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Show of the Month October 2012
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The U.S. Drug Enforcement Administration classifies ADHD drugs as Scheudle ll
Modulation of apoptosis in human hepatocellular carcinoma
Sesame and Rice Bran Oil Lowers Blood Pressure, Improves Cholesterol
Chlorophyll revisited- anti-inflammatory activities of chlorophyll a and inhibition of expression of TNF-α gene by the same
Bacterial Cause Found for Skin Condition Rosacea
The U.S. Drug Enforcement Administration classifies ADHD drugs as Scheudle ll,
in the same class of highly addictive drugs as morphine, opium and cocaine.
Common brand name stimulants, also known as ADHD drugs, include Ritalin, Concerta, Adderall, Metadate, Vyvanse, Provigil.
A) Drug Agency Regulatory Warnings on Stimulants/ADHD drugs – There have 31 drug regulatory agency warnings from eight countries including warnings of stimulant induced heart problems, suicide, violence, depression, mania, psychosis, hallucinations and death. See Tab A
B) Drug Studies on Stimulants – There have been 119 studies in twelve countries on stimulant induced side effects including birth defects, heart problems, depression, suicidal ideation, violence, hallucinations, mania, psychosis, homicidal ideation and death. See Tab B
C) Adverse Reaction Reports filed with the US FDA -- There have been 14,158 adverse reactions reported to the US FDA in connection with stimulants. See Tab C
Tab A) Stimulant Drug Warnings:
There have been 31 warnings from eight countries (United States, United Kingdom, Canada, Japan, Australia, New Zealand, France and Singapore) warning that stimulants cause harmful side effects, which include:
12 warnings on stimulants causing heart problems
8 warnings on stimulants causing mania/psychosis
8 warnings on stimulants causing death
3 warnings on stimulants causing hallucinations
2 warnings on stimulants causing depression
2 warnings on stimulants causing violence, hostility or aggression
2 warnings on stimulants causing seizures
1 warning on stimulants causing suicide risk/attempts
1 warning on stimulants causing anxiety
Back to Top
Tab B) Stimulant Drug Studies:
There are 20 studies from four countries (United States, Australia, Denmark and Italy) showing that stimulants cause harmful side effects, including:
5 studies on stimulants causing medication abuse
3 studies on stimulants causing heart problems
2 studies on stimulants causing death
1 study on stimulants causing suicide risk/attempts
1 study on stimulants causing birth defects
1 study on stimulants causing violence
1 study on stimulants causing homicidal ideation
1 study on stimulants causing depression
1 study on stimulants causing mania, psychosis and hallucinations
Back to Top
Tab C – Stimulant Drug Side Effects Reported to the FDA:
The Adverse Drug Reactions that have been reported to the FDA's Adverse Event Reporting System (MedWatch), between 2004 and 2011 include:
871 cases of stimulants causing reactions related to suicide (completed suicides, suicide attempts, suicidal ideation and suicidal behavior)
636 cases of stimulants causing aggression
593 cases of stimulants causing hallucinations
499 cases of stimulants causing anxiety
495 cases of stimulants causing abnormal behavior
464 cases of stimulants causing depression
220 cases of stimulants causing death/sudden death
147 cases of stimulants causing mania
52 cases of stimulants causing homicidal ideation
44 cases of stimulants causing diabetes
30 cases of stimulants causing hostility
25 cases of stimulants causing coma
23 cases of stimulants causing physical Assault
21 cases of stimulants causing birth defects
13 cases of stimulants causing violence-related symptoms
12 cases of stimulants causing psychosis
11 cases of stimulants causing homicide
9 cases of stimulants causing sexual dysfunction
1 case of stimulants causing stillbirth
Search CCHR's Psychiatric Drug Side Effects database for more information
Modulation of apoptosis in human hepatocellular carcinoma (HepG2 cells) by a standardized herbal decoction of Nigella sativa seeds, Hemidesmus indicus roots and Smilax glabra rhizomes with anti- hepatocarcinogenic effects.
BMC Complement Altern Med. 2012;12:25
Authors: Samarakoon SR, Thabrew I, Galhena PB, Tennekoon KH
BACKGROUND: A standardized poly-herbal decoction of Nigella sativa seeds, Hemidesmus indicus roots and Smilax glabra rhizome[U1] s used traditionally in Sri Lanka for cancer therapy has been demonstrated previously, to have anti-hepatocarcinogenic potential. Cytotoxicity, antioxidant activity, anti-inflammatory activity, and up regulation of p53 and p21 activities are considered to be some of the possible mechanisms through which the above decoction may mediate its anti-hepatocarcinogenic action. The main aim of the present study was to determine whether apoptosis is also a major mechanism by which the decoction mediates its anti-hepatocarcinogenic action.
METHODS: Evaluation of apoptosis in HepG2 cells was carried out by (a) microscopic observations of cell morphology, (b) DNA fragmentation analysis, (c) activities of caspase 3 and 9, as well as by (d) analysis of the expression of pro-apoptotic (Bax) and anti-apoptotic (Bcl-2) proteins associated with cell death.
RESULTS: The results demonstrated that in HepG2 cells, the decoction can induce (a) DNA fragmentation and (b) characteristic morphological changes associated with apoptosis (nuclear condensation, membrane blebbing, nuclear fragmentation and apoptotic bodies). The decoction could also, in a time and dose dependent manner, up regulate the expression of the pro-apoptotic gene Bax and down regulate expression of anti-apoptotic Bcl-2 gene (as evident from RT-PCR analysis, immunohistochemistry and western blotting). Further, the decoction significantly (p < .001) enhanced the activities of caspase-3 and caspase-9 in a time and dose dependent manner.---CONCLUSIONS: Overall findings provide confirmatory evidence to demonstrate that the decoction may mediate its reported anti-hepatocarcinogenic effect, at least in part, through modulation of apoptosis.---PMID: 22458551 [PubMed - indexed for MEDLINE]
Recipe for making this decoction of Black seed and Smilax ( sarsaparilla)—take equal parts of each herb and boil them down to at least half of the volume of water you put in— I.E 2 pint down to 1 pint or less ( 500mls for the metric to 250 mls)—and then use small amounts 1-2 oz increments 4-5 times daily
Sesame and Rice Bran Oil Lowers Blood Pressure, Improves Cholesterol
ScienceDaily (Sep. 18, 2012) — People who cooked with a blend of sesame and rice bran oils saw a significant drop in blood pressure and improved cholesterol levels, according to new research presented at the American Heart Association's High Blood Pressure Research 2012 Scientific Sessions.---The researchers found cooking with a combination of these oils in a variety of ways worked nearly as well as a commonly prescribed high blood pressure medication, and that the use of the oil blend with medication yielded even more impressive results.---"Rice bran oil, like sesame oil, is low in saturated fat and appears to improve a patient's cholesterol profile," said Devarajan Sankar, M.D, Ph.D., a research scientist in the Department of Cardiovascular Disease at Fukuoka University Chikushi Hospital in Chikushino, Japan. "Additionally, it may reduce heart disease risk in other ways, including being a substitute for less healthy oils and fats in the diet[U2] ."--The 60-day study in New Delhi, India, divided 300 people with mild to moderately high blood pressure into three groups. One group was treated with a commonly used blood pressure lowering medication called a calcium-channel blocker (nifedipine). The second group was given the oil blend and told to use about an ounce each day in their meals.---The final group received the calcium channel blocker and the oil blend.----All three groups, with approximately an equal number of men and women, average age of 57, saw drops in their systolic blood pressure. Systolic blood pressure is the top number in a blood pressure reading and measures the force of blood against your artery walls when the heart is pumping.---Systolic blood pressure dropped an average of 14 points for those using only the oil blend and 16 points for those taking medication. Those using both saw a 36-point drop.---Diastolic blood pressure also dropped significantly: 11 points for those eating the oil, 12 for those on medication and 24 for those using both. Diastolic blood pressure is the bottom number in a blood pressure reading that measures the force of blood against your artery walls when your heart is at rest between beats.---As for cholesterol, those using the oils saw a 26 percent drop in their LDL ("bad" cholesterol) and a 9.5 percent increase in the HDL ("good" cholesterol[U3] ), while no changes in cholesterol were observed for the patients who used only the calcium-channel blocker. Those who took the calcium channel blocker and the oils had a 27 percent drop in LDL levels and a 10.9 percent increase in the HDL[U4] . Healthier fatty acids and antioxidants, such as sesamin, sesamol, sesamolin and oryzanol, in the oil blends may be responsible for the results, Sankar said. These antioxidants, mono and poly unsaturated oils are compounds found in plants and have been linked with lower blood pressure and total cholesterol in earlier studies.--Additional studies are needed to determine if the oil blend is as beneficial as it seems. The combination was made specifically for this study, and there are no plans to market it commercially, Sankar said. Blending these oils yourself would not necessarily produce these effects.--Co-authors are.Ravinder Singh, M.B.B.S., and Biprabuddha Chatterjee, M.Sc.-Story Source-The above story is reprinted from materials provided by American Heart Association.
Chlorophyll revisited~~ anti-inflammatory activities of chlorophyll a and inhibition of expression of TNF-α gene by the same.
Inflammation. 2012 Jun;35(3):959-66
Authors: Subramoniam A, Asha VV, Nair SA, Sasidharan SP, Sureshkumar PK, Rajendran KN, Karunagaran D, Ramalingam K
Abstract--In view of the folklore use of green leaves to treat inflammation, the anti-inflammatory property of chlorophylls and their degradation products were studied. Chlorophyll a and pheophytin a (magnesium-free chlorophyll a) from fresh leaves showed potent anti-inflammatory activity against carrageenan-induced paw edema in mice and formalin-induced paw edema in rats.[U5] Chlorophyll a inhibited bacterial lipopolysaccharide-induced TNF-α (a pro-inflammatory cytokine) gene expression in HEK293 cells, but it did not influence the expression of inducible nitric acid synthase and cyclooxygenase-2 genes. Chlorophyll b only marginally inhibited both inflammation and TNF-α gene expression. But both chlorophyll a and chlorophyll b showed the same level of marginal inhibition on 12-O-tetradecanoyl-phorbol-13-acetate-induced NF-κB activation. Chlorophylls and pheophytins showed in vitro anti-oxidant activity. The study shows that chlorophyll a and its degradation products are valuable and abundantly available anti-inflammatory agents and promising for the development of phytomedicine or conventional medicine to treat inflammation and related diseases.---PMID: 22038065 [PubMed - indexed for MEDLINE]
Chlorophyll is a chemoprotein commonly known for its contribution to the green pigmentation in plants, and is related to protoheme, the red pigment of blood. It can be obtained from green leafy vegetables (broccoli, Brussel sprouts, cabbage, lettuce, and spinach), algae (Chlorella and Spirulina), wheat grass, and numerous herbs (alfalfa, damiana, nettle, and parsley).--Chlorophyll has been used traditionally to improve bad breath and other forms of body odor including odors of the urine, feces, and infected wounds. More recently chlorophyll has been used to aid in the removal of various toxins via the liver and remains a key compound for improving the function of essential detoxification pathways. Supportive evidence suggests it may be used as an anti-inflammatory agent for conditions, such as pancreatitis as well as exhibiting potent antioxidant and chemoprotective activities. Scientific research has demonstrated it may be an effective therapeutic agent in the treatment of herpes simplex, benign breast disease, chemoprevention, tuberculosis, and rheumatoid arthritis. Type 2 diabetes and obesity are also being explored as areas where chlorophyll can also be used.
Bacterial Cause Found for Skin Condition Rosacea
ScienceDaily (Aug. 28, 2012) — Scientists are closer to establishing a definitive bacterial cause for the skin condition rosacea. This will allow more targeted, effective treatments to be developed for sufferers, according to a review published in the Journal of Medical Microbiology.---Rosacea is a common dermatological condition that causes reddening and inflammation of the skin mostly around the cheeks, nose and chin. In severe cases skin lesions may form and lead to disfigurement[U6] . Rosacea affects around 3% of the population -- usually fair-skinned females aged 30-50 and particularly those with weak immune systems. The condition is treated with a variety of antibiotics, even though there has never been a well-established bacterial cause.[U7] --A new review carried out by the National University of Ireland concludes that rosacea may be triggered by bacteria that live within tiny mites that reside in the skin.--The mite species Demodex folliculorum is worm-like in shape and usually lives harmlessly inside the pilosebaceous unit which surrounds hair follicles of the face. They are normal inhabitants of the face and increase in number with age and skin damage -- for example, following exposure to sunlight. The numbers of Demodex mites living in the skin of rosacea patients is higher than in normal individuals[U8] , which has previously suggested a possible role for the mites in initiating the condition.---More recently, the bacterium Bacillus oleronius was isolated from inside a Demodex mite[U9] and was found to produce molecules provoking an immune reaction in rosacea patients. Other studies have shown patients with varying types of rosacea react to the molecules produced by this bacterium -- exposing it as a likely trigger for the condition. [U10] What's more, this bacterium is sensitive to the antibiotics used to treat rosacea.---Dr Kevin Kavanagh who conducted the review explained, "The bacteria live in the digestive tracts of Demodex mites found on the face, in a mutually beneficial relationship. When the mites die, the bacteria are released and leak into surrounding skin tissues -- triggering tissue degradation and inflammation."[U11] ---"Once the numbers of mites increase, so does the number of bacteria, making rosacea more likely to occur. Targeting these bacteria may be a useful way of treating and preventing this condition," said Dr Kavanagh. "Alternatively we could look at controlling the population of Demodex mites in the face.. Some pharmaceutical companies are already developing therapies to do this, which represents a novel way of preventing and reversing rosacea, which can be painful and embarrassing for many people."----Story Source-The above story is reprinted from materials provided by Society for General Microbiology, via AlphaGalileo. ---Journal Reference-Stanisław Jarmuda, Niamh O'Reilly, Ryszard Żaba, Oliwia Jakubowicz, Andrzej Szkaradkiewicz and Kevin Kavanagh. The potential role of Demodex folliculorum mites and bacteria in the induction of rosacea. Journal of Medical Microbiology, 2012 DOI: 10.1099/jmm.0.048090-0
Show Of the Month October 5 2012
Diet promotes sleep duration and quality
Short Sleep Duration and Weight Gain-- A Systematic Review
Cell tower regulations frustrate homeowners Towers under 15 metres tall avoid municipal scrutiny
Red wine and components flavonoids inhibit UGT2B17 in vitro
Rhodiola Protects HPG Axis during Exercise or Physical Work
Diet promotes sleep duration and quality.
Nutr Res. 2012 May;32(5):309-19--Authors: Peuhkuri K, Sihvola N, Korpela R
Abstract--Sleep, much like eating, is an essential part of life. The mechanisms of sleep are only partially clear and are the subject of intense research. There is increasing evidence showing that sleep has an influence on dietary choices. Both cross-sectional and epidemiologic studies have demonstrated that those who sleep less are more likely to consume energy-rich foods (such as fats or refined carbohydrates), to consume fewer portions of vegetables, and to have more irregular meal patterns. In this narrative review, we pose the opposite question: can ingested food affect sleep? The purpose of this review is to discuss the evidence linking diet and sleep and to determine whether what we eat and what kind of nutrients we obtain from the food consumed before bedtime matter. In addition, scientific evidence behind traditional sleep-promoting foods such as milk and some herbal products is briefly described. These are reviewed using data from clinical trials, mostly in healthy subjects. In addition, we discuss the possible mechanisms behind these observations. Lastly, we summarize our findings that emerging evidence confirms a link between diet and sleep. Overall, foods impacting the availability of tryptophan, as well as the synthesis of serotonin and melatonin, may be the most helpful in promoting sleep. Although there are clear physiological connections behind these effects, the clinical relevance needs to be studied further.---PMID: 22652369 [PubMed - indexed for MEDLINE]
Short Sleep Duration and Weight Gain-- A Systematic Review
Sanjay R. Patel1 and Frank B. Hu2,3,4
- 1Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, University Hospitals Case Medical Center and Case Western Reserve University, Cleveland, Ohio, USA
- 2Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts, USA
- 3Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA
- 4Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA
Correspondence: Sanjay R. Patel (email@example.com)
Received 18 April 2007; Accepted 19 July 2007; Published online 17 January 2008.
The recent obesity epidemic has been accompanied by a parallel growth in chronic sleep deprivation. Physiologic studies suggest sleep deprivation may influence weight through effects on appetite, physical activity, and/or thermoregulation. This work reviews the literature regarding short sleep duration as an independent risk factor for obesity and weight gain.
Methods and Procedures---A literature search was conducted for all articles published between 1966 and January 2007 using the search "sleep" and ("duration" or "hour" or "hours") and ("obesity" or "weight") in the MEDLINE database. Additional references were identified by reviewing bibliographies and contacting experts in the field. Studies reporting the association between sleep duration and at least one measure of weight were included.
Results---Thirty-six publications (31 cross-sectional, 5 prospective, and 0 experimental) were identified. Findings in both cross-sectional and cohort studies of children suggested short sleep duration is strongly and consistently associated with concurrent and future obesity. Results from adult cross-sectional analyses were more mixed with 17 of 23 studies supporting an independent association between short sleep duration and increased weight. In contrast, all three longitudinal studies in adults found a positive association between short sleep duration and future weight. This relationship appeared to wane with age.
Discussion--Short sleep duration appears independently associated with weight gain, particularly in younger age groups. However, major study design limitations preclude definitive conclusions. Further research with objective measures of sleep duration, repeated assessments of both sleep and weight, and experimental study designs that manipulate sleep are needed to better define the causal relationship of sleep deprivation on obesity.
Introduction---Over the past several decades, the prevalence of obesity has grown to epidemic proportions. Concurrent with this rise in weight there has been a similar epidemic of chronic sleep deprivation. According to annual surveys done by the National Sleep Foundation, by 1998 only 35% of American adults were obtaining 8 h of sleep and that number had fallen to 26% by 2005 (ref. 1[U12] ).-----Evidence has grown over the past decade supporting a role for short sleep duration as a novel risk factor for weight gain and obesity. A number of causal pathways linking reduced sleep with obesity have been posited based on experimental studies of sleep deprivation. Chronic partial sleep deprivation causes feelings of fatigue which may lead to reduced physical activity (2,3). Sleep deprivation may also have neurohormonal effects that increase caloric intake (4). Because of the rapidly accelerating prevalence of sleep deprivation, any causal association between short sleep durations and obesity would have substantial importance from a public health standpoint. We performed a systematic review of the literature to assess the present evidence suggesting that sleep deprivation may represent a novel risk factor for weight gain and obesity.
Methods and Procedures----Relevant original articles were identified by searching the MEDLINE database (National Library of Medicine, Bethesda, MD) of articles published between 1966 and August 2006 examining the relationship between sleep duration and weight gain, obesity, or both. The primary search was performed using the keywords "sleep" and ("duration" or "hour" or "hours") and ("obesity" or "weight"). A subsequent search was also performed using medical subheading terms. The searches were repeated in January 2007 to identify any new publications. Bibliographies of retrieved articles were reviewed, and experts in the field were contacted to further identify relevant works. Articles were restricted to studies conducted in humans presenting original research. Where data from the same cohort were presented in more than one article, only the report that most directly analyzed the sleep–weight association was included. All abstracts obtained from this search were screened. Relevant articles were obtained and evaluated for presentation of data regarding the association between sleep duration and at least one measure of weight (e.g., BMI, BMI z-score, and weight) either cross-sectionally or longitudinally. A meta-analysis was attempted, but the degree of heterogeneity among study designs, particularly with respect to the measure of association and the definition of short sleep duration, was prohibitive, and therefore a more qualitative assessment is presented. Greater weight is given to large studies, prospective cohort studies, and studies which objectively assessed sleep durations. Because of differences in the sleep requirements of children and adults, these groups are considered separately. Where results were presented graphically, authors were contacted to obtain the numeric data (3,5,6).
