Si può desiderare di provare un trattamento naturale disfunzione erettile come un diverso per i problemi di costruzione. Al giorno d oggi ci sono diverse terapie sul mercato, ma un trattamento naturale disfunzione erettile è stato confermato qualche ora e ora di nuovo per dare risultati efficienti e permanenti. Cos è la disfunzione sessuale? L incapacità di sviluppare o sostenere una costruzione abbastanza lungo per fare l amore è chiamato disfunzione erettile, ED https://farmacia-senzaricetta.it/ o (maschio) problemi di erezione. Tutti gli uomini possono avere problemi di costruzione di volta in volta e gli scienziati considerano ED essere presenti se si verificano problemi di costruzione almeno il 25% del tempo. Alcuni fatti duri: ED Può essere dovuto a problemi emotivi. Stress, pressione, giltiness, depressione, bassa autostima e ansia prestazioni può essere la causa dei vostri problemi di costruzione. La ricerca ha confermato che il 90 per cento della disfunzione erettile è fisica in origine, non emotiva. L impotenza colpisce la maggior parte degli uomini durante la loro vita e può essere dovuto a troppo colesterolo, problemi cardiaci, diabete, ipertensione, fumo o alcol. Alcuni rimedi possono essere la ragione. Le questioni legate al movimento sono collegate. Se ti occupi dei tuoi problemi di movimento, hai piu possibilita di risolvere questo problema. Qui ci sono 5 consigli facili su come aumentare la circolazione: 1. Mangia i pasti giusti. Questo ti rendera il flusso sanguigno ovvio. Una grande parte di rimanere sani e anche mantenere il flusso sanguigno ovvio è legato al vostro piano di alimentazione quotidiana e quello che si mangia. Una buona cura per la disfunzione erettile è mangiare un piano a basso contenuto di grassi e grande alimentazione di fibre. Mangiare fibre tutti i giorni e questo viene scoperto in prodotti cerealicoli cereali integrali, frutta e verdura. Evitare il più possibile pasti pronti o pasti non sani. 2. Wonder herbal rimedi. Molti rimedi vegetali per ED eseguire bene come possono migliorare il movimento. Hanno molto meno reazioni avverse rispetto ai farmaci convenzionali e si svolgono in modo efficiente per migliorare hardons e la forza, troppo. Erbe naturali come Ginkgo Biloba sono utilizzati come una strategia per ED. Gli specialisti di erboristeria credono anche che le spezie o le erbe come noce moscata, portano al movimento intorno al corpo, tra cui il pene. 3. Vitamine naturali vitali. Gli scienziati sanitari hanno scoperto che una mancanza di supplemento è tipico tra gli uomini con ED in particolare vitamina A. Se si ha una mancanza del nutriente ossido di zinco, Questo è stato confermato per portare alla disfunzione erettile. Queste inadeguatezze derivano dal fatto che molti valori nutrizionali in quello che mangiamo piano non sono sufficienti. Aggiungere al vostro fabbisogno di nutrienti aumenterà la circolazione del sistema e migliorare questa condizione. Gli integratori alimentari sono completamente naturali, quindi non dovrete preoccuparvi dei rischi di reazioni avverse. Inoltre, queste vitamine naturali sono utili per il vostro benessere over-all. Oltre a questi vantaggi benessere, disfunzione erettile vitamine naturali e integratori costano molto meno di farmaci rimedi. 4. Esercitare. Fai una mossa e non un tablet vibrante. Camminare farà di più per migliorare e sostenere hardons di qualsiasi altra compressa chimica nel lungo periodo. Il fitness fisico manterrà bassi livelli di pressione e mantenere grandi stadi di movimento. Andando per un 20-30 minuti di movimento rapido ogni giorno, può affrontare questo problema e può sostenere la vostra libido senza l uso di qualsiasi farmaco. 5. Sottolineare. Questo è il peggior attaccante per problemi di erezione. Scopri diversi metodi per riposare. Alcuni metodi tipici per riposare includono la lettura di un libro, la meditazione, un bagno rilassante o allenamenti di respirazione. Sto solo imparando alcuni semplici allenamenti di respirazione che possono migliorare significativamente il movimento nel reparto pantaloni. Una naturale disfunzione erettile soluzioni di trattamento stanno diventando sempre più popolare con gli uomini. Questi rimedi a base di erbe sono preferiti perché non hanno reazioni avverse e sono confermati essere efficiente come il farmaco. La maggior parte degli uomini combattere parlano dei loro problemi, in particolare la disfunzione erettile come c è poca discussione sui problemi di erezione. La verita e che ED ha un impatto su piu di dieci milioni di uomini solo negli Stati Uniti. Non siete soli e l aiuto è disponibile.

