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“Pregnant women who drink alcohol may reduce sperm count of sons,”, according to The Guardian. It reported that research has found that pregnant women who drank more than 4.5 alcoholic drinks per week were more likely to have sons who had a lower sperm count than women who drank little alcohol.

This Danish research has analysed the pregnancy drinking habits of 347 women during pregnancy and the quality of their adult sons’ semen. Although the study found a relationship between higher alcohol consumption and lower sperm concentration, semen volume and total sperm count, the trend and its implications are not completely clear. There are numerous limitations to the research, such as the small number of participants and the adaptation of a study design originally devised to examine smoking. Crucially though, male fertility was not directly assessed, meaning it is incorrect to assume that the men involved would have difficulties if they try to father children.

Overall, there are no definite conclusions to draw from this limited research. However, regardless of the study’s limitations, pregnant women are strongly advised to limit or avoid alcohol during pregnancy due to the numerous established harmful effects of excess alcohol during pregnancy.

 

Where did the story come from?

The study was carried out by researchers from Aarhus University Hospital, Denmark, and funded by Danish Medical Research Council. The study was published in the peer-reviewed medical journal, Human Reproduction.

News reports have reflected the findings of this research, but have generally not taken into account several of the study’s important limitations. This means that no firm conclusions can be drawn on this issue. The Daily Mail’s opening paragraph, which says that ‘pregnant women who drink alcohol could be jeopardising their chances of becoming grandmothers,’ is not substantiated by this research or supported by the researchers.

 

What kind of research was this?

This was a cohort study that aimed to investigate the effects of exposing a male foetus to alcohol. Specifically it looked at what effect maternal alcohol consumption during pregnancy has upon sperm quality and levels of reproductive hormones once the child has reached adulthood.

A cohort study is the best design for examining the relationship between a cause (maternal alcohol) and potential effect (reduced fertility in the son). However, to ensure the accuracy of its results a cohort study must take into account all possible confounders that could affect the relationship being studies. A limitation of this particular study is that it was not set up to examine the link between maternal alcohol consumption during pregnancy and sperm quality in the son. The original aim and design was an examination of the effect of smoking in pregnancy on sperm quality.

 

What did the research involve?

This research used participants of a Danish cohort study (the Healthy Habits for Two study), which recruited 11,980 pregnant women between 1984 and 1987. At 36 weeks of pregnancy the women completed a questionnaire on their lifestyle habits including drinking of beer, wine and spirits. Responses were categorised as drinks per week (for each drink type): never, 1, 1–4, 5–9, 10–14, 15–19, 20 or more.

After summing the total of each type of drink, they put each woman into a category of: less than one drink a week, 1-1.5 drinks a week, 2-4 drinks, or 4.5 or more drinks a week. One standard drink in Denmark reportedly corresponded to 12g of pure alcohol. In the UK, one standard drink (unit) contains 8g of pure alcohol.

In 2004, a total of 5,109 sons were identified through the Danish Civil Registration System. Between 2005 and 2006, the researchers collected semen samples from 347 men (48.5% of the 716 invited to participate) and took blood samples (both performed with due laboratory protocols). They analysed semen for sperm concentration and motility, and looked at hormone concentrations in the sample.

The men also provided questionnaires containing health and lifestyle questions, including about their own alcohol consumption. When calculating the associations between maternal alcohol and semen quality the researchers adjusted for maternal smoking, and in the sperm donor’s, smoking, alcohol, history of reproduction infections/disease, and days of sexual abstinence prior to providing the sample.

 

What were the basic results?

Of the mothers of the 347 men who participated in the study, 110 drank less than one drink a week during pregnancy, 127 had 1-1.5 drinks a week, 72 women had 2-4 drinks a week, and 38 drank 4.5 or more drinks a week.

There was a trend for decreasing sperm concentration with increasing alcohol exposure while in the uterus. The researchers calculated that sons of mothers who were in the highest alcohol category during pregnancy (more than 4.5 drinks per week) had a 32% lower sperm concentration than those whose mothers were in the lowest category (less than one drink per week).

Maternal alcohol consumption showed no clear relationship with either semen volume or total sperm count (the 1-1.5 drinks per week group was associated with the highest volume and sperm count). There was no observed association between maternal alcohol consumption and hormone levels, sperm motility or sperm morphology. They also found that higher pregnancy alcohol consumption was independently associated with the mum being of lower BMI, being of older age and being a smoker, and with the son being of lower birth weight.