Results---The keyword search initially identified a total of 1,013 citations. After screening through abstracts for relevance, 36 articles of potential relevance were identified. The medical subheading search identified an additional five articles. Fifteen articles were excluded because, though both sleep duration and weight data were collected, the association between these two factors was not assessed. Another five articles were excluded for presentation of data overlapping with another report, leaving 21 articles. Ten investigations were added after the original extraction from review of references and expert contact. The updated search in January 2007 identified 44 additional citations, of which 5 were relevant for this synthesis. Thus 36 studies were included in this analysis. Of these, 31 are cross-sectional studies, 2 are prospective cohort studies, and 3 report both cross-sectional and prospective findings. No experimental studies with weight as an outcome were identified. There are 13 studies examining the association between sleep duration and weight in pediatric populations and 23 studies of adults.
Cross-sectional studies in children---Eleven studies were identified which assessed the cross-sectional association between sleep duration and weight in children (Table 1). All 11 works reported a positive association between short sleep duration and increased obesity. For the most part, obesity was defined by age-adjusted thresholds of BMI, which was directly measured, while sleep duration was typically obtained from questionnaires completed by parents. Because sleep requirements change through childhood, definitions of short sleep duration varied greatly based on the age of the cohort being studied.--The largest pediatric cohort to date is a Japanese birth cohort of 8,274 children assessed between the ages of 6 and 7 (ref. 7). Compared to children with a sleep duration of 10 h, the odds ratios (ORs) for obesity were 1.49, 1.89, and 2.89 for sleep durations of 9–10, 8–9, or <8 h, respectively. A study of 4,511 Portuguese school children aged 7–9 reported similar findings (8). Compared to a sleep duration of 11 h, the ORs for obesity were 2.27 and 2.56 for sleep durations of 9–10 and 8 h, respectively.----Two studies have analyzed data from children undergoing health screens at school enrollment. A study of 6,645 German children aged 5–6 years found the ORs for obesity were 1.18 and 2.22 for sleep durations of 10.5–11.0 and <10.5 h, respectively, compared to 11.5 h (9). A similar study of 1,031 French 5-year-olds found the OR for obesity was 1.4 for a sleep duration <11 h (10).---Three smaller studies have examined a broader range of grade school children. A study of 422 Canadian children ages 5–10 found that compared to a sleep duration of 12 h, the ORs for obesity were 1.42 and 3.45 for sleep durations of 10.5–11.5 and 10 h (11). Two small case–control studies of children aged 6–10 years, one from Brazil and one from Tunisia, reported similar findings. Giugliano and Carneiro reported obese children had 31 min shorter sleep duration than normal weight children but no significant difference was found between overweight and normal weight children (12). Ben Slama et al. found 58% of obese children had a sleep duration <8 h compared to only 11% of nonobese children (13).
Four studies have examined the relationship between sleep duration and weight in adolescents. Two of these studies, though small, were notable for using objective measures of sleep habits. Measuring sleep duration with wrist actigraphy over a 24-h period in 383 children aged 11–16, Gupta et al. reported one of the strongest associations between short sleep duration and obesity, with the odds of obesity increasing five-fold for every hour reduction in sleep duration (14). Benefice et al., using an accelerometer worn near the hip to assess sleep over 3–4 days in 40 Senegalese girls aged 13–14 years, observed that sleep duration was reduced by 6.85 min for every 1 kg/m2 increase in BMI (15). This work was notable for demonstrating a sleep–weight relationship in a nonobese population—mean BMI was only 16.9 kg/m2. The other adolescent reports included one of 4,486 American teens (mean age 16.6 years), which found short self-reported sleep duration predicted both higher BMI z-score and overweight among boys. However, no relationship was found in girls (16). A study of 656 Taiwanese teenagers (mean age 15.0 years) found that the frequency of obtaining a sleep duration of at least 6–8 h was inversely correlated with obesity risk (17).
The consistent findings from studies spanning five continents suggest that the reported associations are independent of ethnicity, though no formal assessment of effect modification by race has been reported. Several studies suggest boys may be more susceptible to sleep loss than girls. Sekine et al. found the OR for obesity associated with a sleep duration <8 h compared to >10 h was 5.5 in boys and 2.1 in girls (7). Similarly, Chaput et al. found that the OR for obesity associated with a sleep duration of 10 h as opposed to 12 h was 5.7 in boys and 3.2 in girls (11). Knutson found the risk of being overweight increased 10% for each hour reduction in sleep duration among boys, while no significant effect was found among girls (16). A few studies have attempted to identify the causal pathway linking sleep duration to obesity. Von Kries et al. found no relationship between sleep habits and caloric intake obtained from a food frequency questionnaire (9). Gupta et al., using actigraphy, and Benefice et al., using accelerometry to estimate activity levels, each found no relationship between sleep duration and physical activity (14,15).
Cross-sectional Studies in adults---Nineteen studies have focused on the cross-sectional relationship between sleep duration and weight in adults. The findings have been less consistent than the pediatric literature. Eleven studies reported a clear association between short sleep duration and increased weight, and two studies reported mixed findings with an association found in one gender but not in the other. Five studies reported no association between short sleep duration and increased weight, while one found short sleep duration was associated with reduced weight. In addition, six studies have found evidence that long sleep durations are also associated with increased weight resulting in a U-shaped curve between sleep duration and weight. In general, obesity has been defined as a BMI 30 kg/m2 based on either measured or self-reported height and weight. Habitual sleep duration has been typically obtained through questionnaire.----The largest studies reporting on the association between sleep duration and weight were designed as prospective cohort studies to examine the effects of a wide range of behaviors on health outcomes and were not specifically designed to study sleep duration (5,18,19,20). Furthermore, data on the cross-sectional association between sleep duration and weight in these cohorts were presented as part of analyses designed to assess sleep duration as a predictor of mortality and so focused on the potential of weight to confound the sleep–mortality association. As a result, only the marginal associations between sleep duration and BMI were computed. The largest of these studies was a survey by the American Cancer Society of over 1.1 million individuals (5). This study found a U-shaped association between sleep duration and BMI among women with the minimum at 7 h and a monotonic trend in men such that longer sleep durations were associated with a lower BMI. Comparing a sleep duration of 4–7 h, women had a 1.39 kg/m2 greater BMI and men had a 0.57 kg/m2 greater BMI. The next largest study was a Japanese cohort of over 100,000 individuals (19). This is the only study to find short sleep durations associated with reduced weight. Mean BMI in those with sleep durations 4, 5, 6, and 7 h were 22.2, 22.6, 22.9 and 22.7 kg/m2 for men and 22.6, 22.9, 22.9, and 22.9 kg/m2 for women. A second Japanese cohort of over 10,000 individuals found no association between sleep duration and weight (20). On the other hand, a Scottish study of 6,797 individuals found mean BMI was 0.3 kg/m2 greater among men with a sleep duration <7 h compared to 7–8 h (18). Two other studies considered weight as a secondary outcome. The Sleep Heart Health Study, in studying the association of sleep duration with hypertension, found a U-shaped association between sleep duration and weight with BMI 0.7 and 0.4 kg/m2 greater in those with sleep durations <6 and 6–7 h compared to 7–8 h (21). A Swedish study of sleep duration and diabetes found sleep duration was inversely correlated with both BMI (r = -0.06) and waist-to-hip ratio (r = -0.08) (ref. 22).
Two studies using population-based sampling techniques have directly assessed the relationship between short sleep duration and obesity in middle-aged populations. The larger studied 3,158 adults and found an inverse association between sleep duration and obesity with a minimum risk associated with a sleep duration of 8–9 h (23). Compared to this group, the ORs for obesity were 1.85, 1.49, 1.24, and 1.09 for sleep durations 5, 5–6, 6–7, and 7–8 h. A second study of 1,772 Spanish subjects found a similar association with the odds of obesity 39% greater in those with a sleep duration of 6 h compared to a sleep duration of 7 h.
Several studies have examined the sleep–weight association in working populations. A survey of 4,878 Brazilian truck drivers found a sleep duration <8 h per day was associated with a 24% greater odds of obesity (24). Similarly, a survey of 4,793 Hong Kong union members found an inverse correlation between sleep duration and BMI (r = -0.037, P = 0.02) (ref. 25). This relationship was almost exclusively observed in men. In contrast, a French study of 3,127 workers found that while no association between sleep duration and weight was found in men, among women, those with a sleep duration of 6 h had a 0.63 kg/m2 greater mean BMI than those with longer sleep durations (26). In a study of 1,024 government workers in Wisconsin, a U-shaped association was found using sleep duration based on sleep diaries (27). In multivariate modeling, the minimum BMI corresponded to a sleep duration of 7.7 h. A cross-sectional study of 990 employed adults in Iowa found that BMI was 0.42 kg/m2 greater for each hour reduction in sleep duration (28).
Analysis of a Canadian family-based cohort supports the presence of a U-shaped relationship between sleep duration and obesity (29). The ORs for obesity were 1.63 and 1.51 in women with sleep durations of 5–6 and 9–10 h compared to 7–8 h. The corresponding values in men were 1.72 and 1.18. Similar associations were found between sleep duration and waist-to-hip ratio, body fat mass, and skinfold thicknesses.
Two reports have specifically examined the association between sleep duration and weight in geriatric cohorts. Both were designed to define normative sleep habits in the elderly and considered weight as a predictor of sleep duration. The first study recruited 8,091 individuals over the age of 55 from seven European nations (30). Obesity did not predict being in the lowest 5th percentile of sleep durations. A study of 1,026 French subjects over 60 found those with a BMI >27 kg/m2 were 3.6 times more likely to report nocturnal sleep duration in the lowest 5th percentile than those with BMI of 20–25 kg/m2 (31). However, the obese were also more likely to report daytime naps so that no association existed between total sleep duration and obesity.--Only one study of adults has examined the sleep–weight relationship using an objective measure of sleep duration. Lauderdale et al. investigated predictors of sleep duration in 669 individuals and used 72-h actigraphy to assess average sleep duration (32). In multivariate analysis, the study found a weak inverse correlation between sleep duration and BMI that was not statistically significant.---Two studies have examined the association between sleep habits and weight in clinic populations. Among 924 Americans attending a primary care clinic, sleep duration was longest in those with BMI <25 kg/m2 (33). In a study of 453 Japanese clinic patients, the odds of obesity was nearly double in those with a sleep duration <6 h (34).---Overall, the cross-sectional data in adults suggest short sleepers are heavier though the findings are much less consistent than the pediatric data. Several reports have noted a U-shaped association between sleep duration and weight in adults with the lowest BMI associated with a sleep duration of 7–8 h (5,21,27,29). If this relationship is truly U-shaped, studies that force a linear relationship in modeling the sleep–weight association would underestimate the true effect of short sleep duration and might explain the negative findings in some studies. Ethnic differences in susceptibility to sleep deprivation may also explain the disparate findings, as two of the three Japanese studies were negative. Although no study has directly examined differential susceptibility by ethnicity, several studies have noted that both obesity and sleep deprivation are more common among African Americans than whites (23,32). Findings on differences in gender susceptibility have been mixed. While several studies suggested a greater vulnerability in women (5,26,29,33), at least two reports found an association between short sleep duration and obesity existed only in men (18,25).---In terms of understanding the mechanism of any sleep–weight association, four of the studies finding an association between short sleep duration and obesity found this association could not be explained by differences in physical activity (18,26,29,35). In addition, one of the negative studies also found no relationship between sleep duration and physical activity (32). None of the studies assessed caloric intake. However, two studies examined biomarkers that may be relevant to appetite. Short sleep durations were associated with suppressed leptin levels in both the Quebec Family Study and the Wisconsin Sleep Cohort Study after adjusting for obesity (27,29). Short sleep durations were also associated with elevated ghrelin levels in the Wisconsin cohort (27).
Cell tower regulations frustrate homeowners Towers under 15 metres tall avoid municipal scrutiny
Cellular towers sprouting around Canadian churches
Cell tower in church parking lot draws ire of neighbours
Health Canada: Safety of cellphones and cellphone towers
Do you live near an unexpected cellphone tower?
Suburban cell tower woes4:30
Homeowners across Canada are discovering cellphone towers popping up in residential neighbourhoods that slip just under height regulations that would require the company to notify those living nearby. Oakville[U13] , Ont., resident Lisa Guglietti was in the midst of building her dream home when the mother of three noticed eight cellular network antennas strapped to the chimney of a Bell Canada building, a short distance from her son's bedroom. "We were surprised that we weren't notified," she said. "We asked some of the neighbours. None of the neighbours had any clue that these cellular antenna had been put up." Under federal regulations, cellphone companies must notify the municipality for towers at least 15 metres high, but many new installations are coming up short of the limit, at just 14.9 metres. Homeowners say the rule undermines their ability to weigh in on installations in the community. Though the antennas are an eyesore, Guglietti's primary concern is possible health effects. Experts disagree on the impact caused by cell towers. The International Agency for Research on Cancer classifies radiofrequency electromagnetic fields, which are emitted by wireless phones and cell towers, as a possible human carcinogen. Health Canada states that radiofrequency fields given off by cellphone towers are safe as long as the facility adheres to federal regulatory requirements limiting human exposure. In an email to CBC News, a Bell spokesperson wrote that all its sites, including the Oakville, Ont., one near Guglietti's house, "meet or exceed all federal safety and other operating requirements."
City councillor struggles with issue---In June, construction began on a 14.9-metre cellphone tower in a Barrie, Ont. neighbourhood that triggered a backlash over potential health concerns for those living across the street and students walking to nearby schools. "Telecommunications companies are able to come in and put these things basically wherever they want: as close to any residents, as close to any schools, and as close to any community centre they want," Barrie, Ont. city councillor John Brassard told CBC News. "Why not make it 14.99 metres?" he asked. Since the incident, the Barrie city councillor has begun working to change federal regulations to give Canadians a voice over the placement of cell towers in their neighbourhoods. "Authority and a large part of that decision making should be made by the municipality and in consultation with Industry Canada. Not just Industry Canada alone."
Government, company response---CBC News requested government data on the number of towers under 15 metres erected across Canada, but Industry Canada said the department doesn't keep a database of that information[U14] . In the last year, Ottawa has collected about $582 million in revenue from telecommunications companies rolling out their networks of cell towers[U15] . Industry Canada told CBC News that companies are required to consult with the municipality and public before installing antenna towers, unless the towers fall within a certain height. "Certain installations, including towers less than 15 metres, generally have minimal local impact and so may be excluded from municipal consultation," an Industry Canada spokesperson said in a written statement to CBC News. After discovering the cell antennas on the large brick building next door to her new house, Guglietti contacted the federal agency. An Industry Canada official responded in an email to Guglietti on June 8, 2012 that "given that the installation at the Bell central office building on Balsam Street complies with all procedural and technical requirements, Industry Canada is not in a position to order Bell to relocate the facility." Cell tower antennas were strapped to a chimney that was 13 metres away from the bedroom of Lisa Guglietti's son[U16] . (Angela Gilbert/CBC) Guglietti also contacted Bell Canada, which owns the building next door, and says she was initially told it would try to find an alternative location. However, the eight cell antennas remain attached to the chimney next door.
'Don't want to be a guinea pig' --The scientific uncertainty over the health impact of cellphone towers doesn't sit well with Guglietti. "I'm supposed to be OK with that?" asked Guglietti. "I'm supposed to have my son exposed to these frequencies day in and day out and I have to wait. Maybe in 10 years from now I'm going to find out, 'Oh yeah there is, there can be health hazards in living so close to a cell tower.' " "I don't want to be a guinea pig," said Guglietti. A Bell spokesperson said in an email to CBC News that cellphone towers are being installed to meet customer demand[U17] . Guglietti said she's certain other homeowners are dealing with similar concerns. If you have any information on this story, or other cellphone tower stories, please contact us at firstname.lastname@example.com. "I need to protect myself and I need to protect my family. I'm a mother and I'm sure anyone would do the same thing in our situation." If you have any information on this story, or other cellphone tower stories, please contact us at firstname.lastname@example.com.
Red wine and components flavonoids inhibit UGT2B17 in vitro.
Jenkinson C, Petroczi A, Naughton DP.
BACKGROUND: -The metabolism and excretion of the anabolic steroid testosterone occurs by glucuronidation to the conjugate testosterone glucuronide which is then excreted in urine. Alterations in UGT glucuronidation enzyme activity could alter the rate of testosterone excretion and thus its bioavailability. The aim of this study is to investigate if red wine, a common dietary substance, has an inhibitory effect on UGT2B17.
METHODS-Testosterone glucuronidation was assayed using human UGT2B17 supersomes with quantification of unglucuronidated testosterone over time using HPLC with DAD detection. The selected red wine was analysed using HPLC and the inhibitory effects of the wine and phenolic components were tested independently in a screening assay. Further analyses were conducted for the strongest inhibitors at physiologically relevant concentrations. Control experiments were conducted to determine the effects of the ethanol on UGT2B17.
RESULTS-Over the concentration range of 2 to 8% the red wine sample inhibited the glucuronidation of testosterone by up to 70% over 2 hours[U18] . The ethanol content had no significant effect. Three red wine phenolics, identified by HLPC analyses, also inhibited the enzyme by varying amounts in the order of quercetin (72%), caffeic acid (22%) and gallic acid (9%); using a ratio of phenolic: testosterone of 1:2.5. In contrast p-coumaric acid and chlorogenic acid had no effect on the UGT2B17. The most active phenolic was selected for a detailed study at physiologically relevant concentrations, and quercetin maintained inhibitory activity of 20% at 2 M despite a ten-fold excess of testosterone.
CONCLUSION-This study reports that in an in vitro supersome-based assay, the key steroid-metabolising enzyme UGT2B17 is inhibited by a number of phenolic dietary substances and therefore may reduce the rate of testosterone glucuronidation in vivo. These results highlight the potential interactions of a number of common dietary compounds on testosterone metabolism. Considering the variety of foodstuffs that contain flavonoids, it is feasible that diet can elevate levels of circulating testosterone through reduction in urinary excretion. These results warrant further investigation and extension to a human trial to delineate the health implications.
Rhodiola Protects HPG Axis during Exercise or Physical Work
[Salidroside protects the hypothalamic-pituitary-gonad axis of male rats undergoing negative psychological stress in experimental navigation and intensive exercise].
[Article in Chinese]
Wang Q, Wang J, Sun LJ, Hu LP, Li J, Shao JQ, Lu B, Wang YT, Wu B, Wang GH.
Source-Department of Endocrinology, Nanjing University School of Medicine/Nanjing General Hospital of Nanjing Military Region, Nanjing, 210002 Jiangsu, China.
OBJECTIVE-To study the effects of salidroside on the function and ultramicro-pathological change of the hypothalamic-pituitary-gonadal (HPG) axis of male rats in experimental navigation and intensive exercise.
METHODS-Six-week SD rats were randomized into 3 groups: non-stress control (NC, n = 10), training control (TC, n = 12) and salidroside treatment (ST, n = 12) group. Blood samples were collected from the NC rats that did not receive any stimulus after a 7-day intragastric administration of saline. The TC rats underwent a 10-day running training with increasing load on the treadmill followed by a 7-day intragastric administration of saline. The ST rats were subjected to the same process of running training as the TC group and received intragastric administration of salidroside. Then blood samples were immediately obtained and the levels of testosterone (T), corticosterone (CORT), adrenocorticotropic hormone (ACTH), luteinizing hormone (LH) and gonadotropin-releasing hormone (GnRH) measured by radioimmunoassay. The testis histopathology was observed by HE staining, and the ultrastructural changes of the pituitaries and testes investigated by electron microscopy.
RESULTS-The serum T level was significantly lower in the TC than in the NC group, but showed no significant difference between the ST and NC groups. HE staining revealed no significant difference in testis histopathology among the 3 groups. Ultramicro-pathology showed that the secretory granules of the pituitary cells were significantly reduced in the TC rats compared with the NC ones; the number of the granules significantly increased in the ST group compared with the TC rats; and mitochondrial swelling, increase of electron density and decrease/disappearance of mitochondrial cristae were observed in the Leydig cells of the TC rats. But no significant differences were found in the testicular cells between the ST and NC groups.
CONCLUSION-Negative psychological stress and intensive exercise can significantly suppress the function of the HPG axis in rats. Salidroside therapy has protective effect on the HPG axis.
