Interesting... another blood pressure med, Lisinopril, is also being looked at as a possible ms treatment.http://www.webmd.com/multiple-sclerosis/news/20090817/blood-pressure-drug-may-help-treat-ms
I have been following almost ALL the published research of "Larry" - Lawrence Steinman, MD, of Stanford University since Sep 93.
I bought a SCIENTIFIC AMERICIAN Specl edition Sep 93 on The Immune System at my local supermarket two years before I was Dxd with MS.
I found an article in it by him on "HOW MS PROGRESSES
". The tech terms are a little different but he maps it out quite well.
He even indicated 5 points in which meds could be made to STOP the progression.http://home.ix.netcom.com/~jdalton/autoimmunity.pdf
I think he later went on to help develope two of them.
His later article on the two stages of MS is fantastic.http://home.ix.netcom.com/~jdalton/ms-two-stages.pdf
It appears "Larry" has high blood pressure so when his doctor put him on the ACE Inhibitor Lisinopril he did a search on it to get the med facts on it.
He had his computer add "Multiple Sclerosis" to all his searches automatically so was quite surprised when he found that it had positive effect on slowing MS activity.
As I posted above, I am taking the ACE drug Captopril which seems to have the same effect. I must take it three times a day. The Lisinopril is a one pill a day ACE drug.
The three times a day is a bit of a pain but I am going to stick with it because my research reveals OTHER BIG advantages for ME with the Captopril.
I have real BIG chance of having Prostate Cancer. My biopsy found ASAP cells which means I have a 40% chance of having it now or a 60% chance of getting it in the near futue.
Captopril is the ONLY ACE drug that seems to be VERY anti-cancer.
Prostate. 2004 Jan 1;58(1):50-6.
Association between captopril, other antihypertensive drugs and risk of prostate cancer.
Ronquist G, Rodríguez LA, Ruigómez A, Johansson S, Wallander MA, Frithz G, Svärdsudd K.
SourceDepartment of Medical Sciences, Clinical Chemistry, University Hospital, Uppsala, Sweden.
BACKGROUND: There has been some debate on the existence of an association between hypertension, antihypertensive medications and cancer risk.
METHODS: We performed a nested case-control study to assess the association between the risk of prostate cancer and the use of the angiotensin converting enzyme (ACE)-inhibitor captopril, and other antihypertensive drugs. We used data from the General Practice Research Database in UK.
RESULTS: We found an incidence rate of prostate cancer of 1.61 per 1,000 person-years among male patients aged 50-79 years old.
Patients with a history of benign prostatic hyperplasia and/or prostatism carried a two-fold greater risk of prostate cancer than those without such antecedents.
None of the other studied co-morbidities were associated with prostate cancer. We found that users of captopril had a relative risk of 0.7 (95% CI: 0.4-1.2) to develope prostate cancer.
None of the other studied individual ACE-inhibitors shared a similar effect with the one observed for captopril
CONCLUSIONS: No clear association was apparent between the use of antihypertensive drugs and prostate cancer. However, specific focus on users of captopril showed a lower risk of subsequent prostate cancer.
Further research is needed to explore this association.
Copyright 2003 Wiley-Liss, Inc.
PMID:14673952[PubMed - indexed for MEDLINE]
Scand J Urol Nephrol. 2009;43(1):32-6.
Captopril may reduce biochemical (prostate-specific antigen) failure following radical prostatectomy for clinically localized prostate cancer.
Ronquist G, Frithz G, Wang YH, Lindeborg T.
SourceDepartment of Medical Sciences, Clinical Chemistry, Uppsala University, Uppsala, Sweden.
OBJECTIVE: A prior report suggested that individuals medicated with captopril showed a decreased incidence of prostate cancer. This study therefore investigated whether captopril given postoperatively had any preventive effect on biochemical recurrence for patients treated with radical prostatectomy.
MATERIAL AND METHODS: Data were prospectively reviewed for 62 men subjected to radical retropubic prostatectomy due to biopsy-confirmed, clinically localized prostate cancer and comparisons were made between two groups, those receiving captopril postoperatively (12.5 mg twice daily; captopril group, n=32) and those not receiving any captopril (control group, n=30). One surgeon carried out the surgery.
RESULTS: The two groups were comparable as regards age at surgery, prostate volume, preoperative prostate-specific antigen values, pathological stage, Gleason score, organ-confined disease, occurrence of positive surgical margins and extraprostatic extension. The incidence of biochemical failure was three out of 32 patients in the captopril group and 10 out of 30 in the control group (p=0.034) during a mean observational time of 29 months.
CONCLUSIONS: A lower rate of biochemical recurrence was observed in men subjected to radical prostatectomy treated with captopril postoperatively than in those not receiving captopril. These results were based on only 32 observations; a larger study may show no evidence of an association.
PMID:18932051[PubMed - indexed for MEDLINE] THIS ANTI-CANCER EFFECT OF CAPTOPRIL SEEMS TO EXTEND TO OTHER CANCERS
Ann N Y Acad Sci. 2008 Sep;1138:65-72.Captopril as a potential inhibitor of lung tumor growth and metastasis.
Attoub S, Gaben AM, Al-Salam S, Al Sultan MA, John A, Nicholls MG, Mester J, Petroianu G.
SourceDepartment of Pharmacology, Faculty of Medicine and Health Sciences, UAE University, Al Ain, United Arab Emirates.
AbstractLung cancer is the most common form of cancer in the world, and 90% of patients die from their disease.
The angiotensin converting enzyme (ACE) inhibitors are used widely as antihypertensive agents, and it has been suggested that they decrease the risk of some cancers, although available data are conflicting. Accordingly, we investigated the anticancer activity of the ACE inhibitor, captopril, in athymic mice injected with highly tumorigenic LNM35 human lung cells as xenografts.Using this model, we demonstrated that daily IP administration of captopril (2.8 mg/mouse) for 3 weeks resulted in a remarkable reduction of tumor growth (58%, P < 0.01) and lymph node metastasis (50%, P= 0.088).
There were no undesirable effects of captopril treatment on animal behavior and body weight. In order to determine the mechanism by which captopril inhibited tumor growth, we investigated the impact of this drug on cell proliferation, apoptosis, and angiogenesis. Immunohistochemical analysis demonstrated that captopril treatment significantly reduced the number of proliferating cells (Ki-67) in the tumor samples but was not associated with inhibition of tumor angiogenesis (CD31). Using cell viability and fluorescent activated cell sorting analysis tests, we demonstrated that captopril inhibited the viability of LNM35 cells by inducing apoptosis, providing insight about the mechanisms underlying its antitumorigenic activities.In view of these experimental findings, we conclude that captopril could be a promising option for the treatment of lung cancer.
PMID:18837885[PubMed - indexed for MEDLINE]