 

How did the researchers interpret the results?

The researchers conclude that their results indicate that prenatal exposure to alcohol may have an adverse effect on sperm production, and if this were a causal relationship it could explain some of the reported differences in semen quality between populations and across generations.

 

Conclusion

This research has found some association between semen quality in sons and their mothers’ alcohol consumption during pregnancy. However, there are several important limitations to this research:

• As the researchers say, ‘the participants were selected according to levels of maternal smoking during pregnancy’. Carrying out a post hoc analysis that was not the primary aim of the study increases the risk of chance findings. This may be particularly problematic in this instance as the initial research had a preference for selecting women who smoked and therefore may not have been a typical representative sample of pregnant women.
• Although the cohort of pregnant women was very large (11,980), there were only a total of 347 sets of mothers and sons across the four categories of alcohol consumption analysed. With this small number there is a high possibility of chance findings, particularly with the association found for drinking more than 4.5 drinks a week as there were only 38 women and their sons in this category. The findings based on the analyses of these small numbers may be by chance.
• Additionally, only half of the men invited to participate chose to do so. There may be important differences between the population studied and those who chose not to participate.
• An association was found between higher and drink consumption and decreasing sperm concentration, semen volume and sperm count. However, these relationships were not completely clear, with the highest values being in sons of mothers who drank 1-1.5 drinks per week rather than in those who drank more or less than this. There was also no relationship with hormone levels, sperm motility or sperm morphology. Therefore the actual implications of these findings are not clear.
• It is not known whether any of the differences in sperm quality seen across the groups would cause any actual fertility problems for the man.
• Alcohol consumption was assessed at the end of pregnancy. It is unclear whether the answer reflected the whole of the pregnancy, or just at the time of assessment. Also with any assessment like this, the number of drinks and size and strength of a drink will mean different things to different people.
• There is a possibility that other confounders have not been adjusted for or not fully adjusted. For example, the reporting of alcohol consumption by the men themselves was adjusted for but there may have been insufficient data to do this reliably.

Regardless of the limitations of this research and uncertainty over its findings, there are numerous other established harmful effects of consuming alcohol during pregnancy. NICE recommendations on alcohol consumption (based on one unit being 8g of pure alcohol instead of the 12g used in this study) during pregnancy advise that:

• Pregnant women and women planning a pregnancy should avoid drinking alcohol in the first three months of pregnancy if possible because it may be associated with an increased risk of miscarriage.
• If women choose to drink alcohol during pregnancy they should be advised to drink no more than 1 to 2 UK units once or twice a week (1 unit equals half a pint of ordinary strength lager or beer, or one shot [25ml] of spirits. One small [125ml] glass of wine is equal to 1.5 UK units). Although there is uncertainty regarding a safe level of alcohol consumption in pregnancy, at this low level there is no evidence of harm to the unborn baby.
• Women should be informed that getting drunk or binge drinking during pregnancy (defined as more than five standard drinks or 7.5 UK units on a single occasion) may be harmful to the unborn baby.

Links To The Headlines

Pregnant drinking ‘affects sperm’. BBC News, 30 June 2010

Pregnant women who drink alchohol may reduce the sperm count of sons. The Guardian, 30 June 2010

Women who drink alcohol during pregnancy ‘could damage their sons’ fertility’. Daily Mail, 30 June 2010
 

“There are far more people with Huntington’s disease in the UK than has been assumed,” said The Guardian. However, stigma and fear of insurance companies leads many to keep their condition a secret, it added.

The news is based on two articles about Huntington’s disease, a progressive, inherited disorder that affects the nervous system, for which there is presently no cure. The disease typically appears in middle age, affecting muscle co-ordination and leading to cognitive decline. One article discusses the negative medical and scientific attitudes towards Huntington’s, which, in the past, had supported the sterilisation of families who carry the gene. The other is a commentary that argues that the estimated prevalence of Huntington’s may be double the standard estimates of about six to seven in 100,000, but that stigmatisation and financial penalties in insurance policies may lead people to conceal the condition.

The articles are timed to coincide with the launch of an all-party parliamentary group to promote greater understanding and awareness of Huntington’s. While both are based to some extent on personal opinion, they highlight a serious issue for sufferers of the disease and their families and will perhaps lead to advances in both treatment and perceptions of this devastating illness.

 

Where did the story come from?

