"Cancer cell enzymes shown to act as 'good cops'," is the headline on the BBC News website.

The BBC reports on laboratory research into an enzyme called MMP-8 and its effects on breast cancer. The research reveals that while MMP-8 appears to stimulate the growth of breast cancer cells in the short-term, it may slow tumour growth in the long-term.

Scientists are likely to want to explore new treatments that use MMP-8’s ability to slow tumour growth in this way. However, this study used laboratory-grown cells, which don’t behave in the same way as tumour cells within the body. It could be the case that the effect of MMP-8 is different when studied in people.

Nonetheless, this research provides new understanding about how the MMP-8 enzyme influences the growth and development of laboratory-grown breast cancer cells. And while this research has limited immediate implications for people with breast cancer it does contribute new understanding that may help to treat the disease in the future.

Where did the story come from?

The study was carried out by researchers from the University of East Anglia (UK) and the University of Vermont College of Medicine (USA) and was funded by Breast Cancer Campaign, Cancer Research UK, the European Union Framework Programmes 6 and local Norfolk fundraisers.

The study was published in the Journal of Biological Chemistry, a peer-reviewed science journal. It was published as an open-access article so it is free to download.

The reporting of the research was mixed. While the Mail Online exaggerated the results of the study by describing a “breakthrough” that “turns previous thinking on its head”, the BBC coverage was more restrained, including comment from Cancer Research UK on how the research provides "very early clues" about how the enzyme might recruit cells to fight breast cancer.

What kind of research was this?

This was a laboratory study exploring the role of an enzyme called matrix metalloproteinase-8 (MMP-8) in the growth of breast cancer tumour cells.

MMP-8 performs many essential jobs in a normal cell. The researchers say it is known to activate certain immune system signals (called interleukin-6 and interleukin-8), which are types of molecules that regulate and orchestrate the actions of the immune system.

The researchers comment that, traditionally, scientists thought MMP-8 helped cancer cells grow and spread, but more recent research has suggested it may also prevent cancer cell growth.

This research sought to find out if, and how, MMP-8 inhibited tumour cell growth in laboratory-grown breast cancer cells.

Understanding the biology and chemistry of processes involved in diseases such as cancer through laboratory studies is essential if we want to discover new ways to prevent and treat them.

What did the research involve?

The researchers grew human breast cancer tumour cells in a laboratory. Some cancer cells were deliberately engineered to lack a properly functioning MMP-8 enzyme (called “mutant MMP-8”), whereas others had a fully functional version (known as the “wild-type” version). The intention was to see what effect this had on the ability of the cancer cells to grow and develop.

The researchers paid particular attention to the effect of this manipulation on the immune system signalling molecules interleukin-6 (IL-6) and IL-8, which are known to be involved in the growth and development of cancer cells. Genetic changes within the cells were also measured. 

All the research was carried out in artificially grown laboratory cells and no tests were done in people with cancer.

What were the basic results?

The research found tumour cells containing the wild-type MMP-8 had elevated levels of IL-6 and IL-8 and that, in the short-term, this was associated with higher levels of tumour cell growth. Cells lacking a working MMP-8 enzyme had lower levels of IL-6 and IL-8 and did not grow as well.

However, in the longer term, activity of the MMP-8 enzyme was found to inhibit the growth of the tumour cells and it was found that the IL-6 and IL-8 levels were no longer elevated.

Interestingly, the small number of cells with a working MMP-8 enzyme that did keep on growing in the long-term had somehow maintained their elevated levels of IL-6 and IL-8 but these were no longer dependent on MMP-8 activity. The relationship had changed from the short- to the long-term.

This showed that in the early stages of tumour growth MMP-8 activity stimulated IL-6 and IL-8, which helped the tumour grow, but, later on, MMP-8 activity limited tumour growth and the IL-6 and IL-8 levels returned to normal.

Only cancer cells where MMP-8 activity had become disconnected from IL-6 and IL-8 levels were able to keep growing in the longer term. 

How did the researchers interpret the results?

The researchers concluded that their research showed a “causal connection” between “MMP-8 activity and the IL-6/IL-8 network”, which showed MMP-8 influences the signalling of pro-inflammatory factors (IL-6 and IL-8) that “conventionally promote tumour cells’ growth and development”.

Conclusion

This laboratory study provides new understanding about how the MMP-8 enzyme interacts with inflammatory signals (IL-6 and IL-8). MMP-8 might be something of a double-edged sword. While it stimulates the growth of cancerous cells in the short-term, it may also suppress growth in the long-term.

As with all laboratory studies, new or different discoveries need to be replicated by other research groups to ensure they are accurate and the results weren’t due to chance.