Show Of the Month October 8 2012
Black Seed Plus Sarsparilla-Liver Protection
Recipe for making this decoction of Black seed and Smilax ( sarsaparilla )
Your filter specification- Drug Class~~Name- Mood Stabilizer
Your filter specification- Drug Class-Name- Antidepressant
Black Seed Plus Sarsparilla-Liver Protection
Modulation of apoptosis in human hepatocellular carcinoma (HepG2 cells) by a standardized herbal decoction of Nigella sativa seeds, Hemidesmus indicus roots and Smilax glabra rhizomes with anti- hepatocarcinogenic effects.
BMC Complement Altern Med. 2012;12:25
Authors: Samarakoon SR, Thabrew I, Galhena PB, Tennekoon KH
BACKGROUND: A standardized poly-herbal decoction of Nigella sativa seeds, Hemidesmus indicus roots and Smilax glabra rhizome[U19] s used traditionally in Sri Lanka for cancer therapy has been demonstrated previously, to have anti-hepatocarcinogenic potential. Cytotoxicity, antioxidant activity, anti-inflammatory activity, and up regulation of p53 and p21 activities are considered to be some of the possible mechanisms through which the above decoction may mediate its anti-hepatocarcinogenic action. The main aim of the present study was to determine whether apoptosis is also a major mechanism by which the decoction mediates its anti-hepatocarcinogenic action.
METHODS: Evaluation of apoptosis in HepG2 cells was carried out by (a) microscopic observations of cell morphology, (b) DNA fragmentation analysis, (c) activities of caspase 3 and 9, as well as by (d) analysis of the expression of pro-apoptotic (Bax) and anti-apoptotic (Bcl-2) proteins associated with cell death.
RESULTS: The results demonstrated that in HepG2 cells, the decoction can induce (a) DNA fragmentation and (b) characteristic morphological changes associated with apoptosis (nuclear condensation, membrane blebbing, nuclear fragmentation and apoptotic bodies). The decoction could also, in a time and dose dependent manner, up regulate the expression of the pro-apoptotic gene Bax and down regulate expression of anti-apoptotic Bcl-2 gene (as evident from RT-PCR analysis, immunohistochemistry and western blotting). Further, the decoction significantly (p < .001) enhanced the activities of caspase-3 and caspase-9 in a time and dose dependent manner.---CONCLUSIONS: Overall findings provide confirmatory evidence to demonstrate that the decoction may mediate its reported anti-hepatocarcinogenic effect, at least in part, through modulation of apoptosis.---PMID: 22458551 [PubMed - indexed for MEDLINE]
Recipe for making this decoction of Black seed and Smilax ( sarsaparilla)—take equal parts of each herb and boil them down to at least half of the volume of water you put in— I.E 2 pint down to 1 pint or less ( 500mls for the metric to 250 mls)—and then use small amounts 1-2 oz increments 4-5 times daily
Symptoms of chemtrail spraying
@ 20.08.10 – 19:05:47
We've covered this before on this blog but I believe that one way to put an end to this is to educate people how they are being poisoned. Who in their right mind wouldn't want spraying to cease once they realize their health is being compromised? So here's a new article and a few links to refresh everyone.
Chemtrails – Health Effects on the General Population
by Claude-Michel Prévost
Over the past ten years, through research and the personal accounts of many individuals, it has become readily apparent that the aluminum and barium salt mixtures, polymer fibers, toxic chemicals and biologicals sprayed in the atmosphere are the irritants that are either directly or indirectly responsible for health problems on the rise in the United States and elsewhere.
These toxic particulates are rapidly absorbed from the respiratory system and / or the gastrointestinal tract and are deposited in the lungs, muscles, and bone.
This illegal aerial spraying is producing atmospheric and ground conditions detrimental to human and animal health but favorable to the growth of harmful molds / fungus.
This overview is a partial list of health problems reported by private citizens to Chemtrail researchers.
1.Nose and lung bleeds (the latter including several reports from nursing homes of elderly dying from lung bleed outs, we believe being directly attributable to atmospheric aerosols);
2.Asthma and allergies;
3.Allergic bronchopulmonary aspergillosis (ABPA) (fungus on the lungs in both infants and adults),
4.Flu, Bronchitis and Pneumonia (in epidemic proportions, with doctors commenting to their patients on the many weeks it sometimes takes to improve and the lack of effective antibiotics to treat, including reports of pets having the flu, whole families being decimated), meningitis (inflammation / infection of the brain);
5.Upper respiratory symptoms (wheezing, dry cough), including Pulmonary Distress Syndrome (PDS) (in newborns, infants and adults alike), Sudden Infant Death (SIDS), and increased nationwide reports of the sudden death of athletes (reported in the news media as having possibly been attributable directly to air particulates / pollution);
6.Deaths from black mold; black or red mold on food crops (farmers reporting pH changes of soil and water), in buildings and ventilation systems (including school buildings);
7.Arthritis-like symptoms and muscular pain (young and old alike, sometimes crippling, and in pets);
8.Gastrointestinal distress (young and old alike, and in pets);
9.Bladder and yeast infections (includes bed wetting, not just in infants but adults);
10.Extreme fatigue (young and old alike);
11.Ringing of the ears, dizziness (increasingly reported immediately preceding or after a storm or weather system);
12.Eye problems – pink eye, blurred and deteriorating vision / nervous tics after exposure to the air outdoors;
13.Dry / cracking skin and lips, rashes, sores and fungal infections, aging of the skin;
14.Mental confusion / slow thinking and / or the feeling of mentally "being in a fog" (young and old alike, increasingly reported after actually being in heavy mists and fog banks);
15.Autoimmune disorders (Lupus, Crohn's, Addison's Disease, Rheumatoid Arthritis, etc.)
Note: Some of the above symptoms / illnesses can be related to other physical / environmental factors such as dehydration.)
by Remarkable-recovery.com
Aluminum Symptoms
Excessive amounts of aluminum can result in symptoms of poisoning. The symptoms include constipation, colic, loss of appetite, nausea, skin ailments, twitching of leg muscles, excessive perspiration, and loss of energy. People with aluminum poisoning should discontinue the use of aluminum cookware and the drinking of tap water. Small quantities of soluble salts of aluminum present in the blood causes slow form of poisoning characterized by motor paralysis and areas of local numbness, with fatty degeneration of kidney and liver. There are also anatomical changes in the nerve centres and symptoms of gastro intestinal inflammation.
In the last few years there has been much publicity about aluminum, as well as a tentative connection of aluminum to Alzheimer Disease. According to Dr. Terry L. Franks the clinical picture is clear that Alzheimers is concurrently involved with aluminum toxicity and he also believe it is the major contributing factor to Alzheimers. It will progressively worsen in North America in the coming year because of the pervasive use of aluminum. Aluminum has the tendency to freeze up or irritate nerve endings, producing spasm and contracture. When someone is going through aluminum detoxification can actually look like an advanced case of Alzheimers Disease.
Cooking utensils, antacids, baking powders, antiperspirants, some soft water, aluminum foils, concrete and process foods contain aluminum (table salt, cheese slices individually wrapped), bleached flour, fluoridated water increases leaching of aluminum.
How Aluminum Affects Health
Nervous system
In animal studies, aluminum blocks the action potential or electrical discharge of nerve cells, reducing nervous system activity. Aluminum also inhibits important enzymes in the brain (Na-K-ATPase and hexokinase). Aluminum may also inhibit uptake of important chemicals by nerve cells (dopamine, norepinephrine, and 5-hydroxytryptamine).
Behavioural Effects
Dementia resulting from kidney dialysis related to aluminum toxicity causes memory loss, loss of coordination, confusion and disorientation.
Symptoms of Aluminum Toxicity
Early symptoms of aluminum toxicity include: flatulence, headaches, colic, dryness of skin and mucous membranes, tendency for colds, burning pain in the head relieved by food, heartburn and an aversion to meat.
Later symptoms include paralytic muscular conditions, loss of memory and mental confusion. Other symtpoms may include:
Alzheimer's disease, amyotrophic lateral sclerosis, anaemia, haemolysis, leukocytosis, porphyra, colitis, dental cavities, dementia dialactica, hypo-parathyroidism, kidney dysfunction, neuromuscular disorder, osteomalacia, Parkinson's disease, ulcers.
Digestive system
Aluminum reduces intestinal activity, and by doing so can cause colic.
Treatmnet of Toxicity
Decreasing contact with and use of aluminum-containing substances will reduce intake and allow more aluminum to leave the body. Oral chelating agents will also help clear aluminum more rapidly. Calcium disodium edetate (EDTA) binds and clears aluminum from the body; this substance is fairly nontoxic and used as the agent for "chelation therapy,: an intravenous treatment used to pull metals such as lead from the body, and more recently used in the treatment of atherosclerosis and cardiovascular diseases.
Deferoxamine, an iron chelator, also binds aluminum. In a study with Alzheimer's patients, nearly 40 percent of the patients showed an improvement in symptoms with deferoxamine treatment. There is some evidence that intravenous chelation with EDTA helps Alzheimer's patients. More research is needed to evaluate aluminum's involvement with this disease. Recovery is excellent for removing heavy metals.
Vitamin C
Has been found to bind aluminum. The average dose, if the patient is relatively comfortable, is about six grams a day. Up to twelve grams is not excessive. The average time on an aluminum detoxification is three to four weeks.
The best way to prevent aluminum buildup is to avoid the sources of aluminum. Eliminating foods that have aluminum additives is probably healthier overall. Not using common table salt is a positive health step as well. Some tap waters contain aluminum, this can be checked. Avoiding aluminum cookware and replacing it with stainless steel, ceramic, or glass is a good idea. Blocking skin and sweat pores with aluminum anti-perspirants.
by Testcountry.org
The possibility of barium poisoning is a reality among people working in and living near heavy industrial sites such as chemical plants, factories that produce rubber products and other such places. That is because barium is one of the components used in manufacturing the products created in these plants.
However, because many of these products end up in ordinary households, it is also possible for a person who does not work in or live near an industrial plant to experience barium poisoning. Rat poison, for instance, contains barium compounds. Some fluorescent bulbs have coatings made from barium oxide. Fish caught in waters near industrial sites may have absorbed barium from the water.
Given the considerable probability of a person becoming afflicted with barium poisoning, how would you know for sure if you or someone living with you ingested barium at toxic levels? If you find yourself or someone living in your household with symptoms of barium poisoning, then you should act immediately.
What Is Barium?
In order to understand how serious barium poisoning is, we need first to understand what barium is in the first place. Barium is a heavy metal that naturally occurs in the environment. It is silvery white in appearance.
Barium is valuable in many industries that make use of heavy metal because it can remove traces of oxygen in some chemical compounds. It also increases the luster of glass. However, barium is explosive and can react violently when mixed with water. Also, it cannot be digested by the body; barium can be poisonous if the amount the body contains exceeds tolerable levels.
Symptoms of Barium Poisoning to Look For
When barium accumulates in the body, it usually affects the functions of the nervous system. Barium poisoning displays symptoms that are similar to flu, which is why it is not strange to find the condition misdiagnosed as flu. Common symptoms of barium poisoning include:
1. Muscle weakness and tremors
2. Difficulty in breathing
3. Stomach irritations accompanied by diarrhea
4. Anxiety
5. Cardiac irregularities such as abnormally high blood pressure and rapid heartbeat
6. Paralysis
What to Do in Case of Barium Poisoning
In case someone in your household has just ingested something that contains barium, the first thing you need to do is to induce him or her to vomit. This will get some of the barium out of the victim's system. You can also mix a tablespoon of Epsom salts (sodium sulfate or magnesium sulfate) with a glass of water and get the victim to drink it. Afterwards, you should bring the victim to the emergency room of the nearest hospital to make sure that he or she does not succumb to barium poisoning.
You can also prevent barium poisoning from happening in your home. For one, you should keep your rat poison or any other chemical substances in your house that contains barium out of reach of children. Make sure that you have labeled their containers properly.
You should also avoid eating fish that was caught near industrial sites and ascertain that the fish and seafood you eat does not contain barium or any other heavy metal. This will prevent you from accumulating barium in your system and suffer from barium poisoning later on.
[U1]East indian Sarsparilla-chinese Sarsparilla and Black seed-decoction would be a tea boiled down to a complete extract
[U2]The less healthy oils would be soy and vegetable and canola oils or anything hydrogenated---these are toxic and become more so when heated and literally cause Genetic damage to the body
[U3]This is outdated there is no such thing as good or bad cholesterol in fact this study shows that using these oils you're better at regulating any blood pressure issues
[U4]So for thos of you consuming a high carb starch type diet with sugar you are going to benefit the most from this
[U5]Possible diuretic
[U6]This is usually caused by pollutant fall outs that stimulate bacterial or fungal growth due to lack of oxygen anddd the consumption of foods with Disodium guaynalte and Disodium Inosinate—other places call this ribo rash as well
[U7]Chemtrails have been being dumped on us with bacterial and microbial ,fungal and virals of all kinds they are a genetic anomaly which can impact the system with skin lesions as well
[U8]Now if this is the case then you would have to consider what is activating them ---what is stimulating there growth-is it something from the air---is there pollutants specific causing this---remember 50 years ago this was not a common issue ---not until the atmospheres was completely polluted and now being chemtrailed
[U9]Inside---was it put there genetically in a lab---was it put there due to the genetics of our foods causing there DNA to alter and become a infection carrying mite?? Something to ponder
[U10]Planned attack?—"trigger"
[U11]A Trojan Horse---something like a virus on a cpu looks like one thing then releases something unwanted
[U12]Wonder if the increasing of HAARP and Chemtails have anything to do with this---or possibly a invading of our Planetary Space things doing things to take away our access to the planet ---
[U13]THIS IS WHY SO many people are not sleeping any more between the hours of 2-4 am the critical time of sleep and regeneration---this is in part one of the reason we are having a Obesity issue going on globally and the fact that the consumption or gmo's causing GE diseases
[U14]Very in efficient for a major Company of global Standing eh!!
[U15]Now is this not Hilarious---they know how to collect exactly X amount of dollars but cannot determine the number of cell towers because they do not keep an inventory soooo how do they determine the tax?? makes me want to hmmm
[U16]40 feet away
[U17]The question I ask with these kind of statements---what customer---who demanded it---it would appear there is a higher position clientele that seem to be able so supercede the will of the people—makes you ponder the thought of who would want to violate human rights and place a dangerous bit of technology in a residential area
[U18]Could improve the exercising-working or sex at home—both men and women have testosterone—males are 97% woman 3% it is ean essential hormone for Males in regard to brain –heart and muscle function and the reproductive system
[U19]East indian Sarsparilla-chinese Sarsparilla and Black seed-decoction would be a tea boiled down to a complete extract
Show of the Month October 12 2012
How to Self-Test for an Iodine Deficiency
List of factors that impairs thyroid function
Adrenal Support
Exploring many uses for topical iodine solution
Inactivation of human viruses by povidone-iodine in comparison with other antiseptics
How to Self-Test for an Iodine Deficiency
1. Dip a cotton ball into USP Tincture of Iodine.
2. Paint a 2 inch circle of iodine on your soft skin, like the inner part of your thigh or upper arm.
3. Wait. -- If the yellowish stain disappears in less than an 4 hours; it means your body is lacking crucial iodine and has soaked it up. If the stain remains for more than 4-8 hours, you iodine levels are fine.
Why check your iodine levels?---Low iodine levels can zap your energy and make you feel tired, edgy and worn out. Low iodine levels can even prevent you from getting a good night's sleep. Before you go to your doctor with complaints of tossing and turning all night, aches and pains, and just feeling "blah," you may want to perform this self-test.---Because the symptoms of an iodine deficiency are classically identical to so many other illnesses (like depression, stress, chronic fatigue, or fibromyalgia,) many doctors either misdiagnose it or miss it completely and tell you there is nothing wrong.
Why are iodine levels so important?--Low levels of iodine mean your thyroid may not be functioning properly. The thyroid needs iodine to function as it helps balance hormones, regulate heartbeats, stabilize cholesterol, maintain weight control, encourage muscle growth, keep menstrual cycles regular, provide energy, and even helps you keep a positive mental attitude.----Women are naturally prone to iodine deficiencies. That's because the thyroid gland in women is twice as large as in men -- so under normal circumstances, women need more iodine. However, when women are under stress, the need for iodine can double or triple. Yet the foods we eat contain less and less dietary iodine. For example, back in 1940, the typical American diet contained about 800 micrograms of iodine. By 1995, that amount plunged to just 135 micrograms. That's an 83% decline.----Two thirds of the body's iodine is found in the thyroid gland. One of the best ways to boost your iodine levels is to add seaweed -sea vegetables to your diet. Just one teaspoon of sea vegetables a day can help you regain normal iodine levels. Incorporating seafood and fish into your diet can also help[U1] . Other foods that contain iodine are eggs and dairy products, including milk, cheese and yogurt, onions, radishes[U2] , and watercress. Some foods, called goitrogens, should be omitted for awhile as they hinder iodine utilization. These included kale, cabbage, peanuts, soy flour, Brussels sprouts, cauliflower, broccoli, kohlrabi and turnips.---[U3] To reactivate the thyroid gland, tyrosine, iodine, zinc, copper and selenium are needed so make sure that foods containing these nutrients are included in your diet. However, if you have the immune system deficiency called Hashimoto's Thyroiditis, you should not supplement your diet with iodine as it may aggravate the condition.
List of factors that impairs thyroid function.
1. Aging linked to a gradual decline of both thyroid and adrenal hormones.
2. Alpha Lipoic Acid (does not affect everyone)
3. Alcohol
4. Chronic illness
5. Cigarette smoking
6. Diet factors. Soy products and cruciferous vegetables dose dependent (avoid large quantities). Studies in animals show soy impairs T4 to T3 conversion.
7. Drugs (Birth control pills, Lithium, Estrogens, Propranolol, Beta blockers, Dexamethasone, Methimazole and Propylthiouracil)
8. External radiation[U4]
9. Growth hormone deficiency
10. Heavy metal toxicity including mercury and lead, pesticides, sodium chloride as well as sodium fluoride in city water.
11. Hemochromatosis
12. High Stress
13. Low adrenal states
14. Malnutrition (mineral deficiencies) consumption of trans fats and hydrogenated fats and a lack of good fats monounsaturated avocados, olive oil, palm, omega 3.
15. Mineral and vitamin deficiencies (selenium, Vitamin A, B6 and B12)
16. Postoperative state
17. Physical trauma.
Besides the above list research views that in a state of hypothyroidism, hydrocortisone production and metabolism is usually low. Hypothyroidism can be established by chronic low basal body temperature as measured by the Barnes method upon rising. Thus a direct link has been established between subnormal thyroid and inadequate adrenal production of hormones.
Toxemia or the buildup of toxins in the body and an impairment of the detoxification pathways can be a major cause of impaired thyroid function. Link by link, the health of one organ affects the health of another. The liver, the organ through which most detoxification occurs, has the greatest burden of all.
Today, I reasonably estimate that due to toxins in the diet, air pollution and contaminants in the water we drink and electromagnetic pollution, that the combined effect contributes to overworked adrenal and subnormal thyroid activity in at least a third or more of the population in the United States.
Adrenal Support
Degeneration of the Adrenal Glands may occur as a symptom of Choline deficiency. [more info]
Vitamin A concentrates in the Adrenal Glands and may improve the function of the Adrenal Glands. references
Vitamin B5 may activate the Adrenal Glands and may "revive" exhausted Adrenal Glands.
Vitamin C is essential for the function of the Adrenal Glands - the Adrenal Glands (especially the Adrenal Medulla) contain approximately 30 mg of Vitamin C - the second highest concentration of Vitamin C of any component of the body.
Vitamin E concentrates in the Adrenal Glands (within the Adrenal Cortex). The Adrenal Glands contain 132 mcg of Vitamin E per gram).
Adrenal Extract may improve the function of the Adrenal Glands in persons with impaired Adrenal Gland function.
