"four fifths of men with prostate cancer are also on blood pressure medication."
Is that really so?
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"Those who were taking angiotensin II receptor blockers (known as ARBs) – which include common pills such as Valsartan and Losartan – had the lowest chance of death during the study period."
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I wish I could find an account of the presentation not linked to the Daily Mail [1].
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There was a Murtola paper published in November [2]:
"Antihypertensive drugs and prostate cancer survival after radical prostatectomy in Finland-A nationwide cohort study."
***
[1]:
"Cheap blood pressure drugs taken by thousands of people could increase survival chances for men with prostate cancer, research suggests.
A study of nearly 8,300 men with prostate cancer found that a particular class of blood pressure pills cuts the chance of an early death by up to 42 per cent.
Other types of blood pressure drugs, on the other hand, may actually increase the risk of death.
Certain types of blood pressure medication – angiotensin II receptor blockers (ARBs) – improve prostate cancer survival rates, according to research ... (?)
The researchers – presenting their findings at the European Association of Urology Conference in Barcelona – said the findings are crucial because four fifths of men with prostate cancer are also on blood pressure medication.
So it is vital that doctors select a type of pill that could extend their life, rather than potentially shorten it.
The researchers, from the University of Tampere in Finland, tracked 8,253 men with prostate cancer for seven and a half years after they were diagnosed.
Most of the men, who had an average age of 68 at the start of the study, also happened to be taking pills for high blood pressure.
The researchers compared the type of blood pressure medication with the participants’ death rates, and found they varied significantly depending on the class of the drug.
Those who were taking angiotensin II receptor blockers (known as ARBs) – which include common pills such as Valsartan and Losartan – had the lowest chance of death during the study period.
Men who been taking the pills before they were diagnosed had a 30 per cent lower chance of dying from their prostate cancer than those who were taking no blood pressure medication, and those who started taking them after diagnosis had a 42 per cent reduced risk.
ACE-inhibitors – another common drug – also seemed to have a protective effect, with an 18 per cent lower death risk if they started on the pills after diagnosis.
But other treatments, such as diuretics, seemed to increase the risk of mortality by up to 161 per cent.
Angiotensin II receptor blockers – which cost as little as 70p a day – have been used for blood pressure for more than 30 years and come with few side effects.
Researcher Professor Teemu Murtola said the method by which Valsartan and similar treatments lower blood pressure may slow the growth of prostate tumours.
Other drugs work in different ways, so may not have the same effect.
He said he doubts any blood pressure drugs actually increase the risk of death by themselves – it may just be that men on those drugs are at greater risk because they have underlying heart problems which make them more vulnerable to cancer.
But he stressed that with so many prostate cancer patients taking blood pressure pills, the choice of treatment could make a big difference.
‘Up to 80 per cent of men in our study population had at least one prescription for antihypertensive drugs, demonstrating how common the usage is among men with prostate cancer,’ Professor Murtola said.
‘Therefore, it is essential to know their potential impact on cancer prognosis.
‘Of course other studies are needed to confirm these results – but there could be real benefits to selecting certain medication rather than others. It is definitely worth studying further.’
Here is a paper from last year. the Discussion is pasted below. -Patrick
DISCUSSION
Many studies have sought a relationship between use of CCBs and the development of PCa but this study is the first to evaluate the association between CCB usage and PCa aggressiveness, PFS and OS. Perron et al. [6] found no association between use of CCBs and incidence of PCa in a case–control population study on 13,326 men. Debes et al. [4], on the other hand, reported an inverse relationship between CCB usage and the probability of developing PCa. Similarly, data from the Cardiovascular Health Study indicated a 40% reduced PCa risk in men taking CCBs [1]. While the Cancer Prevention Study II Nutritional Cohort study reported that patients on antihypertensive medications were at a decreased risk for low grade PCa, when data were stratified by CCB use, no significant association remained between the use of the CCB class of antihypertensives and PCa incidence or aggressiveness [7]. Data from the General Practice Research Database in the UK identified 1,093 patients with a new diagnosis of PCa over a 4-year period. When stratified by CCB use there was no difference in PCa incidence between the two groups [5]. Vezina et al. [8] evaluated the risk of PCa in Massachusetts tumor registry population and found no difference in incidence between CCB users non-users.
