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
Abstract
BACKGROUND: A standardized poly-herbal decoction of Nigella sativa seeds, Hemidesmus indicus roots and Smilax glabra rhizome[U1]s used traditionally in Sri Lanka for cancer therapy has been demonstrated previously, to have anti-hepatocarcinogenic potential. Cytotoxicity, antioxidant activity, anti-inflammatory activity, and up regulation of p53 and p21 activities are considered to be some of the possible mechanisms through which the above decoction may mediate its anti-hepatocarcinogenic action. The main aim of the present study was to determine whether apoptosis is also a major mechanism by which the decoction mediates its anti-hepatocarcinogenic action.
METHODS: Evaluation of apoptosis in HepG2 cells was carried out by (a) microscopic observations of cell morphology, (b) DNA fragmentation analysis, (c) activities of caspase 3 and 9, as well as by (d) analysis of the expression of pro-apoptotic (Bax) and anti-apoptotic (Bcl-2) proteins associated with cell death.
RESULTS: The results demonstrated that in HepG2 cells, the decoction can induce (a) DNA fragmentation and (b) characteristic morphological changes associated with apoptosis (nuclear condensation, membrane blebbing, nuclear fragmentation and apoptotic bodies). The decoction could also, in a time and dose dependent manner, up regulate the expression of the pro-apoptotic gene Bax and down regulate expression of anti-apoptotic Bcl-2 gene (as evident from RT-PCR analysis, immunohistochemistry and western blotting). Further, the decoction significantly (p < .001) enhanced the activities of caspase-3 and caspase-9 in a time and dose dependent manner.—CONCLUSIONS: Overall findings provide confirmatory evidence to demonstrate that the decoction may mediate its reported anti-hepatocarcinogenic effect, at least in part, through modulation of apoptosis.—PMID: 22458551 [PubMed – indexed for MEDLINE]
Recipe for making this decoction of Black seed and Smilax ( sarsaparilla)—take equal parts of each herb and boil them down to at least half of the volume of water you put in— I.E 2 pint down to 1 pint or less ( 500mls for the metric to 250 mls)—and then use small amounts 1-2 oz increments 4-5 times daily
*************************************************************************
Sesame and Rice Bran Oil Lowers Blood Pressure, Improves Cholesterol
ScienceDaily (Sep. 18, 2012) — People who cooked with a blend of sesame and rice bran oils saw a significant drop in blood pressure and improved cholesterol levels, according to new research presented at the American Heart Association’s High Blood Pressure Research 2012 Scientific Sessions.—The researchers found cooking with a combination of these oils in a variety of ways worked nearly as well as a commonly prescribed high blood pressure medication, and that the use of the oil blend with medication yielded even more impressive results.—“Rice bran oil, like sesame oil, is low in saturated fat and appears to improve a patient’s cholesterol profile,” said Devarajan Sankar, M.D, Ph.D., a research scientist in the Department of Cardiovascular Disease at Fukuoka University Chikushi Hospital in Chikushino, Japan. “Additionally, it may reduce heart disease risk in other ways, including being a substitute for less healthy oils and fats in the diet[U2] .”–The 60-day study in New Delhi, India, divided 300 people with mild to moderately high blood pressure into three groups. One group was treated with a commonly used blood pressure lowering medication called a calcium-channel blocker (nifedipine). The second group was given the oil blend and told to use about an ounce each day in their meals.—The final group received the calcium channel blocker and the oil blend.—-All three groups, with approximately an equal number of men and women, average age of 57, saw drops in their systolic blood pressure. Systolic blood pressure is the top number in a blood pressure reading and measures the force of blood against your artery walls when the heart is pumping.—Systolic blood pressure dropped an average of 14 points for those using only the oil blend and 16 points for those taking medication. Those using both saw a 36-point drop.—Diastolic blood pressure also dropped significantly: 11 points for those eating the oil, 12 for those on medication and 24 for those using both. Diastolic blood pressure is the bottom number in a blood pressure reading that measures the force of blood against your artery walls when your heart is at rest between beats.—As for cholesterol, those using the oils saw a 26 percent drop in their LDL (“bad” cholesterol) and a 9.5 percent increase in the HDL (“good” cholesterol[U3] ), while no changes in cholesterol were observed for the patients who used only the calcium-channel blocker. Those who took the calcium channel blocker and the oils had a 27 percent drop in LDL levels and a 10.9 percent increase in the HDL[U4] . Healthier fatty acids and antioxidants, such as sesamin, sesamol, sesamolin and oryzanol, in the oil blends may be responsible for the results, Sankar said. These antioxidants, mono and poly unsaturated oils are compounds found in plants and have been linked with lower blood pressure and total cholesterol in earlier studies.–Additional studies are needed to determine if the oil blend is as beneficial as it seems. The combination was made specifically for this study, and there are no plans to market it commercially, Sankar said. Blending these oils yourself would not necessarily produce these effects.–Co-authors are.Ravinder Singh, M.B.B.S., and Biprabuddha Chatterjee, M.Sc.-Story Source-The above story is reprinted from materials provided by American Heart Association.
******************************************************************************
Chlorophyll revisited~~ anti-inflammatory activities of chlorophyll a and inhibition of expression of TNF-α gene by the same.