Tyrosine may relieve excessive stress on the Adrenal Glands
Pregnenolone production (from Cholesterol) occurs primarily in the Adrenal Glands (but is also produced in smaller quantities in other areas of the body, including the Liver, Brain, Skin and Retina of the Eye).
Could painting a circle of iodine solution on the skin daily help get rid of the candida albicans, parasites, HHV-6, herpes, hepatitis and multiple other bacterial, fungal, parasitic and viral infections including HIV?
Exploring many uses for topical iodine solution
Iodine for HIV - to directly kill the virus
Iodine to treat opportunistic infections in AIDS
Iodine for chronic Candidiasis, EBV and CMV
Iodine for viral hepatitis A, B, C and D
Iodine for HHV-6 infection
Iodine for parasites
Iodine for herpes
Iodine for strep and staff infections
Iodine for sore joints and arthritis
Iodine for rheumatism
Iodine for the flu
Iodine for a sore throat
Iodine for almost any bacterial, fungal, parasitic or viral infection that exists.
Iodine to increase the thyroid's production of thyroxin
Iodine to help restore normal body temperature
Iodine to prevent and treat metabolic syndrome (obesity, diabetes and heart disease)
Iodine is cheap, plentiful and safe to use.
Here is how to do iodine testing and use
1. Dip a cotton ball into USP Tincture of Iodine –Lugols will do as well
2. Paint a 2 inch circle of iodine on your soft skin, like the inner part of your thigh or upper arm.
3. Wait. -- If the yellowish stain disappears in less than an hour; it means your body is lacking crucial iodine and has soaked it up. If the stain remains for more than 4-8 hours, your iodine levels are fine.
Why check your iodine levels? ---Low iodine levels can zap your energy and make you feel tired, edgy and worn out. Low iodine levels can even prevent you from getting a good night's sleep. Before you go to your doctor with complaints of tossing and turning all night, aches and pains, and just feeling "blah," you may want to perform this self-test.
Because the symptoms of an iodine deficiency are classically identical to so many other illnesses (like depression, stress, chronic fatigue, or fibromyalgia,) many doctors either misdiagnose it or miss it completely and tell you there is nothing wrong. ---About 60% of all iodine in the human body is stored in the thyroid gland at the base of the neck. A Goiter, an enlargement of the thyroid gland, can occur when iodine deficiency is prolonged over a period of time. Iodine is the most important mineral used by the thyroid gland to produce thyroxin, a hormone that regulates the metabolic rate of energy production in the cells. ---Iodine deficiency and a resulting insufficient production of thyroxin is linked to a wide range of illness form chronic infection of all types including candidiasis, herpes, bacterial, fungal and viral infections. ---Table salt is iodized and is a source of iodine[U5] . However, excess sodium intake from salt consumption is a toxin and impairs the production of energy in the cells. Excess sodium intake is linked to metabolic syndrome including obesity, high blood pressure, heart disease and cancer. [U6] The best sources of iodine are from sea vegetables and seafood including ocean fish[U7] . Unfortunately, most people do not consume iodine rich foods on a daily basis. Low body temperature and long term chronic infections may be directly linked to a deficiency of iodine and an impaired thyroid function.
How much iodine to consume ----Why are iodine levels so important? Low levels of iodine mean your thyroid isn't functioning properly. The thyroid helps balance hormones, regulate heartbeats, stabilize cholesterol, maintain weight control, encourage muscle growth, keep menstrual cycles regular, provide energy, and even helps you keep a positive mental attitude. ---Women are naturally prone to iodine deficiencies. That's because the thyroid gland in women is twice as large as in men -- so under normal circumstances, women need more iodine. However, when women are under stress, the need for iodine can double or triple. Yet the foods we eat contain less and less dietary iodine. For example, back in 1940, the typical American diet contained about 800 micrograms of iodine. By 1995, that amount plunged to just 135 micrograms. That's an 83% decline. ----Two thirds of the body's iodine is found in the thyroid gland. One of the best ways to boost your iodine levels is to add seaweed sea vegetables to your diet. Just one teaspoon of sea vegetables a day can help you regain normal iodine levels[U8] . Incorporating seafood and fish into your diet can also help. Other foods that contain iodine are eggs and dairy products, including milk, cheese and yogurt, onions, and watercress. Some[U9] foods, called goitrogens, should be omitted for awhile as they hinder iodine utilization. These included kale, cabbage, peanuts, radishes, soy flour, Brussels sprouts, cauliflower, broccoli, kohlrabi and turnips. ----To reactivate the thyroid gland, tyrosine, iodine, zinc, copper and selenium are[U10] needed so make sure that foods containing these nutrients are included in your diet. ---Editor's note: The RDA of iodine is 150 mcg. That is just too little, in my opinion. Ideally, the average daily intake of iodine should be closer to 1000 mcg daily and higher than that for stress conditions that rapidly deplete iodine levels[U11] . Persons with systemic infections will need higher amount of iodine as this trace mineral will be rapidly bound to the infectious agents (bacterial, fungal or viral) in the process of destroying them thus leaving less iodine for the thyroid to pick up. While most people have an under active thyroid, a few people have an overactive thyroid but there is no research linking this to excess iodine intake.
Inactivation of human viruses by povidone-iodine in comparison with other antiseptics.
Kawana R, Kitamura T, Nakagomi O, Matsumoto I, Arita M, Yoshihara N, Yanagi K, Yamada A, Morita O, Yoshida Y, Furuya Y, Chiba S.
Dermatology . 1997;195 Suppl 2:29-35.
Morioka Yuuai General Hospital, Japan.
Inactivation of a range of viruses, such as adeno, mumps, rota-, polio- (types 1 and 3), coxsackie-, rhino-, herpes simplex, rubella, measles, influenza and human immunodeficiency viruses, by povidone-iodine (PVP-I) and other commercially available antiseptics in Japan was studied in accordance with the standardized protocol in vitro. In these experiments, antiseptics such as PVP-I solution, PVP-I gargle, PVP-I cream, chlorhexidine gluconate, alkyldiaminoethyl-glycine hydrochloride, benzalkonium chloride (BAC) and benzethonium chloride (BEC) were used. ----PVP-I was effective against all the virus species tested. PVP-I drug products, which were examined in these experiments, inactivated all the viruses within a short period of time. Rubella, measles, mumps viruses and HIV were sensitive to all of the antiseptics, and rotavirus was inactivated by BAC and BEC, while adeno-, polio- and rhinoviruses did not respond to the other antiseptics. PVP-I had a wider virucidal spectrum, covering both enveloped and nonenveloped viruses, than the other commercially available antiseptics.
Script of the Show October 15-2012
Inactivation of human immunodeficiency virus by Betadine products & chlorhexidine.
The action of three antiseptics/disinfectants against enveloped and non-enveloped viruses
Aloe + Bioflavonoid ( Pectin )
PARSLEY, THE NEW PREDNISONE--- Parsley- Antiinflammatory
Inactivation of human immunodeficiency virus by Betadine products & chlorhexidine.
Harbison MA, Hammer SM.
J Acquir Immune Defic Syndr . 1989;2(1):16-20.
Infectious Disease Section, New England Deaconess Hospital, Boston, Massachusetts.
Eleven povidone-iodine-containing products (Betadine) and chlorhexidine gluconate solution were tested for their ability to inactivate human immunodeficiency virus (HIV) in a cell culture system. All Betadine products completely inactivated the virus at povidone-iodine concentrations of greater than or equal to 0.5% (10- to 20-fold dilutions of stock) except for Betadine Lubricating Antiseptic Gel, which required 2.5% for efficacy (1:2 dilution).
The action of three antiseptics/disinfectants against enveloped and non-enveloped viruses.
Wood A, Payne D.
J Hosp Infect . 1998 Apr;38(4):283-95.
Results indicate that all products were effective in inactivating the enveloped viruses herpes simplex virus type 1 and human immunodeficiency virus type 1, whilst being ineffective in inactivating human coronavirusŠ..Four antiseptic/disinfectant solutions with chloroxylenol, benzalkonium chloride, cetrimide/chlorhexidine and povidone-iodine were also assessed for antiviral effect against human immunodeficiency virus in the presence of whole human blood. All four solutions proved to be effective within 1 min despite the cytotoxic nature of the compounds to the detection system. ---Note from Mark Konlee: A few years ago I talked with 2 persons from different parts of the country who have been on an unusual diet for several years with striking similarities and results. They ate no meat and ate seafood, fish and or sea vegetables daily for several years. They were also both HIV positive and non-progressors and neither person had used prescribed antiviral drugs for HIV. Could the iodine and other trace minerals in the seafood they consumed have had something to do with their status as non-progressors? Could eating sea vegetables and ocean fish daily help stop HIV
Andrew Goldsworthy July 2011
There is increasing evidence that wireless transmissions have biological effects, some of which are harmful, at levels that may be orders of magnitude below present safety guidelines. These guidelines were drawn up on the assumption that the radiation could only damage living tissues if it generated significant heat. It has since been shown that radiation at much lower levels has direct electrical effects. These are mainly on electrically charged cell membranes, where the low frequency pulses from the modulated microwaves make them vibrate and leak. This can give rise to many "modern illnesses" ranging from electromagnetic hypersensitivity to cancer and disorders of the immune system. The most dramatic increase in the incidence of autism due to damage to the developing brains of the fetus and young children. Modulated microwaves, such as those from cell phones, portable phones, WiFi, baby monitors and wireless smart meters are sources of potentially damaging radiation. The strength of the radiation appears to be less important than the duration and pattern of the exposure, with intermittent and repeated exposure being the most damaging. The strong regular transmissions from wireless smart meters are particularly harmful and more likely to lead to DNA damage, cancer and autism.
Sub-thermal effects of electromagnetic radiation.
There are thousands of scientific papers showing biological effects of non-ionizing electromagnetic radiation occurring well below the levels at which them can generate significant heat. Many of these have been reviewed at by expert scientist at www.bioinitiative.org and http://www.neilcherry.com/documents.php . They include harmful effects such as damage to DNA in living cells that can lead to cancer, loss of fertility, brain damage due to the disruption of the blood-brain barrier and neuronal hyperactivity leading to autism in children. Many of these effects can be attributed to the loss of structurally important calcium from cell membranes, which makes them leak. This can disrupt normal metabolism and also release DNase (which destroys DNA) from the internal structures (lysosomes) that normally recycle waste into the rest of the cell http://www.hese-project.org/hese-uk/en/papers/cell_phone_and_cell.pdf .
Prolonged and intermittent radiation causes more damage
The duration of the radiation seems to be more important than its strength, with the effects being cumulative as more and more cells are damaged. Interestingly, DNA damage from cell phone radiation is greater when the exposure is intermittent (5 minutes on, 10 minutes off) than when continuous (Diem et al 2005). This may be because the cells are constantly adapting and using energy to defend themselves; they drop their guard during the off period and are caught unawares when it goes on again. This constant switching uses more energy, which eventually leaves the cells less able to counteract the effects of the radiation.
Diem et al. (2005) also found that the effect on DNA damage was still greater if the microwaves were pulsed or modulated to carry information (modulation involves sudden stops and starts of the signal, which are even more damaging).
Smart meters, which operate 24/7 and radiate modulated microwaves intermittently, can therefore be expected to be particularly harmful to DNA.
Microwave radiation causes cancer
There is already evidence that heavy cell phone users are more prone to brain cancers. This has resulted in cell phones now being rated by the World Health Organisation as class 2B carcinogens. This rating may later be increased, since brain tumours normally take decades to develop and few people have been regularly using a cell phone for more than a single decade. Particularly worrying is the finding by Hardell and Carlberg (2009 ) that young people were about 5-times more likely to get brain cancer both from cordless and cell phones if they began using them before the age of 20. The regular transmissions from wireless smart meters can be expected to have much the same effect, with younger people being more at risk. This is possibly because their brain structure is still growing and developing and therefore more susceptible to damage leading to cancer.
The effect of microwaves on autism is far worse
The greatest damage from microwaves is when the brain is first developing in the foetus and the very young child, when it can lead to autism. Dr Dietrich Klinghardt has recently shown the relationship between microwaves and autism; a summary of his work can be found at http://electromagnetichealth.org/media-stories/#Autism .
What is autism?
Autism is in fact a group of life-long disorders (autistic spectrum disorders or ASD) caused by brain malfunctions and is associated with subtle changes in brain anatomy (see Amaral et al. 2008 for a review). The core symptoms are an inability to communicate adequately with others and include abnormal social behaviour, poor verbal and non-verbal communication, unusual and restricted interests, and persistent repetitive behaviour. There are also non-core symptoms, such as an increased risk of epileptic seizures, anxiety and mood disorders. ASD has a strong genetic component, occurs predominantly in males and tends to run in families.
Genetic ASD may be caused by calcium entering neurons
It has been hypothesised that some genetic forms of ASD can be accounted for by known mutations in the genes for ion channels that result in an increased background concentration of calcium in neurons. This would be expected to lead to neuronal hyperactivity, the formation of sometimes unnecessary and inappropriate synapses, which in turn can lead to ASD (Krey and Dolmetsch 2007).
Electromagnetic fields let calcium into neurons too
There has been a 60-fold increase in ASD in recent years, which cannot be accounted for by improvements in diagnostic methods and can only be explained by changes in the environment. This increase corresponds in time to the proliferation of mobile telecommunications, WiFi, and microwave ovens as well as extremely low frequency fields (ELF) from mains wiring and domestic appliances. We can now explain this in terms of electromagnetically-induced membrane leakage leading to brain hyperactivity and abnormal brain development.
Non-ionising radiation makes cell membranes leak
The first effect of non-ionising electromagnetic radiation is to generate small alternating voltages across the cell membranes, which destabilize them and make them leak. This can have all sorts of consequences as unwanted substances diffuse into and out of cells unhindered, and materials in different parts of the cell that are normally kept separate, become mixed.
Why weak fields are more damaging than strong ones
We have known since the work of Suzanne Bawin and her co-workers (Bawin et al. 1975) that modulated radio-frequency electromagnetic radiation that is far too weak to cause significant heating can nevertheless remove calcium ions (positively charged calcium atoms) from cell membranes in the brain. Later, Carl Blackman showed that this also occurs with extremely low frequency electromagnetic radiation (ELF) but only within one or more "amplitude windows", above and below which there is little or no effect (Blackman et al. 1982; Blackman 1990). A proposed molecular mechanism for this can be found in Goldsworthy (2010). In particular, it explains why weak electromagnetic fields can have a greater effect than strong ones and why prolonged exposure to weak fields (where cells are maintained in the unstable condition for longer) is potentially more damaging than relatively brief exposure to much stronger ones.
How calcium ions stabilize cell membranes
This loss of calcium is important because calcium ions bind to and stabilize the negatively charged membranes of living cells. They sit between the negatively charged components of the cell membrane and bind them together rather like mortar binds together the bricks in a wall. Loss of just some of these calcium ions destabilize the membrane and make it more inclined to leak, which can have serious metabolic consequences. Among these are the effects of membrane leakage on the neurons of the brain.
How membrane leakage affects neurons
Neurons transmit information between one another in the form of chemical neurotransmitters that pass across the synapses where they make contact. However, the release of these is normally triggered by a brief pulse of calcium entering the cell. If the membrane is leaky due to electromagnetic exposure, it will already have a high internal calcium concentration as calcium leaks in from the much higher concentration outside. The effect of this is to put the cells into hair-trigger mode so that they are more likely to release neurotransmitters and the brain as a whole may become hyperactive (Beason and Semm 2002; Krey and Dolmetsch 2007, Volkow et al. 2011). This may not be a good thing since the brain may become overloaded leading to a loss of concentration and what we now call attention deficit hyperactive disorder (ADHD).
How does this impact on autism?
Before and just after its birth, a child's brain is essentially a blank canvas, and it goes through an intense period of learning to become aware of the significance of all of its new sensory inputs, e.g. to recognise its mother's face, her expressions and eventually other people and their relationship to him/her (Hawley & Gunner 2000). During this process, the neurons in the brain make countless new connections, the patterns of which store what the child has learnt. However, after a matter of months, connections that are rarely used are pruned automatically (Huttenlocher & Dabholkar 1997) so that those that remain are hard-wired into the child's psyche. The production of too many and often spurious signals due to electromagnetic exposure during this period will generate frequent random connections, which will also not be pruned, even though they may not make sense. It may be significant that autistic children tend to have slightly larger heads, possibly to accommodate unpruned neurons (Hill & Frith 2003).
Because the pruning process in electromagnetically-exposed children may be more random, it could leave the child with a defective hard-wired mind-set for social interactions, which may then contribute to the various autistic spectrum disorders. These children are not necessarily unintelligent; they may even have more brain cells than the rest of us and some may actually be savants. They may just be held back from having a normal life by a deficiency in the dedicated hard-wired neural networks needed for efficient communication.
Autism and the economy
The incidence of autism has increased 60-fold, in parallel with the increase in electromagnetic pollution over the last thirty years. The chance of having an autistic child may now be as high as one in fifty. Apart from the personal tragedies for the affected children and their families, autism is of enormous economic importance. In the UK alone, the annual cost to the Nation in care and lost production exceeds the annual tax revenue from the entire mobile phone industry, which is about 20billion UK pounds. http://www2.lse.ac.uk/newsAndMedia/news/archives/2009/05/MartinKnappAutism.aspx In theory the Government could close down the entire mobile phone industry and actually show a profit!
There are ways in which the modulation of the signal can be changed to avoid this, but in the meantime, the compulsory introduction of smart meters can only contribute further to autism on a grand scale. This will be a further burden on the economy and increase the National deficit. This will far outweigh any possible advantages from the use of these meters.
There is also a risk of legal complications for the utility companies. If it can be shown that that the consumer has taken reasonable precautions to minimise their microwave exposure by eliminating WiFi, cordless phones and wireless baby monitors from their house, the utility company could be held legally responsible for any autistic children that they may have.
In the UK, the lifetime cost of caring for an autistic child is in the region of one million pounds. It would be reasonable to claim compensation for this amount. In the United States, it may also be possible to claim punitive damages if it can be shown that the utility company knew of this risk when they installed or refused to remove a smart meter when requested.
Dr Andrew Goldsworthy
Lecturer in Biology (retired)
Imperial College London
Amaral DG, Schumann CM, Nordahl CW (2008), Neuroanatomy of Autism, Trends in Neurosciences 31: 137-145
Bawin SM, Kaczmarek KL, Adey WR (1975), Effects of modulated VHF fields on the central nervous system. Ann NY Acad Sci 247: 74-81
Beason RC, Semm P (2002), Responses of neurons to an amplitude modulated microwave stimulus. Neuroscience Letters 333: 175-178
Blackman CF (1990), ELF effects on calcium homeostasis. In: Wilson BW, Stevens RG, Anderson LE (eds) Extremely Low Frequency Electromagnetic Fields: the Question of Cancer. Battelle Press, Columbus, Ohio, pp 189-208
Blackman CF, Benane SG, Kinney LS, House DE, Joines WT (1982), Effects of ELF fields on calcium-ion efflux from brain tissue in vitro. Radiation Research 92: 510-520
Diem E, Schwarz C, Adlkofer F, Jahn O, Rudiger H (2005). Non-thermal DNA breakage by mobile-phone radiation (1800 MHz) in human fibroblasts and in transformed GFSH-R17 rat granulosa cells in vitro. Mutation Research 583: 178-183
Goldsworthy A (2010) , Witness Statement, http://mcs-america.org/june2010pg910111213141516.pdf
Hardell L, Carlberg M (2009), Mobile phones, cordless phones and the risk for brain tumours. Int J Oncology 35: 5-17 DOI: 10.3892/ijo_00000307
Hawley T, Gunner M (2000), How early experiences affect brain development. http://tinyurl.com/5u23ae
Hill EL, Frith U (2003), Understanding autism: insights from mind and brain. Phil Trans R Soc Lond B 358 281-289
Huttenlocher PR, Dabholkar AS (1997) Regional differences in synaptogenesis in human cerebral cortex. J Comparative Neurology 387 167-178
Krey JF, Dolmetsch RE (2007) Molecular mechanisms of autism: a possible role for Ca2+ signaling. Current Opinion in Neurobiology. 17: 112-119
Volkow ND, Tomasi D, Wang G, Vaska P, Fowler JS, Telang F, Alexoff D, Logan J, Wong C (2011), Effects of Cell Phone Radiofrequency Signal Exposure on Brain Glucose Metabolism. JAMA. 305 (8):808-813. doi: 10.1001/jama.2011.186
Aloe + Bioflavonoid ( Pectin )
Aloe vera in dermatology- a brief review.