The narrative review was written by Alice Wexler, an historian from the UCLA Center for the Study of Women in Los Angeles, whose sister led the discovery of the underlying genetic abnormality that causes Huntington’s disease. The accompanying commentary is written by Sir Michael Rawlins, honorary professor at the London School of Hygiene and Tropical Medicine and chairman of the National Institute for Health and Clinical Excellence, who has helped establish the new all-party group on Huntington’s disease. Both articles were published in the peer-reviewed medical journal, The Lancet.

The articles were covered accurately in the media, with the BBC saying that this ‘devastating brain condition’ is ‘at least twice as common as previously thought’. The Guardian focused in particular on the insurance penalties faced by families who carry the gene. People who have tested positive for the Huntington’s gene are required to declare their status when applying for life insurance policies over £500,000.

 

What kind of research was this?

Both these articles present evidence to support their views that Huntington’s is and has been stigmatised by scientists and clinicians and that its prevalence has been underestimated. The commentary, on which most news stories are based, looks at the evidence on the numbers of people with Huntington’s in the UK and argues on the basis of this evidence that prevalence is far higher than has so far been estimated. The other article is a narrative review of both social and scientific attitudes towards Huntington’s that assesses a range of historical evidence from over the last century.

 

What did the articles say?

Alice Wexler’s article begins on a personal note, explaining that although the disease had killed several members of her mother’s family, it was never mentioned until her mother herself was diagnosed. This ‘missing family history’ she says, may explain why she became a historian, to understand her ‘mother’s shame’ and ‘the origins of her devastating silence’.

She describes how the discovery that Huntington’s was an autosomal dominant disease (one in which the gene only needs to be passed to a child from one parent in order for it to be inherited) at the beginning of the century, coincided with emergence of the eugenics movement, which supported selective breeding as a way ‘to improve the species’. As a result, there were calls for immigration restrictions, surveillance and compulsory sterilisation of families with a history of the condition. She cites evidence to show that scientists and physicians have historically linked the disease with ‘feeblemindedness, insanity, suicide, criminality and drug addiction’. One much-admired paper by a US psychiatrist, published in 1932, linked sufferers to ancestors accused of witchcraft.

Wexler says that such stereotyping gave a rationale for doctors to endorse celibacy or even sterilisation for people at risk, and it was only with the advent of civil rights in the 1960’s and 70’s that research priorities and representations of people with Huntington’s began to change. It was only at this point that the witchcraft link was discredited .

The accompanying commentary points out that each child of a parent with Huntington’s has a 50% chance of developing the disease, so the stigma attaches to those who are at risk as well as those with symptoms. It says that local UK studies have found the prevalence of Huntington’s to be on average six to seven per 100,000 of the population, but it argues the true prevalence is unquestionably far greater.

About 6,700 people diagnosed with the disease are currently being cared for by the Huntington’s Disease Association, meaning the minimum prevalence is at least 12.4 per 100,000. It argues that since an unknown number of patients with the disease have never been referred to the association, this is ‘unquestionably an underestimate’.

The most important reason for this underestimate, says the commentary, is the stigma associated with the condition. Huntington’s disease is the only genetic condition for which the insurance industry financially penalises those at risk.

 

How did the researchers interpret the results?

The narrative review concludes that ‘medical histories matter’ and scientists and clinicians have created ‘historical narratives’ that have deepened the stigmatisation of people with Huntington’s and lead to harmful psychological and social legacies. The accompanying commentary concludes that this stigmatisation means its prevalence has been underestimated and families with a member who have this distressing disease often try to conceal its ‘true nature’, even from their own doctors.

Reliable estimates of prevalence are needed for two reasons, the commentary argues. Firstly, so that appropriate health services can be provided, both now and in the future, for both sufferers and their families and secondly, so that any possible future treatments can be started in those at risk, before neuropsychiatric changes have occurred and symptoms of this deadly condition develop.

 

Conclusion

Huntington’s disease is a distressing disorder for which at present there is no cure. Therefore any articles that can promote awareness of the disease or shed light on its prevalence and historical attitudes, are to be welcomed.

Although both these articles present personal opinions, based on an assessment of the evidence, it seems possible, as the commentary points out, that the prevalence of Huntington’s has been underestimated and that more research into this area is needed. This is an important issue, in terms of the provision of services and also of research into treatments, especially treatments for those who might be at risk.

