Like many of you, the Nerd not able to do basic
medline research. I have simplified the process.
Go to www.maloneymedical.com. Scroll to the bottom of the page and click on Quackery. Click on PHARYGULA POSTS FOR READERS UNABLE TO FOLLOW THE THREAD and read down to
the section on placebo effects. For those, like Nerd, who are too lazy to even
do this: “According to The Cochrane Collaborative Cochrane Database Syst
Rev. 2010 Jan 20;(1):CD003974 the “sugar pill” placebo effect doesn’t really exist anymore.” In other words, the concept that you are promoting doesn’t have any effect in
modern medical studies. While it currently continues to be used in drug trials,
I would hope we would move to more effective drug vs. drug trials.
Several of you took umbrage at my mentioning
of either Taxol or aromatase inhibitors. My answer is show the data or accept
mine. Do not prevent women who have this illness from getting proper care because
you don’t like the source of the information. The following is the meta-analysis of aromatase inhibitors versus tamoxifen.
I believe the cancer in question was estrogen negative (which is rarer), in which case the standard therapies are still
used, but less effectively.
Ambulocetacean seems to be under the misapprehension
that I am not a licensed naturopathic doctor. Please take a moment to have a
look at my website. All the relevant information is there, and at this point
I can confidently claim I have had more medical training than the majority of individuals on this endless thread. As I mention on my website, I maintain a license, malpractice insurance, and have a community of M.D.s
and D.O.s within which we cross refer.
I’ve never been a fan of chelation, and I don’t frighten people.
I give the best data available when panicked parents are told to get things like the H1N1 vaccine WHEN NONE OF IT IS
AVAILABLE. The whole idea of me being a quack was based on my editorial printed
at a time when there was no vaccine and parents were literally quarantining themselves and their children in their homes out
of fear. So no, I’m not the fear monger in this situation. I support parents in making informed decisions, giving them both the positive and the negative information. It’s called informed consent, and is required of all doctors.
Bride of Shrek is arguing for a study that she hasn’t
provided any link to. But let’s all give credit here, because the rest
of you haven’t provided a shred of objective evidence for your terribly virulent opinions.
David,
if Josh has not experienced anything from alternative medicine first hand, we are all to assume he is some sort of a benevolent
hater? Sort of his gift to the world, hating things randomly? Someone should get him a Gandhi award. Oh, wait, that would
be a KKK hood. Gay…hating randomly… no irony bells going off in the
ol’ Joshosphere?
Menopause is not only classified medically,
it has its own medical journal: Menopause.
I’m sorry, let me send patients to your house who are hot flashing every six minutes. I’ll let you explain to them how they don’t have a disease, but make it quick because they
will kill you.
The taxol comments are random, my point was that
if you lot had your way, we wouldn’t look into the effects of herbs at all. The
botanical world is where we will find the cures for things, and the first step to that is figuring out which herbs are most
effective.
Ol’ Greg, have you never talked to a
woman who is doubled up in agony for a week every month? Any body process that
gets out of hand, whether it is the immune system or the hormonal systems, becomes a disease.
I shouldn’t need to explain basic medical information to you all. Take
the time to educate yourselves. It’s called dysmenorrhoea for those English
and Aussies out there.
The citations on this post are another five
pages, so I’m putting them under Quackery on my website rather than “force” you all to read some actual
research.
Menopause. 2010 Mar;17(2):295-302.
Hormone therapy and physical function change
among older women in the Women's Health Initiative: a randomized controlled trial.
Michael YL, Gold R, Manson JE, Keast EM, Cochrane
BB, Woods NF, Brzyski RG, McNeeley SG, Wallace RB.
Department of Epidemiology, Drexel University
School of Public Health, Philadelphia, PA 19102, USA. michaely@drexel.edu
Comment in:
Menopause. 2010 Mar;17(2):235-6.
OBJECTIVE: Although estrogen may be linked
to biological pathways that maintain higher physical function, the evidence is derived mostly from observational epidemiology
and therefore has numerous limitations. We examined whether hormone therapy affected physical function in women 65 to 79 years
of age at enrollment. METHODS: This study involves an analysis of the Women's Health Initiative randomized controlled trials
of hormone therapy in which 922 nondisabled women who had previous hysterectomies were randomized to receive estrogen therapy
or a placebo and 1,458 nondisabled women with intact uteri were randomized to receive estrogen + progestin therapy or a placebo.
Changes in physical function were analyzed for treatment effect, and subgroup differences were evaluated. All women completed
performance-based measures of physical function (grip strength, chair stands, and timed walk) at baseline. These measures
were repeated after 1, 3, and 6 years. RESULTS: Overall, participants' grip strength declined by 12.0%, chair stands declined
by 3.5%, and walk pace slowed by 11.4% in the 6 years of follow-up (all P values <0.0001). Hormone therapy, as compared
with placebo, was not associated with an increased or decreased risk of decline in physical function in either the intention-to-treat
analyses or in analyses restricted to participants who were compliant in taking study pills. CONCLUSIONS: Hormone therapy
provided no overall protection against functional decline in nondisabled postmenopausal women 65 years or older in 6 years
of follow-up. This study did not address the influence of hormone therapy for women of younger ages.
PMID: 19858764
Cochrane Database Syst Rev. 2010 Jan 20;(1):CD001751.
Nonsteroidal anti-inflammatory drugs for dysmenorrhoea.
Marjoribanks J, Proctor M, Farquhar C, Derks
RS.
Obstetrics and Gynaecology, Cochrane Menstrual
Disorders and Subfertility Group, Park Rd, Grafton, Auckland, New Zealand, 1003.
Update of:
Cochrane Database Syst Rev. 2003;(4):CD001751.