Feily A, Namazi MR.
Source--Department of Dermatology, Jondishapur University of Medical Sciences, Ahvaz, Iran. email@example.com
Abstract---Aloe vera Linne or aloe barbadensis Miller is a succulent from the Aloe family (400 different species), a tropical plant which is easily grown in hot and dry climates and widely distributed in Asia, Africa and other tropical areas. The use of aloe vera is being promoted for a large variety of conditions. The aim of this systematic review was to summarize all dermatology-oriented in vitro and in vivo experiments and clinical trials on aloe vera preparations. Extensive literature search were carried out to identify all in vitro and in vivo studies as well as clinical trials on the subject. Data were extracted from these in a predefined standardized manner. Forty studies were located. The results suggest that oral administration of aloe vera in mice is effective on wound healing, can decrease the number and size of papillomas and reduce the incidence of tumors and leishmania parasitemia by >90% in the liver, spleen, and bone marrow. Topical application of aloe vera is not an effective prevention for radiation-induced injuries and has no sunburn or suntan protection. It can be effective for genital herpes, psoriasis, human papilloma virus, seborrheic dermatitis, aphthous stomatitis, xerosis, lichen planus, frostbite, burn, wound healing and inflammation. It can also be used as a biological vehicle and an anti-microbial and antifungal agent and also as a candidate for photodynamic therapy of some kinds of cancer. Even though there are some promising results with the use of aloe vera for diverse dermatologic conditions, clinical effectiveness of oral and topical aloe vera is not sufficiently and meticulously explored as yet.
Parsley has been used for years as a folk remedy for water retention, coughs, allergy, autoimmune, and chronic inflammatory disorders. Although it is one of the most potent disease-fighting plants little is known about how parsley works its magic….that is, until now. Recently, scientists set out to examine just one of the many wonders of parsley, its immune effects, in rigorous scientific detail. They looked at how parsley oil interacts with T-cells and B-cells (both types of white blood cells) and macrophages (cells that engulf and eliminate other cells). Conclusion: parsley oil acted in a similar way to drugs that suppress the immune system, like prednisone, but without the harmful side effects. As if that weren't enough, other studies have shown that parsley has antitumor, antibacterial, and antioxidant properties.
Karimi MH et al. "Parsley and immunomodulation." Expert Rev Clin Immunol. 2012 May;8(4):295-7. http://www.expert-reviews.com/doi/pdf/10.1586/eci.12.12
It is believed that parsley is one of the world's seven most potent disease-fighting spices [8]. Although parsley has been used to treat allergy, autoimmune and chronic inflammatory disorders, the mechanism underlying its beneficial effects in these immune-mediated diseases have been rarely investigated. Of the various therapeutically beneficial aspects of parsley, we decided to examine the immunomodulatory effects of this plant.
Parsley- Antiinflammatory
Throughout history, herbs have been utilized as an important constituent of foods, industry and folk medicine. One of the widely used vegetal species in various nations' medicine is parsley (Petroselinum crispum), which has remedial effects as a powerful diuretic agent [1,2], an abortifacient [3–5] and an expectorant [6,7]. Parsley is a native herb of the central Mediterranean region (southern Italy, Algeria and Tunisia), which is in the Apiaceae family, and is a species of Petroselinum [8]. It is believed that parsley is one of the world's seven most potent disease-fighting spices [8]. Although parsley has been used to treat allergy, autoimmune and chronic inflammatory disorders, the mechanism underlying its beneficial effects in these immune-mediated diseases have been rarely investigated. Of the various therapeutically beneficial aspects of parsley, we decided to examine the immunomodulatory effects of this plant. In our study, the effects of parsley essential oil on phytohemagglutinin (PHA)-stimulated splenocytes (T cells) and lipopolysaccharide (LPS)-stimulated B cells, as the main effector cells in adaptive immune system, was examined. In addition, the suppressive activity of different concentrations (0.01–100 μg/ml) of parsley essential oil on macrophages and LPS-stimulated macrophages for evaluation of nitric oxide (NO) was studied [9]. The methyl tetrazolium method was performed to survey the proliferation of mitogen-stimulated splenocytes as well as the viability of pretreated macrophages [9]. NO production of both macrophage groups was determined in the Griess reaction [9]. Parsley essential oil suppressed the proliferation of PHA-stimulated splenocytes at all applied concentrations. Similarly, it had a suppressive effect on the unstimulated and LPS-stimulated splenocytes, but only at high concentrations (10 and 100 μg/ml). NO production by unstimulated and stimulated macrophages was reduced by parsley essential oil; although, in all concentrations, unstimulated ones produced lower amounts of NO compared to the control group. These results can propose the suppressive effect of parsley essential oil on macrophages, as the major cells involved in the innate immune system [9].--The use of immunosuppressive drugs to control unwanted immune responses such as allergies, autoimmune disease and transplant rejection has grown over the past few years. The disadvantages and side effects of any immunosuppressive treatment are a significant and growing anxiety [10]. Some serious side effects including nephrotoxicity, hepatotoxicity, induction of diabetes, hypertension and neurotoxicity have been stated for various immunosuppressive drugs [10,11]. Thus, healthier and lower risk therapeutics are required. In this regard, more attention has been recently made on natural products. For example, the immunosuppressive activity of various herbal plants and ingredients including Achillea talagonica, [12] Plantago ovata [13], Boerhaavia diffusa [14], Stachys obtsicrena [15], Pollen Typhae [10] and Silymarin [16] has been explored. Parsley has also been shown to possess other biological activities than these described here. Several studies have suggested anticancer potential of parsley. By means of ascorbic acid‑induced lipid peroxidation, the antilipoperoxidant activity of parsley extracts has been shown [10,17,18]. The antioxidant activity of parsley essential oil has been confirmed in other investigations. Wong et al. indicated that the phenolic compounds of parsley were responsible for its antibacterial and antioxidant activity [19]. Zhang and his coworkers demonstrated the antioxidant activity of this herb in terms of b-carotene bleaching capacity and free radical scavenging activity [7]. This concept was then supported by further studies [20]. Parsley possesses several flavonoids such as apiin and luteolin, and its essential oil contains apiol and myristicin. These components are believed to be responsible for the therapeutic effects of parsley [17,21]. Kandaswami et al. indicated the direct and indirect effects of flavonoids on tumor cells. Their studies showed that the hydroxylation pattern of the B-ring of the flavons and flavonols, such as luteolin and quercetin, seemed to affect their angionesis and anticancer activity, especially the inhibition of protein kinase activity and antiproliferation [22]. Robak and his coworkers believe that flavonoids are the superoxide anion scavengers of the media and this effect can also lead to their anti-inflammatory effects [23]. Daly et al. observed bioactive phytochemicals, including carotenoids, in parsley [6]. Carotenoids were shown to be associated with a low risk of several human chronic disorders including age-related macular degeneration and certain cancers. Matching the wide use of this vegetal species as a diuretic in folk medicine, natriuretic and hypotensive effects of parsley were demonstrated in studies by Kreydiyyeh and Usta, and de Campos et al. [1,2]. Further studies indicated more biological effects of parsley plants, such as provitamine A activity, and influencing the cell signaling pathways [22,23]. In summary, parsley is a plant with various biological activities. With respect to its immunomodulatory effects, we found that its inhibitory effect on PHA-stimulated splenocytes might be due to the production of cytokines such as IFN-g and IL-2, which are vital for T-cell proliferation or it may influence the signaling pathways. Our results indicated that parsley essential oil can modulate the activity of macrophages without exerting cytotoxic effect. The immunomodulatory effect of parsley essential oil and its modulatory effects on NO production and function of macrophages may identify it as a useful natural candidate to treat some autoimmune and allergic diseases; however, its further application needs more investigation.
1 Kreydiyyeh SI, Usta J. Diuretic effect and mechanism of action of parsley. J. Ethnopharmacol. 79, 353–357 (2002).
2 de Campos KE, Balbi APC, De Freitas Alves MJQ. Diuretic and hypotensive activity of aqueous extract of parsley seeds (Petroselinum sativum Hoffm.) in rats. Braz. J. Pharmacog. 19(1A), 41–45 (2009).
3 Tyler VE. The Honest Herbalist (3rd Edition). Pharmaceutical Products Press, London, UK, 235–236 (1993).
4 Anderson LA, Newall CA, Phillipson JDA. Guide for Health-care Professionals. The Pharmaceutical Press, London, UK, 203–204 (1996).
5 Robbers JE, Tyler VE. Tyler's Herbs of Choice. The Therapeutic Use of Phytochemicals. Haworth Herbal Press, NY, USA, 92 (1999).
6 Daly T, Jiwan MA, O'Brein M, Aherne SA. Carotenoid content of commonly consumed herbs and assessment of their bioaccessibility using an in vitro digestion model. Plant. Foods Hum. Nutrit. 65(2), 164–169 (2010).
7 Zhang H, Chen F, Wang X, Yao HY. Evaluation of antioxidant activity of parsley (Petroselinum crispum) essential oil and identification of its antioxidant constituents. Food Res. Int. 39(8), 833–839 (2006).
8 Lopez MG, Sanchez-Mendoza IR, Ochoa-Alejo N. Compartive study of volatile components and fatty acids of plants and in-vitro cultures of parsley (Petroselinum crispum [Mill] nym ex hill). J. Agric. Food Chem. 47, 3292–3296 (1999).
9 Yousofi A, Daneshmandi S, Soleimani N, Bagheri K, Karimi MH. Immunomodulatory effect of Parsley (Petroselinum crispum) essential oil on immune cells: mitogen-activated splenocytes and peritoneal macrophages. Immunopharmacol. Immunotoxicol. 34(2), 303–308 (2012).
10 Vial T, Descotes J. Immunosuppressive drugs and cancer. Toxicology 185(3), 229–240 (2003).
11 Qin F, Sun HX. Immunosuppressive activity of pollen typhae ethanol extract on the immune responses in mice. J. Ethnopharmacol. 102, 424–429 (2005).
12 Rezaeipoor R, Saeidnia S, Kamalinejad M. Immunosuppressive activity of Achillea talagonica on humoral immune responses in experimental animals. J. Ethnopharmacol. 65, 273–276 (1999).
13 Rezaeipoor R, Saeidnia S, Kamalinejad M. The effect of Plantago ovata on humoral immune responses in experimental animals. J. Ethnopharmacol. 72, 283–286 (2000).
14 Mehrotra S, Mishra KP, Maurya R, Srimal RC, Singh VK. Immunomodulation by ethanolic extract of Boerhaavia diffusa roots. Int. Immunopharmacol. 2, 987–996 (2002).
15 Amirghofran Z, Bahmani M, Azadmehr A, Javidnia K. Immunomodulatory and apoptotic effects of Stachys obtusicrena on proliferative lymphocytes. Med. Sci. Monit. 13(6), BR145–BR150 (2007).
16 Gharagozloo M, Velardi E, Bruscoli S et al. Silymarin suppress CD4+ T cell activation and proliferation: effects on NF-kB activity and IL-2 production. Pharmacol. Res. 61(5), 405–409 (2010).
17 Mimica-Dukić N, Popović M. Apiaceae species. A promising sources of pharmacologically active compounds I: Petrosellinum crispum, Apium greveolens and Pastinaca sativa. In: Recent Progress in Medicinal Plants. Govil JN, Singh VK (Eds). Studium Press LLC, TX, USA (2007).
18 Fejes S, Blázovics A, Lemberkovics E, Petri G, Szöke E, Kéry A. Free radical scavenging and membrane protective effects of methanol extracts from Anthriscus cerefolium L. (Hoffm.) and Petroselinum crispum (Mill.) Nym. ex A. W. Hill. Phytother. Res. 14(5), 362–365 (2000).
19 Wong PYY, Kitts DD. Studies on the dual antioxidant and anti bacterial properties of parsley (Petroselinum crispum) and cilantro (Coriandrum sativum) extracts. Food Chem. 97, 505–515 (2006).
20 Kolarovic J, Popovic M, Zlinská J, Trivic S, Vojnovic M. Antioxidant activities of celery and parsley juices in rats treated with doxorubicin. Molecules 15, 6193–6204 (2010).
21 Lombaert GA, Siemens KH, Pellaers P, Mankotia M, Ng W. Furanocoumarins in celery and parsnips: method and multiyear Canadian survey. J. AOAC Int. 84, 1135–1143 (2001).
22 Kandaswami C, Lee LT, Lee PP et al. The antitumor activities of flavonoids. In Vivo 19(5), 895–909 (2005).
23 Robak J, Rys Z, Gryglewski J. Flavonoids are scavengers of super oxide anions. Biochem. Pharm. 37, 837–841 (1998)
[U1]Again this information is somewhat outdated—since mercury is in most fish consumed today it is arguably that the mercury can further diminish your low iodine levels—so again an alternative maybe eating grass fed beef which will have iodine in them based on the feed and without the mercury or seek other sources of aquatic life that may feed on seaweed to obtain the iodine
[U2]Radishes can be goiterogenic so again if you do consume them not often and should be utilizing seaweed or watercress with it
[U3]These are the goiterogenic goods
[U4]Smart Meter-Cell Phone—HAARP -Microwaves
[U5]A bad source---you would need to take 650grams -1 lb 7oz-to get the equivalent 1 drop of lugols
[U6]The key word is EXCESS!!
[U7]AGAIN this is only if the pollution is low and fish all has some form of arsenic and mercury so if you eat fish make sure that it is marinated properly with anti mercury substances—so that when being consumed the toxins are neutralized
[U8]Now this is where it gets tricky---it does not say how long it will take---but it gives the feeling or perspective that it will be quick---this IS NOT SO---it will be contingent on health---how much you are lacking---and what other complimentary minerals or aminos you may be missing as well
[U9]Other then Watercress the rest of the foods mentioned will be determined in there geographical areas which will determine how much is in the soil And how much is absorbed if any---the iodine that is
[U10]ACTIVATE the Thyroid
[U11]Even this is to low way to low-1000mcgs = 1mg the suggested daily dose is 13 mgs to sustain adequate levels---and use more depending on life style and exposure to environments
Show of the Month October 19-2012
Coffee Drinkers Have Lower Risk of Death- Study Suggests
Potato Storage- Essential Oils as Antigerminants
Top 10 Foods Highest in Potassium
EFSA publishes initial review on GM maize and herbicide study
Claims on many supplements don't comply with law, report says
Coffee Drinkers Have Lower Risk of Death- Study Suggests
A new study found that older adults who drank coffee -- caffeinated or decaffeinated -- had a lower risk of death overall than others who did not drink coffee.
ScienceDaily (May 19, 2012) — Older adults who drank coffee -- caffeinated or decaffeinated -- had a lower risk of death overall than others who did not drink coffee, according a study by researchers from the National Cancer Institute (NCI), part of the National Institutes of Health, and AARP.---Coffee drinkers were less likely to die from heart disease, respiratory disease, stroke, injuries and accidents, diabetes, and infections, although the association was not seen for cancer. These results from a large study of older adults were observed after adjustment for the effects of other risk factors on mortality, such as smoking and alcohol consumption. Researchers caution, however, that they can't be sure whether these associations mean that drinking coffee actually makes people live longer. The results of the study were published in the May 17, 2012 edition of the New England Journal of Medicine.---Neal Freedman, Ph.D., Division of Cancer Epidemiology and Genetics, NCI, and his colleagues examined the association between coffee drinking and risk of death in 400,000 U.S. men and women ages 50 to 71 who participated in the NIH-AARP Diet and Health Study. Information about coffee intake was collected once by questionnaire at study entry in 1995-1996. The participants were followed until the date they died or Dec. 31, 2008, whichever came first.---The researchers found that the association between coffee and reduction in risk of death increased with the amount of coffee consumed. Relative to men and women who did not drink coffee, those who consumed three or more cups of coffee per day had approximately a 10 percent lower risk of death. Coffee drinking was not associated with cancer mortality among women, but there was a slight and only marginally statistically significant association of heavier coffee intake with increased risk of cancer death among men.--"Coffee is one of the most widely consumed beverages in America, but the association between coffee consumption and risk of death has been unclear. We found coffee consumption to be associated with lower risk of death overall, and of death from a number of different causes," said Freedman. "Although we cannot infer a causal relationship between coffee drinking and lower risk of death, we believe these results do provide some reassurance that coffee drinking does not adversely affect health."---The investigators caution that coffee intake was assessed by self-report at a single time point and therefore might not reflect long-term patterns of intake. Also, information was not available on how the coffee was prepared (espresso, boiled, filtered, etc.); the researchers consider it possible that preparation methods may affect the levels of any protective components in coffee.---"The mechanism by which coffee protects against risk of death -- if indeed the finding reflects a causal relationship -- is not clear, because coffee contains more than 1,000 compounds that might potentially affect health," said Freedman. "The most studied compound is caffeine, although our findings were similar in those who reported the majority of their coffee intake to be caffeinated or decaffeinated."---Story Source-The above story is reprinted from materials provided by National Institutes of Health. --Journal Reference-Neal D. Freedman, Yikyung Park, Christian C. Abnet, Albert R. Hollenbeck, Rashmi Sinha. Association of Coffee Drinking with Total and Cause-Specific Mortality. New England Journal of Medicine, 2012; 366 (20): 1891 DOI: 10.1056/NEJMoa1112010
Potato Storage- Essential Oils as Antigerminants
ScienceDaily (Oct. 5, 2012) — One of the critical moments in the final quality of the potato occurs during its storage, as there exists the risk of sprouting or rotting due to pathogenic agents such as bacteria and fungi. In order to avoid this, agricultural engineer David Gómez Castillo carried out research for his PhD on the possibility of substituting the current use of chemical products by treating the tuber with essential oils of mint, caraway, coriander, eucalyptus and clove, "which have proved to be great potential inhibitors in the main problems detected."---The chemical product Clorprofam (CIPC) is the most commonly used as a sprout suppressant on stored potatoes. Nevertheless, possible reductions in permitted dosages, market and consumer pressures seeking healthier and, moreover, more environmentally-friendly products, have made it necessary to find alternatives to these synthetic products, with the market, culinary and technological quality of the potato remaining unaltered.---This is the context of the research by David Gómez Castillo, who has evaluated alternative treatment using essential oils of mint, caraway, coriander, eucalyptus and clove. In concrete, he studied the effect of applying these oils with table-stock varieties of the potato (Agata and Monalisa) and industrial ones (Agria and Kennebec), and compared the results thereof with those that had been treated chemically.
A good alternative---The research analysed two parameters: the commercial quality (germination, texture and colour of the tuber) and the culinary and technological quality (colour and texture of slices of the potato, dry material, total soluble solids, reductor sugars and sensorial analysis). Evaluations at 10, 25, 40, 55 and 70 days in storage were also undertaken, the antimicrobial effect of essential oils being assessed for the principal phytopathogens (fungi and bacteria).---According to Mr Gómez, "we found a high antigerminant capacity with treatment using the essential oil of coriander for industrial crops, and with the essential oil of mint for both industrial and table-stock crops. These showed great inhibitory potential on the principal phytopathogenic problems studied and all this makes a good alternative to CPIC use for storage of potatoes."---It was also shown that the essential oil of eucalyptus, for its high antigerminant capacity with table-stock potatoes, "could be another alternative for reducing post-harvest losses due to phytopathogenic problems, obtaining even better results if the treatment is accompanied by the essential oil of clove."--In the opinion of this researcher, the use of treatment with essential oils in the storage of potatoes "can provide added value in the application of antigerminant treatment, due to its efficacy in controlling the progress of important phytopathogens."---Story Source-The above story is reprinted from materials provided by Basque Research.