Links To The Headlines

Huntington’s ‘far more prevalent’. BBC News, June 30 2010

Fear of insurance penalties keeps Huntington’s sufferers in the shadows. The Guardian, June 30 2010

Links To Science

Rawlins M. Huntington’s disease out of the closet? The Lancet, Early Online Publication, 30 June 2010

Wexler A. Stigma, history, and Huntington’s disease. The Lancet, Early Online Publication, 30 June 2010

Beetroot juice “could save your life” claimed the Daily Mail. It said that the juice contains nitrate, a chemical that reduces blood pressure and therefore cuts the risk of heart disease and strokes.

The research behind this story aimed to look at whether nitrates may be responsible for the blood pressure-lowering effects of beetroot juice. It found that drinking beetroot juice or taking nitrate capsules resulted in short-term reductions in blood pressure in healthy volunteers with normal blood pressure.

The study is limited in that it was in a small number of healthy volunteers (only nine people drank beetroot juice) who were only monitored for three hours. It did not look at long-term outcomes such as heart disease or stroke.

High blood pressure is a risk factor for cardiovascular disease, and therefore reducing it is often assumed to reduce the risk of cardiovascular disease. However, whether this is the case will depend on if the effect is great enough, and if the reduction can be sustained over time. Whether drinking beetroot juice can reduce risk of cardiovascular disease would therefore need to be tested in long-term studies that assessed outcomes such as heart disease or stroke.

 

Where did the story come from?

The study was carried out by researchers the Queen Mary University of London, University College London and the University of Exeter and Plymouth. The research was funded by the British Heart Foundation. Two of the researchers report that they are directors of Heartbeet Ltd, a company linked to commercial producers of organic beetroot juice. The study was published in the peer-reviewed medical journal: Hypertension.

The BBC News and Daily Mail covered this story. The BBC News headline of, ‘Nitrate content ‘behind benefits of beetroot juice’’ is a more accurate reflection of the aims and findings of the study than the Mail’s headline, ’Drinking beetroot juice dramatically lowers risk of heart disease and strokes’. The study has not looked at the effects of beetroot juice on either heart disease or strokes, so we cannot say whether it reduces the risk of these outcomes or saves lives. The Mail also suggests that the effects of nitrate tablets and beetroot juice were directly compared, which was not the case.

 

What kind of research was this?

This randomised crossover trial investigated whether taking nitrate, either within nitrate-rich food or as a supplement capsule, affects blood pressure. The researchers’ previous study found that drinking beetroot juice reduced blood pressure in healthy people. Beetroot is high in the chemical nitrate that, when mixed with saliva in the body, is converted into nitrite, a chemical that causes blood vessels to dilate.

The aim of this research was to test whether the nitrate content of beetroot was responsible for this blood pressure-lowering effect. The researchers say that, ‘determining how vegetables confer protection against [cardiovascular disease] and exploiting this to therapeutic advantage are likely to have considerable health and economic implications’.

The study design involves participants receiving different interventions in a random order. This is an appropriate design for looking at treatments that have only short-term effects. The researchers arranged a minimum break of seven days between each treatment, to reduce the chances that the treatment given first would still be having an effect when the second was given.

 

What did the research involve?

The researchers enrolled healthy volunteers and gave them capsules containing nitrate (potassium nitrate), capsules without nitrate (potassium chloride – to rule out an effect of potassium), beetroot juice, or water. The effects of each treatment on the levels of nitrite in the blood and blood pressure were then monitored for up to 24 hours.

The volunteers were 18 to 45 years old, non-smokers, with BMI of 18 to 31kg/m2. They were not on medication to treat any medical condition and had normal blood pressure. They were asked to eat a diet low in nitrates during the study (no processed meat or leafy green vegetables).

There were three parts to the study. In each part, volunteers received two different treatments in a random order. The three parts of the study compared:

• potassium nitrate capsules (containing 1488mg nitrate) and potassium chloride capsules in 21 volunteers; participants and researchers did not know which type of capsule was being received
• a lower dose capsule of potassium nitrate and a higher dose capsule of potassium nitrate in six additional volunteers; participants and researchers knew which dose was being received
• 250ml of beetroot juice and 250ml water in nine different volunteers who were monitored for three hours after each drink; participants and researchers knew which drink was being received

There was a minimum of seven days between each treatment received.

Data was analysed by a person who did not know which treatment had been taken before each measurement of nitrite and blood pressure.

 

What were the basic results?