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Effect of Different Antilipidemic Agents
and Diets on Mortality
A Systematic Review
Marco Studer, MD; Matthias Briel, MD; Bernd Leimenstoll, MD; Tracy R. Glass, MSc; Heiner C. Bucher, MD, MPH Background: Guidelines for the prevention and treat-
CI, 0.91-1.11), 0.84 for resins (95% CI, 0.66-1.08), 0.96 ment of hyperlipidemia are often based on trials using for niacin (95% CI, 0.86-1.08), 0.77 for n-3 fatty acids combined clinical end points. Mortality data are the most (95% CI, 0.63-0.94), and 0.97 for diet (95% CI, 0.91- reliable data to assess efficacy of interventions. We aimed 1.04). Compared with control groups, risk ratios for car- to assess efficacy and safety of different lipid-lowering diac mortality indicated benefit from statins (0.78; 95% interventions based on mortality data.
CI, 0.72-0.84), resins (0.70; 95% CI, 0.50-0.99) and n-3fatty acids (0.68; 95% CI, 0.52-0.90). Risk ratios for non- Methods: We conducted a systematic search of ran-
cardiovascular mortality of any intervention indicated no domized controlled trials published up to June 2003, com- association when compared with control groups, with the paring any lipid-lowering intervention with placebo or exception of fibrates (risk ratio, 1.13; 95% CI, 1.01- usual diet with respect to mortality. Outcome measures were mortality from all, cardiac, and noncardiovascularcauses.
Conclusions: Statins and n-3 fatty acids are the most fa-
vorable lipid-lowering interventions with reduced risks
Results: A total of 97 studies met eligibility criteria, with
of overall and cardiac mortality. Any potential reduc- 137 140 individuals in intervention and 138 976 indi- tion in cardiac mortality from fibrates is offset by an in- viduals in control groups. Compared with control groups, creased risk of death from noncardiovascular causes.
risk ratios for overall mortality were 0.87 for statins (95%confidence interval [CI], 0.81-0.94), 1.00 for fibrates (95% LIPID-LOWERINGAGENTSARE theefficacyofthesedrugsinvariousrisk
groups and settings as well as in generally analyses of randomized controlled trials are drugs with proven efficacy to lower both car- benefit of interventions and to explore effect diovascular morbidity and overall mortal- ity in a large-scale clinical trial were 3-hy- present meta-analysis is to investigate the reductase inhibitors (statins).1 In previous meta-analyses, only statins showed statis- lowering interventions in the primary and tically significant and clinically relevant re- Author Affiliations: Basel
and overall mortality.2,3 In addition to the potent lipid-lowering capacity of statins, more recent findings indicate that the posi- tive effects of statins could also be the re- SEARCH FOR RELEVANT STUDIES
sult of reductions in platelet aggregability We included references from previous meta- Over the past 5 years, large trials of sev- analyses2,6 and 2 of us (M.S. and M.B.) searched eral statins and other lipid-lowering inter- Financial Disclosure: None.
ventions provided important information on Cochrane Controlled Trials Register together (REPRINTED) ARCH INTERN MED/ VOL 165, APR 11, 2005 2005 American Medical Association. All rights reserved.
with a professional librarian to identify s e e h t t p : / / w w w . b i c e . c h / e n g l all benefit of lipid-lowering interven-tions were overall mortality and cardiac STUDY SELECTION
AND DATA ABSTRACTION
farction, sudden death, or heart failure) meta-analysis if they compared any lipid- STATISTICAL ANALYSIS
a follow-up of at least 6 months, and re- ported mortality data. We excluded trials recipients; trials in coronary artery by- groups by using a random effects model.