Recipe for AntiPhytopathegenic for Potato's---take either a combination of peppermint and coriander add 2 drops each to either a Sprayer with water---make sure the Essential oils are dispersed well in the water---blend in a blender for about 2 minutes to mix---once done then spray the potatoes being stored---or take a vaporiser and add the oils into the vaporiser and allow it to mist the air as well---this will cause the components to be air borne and will reduce the break down----this same principle can be done with other things as well or even utilize this principle to do a room or household to eliminate pathogens that might be airborne---keep the potatoes in a cool place for storage as well will reduce spoilage
Top 10 Foods Highest in Potassium
Potassium is an essential nutrient used to maintain fluid and electrolyte balance in the body. A deficiency in potassium causes fatigue, irritability, and hypertension (increased blood pressure). Overdose of potassium from natural sources is nearly impossible, however, it is possible to consume too much potassium via potassium salts which can lead to nausea, vomiting, and even heart attack. Potassium from natural food sources, like the ones listed below, are considered safe and healthy. The current percent daily value for potassium is a whopping 3.5 grams, below is a list of high potassium foods. For more foods high in potassium please see the lists of potassium rich foods, fruits high in potassium, and vegetables high in potassium.
#1: Dried Herbs
Long used for medicinal purposes, herbs are packed with nutrients and potassium is no exception. Dried Chervil contains the most potassium with 4.7g (135% DV) per 100g serving, or 95mg (3% DV) per tablespoon. It is followed by Dried Coriander (3% DV) per tblsp, Dried Parsley (2% DV), Dried Basil, Dried Dill, Dried Tarragon, Ground Turmeric, Saffron, and finally Dried Oregano with 50mg (1% DV).
Click to see complete nutrition facts
#2: Avocados
Avocados are great when made into guacamole or in a salad. 100 grams will provide 485mg of potassium or 14% of the DV. That is 1.1g (32% DV) in one cup pureed, and 975mg (28% DV) in a single avocado (201 grams).
Click to see complete nutrition facts || More Fruits High in Potassium
#3: Paprika and Red Chili Powder
Either paprika or red chili powder add a nice kick to any dish, and with all the potassium they provide you have good reason to start adding them. Paprika provides the most potassium with 2.3g (67% DV) per 100 gram serving, or 164mg (5% DV) per tablespoon. Chili powder will provide 1.9g (55% DV) per 100 gram serving or 153mg (4% DV) per tablespoon. Click to see complete nutrition facts
#4: Cocoa Powder and Chocolate
Dark chocolate is an excellent source of iron and zinc in addition to potassium. Pure cocoa powder without any fat, milk, or sugar, provides the most potassium with 1.5 grams (44% DV) in a 100g serving, or 1.3g (37% DV) per cup, and 76mg (2% DV) per tablespoon. Unsweetened baking chocolate provides 830mg (24% DV) per 100 gram serving or 241mg (7% DV) per square. Most sweetened milk chocolates will provide around 272mg (11% DV) per 100 gram serving, and 164mg (5% DV) per bar (1.5oz). Click to see complete nutrition facts
#5: Dried Apricots, Prunes, Zante Currants, and Raisins
Most common as a snack, dried apricots and prunes can also be chopped and served in a salad. A good source of fiber and many other vitamins, apricots provide 1.9g (53%DV) of potassium per 100g serving (about 20 dried apricots). Prunes provide 1g (30% DV) per 100g serving, or 1.4g (40% DV) per cup. Zante currants are really a type of grape and taste very similar to raisins. Zante currants provide 892mg (25% DV) of potassium per 100g serving, or 1.3g (37% DV) per cup. Raisins provide almost the same amount with 825mg (24% DV) per 100 gram serving, or 1.2g (24% DV) per cup. Click to see complete nutrition facts
#6: Pistachios and Other Nuts
Pistachios are a delicious snack, and a great addition to salads. 100 grams (~3/4cup) will provide 1g (30% DV) of potassium. Other nuts high in potassium include Beechnuts (29% DV per 100g), Ginko nuts (29% DV), Chestnuts (28% DV), Almonds (21% DV), Hazelnuts (19% DV), Cashews (18% DV), Pine nuts (17% DV), Coconuts (16% DV), and Walnuts (15% DV).
Click to see complete nutrition facts
#7: Seeds (Pumpkin, Squash, Sunflower, and Flax)
A popular food in the Middle East and East Asia pumpkin and squash seeds contain about 919mg (26% DV) of potassium per 100g serving, 588mg (17% DV) per cup. If you can't find these in your local supermarket you will surely find them in Middle Eastern or East Asian specialty stores. Alternatively, you can also save any pumpkin and squash seeds you have and roast them in your oven. The seeds are typically eaten by cracking the outer shell and eating the seed inside. Sunflower seeds are also a good source of potassium, providing 850mg (24% DV) per 100 gram serving, or 1.1g (31% DV) per cup. Flax seeds provide 813mg (23% DV) of potassium per 100 gram serving, or 1.4g (39% DV) per cup, and 81mg (2% DV) per tablespoon.
Click to see complete nutrition facts. Buy Pumpkin Seeds from Amazon.com
#8: Fish (Pompano, Salmon, Halibut, Tuna)
Fish has many health benefits and is a great source of potassium. Pompano provides the most with 636mg (18% DV) per 100 gram serving, or 540mg (15% DV) per fillet (3 ounces, 85 grams). It is followed by Salmon which provides 534mg (15% DV) per 3 ounce serving, Halibut, Yellow Fin Tuna, Lingcod, Mackerel, Anchovies, Herring, Cod, Snapper, Rockfish, Tilefish, Grouper, and finally Trout with 394mg (11% DV) in a 3 ounce serinvg. Cooking fish with dry heat is the best way to preseve the potassium content. Click to see complete nutrition facts
#9: Beans
White beans provide the most potassium with 561mg (16% DV) per 100 gram serving, 1g (29% DV) per cup cooked. White beans are followed by Adzuki Beans, Soy Beans, Lima Beans, Pinto Beans, Kidney Beans, Great Northern Beans, Navy Beans, Pigeon Peas, Cranberry (Roman) Beans, French Beans, Lentils, Split Peas, Black Beans, Hyancinth, and finally Yardlong Beans with 539mg (15% DV) per cup cooked.
Click to see complete nutrition facts
#10: Dates (Medjool)
Dates are great as a snack, as an addition to fruits salads, or even savory stews. Medjool dates provide 696mg (20% DV) per 100 gram serving, or 167mg (5% DV) in a single date.
Click to see complete nutrition facts
Read more at http://www.healthaliciousness.com/articles/food-sources-of-potassium.php#cTUeesXT5EcLhruM.99
EFSA publishes initial review on GM maize and herbicide study
The European Food Safety Authority has concluded that a recent paper raising concerns about the potential toxicity of genetically modified (GM) maize NK603 and of a herbicide containing glyphosate is of insufficient scientific quality to be considered as valid for risk assessment.---EFSA's initial review found that the design, reporting and analysis of the study, as outlined in the paper, are inadequate. To enable the fullest understanding of the study the Authority has invited authors Séralini et al to share key additional information.--Such shortcomings mean that EFSA is presently unable to regard the authors' conclusions as scientifically sound. The numerous issues relating to the design and methodology of the study as described in the paper mean that no conclusions can be made about the occurrence of tumours in the rats tested.---Therefore, based on the information published by the authors, EFSA does not see a need to re-examine its previous safety evaluation of maize NK603 nor to consider these findings in the ongoing assessment of glyphosate.---EFSA assessed the paper against recognised good scientific practices, such as internationally agreed study and reporting guidelines.----Per Bergman, who led EFSA's work, said: "Some may be surprised that EFSA's statement focuses on the methodology of this study rather than its outcomes; however, this goes to the very heart of the matter. When conducting a study it is crucial to ensure a proper framework is in place. Having clear objectives and the correct design and methodology create a solid base from which accurate data and valid conclusions can follow. Without these elements a study is unlikely to be reliable and valid."---The Director of Scientific Evaluation of Regulated Products added that the consideration of possible long-term effects of GMOs has been, and will continue to be, a key focus of EFSA's work to protect animals, humans and the environment.----EFSA's preliminary review issued today is the first step in a two-stage process. A second analysis will be delivered by the end of October 2012. This will take into account any additional information from the study authors, who will be given an opportunity to supply study documentation and procedures to the Authority to ensure the broadest possible understanding of their work. It will also include an overview of Member State assessments of the paper and an analysis from the German authorities responsible for the assessment of glyphosate.
Main findings of Initial Review---The task force, whose members were drawn from the Authority's GMO, pesticide and scientific assessment units, has outlined a list of issues about the paper that would need to be resolved before it could be viewed as well-conducted and properly-reported study.
- The strain of rat used in the two-year study is prone to developing tumours during their life expectancy of approximately two years. This means the observed frequency of tumours is influenced by the natural incidence of tumours typical of this strain, regardless of any treatment. This is neither taken into account nor discussed by the authors.
- The authors split the rats into 10 treatment sets but established only one control group. This meant there was no appropriate control for four sets – some 40% of the animals - all of whom were fed GM maize treated or not treated with a herbicide containing glyphosate.
- The paper has not complied with internationally-recognised standard methods – known as protocols - for setting up and carrying out experiments. Many of these procedures are developed by the OECD (Organisation for Economic Cooperation and Development).
- For a study of this type, the relevant OECD guideline specifies the need for a minimum of 50 rats per treatment group. Séralini et al used only 10 rodents per treatment set. The low number of animals used is insufficient to distinguish between the incidence of tumours due to chance rather than specific treatment effects.
- The authors have not stated any objectives, which are the questions a study is designed to answer. Research objectives define crucial factors such as the study design, correct sample size, and the statistical methods used to analyse data - all of which have a direct impact on the reliability of findings.
- No information is given about the composition of the food given to the rats, how it was stored or details of harmful substances – such as mycotoxins – that it might have contained.
- It is not possible to properly evaluate the exposure of the rats to the herbicide as intake is not clearly reported. The authors report only the application rate of the herbicide used to spray the plants and the concentration added to the rats' drinking water but report no details about the volume of the feed or water consumed.
- The paper does not employ a commonly-used statistical analysis method nor does it state if the method was specified prior to starting the study. The validity of the method used is queried and there are questions over the reporting of tumour incidence. Important data, such as a summary of drop outs and an estimation of unbiased treatment effects have not been included in the paper.
- Many endpoints – what is measured in the study – have not been reported in the paper. This includes relevant information on lesions, other than tumours, that were observed. EFSA has called on the authors to report all endpoints in the name of openness and transparency.
- Review of the Séralini et al. (2012) publication on a 2-year rodent feeding study with glyphosate formulations and GM maize NK603
- Letter to Prof. Séralini regarding EFSA's Review of the Séralini et al. (2012) publication on a 2-year rodent feeding trial with Glyphosate Formulations and GM maize NK603 as published online on 19 September 2012 in Food and Chemical Toxicology, 4 October 2012
Notes to editors:
EFSA set up a multi-disciplinary task force in response to an urgent request from the European Commission to evaluate a paper by Séralini et al to assess whether its findings could lead the Authority to reconsider its previous opinion on maize NK603. The two-year study, published in the journal Food and Chemical Toxicology on 19 September 2012, has suggested that consumption of the GM maize and a herbicide containing glyphosate at levels below officially-safe limits are linked to a reported increase in incidence of tumours in rats.
Claims on many supplements don't comply with law, report says
The structure function claims on many dietary supplement products do not comply with federal law,powers for FDA to bring products into compliance[U2] .---Industry sources reacted negatively to the assertion
that FDA needs new statutory powers, but were more accommodating on the report's suggestions on howthe claims notification process should be tightened up[U3] . The report, conducted by the Office of Inspector
General of the United States Department of Health and Human Services, looked at the claims on 127 dietary s
upplements in the weight loss and immune support The report looked at the label language and what kind
of evidence was cited to back up the claims, to judge compliance with FDA-mandated notifications and disclaimers
and to see how many claims trended over into prohibited disease claim territory. The report said that the
popularity of structure function claims is on the rise, and maintains that problems with the use
of these claims is on the rise, too. Report cites thin supporting evidence The report's broad conclusions
supplied by manufacturers in response to HHS requests, few appeared to satisfy FDA recommendationsin every respect in terms of study design and relevance to the meaning of the claim[U5] . It also found
that 20% of the supplements in the sample were making prohibited disease claims and that 7% lacked
the disclaimer that is supposed to accompany every structure function claim. The report went on to
recommend that FDA should seek additional statutory authority to regulate label claims to make sure
that suitable evidence exists to back up the claim, to make sure that proper label notifications arein place and to make sure companies are not making illegal disease claims In[U6] addition, it said FDA
needs to clean up its tracking of who is making what claims, and who has complied with the requirement of a 30-day
prior notification of the use of a claim on a product. Immediate reaction Report overreaches Reaction from trade
groups and industry observers was swift and decisive. The Office of Inspector General reviewed just 127 supplements
out of an estimated 29,000 products on the market. This small sample of supplements shouldn't smear the entire industry,
said John Shaw, executive director and CEO of the Natural Products Foundation. The president and CEO of the
organization, said, What's most disappointing is that this was not a random sampling [of the industry].The vast majority
of the industry, including our members, is doing the right thing. These reports give good companies a black eye,
he said.The small sample size and big conclusions also was an issue for Marc Ullman, who has worked with the
" Natural Products Foundation's Truth in Advertising industry self-regulation effort. They are recommended sweeping
changes to the law, the imposition of vast new regulatory burdens on FDA based on the fact that (a small number)
of dietary supplements didn't pass substantiation. To me it seems quite a reach, Ullman, an attorney with the New
York-based firm Ullman, Shapiro Ullman, told a reporter. I cannot fathom the kind of broad generalizations they
made based on this kind of sample size. Nuanced response to report's recommendations Regarding the recommendations,
Mister said CRN was very supportive of FDA to do more, especially when it came keeping better
track of health claim notifications, which companies are supposed to send in 30 days prior to a
product hitting the But the first recommendation, calling for FDA to 'statutory authority to review
substantiation for structure/function claims to determine whether they are truthful and notmisleading[U7] ,' is a non-starter, he said.This sounds like pre-market approval to us, Mister said. I do hope that
FDA sees that some of this is targeted towards them, he added. The agency needs to manage the information they
already have. Structure/function claims and registrations need to be catalogued to be accessible.The methodology
of the report divided up the supplements more or less equally between the weight loss and immune sectors, and
also about equally between supplements purchased in retail outlets on the Internet. This last detail interested Tony
Young, legal counsel for the American Herbal Products Association, especially in relation to the finding that 20% of
products were making disease claims. An interesting question would be whether those were products purchased off the
Internet or in retail stores. We expect that there is a higher standard out there to get products on retail shelves and
that most of the major retailers don't carry products that make that kind of claim, he said. No public health risk At
the end of the day, Young said, there is no imminent public health risk in the report's findings. Whether FDA should
expend substantial resources doing the kinds of things that were suggested is a decision that FDA would have to make
with regard to all of the other public health priorities," he said.The report might go overboard in its enforcement
recommendations, Ullman said, but that doesn't obviate legitimate questions about how some companies market their
products As an industry we need to recognize—and we do recognize—that there is a problem, he said, going on to cite NPF's
Truth in Advertising effort and CRN's cooperation with the "http://www.bbb.org/us/national-advertising-division/"
National Advertising Division as appropriate ways to self-police label claims.Everybody in our industry argues that there
should be more enforcement with respect to unlawful disease claims so there is pretty much unanimity on that,
[U1] A new attack on supplements
[U2]Drug Companies want to debilitate the industry further for easier acquisition of that health food industry market---where the owners will surrender there companies and sell out
[U3]This is the HFI-health food industry caving in and surrendering---the industry should be looking after itself without gov't interference---
[U4]This is the EFSA—european food and safe authority nonsence---this is the FDA compliance with the EFSA
[U5]Again EFSA
[U6]Gov't interference—again to debilitate the industry to a point where they either bail out or surrender---the health food industry as well a the consumers need to collaborate and get rid of the common enemy Gov't
[U7]Is this not the dumbest thing you ever heard? The wolf guarding the hen house---the industry is going to ask the gov't to monitor the competition??? What a deception here
[U8]This is really disappointing---the big players what the FDA to do there dirty work for them so they can eliminate all competition and have it all under 1 umbrella this is what is really going on a destruction of a free enterprise effect and everyone has to comply and the independent is going to either be absorbed or eliminated from the market
[U1]Smart Meter-Cell Phone—HAARP -Microwaves
[U2] A new attack on supplements
[U3]Drug Companies want to debilitate the industry further for easier acquisition of that health food industry market---where the owners will surrender there companies and sell out
[U4]This is the HFI-health food industry caving in and surrendering---the industry should be looking after itself without gov't interference---
[U5]This is the EFSA—european food and safe authority nonsence---this is the FDA compliance with the EFSA
[U6]Again EFSA
[U7]Gov't interference—again to debilitate the industry to a point where they either bail out or surrender---the health food industry as well a the consumers need to collaborate and get rid of the common enemy Gov't
[U8]Is this not the dumbest thing you ever heard? The wolf guarding the hen house---the industry is going to ask the gov't to monitor the competition??? What a deception here
[U9]This is really disappointing---the big players what the FDA to do there dirty work for them so they can eliminate all competition and have it all under 1 umbrella this is what is really going on a destruction of a free enterprise effect and everyone has to comply and the independent is going to either be absorbed or eliminated from the market
Show of the Month October 22-2012
Antioxidant May Prevent, Even Cure, Cataracts and Other Degenerative Eye Disorders
Caffeine May Block Inflammation Linked to Mild Cognitive Impairment
Cannabis Extract Eases Muscle Stiffness Typical of Multiple Sclerosis
Cannabis as Painkiller
Mushroom Compound Suppresses Prostate Tumors
Antioxidant May Prevent, Even Cure, Cataracts and Other Degenerative Eye Disorders
Cataract formation in rats. Top left (control lens): The lenses in this group were found to contain no detectable cataracts. (BSO-only lens): All lenses in this group developed very distinct cataracts, with most being nearly completely opaque (NACA-only lens): Results similar to those in the control group were obtained, with no detectable signs of cataract formation. (NACA+BSO lens): The lens depicted has a Grade 1 opacity which was evident by the amount of scattering light.
ScienceDaily (Oct. 9, 2012) — Researchers at Missouri University of Science and Technology are working with an antioxidant that could prevent or cure cataracts, macular degeneration and other degenerative eye disorders.---The research group, headed by Dr. Nuran Ercal, the Richard K. Vitek/Foundation for Chemical Research Endowed Chair in Biochemistry at Missouri S&T, is studying eye drops prepared with the antioxidant N-acetylcysteine amide (NACA) as a treatment for these eye conditions.--Ercal says NACA is an improvement over another experimental treatment, the antioxidant N-acetylcysteine (NAC), because it passes more easily across cell membranes, allowing the medication to be used in lower doses.--"NACA's characteristics as a drug were improved over NAC by neutralizing the carboxylic group of NAC, which makes the NACA pass cellular membranes easily," says Ercal. "And because NACA can be administered at a lower dose, the drug has a greater therapeutic index and lowers the risk of side effects traditionally associated with NAC.---"NACA is also an excellent source of glutathione, a cell's main antioxidant power, which is diminished during degenerative eye disorders," she adds.---Vision loss from age-related eye disorders affects more than 30 million people in the United States and is expected to double in the coming decades, Ercal says.---In addition, more than $9 billion is spent annually in the U.S. on cataract surgery alone. The total annual cost of all services related to vision problems exceeds $20 billion, she says.---"NACA eye drops could drastically reduce these costs and represent an alternative to costly surgery, while greatly improving the quality of life for those afflicted," says Ercal.---Ercal and her team have been testing NACA on HIV-related problems, lead poisoning and other toxicities for 10 years. About four years ago they began testing it on eye disorders.--Ercal recently received a $378,000 three-year research grant from the National Eye Institute of the National Institutes of Health. The preliminary data submitted for the funding was based on research by her former Ph.D. student, Joshua Carey.--Carey's dissertation involved preliminary studies of the effects of NACA to slow down cataract growth on rats that had been given L-buthionine-S,R-sulfoximine (BSO), a solution that causes cataracts to form. "The NACA solution prevented cataracts from forming," says Ercal. "Our research will build on Josh's research, to see if NACA can actually reverse the degeneration as well."---Ercal, who is also an M.D., says further testing will help establish appropriate dosage and frequency, as well as possible side effects and other factors. She says successful results using animal subjects may eventually support the viability of human usage.--Ercal works closely with Dr. Shakila Tobwala, a post-doctoral fellow in Missouri S&T's chemistry department. Others in the research group include the grant's co-investigator, Dr. Humeyra Karacal from the ophthalmology department at Washington University in St. Louis, and Missouri S&T graduate and undergraduate students.---Story Source-The above story is reprinted from materials provided by Missouri University of Science and Technology.