The researchers found that nitrate capsules were associated with increased levels of nitrite in the blood, and reduced blood pressure over a 24-hour period compared to potassium chloride capsules. Higher-dose nitrate capsules were linked with a greater increase in nitrite concentrations in the blood than lower-dose capsules.

Women had lower blood pressure and higher levels of nitrite in their blood at the start of the study (before any treatment) than men. Women showed a greater increase in nitrite in the blood after taking the nitrate capsules than men, but had smaller reductions in blood pressure.

Drinking beetroot juice also caused the levels of nitrite in the blood to increase over three hours, and systolic blood pressure to decrease by a maximum of 5.4 mmHg compared to drinking water.

 

How did the researchers interpret the results?

The researchers conclude that their findings showed dose-dependent decreases in blood pressure after taking a nitrate supplement or eating a food high in nitrate (beetroot). They say their study ‘suggests that a dietary nitrate approach to [cardiovascular disease] may have therapeutic use’.

 

Conclusion

This small study has shown some reduction in blood pressure with beetroot juice. This finding needs cautious interpretation however, as the study has several features that limit the conclusions that can be drawn from it. These include the fact that it was in only a small number of people (nine who drank beetroot juice) and that all participants were healthy and had normal blood pressure. Another constraint is that the volunteers who drank beetroot juice were only monitored for three hours, so it is unclear how long this effect may last.

The puzzling result of this study – that more women absorbed nitrate and converted it to nitrite better but had a smaller blood pressure changes when compared with men – needs further explanation. The researchers offer theories for why this may have happened. However, the fact that the fall in blood pressure in women taking the nitrate capsules appeared to be minimal compared to men suggests that nitrates (and possibly beetroot juice) may not be effective for everyone, a point not made by the researchers or the newspapers.

High blood pressure is a risk factor for cardiovascular disease, therefore reducing it is assumed to reduce the risk of cardiovascular disease. However, whether drinking beetroot juice regularly can reduce the risk of cardiovascular disease or death would need to be tested in long-term studies. Such a study would ideally be a randomised controlled trial and look at the effects of different levels of beetroot consumption.

Links To The Headlines

Drinking beetroot juice dramatically lowers risk of heart disease and strokes. Daily Mail, June 29 2010

Nitrate content ‘behind benefits of beetroot juice’. BBC News, June 29 2010

Links To Science

Kapil V, Milsom AB, Okorie M, et al. Inorganic Nitrate Supplementation Lowers Blood Pressure in Humans. Role for Nitrite-Derived NO. Hypertension 2010, published online June 28

“Cholesterol-lowering statins taking by millions might help prevent prostate cancer returning,” according to The Daily Telegraph. The newspaper said a study has found that men taking statins before their prostate removal surgery were less likely to show signs of the cancer returning.

The study looked at data on 1,319 men who had their prostate removed as a result of prostate cancer, following them up for approximately two to three years on average. The researchers made statistical adjustments to account for differences between statin users and non-users. After this, they found that men who had been taking statins were at 30% reduced risk of having an increase in levels of prostate-specific antigen (PSA), a protein that can indicate the cancer is coming back. The study did not look at whether statin use was associated with differences in length of survival, or risk of the cancer spreading to other parts of the body.

Although this study took into account a range of factors that could have affected the results, other differences between statin users and non-users could still have contributed to the differences seen. As the researchers suggest, if other studies support their findings, it would need a randomised controlled trial of statins to confirm any potential effect on recurrence rates.

 

Where did the story come from?

The study was carried out by researchers from Duke University School of Medicine and other research centres in the US. It was funded by the US Department of Defence, Department of Veterans Affairs, National Institutes of Health, the Georgia Cancer Coalition, and the American Urological Association.
The study was published in the peer-reviewed medical journal, Cancer.

The Daily Telegraph has reported on this research in a balanced way.

 

What kind of research was this?

This was a cohort study looking at whether statin use was related to risk of prostate cancer recurrence in men whose prostates had been removed (radical prostatectomy).

This type of study is good for identifying associations between a treatment and an outcome that may not have been expected. However, the design of the study makes it difficult to determine whether the treatment is truly responsible for any differences in outcome seen, as potential differences between those taking the treatment and those who did not could have led to the deiiferences seen. In this case, the best way to confirm the hypothesis that statins may reduce the risk of prostate cancer recurrence would be to test the hypothesis using a randomised controlled trial.