vention2,7); trials using any combination of lipid-lowering intervention (not allow- Cochran Q test and measured inconsis- tency (I2; the percentage of total varia- 1%-24%) (Table 1).
drug); and trials with outdated interven- tion across studies that is due to hetero- OVERALL MORTALITY
tails of included and excluded trials are effects across different lipid-lowering in- calculating a z score, the difference in quality blinded to one another’s rating the subgroup logarithmic relative risk di- of heterogeneity, P = .05; I2= 30% ference.13 For sensitivity analysis we ex- stracted in duplicate, and authors of the CI, 0.63-0.94; P = .01; I2= 53% [95% UI, 14%-75%]) (Figure). For stat-
mary and secondary prevention of CHD.
quality of included trials with respect to meta–regression analysis to investigate blinding of patients, caregivers, or asses- ness of follow-up.8 When the article failed tion, items about trial quality, percent- p r i m a r y p r e v e n t i o n o f C H D trials, and the type and duration of lipid- 95% CI, 0.91-1.11; P = .01; I2= 33% istics, we classified trials according to the following groups9: statins (35 trials [A1- e r a t e h e t e r o g e n e i t y ( P < . 1 0 ; A35]), fibrates (17 trials [A36-A52]), res- ins (8 trials [A53-A60]), niacin (2 trials [A39 and A61]), n-3 fatty acids (14 trials category.15 All statistical analyses were ited the analysis to interventions with at cally significant (Table 2). Hetero-
/publications_reports.htm. Trials in pri- (REPRINTED) ARCH INTERN MED/ VOL 165, APR 11, 2005 2005 American Medical Association. All rights reserved.
Table 1. Effects of Different Lipid-Lowering Interventions on Overall Mortality
Follow-up,
Cholesterol
Individuals,
Mean ± SD,
Reduction, Mean
Mortality,
Heterogeneity,
Inconsistency,
Type of Intervention*
(Range), %
RR (95% CI)
P Value
I 2 (95% UI), %
Abbreviations: CHD, coronary heart disease; CI, confidence interval, NA, not applicable; RR, risk ratio; T/C, number of individuals in treatment/control groups; *Trials in primary prevention of CHD were defined as trials with less than 10% of participants with CHD, while secondary prevention trials comprised 100% participants with CHD. There are some trials with mixed study populations (eg, 55% of participants with CHD) that could not be confined to either category; theseare therefore not included in this subgroup analysis.
†Sensitivity analysis without the trial of Burr et al (A79; see http://www.bice.ch/engl/publications_reports.htm): RR for overall mortality, 0.80 (95% CI, 0.69-0.92; P=.40; I 2=6% [95% UI, 0%-69%]).
the remaining n-3 fatty acid trials.
CI, 0.61-0.80; P = .47; I2= 0% [95% META-REGRESSION ANALYSIS
for overall mortality was 0.75 (95%CI, 0.65-0.87), and heterogeneity MORTALITY FROM
was substantially reduced (P = .36; CAUSES OTHER THAN
CARDIOVASCULAR DISEASE
with established CHD (coefficient,–0.001; 95% CI, –0.003 to –0.0003) CARDIAC MORTALITY
0.84; P = .42; I2= 3% [95% UI, 0%- CI, 1.01-1.27; P = .80, I2= 0% [95% 0.99; P = .83; I2= 0% [95% UI, 0%- CI, 0.52-0.90; P=.001; I2=66% [95% decrease in trials of longer duration.
(REPRINTED) ARCH INTERN MED/ VOL 165, APR 11, 2005 2005 American Medical Association. All rights reserved.
Risk Ratio (95% CI); Heterogeniety (P ); diac mortality in patients with CHD.