Inflammation. 2012 Jun;35(3):959-66
Authors: Subramoniam A, Asha VV, Nair SA, Sasidharan SP, Sureshkumar PK, Rajendran KN, Karunagaran D, Ramalingam K
Abstract–In view of the folklore use of green leaves to treat inflammation, the anti-inflammatory property of chlorophylls and their degradation products were studied. Chlorophyll a and pheophytin a (magnesium-free chlorophyll a) from fresh leaves showed potent anti-inflammatory activity against carrageenan-induced paw edema in mice and formalin-induced paw edema in rats.[U5] Chlorophyll a inhibited bacterial lipopolysaccharide-induced TNF-α (a pro-inflammatory cytokine) gene expression in HEK293 cells, but it did not influence the expression of inducible nitric acid synthase and cyclooxygenase-2 genes. Chlorophyll b only marginally inhibited both inflammation and TNF-α gene expression. But both chlorophyll a and chlorophyll b showed the same level of marginal inhibition on 12-O-tetradecanoyl-phorbol-13-acetate-induced NF-κB activation. Chlorophylls and pheophytins showed in vitro anti-oxidant activity. The study shows that chlorophyll a and its degradation products are valuable and abundantly available anti-inflammatory agents and promising for the development of phytomedicine or conventional medicine to treat inflammation and related diseases.—PMID: 22038065 [PubMed – indexed for MEDLINE]
**********************************************************************
Chlorophyll is a chemoprotein commonly known for its contribution to the green pigmentation in plants, and is related to protoheme, the red pigment of blood. It can be obtained from green leafy vegetables (broccoli, Brussel sprouts, cabbage, lettuce, and spinach), algae (Chlorella and Spirulina), wheat grass, and numerous herbs (alfalfa, damiana, nettle, and parsley).–Chlorophyll has been used traditionally to improve bad breath and other forms of body odor including odors of the urine, feces, and infected wounds. More recently chlorophyll has been used to aid in the removal of various toxins via the liver and remains a key compound for improving the function of essential detoxification pathways. Supportive evidence suggests it may be used as an anti-inflammatory agent for conditions, such as pancreatitis as well as exhibiting potent antioxidant and chemoprotective activities. Scientific research has demonstrated it may be an effective therapeutic agent in the treatment of herpes simplex, benign breast disease, chemoprevention, tuberculosis, and rheumatoid arthritis. Type 2 diabetes and obesity are also being explored as areas where chlorophyll can also be used.
***********************************************************************
Bacterial Cause Found for Skin Condition Rosacea
ScienceDaily (Aug. 28, 2012) — Scientists are closer to establishing a definitive bacterial cause for the skin condition rosacea. This will allow more targeted, effective treatments to be developed for sufferers, according to a review published in the Journal of Medical Microbiology.—Rosacea is a common dermatological condition that causes reddening and inflammation of the skin mostly around the cheeks, nose and chin. In severe cases skin lesions may form and lead to disfigurement[U6]. Rosacea affects around 3% of the population — usually fair-skinned females aged 30-50 and particularly those with weak immune systems. The condition is treated with a variety of antibiotics, even though there has never been a well-established bacterial cause.[U7]–A new review carried out by the National University of Ireland concludes that rosacea may be triggered by bacteria that live within tiny mites that reside in the skin.–The mite species Demodex folliculorum is worm-like in shape and usually lives harmlessly inside the pilosebaceous unit which surrounds hair follicles of the face. They are normal inhabitants of the face and increase in number with age and skin damage — for example, following exposure to sunlight. The numbers of Demodex mites living in the skin of rosacea patients is higher than in normal individuals[U8], which has previously suggested a possible role for the mites in initiating the condition.—More recently, the bacterium Bacillus oleronius was isolated from inside a Demodex mite[U9] and was found to produce molecules provoking an immune reaction in rosacea patients. Other studies have shown patients with varying types of rosacea react to the molecules produced by this bacterium — exposing it as a likely trigger for the condition. [U10]What’s more, this bacterium is sensitive to the antibiotics used to treat rosacea.—Dr Kevin Kavanagh who conducted the review explained, “The bacteria live in the digestive tracts of Demodex mites found on the face, in a mutually beneficial relationship. When the mites die, the bacteria are released and leak into surrounding skin tissues — triggering tissue degradation and inflammation.”[U11]—“Once the numbers of mites increase, so does the number of bacteria, making rosacea more likely to occur. Targeting these bacteria may be a useful way of treating and preventing this condition,” said Dr Kavanagh. “Alternatively we could look at controlling the population of Demodex mites in the face.. Some pharmaceutical companies are already developing therapies to do this, which represents a novel way of preventing and reversing rosacea, which can be painful and embarrassing for many people.”—-Story Source-The above story is reprinted from materials provided by Society for General Microbiology, via AlphaGalileo. —Journal Reference-Stanisław Jarmuda, Niamh O’Reilly, Ryszard Żaba, Oliwia Jakubowicz, Andrzej Szkaradkiewicz and Kevin Kavanagh. The potential role of Demodex folliculorum mites and bacteria in the induction of rosacea. Journal of Medical Microbiology, 2012 DOI: 10.1099/jmm.0.048090-0
TOP
**************************************************************************
TOP A
HOME
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 (srp20@case.edu)
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 greater than or equal to10 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 greater than or equal to11 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 greater than or equal to11.5 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 greater than or equal to12 h, the ORs for obesity were 1.42 and 3.45 for sleep durations of 10.5–11.5 and less than or equal to10 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 less than or equal to10 h as opposed to greater than or equal to12 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 greater than or equal to30 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 less than or equal to4, 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 less than or equal to5, 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 less than or equal to6 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 less than or equal to6 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 investigations@cbc.ca. “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 investigations@cbc.ca.
**************************************************************************
Red wine and components flavonoids inhibit UGT2B17 in vitro.
Jenkinson C, Petroczi A, Naughton DP.
Abstract
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.
TOPA
Tools of Light