Caffeine May Block Inflammation Linked to Mild Cognitive Impairment
ScienceDaily (Oct. 8, 2012) — Recent studies have linked caffeine consumption to a reduced risk of Alzheimer's disease, and a new University of Illinois study may be able to explain how this happens.--"We have discovered a novel signal that activates the brain-based inflammation associated with neurodegenerative diseases, and caffeine appears to block its activity. This discovery may eventually lead to drugs that could reverse or inhibit mild cognitive impairment," said Gregory Freund, a professor in the U of I's College of Medicine and a member of the U of I's Division of Nutritional Sciences.---Freund's team examined the effects of caffeine on memory formation in two groups of mice -- one group given caffeine, the other receiving none. The two groups were then exposed to hypoxia, simulating what happens in the brain during an interruption of breathing or blood flow, and then allowed to recover.--The caffeine-treated mice recovered their ability to form a new memory 33 percent faster than the non-caffeine-treated mice. In fact, caffeine had the same anti-inflammatory effect as blocking IL-1 signaling. IL-1 is a critical player in the inflammation associated with many neurodegenerative diseases, he said.---"It's not surprising that the insult to the brain that the mice experienced would cause learning memory to be impaired. But how does that occur?" he wondered.---The scientists noted that the hypoxic episode triggered the release of adenosine by brain cells.--"Your cells are little powerhouses, and they run on a fuel called ATP that's made up of molecules of adenosine. When there's damage to a cell, adenosine is released," he said.--Just as gasoline leaking out of a tank poses a danger to everything around it, adenosine leaking out of a cell poses a danger to its environment, he noted.---The extracellular adenosine activates the enzyme caspase-1, which triggers production of the cytokine IL-1β, a critical player in inflammation, he said.---"But caffeine blocks all the activity of adenosine and inhibits caspase-1 and the inflammation that comes with it, limiting damage to the brain and protecting it from further injury," he added.---Caffeine's ability to block adenosine receptors has been linked to cognitive improvement in certain neurodegenerative diseases and as a protectant against Alzheimer's disease, he said.--"We feel that our foot is in the door now, and this research may lead to a way to reverse early cognitive impairment in the brain. We already have drugs that target certain adenosine receptors. Our work now is to determine which receptor is the most important and use a specific antagonist to that receptor," he said.--The study appears in the Journal of Neuroscience. Co-authors are Gabriel Chiu, Diptaman Chatterjee, Patrick Darmody, John Walsh, Daryl Meling, and Rodney Johnson, all of the U of I. Funding for the study was provided by the National Institutes of Health.--Story Source-The above story is reprinted from materials provided by University of Illinois College of Agricultural, Consumer and Environmental Sciences. The original article was written by Phyllis Picklesimer. -Journal Reference-G. S. Chiu, D. Chatterjee, P. T. Darmody, J. P. Walsh, D. D. Meling, R. W. Johnson, G. G. Freund. Hypoxia/Reoxygenation Impairs Memory Formation via Adenosine-Dependent Activation of Caspase 1. Journal of Neuroscience, 2012; 32 (40): 13945 DOI: 10.1523/JNEUROSCI.0704-12.2012
Cannabis Extract Eases Muscle Stiffness Typical of Multiple Sclerosis
ScienceDaily (Oct. 8, 2012) — Cannabis seems to ease the painful muscle stiffness typical of multiple sclerosis (MS), indicate phase III trial results, published in the Journal of Neurology Neurosurgery and Psychiatry.---Up to 90 per cent of MS patients endure painful muscle stiffness at some point during the course of their disease, which reduces their mobility and interferes with daily routine activities and sleep quality. But current treatments often fail to resolve symptoms fully, and can be harmful, as a result of which many MS patients have experimented with alternative therapies, including cannabis.---Adult MS patients with stable disease, from 22 different specialist centres across the UK, were either randomly assigned to cannabis extract (tetrahydrocannabinol) daily (144) or a dummy pill (placebo) (135) for a period of 12 weeks.---The treatments were given in gradually increasing doses from 2.5 mg up to a maximum of 25 mg for two weeks, followed by maintenance doses for the remaining 10 weeks. The aim was to see if cannabis extract alleviated or improved muscle stiffness, associated pain, muscle spasms, and sleep quality, using a validated 11 point rating scale. After the first two weeks of treatment, 87 per cent of those taking the placebo were on the maximum daily dose compared with just under half of those (47%) taking the cannabis extract.---After 12 weeks, one in four patients treated with cannabis extract was taking the maximum daily dose compared with over two thirds (69.4%) of those taking the placebo.---At the end of the study period, the rate of relief from muscle stiffness was twice as high among those given the cannabis extract as those given the placebo. Muscle stiffness was alleviated in just under 30 per cent of those given cannabis compared with just under 16 per cent of those treated with the placebo. This difference was evident after 4 and 8 weeks, and also extended to pain, muscle spasms and sleep quality, at all time points, the results showed. The differences were most noticeable among patients not already using antispasmodic treatment, among whom almost 40 per cent of those taking the cannabis extract gained relief compared with just over 16 per cent of those taking placebo. -The rate of side effects was higher among those taking the cannabis extract and highest during the first two weeks of treatment. Nervous system disorders and gut problems were the most commonly reported side effects, but none was severe.--The authors conclude that the results of their trial indicate that cannabis extract could be a useful treatment for the muscle problems typical of MS, and could provide effective pain relief, particularly for those in considerable pain. Story Source-The above story is reprinted from materials provided by BMJ-British Medical Journal. --Journal Reference-J. P. Zajicek, J. C. Hobart, A. Slade, D. Barnes, P. G. Mattison. MUltiple Sclerosis and Extract of Cannabis: results of the MUSEC trial. Journal of Neurology, Neurosurgery & Psychiatry, 2012; 83 (11): 1125 DOI: 10.1136/jnnp-2012-302468
Cannabis as Painkiller
ScienceDaily (Aug. 7, 2012) — Cannabis-based medications have been demonstrated to relieve pain. Cannabis medications can be used in patients whose symptoms are not adequately alleviated by conventional treatment. The indications are muscle spasms, nausea and vomiting as a result of chemotherapy, loss of appetite in HIV/Aids, and neuropathic pain.---This is the conclusion drawn by Franjo Grotenhermen and Kirsten Müller-Vahl in issue 29-30 of Deutsches Ärzteblatt International. --The clinical effect of the various cannabis-based medications rests primarily on activation of endogenous cannabinoid receptors. Consumption of therapeutic amounts by adults does not lead to irreversible cognitive impairment. The risk is much greater, however, in children and adolescents (particularly before puberty), even at therapeutic doses.---Over 100 controlled trials of the effects of cannabinoids in various indications have been carried out since 1975. The positive results have led to official licensing of cannabis-based medications in many countries. In Germany, a cannabis extract was approved in 2011 for treatment of spasticity in multiple sclerosis. In June 2012 the Federal Joint Committee (the highest decision-making body for the joint self-government of physicians, dentists, hospitals and health insurance funds in Germany) pronounced that the cannabis extract showed a slight additional benefit for this indication and granted a temporary license until 2015. Story Source-The above story is reprinted from materials provided by Deutsches Aerzteblatt International, via AlphaGalileo. --Journal Reference-Grotenhermen, F; Müller-Vahl, K. The Therapeutic Potential of Cannabis and Cannabinoids. Dtsch Arztebl Int, 2012; 109(29-30): 495-501 DOI: 10.3238/arztebl.2012.0495
Mushroom Compound Suppresses Prostate Tumors
ScienceDaily (May 24, 2011) — A mushroom used in Asia for its medicinal benefits has been found to be 100 per cent effective in suppressing prostate tumour development in mice during early trials, new Queensland University of Technology (QUT) research shows.--The compound, polysaccharopeptide (PSP), which is extracted from the 'turkey tail' mushroom, was found to target prostate cancer stem cells and suppress tumour formation in mice, according to an article written by senior research fellow Dr Patrick Ling in the online journal PLoS ONE, published by the Public Library of Science.--Dr Ling, from the Australian Prostate Cancer Research Centre-Queensland and Institute for Biomedical Health & Innovation (IHBI) at QUT, said the results could be an important step towards fighting a disease that kills 3,000 Australian men a year.--"The findings are quite significant," Dr Ling said.--"What we wanted to demonstrate was whether that compound could stop the development of prostate tumours in the first place.--"In the past, other inhibitors tested in research trials have been shown to be up to 70 per cent effective, but we're seeing 100 per cent of this tumour prevented from developing with PSP.--"Importantly, we did not see any side effects from the treatment."--Dr Ling said conventional therapies were only effective in targeting certain cancer cells, not cancer stem cells, which initiated cancer and caused the disease to progress.--During the research trial, which was done in collaboration with The University of Hong Kong and Provital Pty Ltd, transgenic mice that developed prostate tumours were fed PSP for 20 weeks.--Dr Ling said no tumours were found in any of the mice fed PSP, whereas mice not given the treatment developed prostate tumours. He said the research suggested that PSP treatment could completely inhibit prostate tumour formation.--"Our findings support that PSP may be a potent preventative agent against prostate cancer, possibly through targeting of the prostate cancer stem cell population," he said.b He said PSP had been previously shown to possess anti-cancer properties, and 'turkey tail' mushrooms (known as Coriolus versicolor or Yun-zhi) had been widely used in Asia for medicinal benefits.--However, Dr Ling said it was the first time it had been demonstrated that PSP had anti-cancer stem cell effects.--Although 'turkey tail' mushrooms had valuable health properties, Dr Ling said it would not be possible to get the same benefit his research showed from simply eating them.--A fundraiser has been organised in September to support further tests for the therapeutic potential of PSP against prostate tumours either alone or in combination with other anti-cancer compounds.---Story Source-The above story is reprinted from materials provided by Queensland University of Technology. --Journal Reference-Sze-Ue Luk, Terence Kin-Wah Lee, Ji Liu, Davy Tak-Wing Lee, Yung-Tuen Chiu, Stephanie Ma, Irene Oi-Lin Ng, Yong-Chuan Wong, Franky Leung Chan, Ming-Tat Ling. Chemopreventive Effect of PSP Through Targeting of Prostate Cancer Stem Cell-Like Population. PLoS ONE, 2011; 6 (5): e19804 DOI: 10.1371/journal.pone.0019804
Show Of The Month October 26 2012
Even Your Fat Cells Need Sleep
Prebiotic May Help Patients With Intestinal Failure Grow New and Better Gut
Special Note as to why not to Consume grains
Non-Medical Prescription Drug Use More Common Among Rural Teens Than City Dwellers
Research Reveals Decline in Illicit Drug Abuse- Prescription Drug Abuse On the Rise
Even Your Fat Cells Need Sleep
ScienceDaily (Oct. 15, 2012) — In a study that challenges the long-held notion that the primary function of sleep is to give rest to the brain, researchers have found that not getting enough shut-eye has a harmful impact on fat cells, reducing by 30 percent their ability to respond to insulin, a hormone that regulates energy.---Sleep deprivation has long been associated with impaired brain function, causing decreased alertness and reduced cognitive ability. The latest finding -- published by University of Chicago Medicine researchers in the Oct. 16 issue of the Annals of Internal Medicine -- is the first description of a molecular mechanism directly connecting sleep loss to the disruption of energy regulation in humans, a process that can lead over time to weight gain, diabetes and other health problems. The study suggests that sleep's role in energy metabolism is at least as important as it is in brain function.--"We found that fat cells need sleep to function properly," said study author Matthew Brady, PhD, associate professor of medicine and vice-chair of the Committee on Molecular Metabolism and Nutrition at the University of Chicago.----Brady said body fat plays an important role in humans.---"Many people think of fat as a problem, but it serves a vital function," he said. "Body fat, also known as adipose tissue, stores and releases energy. In storage mode, fat cells remove fatty acids and lipids from the circulation where they can damage other tissues. When fat cells cannot respond effectively to insulin, these lipids leach out into the circulation, leading to serious complications."--Esra Tasali, MD, assistant professor of medicine at the University of Chicago and co-senior author, led the recruitment of six men and one woman, all young, lean and healthy. Each volunteer went through two study conditions, at least four weeks apart. In one, they spent 8.5 hours a night in bed for four consecutive nights. In the other, they spent 4.5 hours in bed for four nights. Food intake, strictly controlled, was identical under both study conditions.---On the morning after the fourth night following both the long and short sleep conditions, each volunteer took an intravenous glucose tolerance test, which measures total-body insulin sensitivity. The researchers performed a biopsy, removing abdominal fat cells from the area near each volunteer's navel. Then they measured how these fat cells responded to insulin.---The researchers assessed insulin sensitivity at the molecular level by measuring the phosphorylation of a protein called Akt within fat cells. Akt phosphorylation is a crucial early chemical step in the cell's response to insulin.--After four nights of short sleep, total-body insulin response decreased by an average of 16 percent. The insulin sensitivity of fat cells decreased by 30 percent. This reduction is comparable to the difference between cells from obese vs. lean participants or from people with diabetes versus non-diabetic controls.---They found that the sleep-deprived study participants had a decreased response to a range of doses of insulin. It took nearly three times as much insulin to provoke half of the maximum Akt response in volunteers who had been deprived of sleep.
"Sleeping four to five hours a night, at least on work days, is now a common behavior" said study author and sleep specialist Esra Tasali.--"Some people claim they can tolerate the cognitive effects of routine sleep deprivation," said co-author Eve Van Cauter, PhD, the Frederick H. Rawson Professor of Medicine and director of the sleep, metabolism and health center at the University of Chicago. "In this small but thorough study, however, we found that seven out of seven subjects had a significant change in insulin sensitivity. They are not tolerating the metabolic consequences."---The study was one of the first to bring together sleep research experts and biologists focused on energy regulation and metabolism in adipose tissue. The impetus came from a sleep-research graduate student, Josiane Broussard, PhD '10, lead author of the study and now a Society in Science-Branco Weiss fellow at Cedars-Sinai Medical Center in Los Angeles. She wanted to combine her interest in sleep and metabolism with research at the molecular level.---So she pulled together a team for this project that included the two sleep researchers, Tasali and Van Cauter, plus two specialists from the University of Chicago Kovler Diabetes Center, David Ehrmann, MD, and Brady, who studies how insulin regulates energy storage in fat and liver cells.---They focused on fat cells because of their direct links to metabolic disruption and weight gain. These cells store energy for the body, are exquisitely sensitive to insulin and help regulate appetite.---Witnessing the direct effect of sleep deprivation on a peripheral tissue such as fat at the cellular level "was an eye-opener," Broussard said. It helps cement the link between sleep and diabetes and "suggests that we could use sleep like diet and exercise to prevent or treat this common disease[U1] ." Brady said the study opens up many new questions.--"What signals from sleep loss affect the fat cell? What effect does dysfunctional fat have at the whole-body level?" Brady wondered. "And if we can deprive healthy people of sleep and make them worse, can we take sick people, such as those with the common combination of sleep apnea, obesity and diabetes, improve their sleep and make them better? That's the missing link in the sleep-obesity-diabetes connection."--This study is "a valuable contribution to the understanding of the causal pathways by which reduced sleep duration may directly contribute to diabetes and obesity," according to an editorial in the journal by Francesco Cappuccio, MD, DSc, and Michelle Miller, PhD, of the University of Warwick, in Coventry, United Kingdom. "These results point to a much wider influence of sleep on bodily functions, including metabolism, adipose tissue, cardiovascular function, and possibly more."--The paper, "Impaired Insulin Signaling in Human Adipocyes," appears in the Oct. 16, 2012, issue of the Annals of Internal Medicine. Funding for this work was provided by the National Institutes of Health and Society in Science -- The Branco Weiss Fellowship.--Story Source-The above story is reprinted from materials provided by University of Chicago Medical Center, via Newswise. --Journal Reference-Josiane L. Broussard, David A. Ehrmann, Eve Van Cauter, Esra Tasali, Matthew J. Brady. Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction: A Randomized, Crossover Study. Annals of Internal Medicine, 2012; 157 (8): 549-557 [link]
Prebiotic May Help Patients With Intestinal Failure Grow New and Better Gut
ScienceDaily (Oct. 15, 2012) — Adding the right prebiotic to the diets of pediatric patients with intestinal failure could replace intravenous feeding, says a new University of Illinois study. "When we fed the carbohydrate fructooligosacharide (FOS) as a prebiotic, the gut grew and increased in function," said Kelly A. Tappenden, a U of I professor of nutrition and gastrointestinal physiology. "The study showed that using the correct pre- and probiotic in combination could enhance these results even more."--When FOS enters the intestines, bacteria convert it into butyrate, a short-chain fatty acid that increases the size of the gut and its ability to digest and absorb nutrients, she said[U2] .---But today's IV solutions don't contain butyrate and adding it would entail drug development trials and regulatory red tape. She wanted to see if adding this carbohydrate to the diet while continuing to provide most nutrients intravenously would cause the gut to start producing butyrate on its own. It worked According to Tappenden, at least 10,000 U.S. patients are totally reliant on intravenous feeding because their intestines have been surgically shortened. Many of these patients are premature infants who develop necrotizing enterocolitis, a kind of gangrene of the intestine. In the U.S., one in eight infants is a preemie, and removing necrotized, or dead, intestine is the most common surgical emergency in these babies. "Surgery saves their lives, but with so much intestine removed, they're unable to digest or absorb nutrients. These babies are also at risk for long-term complications, such as bone demineralization and liver failure. Our goal is to take kids who've had this resection and cause their gut to grow and adapt," she said.---She tested her hypothesis about butyrate using newborn piglets, an excellent model for the human infant in metabolism and physiology. Piglets with intestinal failure were assigned to one of four groups: a control group; a group whose diet contained FOS, a carbohydrate given as a prebiotic to stimulate the production of butyrate by beneficial bacteria; a probiotic, or actual live bacteria; and a combination of pre- and probiotics. -"We believed that bacteria in the gut would use the prebiotic to make butyrate and support intestinal growth. But we thought that might only happen in the group that received both pre- and probiotics because we didn't know if the newborn gut would have enough bacteria to make this important short-chain fatty acid." Actually, the neonatal piglets did have enough bacteria in their guts, and the prebiotic alone was effective in increasing intestinal function and structure, she said. "In fact, the probiotic that we used in one of the groups eliminated the beneficial effect of the prebiotic. That shows us that we need to be exceptionally careful in selecting the probiotic we use, matching it to the specific disease," she noted. Many consumers believe all probiotics are equal, but the effect of specific bacterial strains is different, she said. "At this point, we can only recommend consumption of the FOS[U3] prebiotic alone," she added.
The article appears in the September 2012 issue of the Journal of Parenteral and Enteral Nutrition. Jennifer L. Barnes of the U of I and Bolette Hartmann and Jens J. Holst of the University of Copenhagen, Copenhagen, Denmark, are co-authors of the study, which was funded by grants from the National Institutes of Health.---Journal References-J. L. Barnes, B. Hartmann, J. J. Holst, K. A. Tappenden. Intestinal Adaptation Is Stimulated by Partial Enteral Nutrition Supplemented With the Prebiotic Short-Chain Fructooligosaccharide in a Neonatal Intestinal Failure Piglet Model. Journal of Parenteral and Enteral Nutrition, 2012; 36 (5): 524 DOI: 10.1177/0148607112444131-K. A. Tappenden. Probiotics Are Not a One-Species-Fits-All Proposition. Journal of Parenteral and Enteral Nutrition, 2012; 36 (5): 496 DOI: 10.1177/0148607112458407
Special Note as to why not to Consume grains--- Amylose is the less easily digested component of Starch (only approximately 40% of dietary Amylose is digested via Amylase). Amylose that escapes digestion is known as Resistant Starch. Several factors influence the percentage of Amylose that escapes digestion--- The physical structure of the Grain protects the starch from digestion (e.g. partly milled grains and pulses). The larger the Grain size, the higher the amount of Resistant Starch.