0.87 (0.81-0.94); P = .05; I 2 = 30 [0-54] 1.00 (0.91-1.11); P = .01; I 2 = 33 [0-63] 0.84 (0.66-1.08); P = .86; I 2 = 0 [0-68] 0.96 (0.86-1.08); P = .81; I 2 = 0 0.77 (0.63-0.94); P = .01; I 2 = 53 [14-75] 0.97 (0.91-1.04); P = .19; I 2 = 23 [0-56] CI, 585-1852) patients in a primaryprevention situation with a mortal- to be treated with a statin for 1 yearto prevent 1 death. For n-3 fatty ac- ids, 140 (95% CI, 87-538) patients ina secondary prevention situation have Risk Ratio (95% CI); Heterogeniety (P ); 0.78 (0.72-0.84); P = .42; I 2 = 3 [0-30] 0.93 (0.81-1.08); P = .13; I 2 = 28 [0-60] 0.70 (0.50-0.99); P = .83; I 2 = 0 [0-68] 0.95 (0.82-1.10); P = .75; I 2 = 0 0.68 (0.52-0.90); P <.001; I2 = 66 [37-81] 0.91 (0.82-1.02); P = .14; I 2 = 27 [0-59] viduals in placebo or control groups.
We found little evidence of hetero-geneity in the summary estimates fornoncardiovascular mortality in fi- Mortality From Causes Other Than Cardiovascular Diseases Risk Ratio (95% CI); Heterogeniety (P ); P=.80; I2=0%), suggesting a consis- 0.97 (0.91-1.04); P = .78; I 2 = 0 [0-43] 1.13 (1.01-1.27); P = .80; I 2 = 0 [0-54] 1.08 (0.74-1.58); P = .82; I 2 = 0 [0-85] 1.13 (0.77-1.67); P = .81; I 2 = 0 0.97 (0.84-1.13); P = .95; I 2 = 0 [0.65] 1.01 (0.96-1.07); P = .71; I 2 = 0 [0-54] rent guidelines recommend the use ofeither drug in patients with hypertri- density lipoproteins, and meta-bolic syndrome.17,18 If used in ap- Figure. Summary estimates for overall mortality (A), cardiac mortality (B), and mortality from causes
other than cardiovascular diseases (C) for different types of lipid-lowering interventions. The CochraneQ test for heterogeneity. I 2 as measure of inconsistency (in percent). CI indicates confidence interval; UI, uncertainty interval; n, number of trials available for analysis; n-3 FA, n-3 fatty acid.
glyceride levels19 but are associatedwith a reduction in overall mortal-ity. However, n-3 fatty acids lower vs trials of interventions other than fi- (REPRINTED) ARCH INTERN MED/ VOL 165, APR 11, 2005 2005 American Medical Association. All rights reserved.
Table 2. Sensitivity Analysis of Quality Components for Statins, Fibrates, and n-3 Fatty Acids
Fibrates
n-3 Fatty Acids
Mortality,
Difference Trials,
Mortality,
Difference Trials,
Mortality,
Difference
Quality Component
RR (95% CI)
P Value
RR (95% CI)
P Value
RR (95% CI)
P Value
Abbreviations: CI, confidence interval; RR, risk ratio.
*Sensitivity analysis without the trial of Burr et al (A79; see http://www.bice.ch/engl/publications_reports.htm): RR for overall mortality, 0.75 (95% CI, 0.60-0.92); †Sensitivity analysis without the trial of Burr et al (A79): RR for overall mortality, 1.25 (95% CI, 0.31-5.07); difference P value, .78.
1. 4S-Group. Randomised trial of cholesterol low- to retrieve all relevant eligible trials.
ering in 4444 patients with coronary heart dis- ease: the Scandinavian Simvastatin Survival Study (4S). Lancet. 1994;344:1383-1389.
for such bias, it cannot be ruled out.
2. Bucher HC, Griffith LE, Guyatt GH. Systematic re- view on the risk and benefit of different cholesterol- lowering interventions. Arterioscler Thromb Vasc be less prone to ascertainment bias.
3. Ross SD, Allen IE, Connelly JE, et al. Clinical out- comes in statin treatment trials: a meta-analysis.
cluded trials (PϽ.001; I2=37% [95% Arch Intern Med. 1999;159:1793-1802.
