling which translates into modulation of neural activity," Chang says. "Acute copper chelation as a result of additional BCS in dissociated hippocampal cultures and intact developing retinal tissue removed the copper which resulted in too much spontaneous activity."--The results of this study suggest that the mismanagement of copper in the brain that has been linked to Wilson's, Alzheimer's and other neurological disorders can also contribute to misregulation of signaling in cell−to-cell communications.--"Our results hold therapeutic implications in that whether a patient needs copper supplements or copper chelators depends on how much copper is present and where in the brain it is located," Chang says. "These findings also highlight the continuing need to develop molecular imaging probes as pilot screening tools to help uncover unique and unexplored metal biology in living systems."--Story Source-The above story is based on materials provided by DOE/Lawrence Berkeley National Laboratory. The original article was written by Lynn Yarris. Note: Materials may be edited for content and length.--Journal Reference-Sheel C. Dodani, Alana Firl, Jefferson Chan, Christine I. Nam, Allegra T. Aron, Carl S. Onak, Karla M. Ramos-Torres, Jaeho Paek, Corey M. Webster, Marla B. Feller, Christopher J. Chang. Copper is an endogenous modulator of neural circuit spontaneous activity. Proceedings of the National Academy of Sciences, 2014; 111 (46): 16280 DOI: 10.1073/pnas.1409796111
Copper can protect against Alzheimer's disease
Date:February 17, 2013
Source: Keele University
Researchers in The Birchall Centre at Keele University, Staffordshire, UK, have provided unequivocal evidence that under conditions which are approximately similar to those found in the brain, copper can only protect against beta amyloid forming beta sheets and as such it is highly unlikely that copper is directly involved in the formation of senile plaques in Alzheimer's disease.--The research, published by Nature's online journal Scientific Reports, may also imply that lower levels of copper in the brain may promote the mechanisms whereby beta amyloid is deposited as senile plaques in Alzheimer's disease.--This research addressed the on-going question as to whether copper in the brain contributes to the formation of the senile plaques in Alzheimer's disease. While previous research at Keele's Birchall Centre pointed towards copper being potentially protective in preventing the protein beta amyloid from aggregating as beta sheets and forming senile plaques it had remained a controversial issue for some.--Story Source--The above story is based on materials provided by Keele University. Note: Materials may be edited for content and length.--Journal Reference--Matthew Mold, Larissa Ouro-Gnao, Beata M Wieckowski, Christopher Exley. Copper prevents amyloid-β1–42 from forming amyloid fibrils under near-physiological conditions in vitro. Scientific Reports, 2013; 3 DOI: 10.1038/srep01256
[F1]Chemtrail Fallout would be more the reality---them dumping tons of nanoparticles and nanometals have accumulated over time and now the water table is being poisoned---in a military exercise this would be considered as “poisoning the wells” where by the water would not be fir for consumption or irrigation and anything it would be exposed to ---spread pathogens –in this case nanopoisoning
[F2]Polymers can ba a lipid or protein mix to create a “Jelly like effect”
[F3]Glyphosates in the region would case this as well –since glyphosates strip out minerals allowing pathogenic materials to become more predomnant
[F4]This sounds fishy---with the amount of GE chemicals such as glyphosates leeching into the water table this would be more credible as the cause and as a result this will now be in the drinking water which will further strip out of people vitals
[F5]Almost sounds like there is another reason to reduce the consumer usage—possible water rationing!!!
[F6]Protects Fat From Breaking down and going bad
[F7]B3 –used ot be used by medicicne to reduce cholesterol in the liver
[F8]And a lot have a B3 deficiency one way to tell is Sleep and rest depeleton---which without B3 you cannot regulate trytophan
[F9]Huge –info here –pancreatic and lung cancers are some of the hardest cancers to reverse---so this canbe effective as well
[F11]Foods with Tryptophan
(mg of Tryptophan per 100 grams)
Algae: Spirulina 929
Velvet Deer Antler
Dairy Products: Cottage Cheese Milk
Yogurt Cheese (cheddar) 340
Swiss Cheese 401 Parmesan Cheese 482
Edam Cheese 352 Gouda Cheese 352
Gruyere Cheese 421 Cheddar Cheese 320
Blue Cheese 312
Eggs: Whole Eggs 210
Fish Crab 330 Tuna (canned) 300
Fruit: Bananas 12 Dates
Beef 400 Turkey 400
Chicken 400 Pork 400
Nuts: Peanuts 340 Brazil Nuts 185
Cashew Nuts 287 Pistachio Nuts 273
Processed Foods: Chocolate Cocoa
Seeds: Sunflower Seeds 350 Pumpkin Seeds 560
Sesame Seeds 388 Mustard Seeds 526
Fenugreek Seeds 391 Poppy Seeds 255
Fennel Seeds 253
Vegetables: Carrots Broccoli
[F12]In medicine, a myopathy is a muscular disease in which the muscle fibers do not function for any one of many reasons, resulting in muscular weakness.
[F13]Glyphosate poisoning removes from the body copper—iron and zinc---and when combo’d with sulphur appears to take away the floaters as well zince zinc+ copper make SOD---which is located in lung –highest –Eyes second highest