BACKGROUND: Dysmenorrhoea is a common gynaecological
problem consisting of painful cramps accompanying menstruation, which in the absence of any underlying abnormality is known
as primary dysmenorrhoea. Research has shown that women with dysmenorrhoea have high levels of prostaglandins, hormones known
to cause cramping abdominal pain. Nonsteroidal anti-inflammatory drugs (NSAIDs) are drugs which act by blocking prostaglandin
production. OBJECTIVES: The purpose of this review is to compare nonsteroidal anti-inflammatory drugs used in the treatment
of primary dysmenorrhoea versus placebo, versus paracetamol and versus each other, to evaluate their effectiveness and safety.
SEARCH STRATEGY: We searched the following databases to May 2009: Cochrane Menstrual Disorders and Subfertility Group trials
register, Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE and Web of Science. The National Research Register
and the Clinical Trials Register were also searched. Abstracts of major scientific meetings and the reference lists of relevant
articles were checked. SELECTION CRITERIA: All randomised controlled comparisons of NSAIDs versus placebo, other NSAIDs or
paracetamol, when used to treat primary dysmenorrhoea. DATA COLLECTION AND ANALYSIS: Two reviewers independently assessed
trials for quality and extracted data, calculating odds ratios (ORs) for dichotomous outcomes and mean differences for continuous
outcomes, with 95% confidence intervals (CIs). Inverse variance methods were used to combine data. MAIN RESULTS: Seventy-three
randomised controlled trials were included. Among women with primary dysmenorrhoea, NSAIDs were significantly more effective
for pain relief than placebo (OR 4.50, 95% CI: 3.85, 5.27). There was substantial heterogeneity for this finding (I(2) statistic
=53%): exclusion of two outlying studies with no or negligible placebo effect reduced heterogeneity, resulting in an odds
ratio of 4.14 (95% CI: 3.52, 4.86, I(2)=40%). NSAIDs were also significantly more effective for pain relief than paracetamol
(OR 1.90, 95% CI:1.05 to 3.44). However, NSAIDS were associated with significantly more overall adverse effects than placebo
(OR 1.37, 95% CI: 1.12 to 1.66). When NSAIDs were compared with each other there was little evidence of the superiority of
any individual NSAID for either pain-relief or safety. However the available evidence had little power to detect such differences,
as most individual comparisons were based on very few small trials. AUTHORS' CONCLUSIONS: NSAIDs are an effective treatment
for dysmenorrhoea, though women using them need to be aware of the significant risk of adverse effects. There is insufficient
evidence to determine which (if any) individual NSAID is the safest and most effective for the treatment of dysmenorrhoea.
PMID: 20091521
Trials. 2008 Jul 29;9:47.
Meta-analysis of trials comparing anastrozole
and tamoxifen for adjuvant treatment of postmenopausal women with early breast cancer.
Aydiner A, Tas F.
Istanbul University, Istanbul Medical School,
Department of Medical Oncology, Istanbul, Turkey. adnanaydiner@superonline.com
OBJECTIVE: It was aimed to review the literature
and make a meta-analysis of the trials on both upfront, switching, and sequencing anastrozole in the adjuvant treatment of
early breast cancer. METHODS: The PubMed, ClinicalTrials.gov and Cochrane databases were systematically reviewed for randomized-controlled
trials comparing anastrozole with tamoxifen in the adjuvant treatment of early breast cancer. RESULTS: The combined hazard
rate of 4 trials for event-free survival (EFS) was 0.77 (95%CI: 0.70-0.85) (P < 0.0001) for patients treated with anastrozole
compared with tamoxifen. In the second analysis in which only ITA, ABCSG 8, and ARNO 95 trials were included and ATAC (upfront
trial) was excluded, combined hazard rate for EFS was 0.64 (95%CI: 0.52-0.79) (P < 0.0001). In the third analysis including
hazard rate for recurrence-free survival (excluding non-disease related deaths) of estrogen receptor-positive patients for
ATAC trial and hazard rate for EFS of all patients for the rest of the trials, combined hazard rate was 0.73 (95%CI: 0.65-0.81)
(P < 0.0001). CONCLUSION: Anastrozole appears to have superior efficacy than tamoxifen in the adjuvant hormonal treatment
of early breast cancer. Until further clinical evidence comes up, aromatase inhibitors should be the initial hormonal therapy
in postmenopausal early breast cancer patients and switching should only be considered for patients who are currently receiving
tamoxifen.
PMID: 18664277
Expert Opin Pharmacother. 2009 Sep;10(13):2081-93.
Pharmacotherapy of triple-negative breast
cancer.
Arslan C, Dizdar O, Altundag K.
Hacettepe University Institute of Oncology,
Department of Medical Oncology, 06100 Sihhiye, Ankara, Turkey.
The term 'triple-negative breast cancer' defines
tumors that do not express estrogen receptors, progesterone receptors or Her2 on immunohistochemical analysis. This subgroup
accounts for 15% of all types of breast cancer. Histologically, triple-negative breast cancers are poorly differentiated and
are characterized by an aggressive clinical history. A significant overlap exists in biological and clinical characteristics
of basal-like breast cancer and triple-negative breast cancer. Treatment options are limited, as these tumors lack a therapeutic
target and are naturally resistant to existing targeted therapies, i.e., endocrine treatment and trastuzumab. As there are
no specific treatment guidelines for this subgroup, triple-negative breast cancers are managed with standard treatment; however,
local and systemic relapse rates are high due to the adverse biology of the disease. Triple-negative breast cancer has many
histological and genetic similarities with BRCA-1-associated breast cancer, suggesting a common pathogenesis and the potential
use of common chemotherapeutics in both cancers. This review discusses current and future treatment options in the light of
the new insights in major proliferative pathways active in the pathogenesis of triple-negative breast cancer.
PMID: 19640211