4. Rosenson RS, Tangney CC. Antiatherothrom- botic properties of statins: implications for car- diovascular event reduction. JAMA. 1998;279: 5. Pogue J, Yusuf S. Overcoming the limitations of current meta-analysis of randomised controlledtrials. Lancet. 1998;351:47-52.
Accepted for Publication: Novem-
6. Smith GD, Song F, Sheldon TA. Cholesterol low- ering and mortality: the importance of consider- Correspondence: Heiner C. Bucher,
ing initial level of risk. BMJ. 1993;306:1367- 7. Rossouw JE, Anderson GL, Prentice RL, et al.
Risks and benefits of estrogen plus progestin in results from the Women’s Health Initiative ran-domized controlled trial. JAMA. 2002;288:321- Funding/Support: Drs Bucher and
8. Juni P, Witschi A, Bloch R, Egger M. The hazards of scoring the quality of clinical trials for meta-analysis. JAMA. 1999;282:1054-1060.
9. McAlister FA, Laupacis A, Wells GA, Sackett DL. Users’ Guides to the Medical Literature, Acknowledgment: We are grateful
XIX: applying clinical trial results B: guidelines for determining whether a drug is exerting(more than) a class effect. JAMA. 1999;282: 10. Egger M, Davey SG, Schneider M, Minder C.
Bias in meta-analysis detected by a simple, graphi- action.9 For example, trials of n-3 fatty cal test. BMJ. 1997;315:629-634.
(REPRINTED) ARCH INTERN MED/ VOL 165, APR 11, 2005 2005 American Medical Association. All rights reserved.
11. Higgins JP, Thompson SG, Deeks JJ, Altman DG.
rived from meta-analysis: a word of caution. ACP 18. Grundy SM, Cleeman JI, Merz CN, et al. Implica- Measuring inconsistency in meta-analyses. BMJ.
tions of recent clinical trials for the National Cho- 16. Din JN, Newby DE, Flapan AD. Omega 3 fatty ac- lesterol Education Program Adult Treatment Panel 12. Higgins JP, Thompson SG. Quantifying hetero- ids and cardiovascular disease—fishing for a natu- III guidelines. Arterioscler Thromb Vasc Biol. 2004; geneity in a meta-analysis. Stat Med. 2002;21: ral treatment. BMJ. 2004;328:30-35.
17. Expert Panel on Detection EaToHBCiA. Execu- 19. Bucher HC, Hengstler P, Schindler C, Meier G.
13. Fleiss JL. The statistical basis of meta-analysis.
N-3 polyunsaturated fatty acids in coronary heart Stat Methods Med Res. 1993;2:121-145.
disease: a meta-analysis of randomized con- 14. Thompson SG, Sharp SJ. Explaining heterogene- (NCEP) Expert Panel on Detection, Evaluation, trolled trials. Am J Med. 2002;112:298-304.
ity in meta-analysis: a comparison of methods. Stat and Treatment of High Blood Cholesterol in 20. Oxman AD, Guyatt GH. A consumer’s guide to sub- Adults (Adult Treatment Panel III). JAMA. 2001; group analyses. Ann Intern Med. 1992;116: 15. Marx A, Bucher HC. Numbers needed to treat de- Omissions in Byline. In the Original Investigation by
Cohen et al titled “Emerging Credentialing Practices, Mal-
practice Liability Policies, and Guidelines Governing
Complementary and Alternative Medical Practices and
Dietary Supplement Recommendations: A Descriptive
Study of 19 Integrative Health Care Centers in the United
States,” published in the February 14 issue of the
ARCHIVES (2005;165:289-295), 2 authors were inadvert-
ently omitted from the byline on page 289. The byline
should have appeared as follows: “Michael H. Cohen, JD;
Andrea Hrbek; Roger B. Davis ScD; Steven C. Schachter,
MD; Kathi J. Kemper, MD, MPH; Edward W. Boyer, MD,
PhD; David M. Eisenberg, MD.”
(REPRINTED) ARCH INTERN MED/ VOL 165, APR 11, 2005 2005 American Medical Association. All rights reserved.

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