Independent analyses of two separate clinical databases, either containing information on men who underwent RP at RPCI or population-based data on men with newly diagnosed PCa, failed to reveal a link between use of these antihypertensives and PCa aggressiveness. In addition, no significant differences in PFS and OS were found between users and non-users in the RPCI patient cohort. Men on CCB, or antihypertensive medication in general, may have better access to health care than those who are not and therefore are more likely to be screened for and diagnosed with PCa [9]. A more intense interaction with the health care system could explain the conflicting results obtained in epidemiological studies that assessed the relationship between CCB use and PCa incidence [15]. Health care access difficulties that confound interpretation of epidemiologic study results are less likely to have influenced this analysis of PCa aggressiveness, PFS and OS: all patients in the PCaP and RPCI cohort had histologically confirmed PCa and follow-up for patients who underwent RP at RPCI was performed consistently.
CCB use in the RP cohorts was associated with an elevated BMI. This is not surprising as BMI has been reported to have a linear correlation with systolic blood pressure [16]. Obesity has been associated also with resistant hypertension, that is, refractory hypertension despite administration of three antihypertensive drugs at full dose [17]. The relationship between resistant hypertension and obesity would lead to an increase in the incidence of CCB usage in obese patients, and an increase in the incidence of concomitant CCB use with other medications, as was found in this study.
A strength of this study is the validation of the findings on PCa aggressiveness between two separate and robust data sets. While the patient populations differed significantly in CCB use (11% in RPCI cohort vs. 24% in the PCaP dataset), analyses of both databases failed to reveal an association between CCB usage and disease aggressiveness. The difference in proportion of patients on CCB may be due to the inclusions of fewer African American men in the RPCI cohort. Approximately half of the participants in the PCaP study were African American, who are more likely to be prescribed CCB as first line treatment for hypertension, compared to only 9% of patients at RPCI. The consistency in the results obtained from a population-based dataset (PCaP) and an RP cohort from a tertiary referral center (RPCI) further strengthens these findings. The results indicate that patients taking CCB alone (n = 23) presented with less aggressive disease than those who combined use of CCB with other antihypertensive medication (n = 81). In view of the small number of patients in each group, the relevance and significance of these observations will need to be assessed in a larger cohort. Similarly, validation of the association between CCB use, family history and PCa aggressiveness that was observed in the PCaP cohort but not for RPCI patients, requires additional analyses of suitable patient cohorts.
The cross-sectional nature of data collection at the time of surgery prevented determination of the duration of CCB use prior to RP. This may have biased the results as patients who were on CCB medication for a short period of time prior to operation are considered CCB users without having experienced necessarily the physiological effects of long term CCB use. In theory, this could affect PCa aggressiveness at time of surgery, but should not affect evaluation of PFS and OS. In an attempt to mitigate this issue, patient records were reviewed to confirm use of CCB at the last follow-up visit. Approximately 70% of patients on CCB medications were still using them at last follow-up. This rate compares favorably to population-based studies. Van Wijk et al. [18] described 10-year discontinuation rates from a large population database of 2,325 antihypertensive users. At 4-year follow-up, approximately 53% of men in the study were using persistently the hypertensive medication prescribed originally. Additionally, data from NHANES demonstrate that in a PSA screening population, mean duration of CCB therapy was 5 years [19]. Therefore, despite the cross-sectional nature of the medication data collection, a large proportion of men in our study group should have had adequate exposure to observe any effect on PCa aggressiveness, PFS, and OS.
PCa aggressiveness was associated with PFS but not OS. The reason for disparity between PFS and OS is likely due to relatively short duration of follow-up. Since the median length of time from operation to PCa-specific mortality and all causes mortality is approximately 9 years, an association between tumor aggressiveness and OS was unlikely to be found [20]. Another limitation is the inability to determine whether there was a dose-dependent response to CCB medication use. Medication dosages were not collected at the time of RP and could not be used to stratify results based upon potential differences in CCB dosage.
I don't have high blood pressure but I do take a high blood pressure med (metoprolol) to help deal with atrial fibrillation. I could see where the effects of long term ADT could lead to the need to take high blood pressure meds.
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