 

What did the research involve?

The researchers looked at data collected on 1,319 men who received radical prostatectomy for prostate cancer. They identified those men who had been taking statins, and looked at whether the time taken for these men to have a recurrence of prostate cancer was different to those not taking statins.

The researchers obtained the data from the Shared Equal Access Regional Cancer Hospital (SEARCH) database. Men who received radical prostatectomy between 1996 and 2008 at five Veterans Association medical centres across the US were eligible. For inclusion, the men also had to have data available on their statin use, the characteristics of their cancer, their length of follow up, and their race.

Recurrence of prostate cancer was defined based on raised PSA levels in the blood. Recurrence was defined as PSA levels higher than 0.2ng/mL on one occasion, two measurements of 0.2ng/mL, or receiving further treatment as a result of detectable PSA levels. Statin use before and after the surgery was assessed, with men taking statins for one or more days before surgery being classed as users. Statin use starting after surgery was not assessed.

The methods the researchers used for their analyses were standard ways of looking at the time for an event to occur in a population. In their analysis they took into account factors that could affect results (confounding factors), such as age at surgery, year of surgery, medical centre, race, body mass index (BMI), clinical stage, and tumour characteristics (Gleason score, preoperative PSA, percentage of biopsy cores containing cancer, extent of cancer spread).

 

What were the basic results?

Among the 1,319 men assessed, 236 (18%) had been taking statins. Statin users had been followed up for a shorter period on average (median 24 months) than non-users (median 38 months). Statin users were also older, were more often white, had higher BMIs, had radical prostatectomy more recently, had presented at earlier clinical stages of their cancer, but had more aggressive tumours according to their biopsy. There was no difference between statin users and non-users in extent of spread of the disease, or in the treatments received after surgery (radiotherapy or hormone therapy).

During follow up, 16% of statin users and 25% of non-users developed a biochemically-detected recurrence of prostate cancer. After taking into account potential confounding factors, statin use was associated with a 30% decrease in risk of biochemically-detected recurrence of prostate cancer (hazard ratio [HR] 0.70, 95% confidence interval [CI] 0.50 to 0.97). There was a tendency for this risk reduction to be greater for the higher doses of statins.

 

How did the researchers interpret the results?

The researchers conclude that: ‘statin use was associated with a dose-dependent reduction in the risk of biochemical recurrence’ of prostate cancer after radical prostatectomy. They say that if their findings are confirmed in other studies a randomised-controlled trial of statins in men undergoing prostatectomy ‘may be warranted’.

 

Conclusion

Some number of points to note about this study:

• As with all studies of this kind there is a possibility that factors other than the factor of interest (i.e. statin use) may be affecting results. For example, the researchers found differences between statin users and non-users, including age, race, BMI, clinical stage and biopsy findings. The researchers took these and other factors into account in their analyses, but unknown or unmeasured factors, such as smoking, diet, physical activity, how often the men were screened and other diseases associated with prostate cancer such as diabetes, may still be having an effect.
• The researchers had to rely on retrospectively analysing data already collected, which can mean that the data is not as reliable as any the study would have collected itself.  There may have been some inaccuracies on this recorded information, or differences in how it was recorded across centres.
• This research defined recurrence based on the levels of PSA in the blood. The researchers say that their previous research has found that statins reduce PSA levels in men without prostate cancer. Future studies will need to focus on whether statins are merely suppressing PSA levels or whether they also reduce other measures of prostate cancer recurrence, including the risk the cancer spreading elsewhere in the body.
• It is not possible to say from this study whether statins are associated with an increase in overall survival.

Overall, these findings suggest that statins may affect risk of biochemically-assessed prostate cancer recurrence in men who have had radical prostatectomy. However, four randomised-controlled trials of statins have been conducted already in an attempt to see if they reduce the onset of prostate cancer, and a meta-analysis of the results in 2006 showed no increase in risk of developing prostate cancer.

If other observational studies confirm an association between statin use and a reduced risk of recurrence after prostatectomy, this would support the need for randomised controlled trials to give a definitive answer about the effects of statins on this outcome.

Links To The Headlines

Statins may reduce risk of prostate cancer returning: research. The Daily Telegraph, June 29 2010

Links To Science

Hamilton RJ, Banez LL, Aronson WJ et al. Results from the Shared Equal Access Regional Cancer Hospital (SEARCH) Database. Cancer, [Early online publication] June 28 2010