- The natural chemical composition of the starch in foods influences the amount of resistant starch. The higher the Amylose content of Starch, the greater its resistance to digestion. Raw Potato, green Bananas, pulses and high amylose Maize starch have a high Amylose content.---When Starch is heated, Starch granules swell and are disrupted. This process, known as gelatinisation, makes the Starch much more accessible to digestive enzymes. Starch with a high Amylose content and Starch which is inaccessible due to the physical structure in which it is located, are less susceptible to gelatinisation and hence are more resistant to digestion.
- When Starch that has been heated, is cooled, retrogradation occurs converting the Starch to a crystalline form which is resistant to digestion. Foods, such as bread, cornflakes, cold cooked potato, rice and pasta, contain retrograded starch which is resistant to digestion.
Non Medical Prescription Drug Abuse-Substance Abuse From Doctors
Non-Medical Prescription Drug Use More Common Among Rural Teens Than City Dwellers
ScienceDaily (Nov. 2, 2010) — Rural teens appear more likely than their urban peers to use prescription drugs for non-medical purposes, according to a report posted online that will appear in the March 2011 print issue of Archives of Pediatrics & Adolescent Medicine, one of the JAMA/Archives journals.--The non-medical use of prescription drugs is common among U.S. adolescents, with about one in eight reporting lifetime non-medical use of prescription opioids, according to background information in the article. "During adolescence, non-medical prescription drug use is particularly problematic given its association with use of other illicit drugs such as cocaine and heroin, as well as engagement in problem behaviors such as gambling, increased sexual activity and impulsivity," the authors write. "Moreover, individuals who use prescription drugs earlier in life have a greater chance of later developing prescription drug dependence[U4] ." Previous studies have examined substance abuse among urban teens, but their conclusions may not apply to those from rural areas, the authors note. Jennifer R. Havens, Ph.D., M.P.H., of University of Kentucky College of Medicine, Lexington, and colleagues analyzed data from 17,872 12- to 17-year-olds participating in the 2008 National Survey on Drug Use and Health. Of these, 53.2 percent lived in urban areas, 51 percent were male and 59 percent were white.---There were no differences between urban and rural youth in rates of any illicit drug use, including marijuana, cocaine, heroin and hallucinogens. However, 13 percent of rural teens reported ever having used prescription drugs for non-medical purposes, compared with 10 percent of urban teens. When the researchers assessed specific medication types, they found rural teens were also more likely to have used pain relievers (11.5 percent vs. 10.3 percent) or tranquilizers (3.5 percent vs. 2.5 percent) non-medically[U5] . --After adjusting for sociodemographic factors, health status and the use of other substances, rural teens remained 26 percent more likely than urban adolescents to say they had used prescription drugs for non-medical purposes. "Data support that one reason for the higher prevalence of non-medical prescription drug use in rural areas may be the lack of availability of drugs such as heroin that are easily accessed in urban areas," the authors write.---Rural teens were more likely to misuse prescription drugs if they reported poorer health, episodes of depression or other substance abuse. "Residing in a household with two parents was associated with a 32 percent reduction in the odds of non-medical prescription drug use," the[U6] authors write. "These results suggest that interventions aimed at family involvement may be beneficial in preventing or reducing non-medical prescription drug use." Enrollment in school was also a protective factor.
"The cultural, structural and social realities of rural life can not only affect the prevalence of drug use but also exacerbate its consequences. The isolation and self-reliance of rural communities can negatively affect careseeking behavior, particularly regarding mental health and substance abuse services[U7] ," the authors write. "While we were able to identify potential targets for intervention such as increased access to health, mental health and substance abuse treatment, this may be difficult for rural areas where such resources are in short supply or non-existent. Research into the causal mechanisms surrounding initiation of non-medical prescription drug use in rural adolescents is necessary to develop tailored interventions for this population."--Story Source-The above story is reprinted from materials provided by JAMA and Archives Journals. ---Journal Reference-Jennifer R. Havens; April M. Young; Christopher E. Havens. Nonmedical Prescription Drug Use in a Nationally Representative Sample of Adolescents: Evidence of Greater Use Among Rural Adolescents. Archives of Pediatrics & Adolescent Medicine, 2010; DOI: 10.1001/archpediatrics.2010.217
Research Reveals Decline in Illicit Drug Abuse- Prescription Drug Abuse On the Rise
ScienceDaily (Oct. 15, 2012) — Research presented at the ANESTHESIOLOGY™ 2012 annual meeting showed while there has been an encouraging decline in illicit drug abuse across most major metropolitan areas in recent years, prescription drug abuse is climbing[U8] .--"Examining trends among various geographical areas, highlighting problem areas and possibly illuminating patterns that may remain otherwise hidden on a larger national level will help determine if we've stemmed the tide of prescription drug abuse or if a national epidemic has surfaced," said study author Asokumar Buvanendran M.D., Rush University Medical Center and Professor, Department of Anesthesiology, Chicago.---About the Study---Emergency department drug abuse-related visits were extracted from the Drug Abuse Warning Network (DAWN) over three years (2007-09) for 11 major metropolitan areas (plus a combined "other" category of various smaller regions). Two types of drug abuse visits were examined; those associated with prescription drugs (e.g., pain medications such as OxyContin®) and those associated with illicit "street" drugs (e.g., heroin, cocaine, etc).---In 2007, the percentage of emergency department visits identifying the involvement of illicit drug abuse (36 percent) was consistently higher than prescription drug abuse (20 percent) for all metro areas except the Phoenix region. Among the metropolitan areas, rates of illicit drug abuse varied in magnitude considerably more than prescription drug abuse. Prescription drug abuse rates were more consistent across metropolitan areas but still displayed a few spikes, with higher rates in Houston (33 percent) and Phoenix (27 percent).
Change over time from 2007-09, for illicit drug abuse, showed a consistent downward trend for all metro areas (8 percent overall), while prescription drug abuse rates over this same time period changed much less, showing a slightly increasing trend (2 percent) with some areas increasing while others decrease.--Overall, in the U.S. the percentage of visits for illicit drug abuse decreased (2007: 36 percent, 2008: 32 percent, 2009: 28 percent) while prescription drug abuse visits increased (2007: 20 percent, 2008: 21 percent, 2009: 22 percent) and the total number of "visits" were: 2007: 301,000; 2008: 352,000; and 2009: 280,000.--"The harsh reality is prescription drug abuse has become a growing problem in our society," said Dr. Buvanendran. "We hope the results of this study will aid physicians in effectively treating patients who struggle with prescription drug abuse, as well as encourage widespread patient education about the safe use, storage and disposal of medications."---Story Source-The above story is reprinted from materials provided by American Society of Anesthesiologists (ASA), via Newswise.
[U1]This is basically stating as well an over worked pancreas and liver---as a result of lack of sleep the other organs have to compensate for this excessive activity
[U2]Dietary Carbohydrates (especially Polysaccharides) are fermented (by Beneficial Bacteria) within the Large Intestine resulting in the manufacture of Butyric Acid: references
- Inulin may enhance the production of Butyric Acid in the Colon. references
- Of all Carbohydrates, Starch produces the greatest concentration of Butyric Acid: references
- The constituent of Starch that most contributes to the production of Butyric Acid is Amylose that escapes digestion (i.e. Resistant Starch). references
Fructooligosaccharides (FOS) (by nourishing Beneficial Bacteria in the Intestines which produce Butyric Acid) may facilitate the endogenous production of Butyric Acid in the digestive tract. references
Larch Arabinogalactan may stimulate the body's production of Butyric Acid. references
Psyllium may increase the production of Butyric Acid in the Intestines (especially in the Colon). This effect occurs from Beneficial Bacteria in the Intestines fermenting Psyllium. references
Acetic Acid may enhance the ability of Butyric Acid to stimulate the absorption of Calcium and Magnesium in the Colon. references
Beneficial Bacteria within the Large Intestine (especially the Colon) are responsible for the fermentation of dietary Carbohydrates that result in the production of Butyric Acid. references
Aspirin may enhances the ability of Butyric Acid to prevent Colon Cancer. references
Resveratrol may enhance the ability of Butyric Acid to prevent Colon Cancer. references
[U3]Chicory (root) Burdock
Vegetables: Leeks Onions
Tomatoes Garlic
Asparagus Jerusalem Artichoke
These foods will increase FOS
[U4]Now here's a thought—what if in early infancy when Teachers working indirectly for the "State" tell you your offspring need a drug-ritalin---as you can see it will lead to an addictive state later on in life---or perhaps a Birth Control pill to offset pregnancy and then later on in life your taking HRT pills to regulate what was shut down
[U5]This research is splitting hairs here –what we have is a stressed or taxed group of people –in this case Caucasians who are looking at these prescriptions to alleviate whatever they are dealing with and it would appear the access is easier to gain in the rural areas--
[U6]In other words a specific level of security in regards not only to access but to the persons stability
[U7]Isolation and the issues of rural living usually are not the issue it is the access ---the more connected a community is the less likely of this kind of behaviour---the less attached a person is or if there is any type of rejection or osterization then this may exacerbate the abuse
[U8]In other words No Real Decline at all –the access is now easier through Doctors
Show Of The Week October 29 2012
GM Crops Destroyed by US Drought but non-GM Varieties Flourish
6-shogaol-rich extract from ginger up-regulates the antioxidant defense
Effect of dietary polyphenols on K562 leukemia cells- a Foodomics approach-Rosemary
50 Reasons to Oppose Fluoridation
GM Crops Destroyed by US Drought but non-GM Varieties Flourish
Non-GM varieties are more drought resistant, yet agritech giants ensure farmers are unable to access them. Dr Eva Sirinathsinghji----The United States is suffering the worst drought in 50 years. But crop damage may well have been avoided if high quality non-GM varieties were available to farmers. Further evidence is emerging that glyphosate-tolerant crops are ill- equipped to deal with drought, while high quality non-GM varieties are flourishing. Monopoly of the seed industry has left farmers unable to get non-GM varieties, despite the drought having global repercussions including steep rises of cereal prices and reduced meat production in many countries. In a commentary circulated by GM Watch (UK), Howard Vlieger, a co-founder and agroecological farming advisor of Verity Farms in drought-stricken South Dakota the US, provides evidence from a farmer who has grown both GM and Verity Farms' non-GM varieties of soybean and corn side by side [1]. Non-GM soybean, grown in agroecological conditions to promote soil biodiversity and nutritional content is shown next to Monsanto's GM triple-stack GM corn, which is glyphosate- tolerant and additionally expresses two Bt insecticidal toxins, grown using conventional chemical industrial methods that include the use of Monsanto's glyphosate-based herbicide, Roundup (Figure 1). As captured in the photograph, non-GM varieties appear greener, fuller, and healthier. These impressions are backed up by the far superior yield reported of non-GM corn, which averaged 100- 120 bushels per acre (BPA) compared to the 8-12 BPA to 30-50 BPA of GM corn. -The large yield differential was confirmed in a new set of harvest data provided by Vlieger (with accompanying photographic identification) for three fields surrounding Verity Farm, all growing Smart Stack RR corn [2]. All were harvested for corn silage as the yields were too poor to harvest the grain. The federal crop insurance adjuster appraised yields were respectively 12 bushels per acre (BPA), 27 BPA, and 28 BPA. The Non-GMO corn on Verity Farm across the road yielded 108 BPA.---The findings were replicated with soybean crops
GM and non-GM soybean crops
Previous studies found glyphosate tolerant crops require more water-- Triple Stack RR corn may be especially drought intolerant, but the new evidence
from the farm is consistent with previous laboratory findings that glyphosate- treated crops are less water efficient than untreated crops. One such study was performed in Brazil when farmers reported "injured-looking" glyphosate-tolerant soybean crops. The team, led by Luis Zobiole from State University of Maringá found that GM glyphosate-tolerant (GT) soybeans absorbed less water, which resulted in reduced water efficiency [3]. The volume of water that non-treated GT soybean plants required to produce 1 g of dry biomass was 204 % and 152 % less than required when the plant is exposed to 2 400 grams acid equivalent (a.e) of glyphosate per hectare, in single or sequential applications
respectively. GT soybean plants receiving a single application of the currently
recommended rates of glyphosate (600–1200 grams a.e per hectare) needed 13–20% more water to produce the same amount of dry biomass than non-glyphosate treated plants. A previous publication by the same lab showed GT soybeans to have reduced lignin content and photosynthesis rates, both possible mechanisms for the reduced water efficiency [4]. Lignin is an essential component of plant cell walls, and contributes to the compression strength of stems and to the efficient transport of water and solutes over long distances within the vascular system. Water deficiency is not the only physiological effect that glyphosate imposes on crops. It has been shown to reduce nutrient availability and immune responses and thus defence against plant diseases (see [5] Glyphosate Tolerant Crops Bring Death and Disease, SiS 47). At least 40 diseases are known to be increased in weed control programmes with glyphosate and the list is growing, affecting a wide range of species: apples, bananas, barley, bean, canola, citrus, cotton, grape, melon, soybean, sugar beet, sugarcane, tomato and wheat [6]. Monopolisation of the seed industry
Contents of chemtrails jets have changed, it is now incl. plutonium
am hearing from all kind of friends who live in various parts of Europe that the contents from the Chemtrails what they used to spray on us has changed recently.
Some of my friends who have a Geiger counter are measuring INCREDIBLE high radiation quickly after those chemtrail planes flew over. This has never happened before that they measured radiation coming from the chemtrail jets a few minutes after they passed !! I have friends in FRANCE, UK, NETHERLANDS, GERMANY, SWITZERLAND. And they all measure these readings !!! This means that the globalist are misusing the situation from Japan and started to bombard the whole world with PLUTONIUM and[U1] such.... NOT BROUGHT BY THE WIND, BUT BY PLANES !!!!! Look at California I mean I just cannot believe that the Wind took this super high concentration of Radiation to this place. Also what I heard in the Netherlands, the radiation in the air is going sky high a few minutes after those chemtrail planes just did their spraying . So high that is almost comparable to measurements close to the area of Fukushima !!
People who I see walking on the streets in my neighborhood are coughing like crazy over here (area in FRANCE)
Yesterday I helped an old woman to get up, she just dropped on the street, she forgot to take her rollator she told me. While she just had in her hand for god sake, it was laying next to her !!! But she did not realize it......
6-shogaol-rich extract from ginger up-regulates the antioxidant defense systems in cells and mice.
Molecules. 2012;17(7):8037-55 Authors: Bak MJ, Ok S, Jun M, Jeong WS
Abstract---The rhizome of ginger (Zingiber officinale Roscoe) is known to have several bioactive compounds including gingerols and shogaols which possess beneficial health properties such as anti-inflammatory and chemopreventive effects. Based on recent observations that 6-shogaol may have more potent bioactivity than 6-gingerol, we obtained a 6-shogaol-rich extract from ginger and examined its effects on the nuclear factor E2-related factor2 (Nrf2)/antioxidant response element (ARE) pathway in vitro and in vivo. 6-Shogaol[U2] -rich extract was produced by extracting ginger powder with 95% ethanol at 80 °C after drying at 80 °C (GEE8080). GEE8080 contained over 6-fold more 6-shogaol compared to the room temperature extract (GEE80RT). In HepG2 cells, GEE8080 displayed much stronger inductions of ARE-reporter gene activity and Nrf2 expression than GEE80RT. GEE8080 stimulated phosphorylations of mitogen-activated protein kinases (MAPKs) such as ERK, JNK, and p38. Moreover, the GEE8080-induced expressions of Nrf2 and HO-1 were attenuated by treatments of SB202190 (a p38 specific inhibitor) and LY294002 (an Akt specific inhibitor). In a mouse model, the GEE8080 decreased the diethylnitrosamine (DEN)-mediated elevations of serum aspartate transaminase and alanine transaminase as well as the DEN-induced hepatic lipid peroxidation. Inductions of Nrf2 and HO-1 by GEE8080 were also confirmed in the mice. In addition, the administration of GEE8080 to the mice also restored the DEN-reduced activity and protein expression of hepatic antioxidant enzymes such as superoxide dismutase, glutathione peroxidase and catalase. In conclusion, GEE8080, a 6-shogaol-rich ginger extract, may enhance antioxidant defense mechanism through the induction of Nrf2 and HO-1 regulated by p38 MAPK and PI3k/Akt pathway in vitro and in vivo.---PMID: 22763741 [PubMed - indexed for MEDLINE]—
Recipe for ginger antioxidant -shogoal—either dehydrate ginger or buy the powder and add it to a alcohol base---if in the USA use ever clear—In Canada depending where you live utilize the polish version of everclear orr get a home made grappa---or buy a 90 proof if you can locate ( Canada has differering laws from province to province unfortunately in Ontario the gov't still feels the need to control the dose of alcohol and access)—what you would do is take this and extract it in the alcohol medium by utilizing a mason jar and the bottom of a blender attachment—seal the jar with a tape and then place the powder and alcohol inside and then twist the bottom of the jar and seal it and proceed to blend this at medium to high speed—for 10-15 minutes then stop the blender and strain off the powder ginger---be careful this will be hot—this will give you this in it's antioxidant levels at the rate they are explaining---if you cannot access the high alcohol then use the 40 or 50 proof it will still work but maybe 3 times stronger rather then 6 times
Effect of dietary polyphenols on K562 leukemia cells- a Foodomics approach-Rosemary
Electrophoresis. 2012 Aug;33(15):2314-27
Authors: Valdés A, Simó C, Ibáñez C, Rocamora-Reverte L, Ferragut JA, García-Cañas V, Cifuentes A
Abstract-- this work, a global Foodomics strategy has been applied to study the antiproliferative effect of dietary polyphenols from rosemary on two human leukemia lines, one showing a drug-sensitive phenotype (K562), and another exhibiting a drug-resistant phenotype (K562/R). To this aim, whole-transcriptome microarray together with an MS-based nontargeted analytical approach (via CE-TOF MS and UPLC-TOF MS) have been employed to carry out transcriptomics and metabolomics analyses, respectively. Functional enrichment analysis was done using ingenuity pathway analysis (IPA) software as a previous step for a reliable interpretation of transcriptomic and metabolomic profiles. Rosemary polyphenols altered the expression of approximately 1% of the genes covered by the whole transcriptome microarray in both leukemia cell lines. Overall, differences in the transcriptional induction of a number of genes encoding phase II detoxifying and antioxidant genes, as well as differences in the metabolic profiles observed in the two leukemia cell lines suggest that rosemary polyphenols may exert a differential chemopreventive effect in leukemia cells with different phenotypes. IPA predictions on transcription factor analysis highlighted inhibition of Myc transcription factor function by rosemary polyphenols, which may explain the observed antiproliferative effect of rosemary extract in the leukemia cells. Metabolomics analysis suggested that rosemary polyphenols affected differently the intracellular levels of some metabolites in two leukemia cell sublines. Integration of data obtained from transcriptomics and metabolomics platforms was attempted by overlaying datasets on canonical (defined) metabolic pathways using IPA software. This strategy enabled the identification of several differentially expressed genes in the metabolic pathways modulated by rosemary polyphenols providing more evidences on the effect of these compounds.---PMID: 22887152 [PubMed - indexed for MEDLINE]
[U1]I stated about a year ago that the chemtrails maybe different in different areas---it would appear I am right and with the newest dumping on the planet it will be used to heat and cause environmental imbalances we are see today
[U2]Shogaol is a antioxidant that comes from the dehydrated part of the ginger---gingerol comes from the fresh part this can be made with both but in this case they are explaining how to make this with the dry form