Assuming the research results are valid they could provide an opportunity for cancer researchers to investigate and possibly devise new methods of using MMP-8 activity to supress breast tumour cell growth. However, the research found that some tumour cells kept growing despite the presence of MMP-8. This highlights that cancer cells differ, and that, often, what works in one place and setting may not work in others.

It is important to remember that the researchers investigated breast cancer cells only, so this study alone does not tell us anything about the role of MMP-8 in other cancer types. Similarly, the research used artificially grown breast cancer cells, which may not behave in exactly the same way as tumour cells within a human body.

This research into a new target for drug development provides new and interesting understanding that other researchers can build on. An improved understanding of the biology underpinning breast cancer may lead to the development of new treatments.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Cancer cell enzymes shown to act as 'good cops'. BBC News, May 24 2013

Breast cancer cells can suppress tumour growth 'by releasing protective proteins'. Mail Online, May 24 2013

Links To Science

Thirkettle S, Decock J, Arnold H, et al. Matrix metalloproteinase-8 (collagenase-2) induces the expression of interleukins-6 and -8 in breast cancer cells. The Journal of Biological Chemistry. Published online May 30 2013

Writing in the New York Times, actress Angelina Jolie has announced that she has recently undergone a double mastectomy (where both breasts are surgically removed) followed by breast reconstruction surgery.

She writes that this is because genetic testing revealed she had a 87% chance of developing breast cancer in later life, as well as a 50% risk of ovarian cancer. This means she took a decision to have ‘preventative surgery’.

Jolie explained: "I decided to be proactive and to minimise the risk as much as I could. I made a decision to have a preventative double mastectomy.

"Cancer is still a word that strikes fear into people’s hearts, producing a deep sense of powerlessness. But today it is possible to find out through a blood test whether you are highly susceptible to breast and ovarian cancer, and then take action."

What genes contribute to breast cancer risk?

A number of genes, associated with breast cancer, have been identified. People often talk about 'having' these genes, which include BRCA1, BRCA2, TP53 or PTEN. In fact, every women has these genes, but if a fault (mutation) develops in one of the genes then it can increase the risk of a women developing breast cancer.

It is estimated that around 1 in 500 women have a high-risk mutation in one of the genes associated with breast cancer. However, having this high risk mutation does not mean that a woman will definitely develop breast cancer.

What is the risk if you have a faulty breast cancer gene?

If you have a faulty gene, it doesn't mean you'll definitely develop breast cancer, but you are at a higher risk.

Having a fault in one of the breast cancer genes raises the risk of developing breast cancer to between 50% and 85%. In other words, out of every 100 women with a faulty gene, between 50 and 85 of them will develop breast cancer in their lifetime.

Are all women routinely tested for faulty genes?

No. Testing, provided by the NHS, is usually only offered to women thought to be at high risk of having a faulty gene. These include:

• women with a strong family history of breast cancer where a living family member with breast or ovarian cancer is available for testing
• women with a family history of several relatives developing early-onset breast cancer (cancer that develops before the age of 50), as this is often associated with having a faulty gene

Gene testing is also available from private clinics. The tests can be expensive, with available prices quoted on the internet ranging from around £2,000 to £3,000. The Pink Lotus Breast Center, where Angelina Jolie had her treatment, states that it screens for BRCA gene mutations in women without cancer who:

• have two or more family members with breast cancer, one under the age of 50
• have a previously identified BRCA mutation in the family at any age
• are of Ashkenazi Jewish descent with a family history of breast or ovarian cancer

Will I need a mastectomy if I am found to have a faulty gene?

No. There is a range of treatment options available to you.

First, there is the option of what is known as active monitoring. This is where you receive annual screening in the form of mammograms or MRI scans (or sometimes both) to monitor the state of your breast tissue.

Changes in your lifestyle can also reduce your individual breast cancer risk. These include taking plenty of exercise and maintaining a healthy diet.

There is also the option of waiting to see if breast cancer develops, and if it does it can be treated using conventional methods as with other breast cancers. Breast cancer cure rates are good and continue to improve. The chance of making a full recovery, especially if the cancer is detected early, are relatively high compared with other forms of cancer.

Ultimately, there is no right or wrong answer about what you should do. Your care team can provide advice that will allow you to make an informed decision about your treatment. But the decision is one only you can make.

What happens if I decide to have a preventative mastectomy?

As much breast tissue as possible is removed through a single cut horizontally or diagonally across the chest under general anaesthetic. It’s a physically and emotionally draining operation. Expect some pain and fatigue afterwards and to spend one or two nights in hospital. It generally takes three to six weeks to recover fully.

What is breast reconstruction?

Basically, new breasts are formed from skin and muscle from your back, stomach or buttocks, or by using implants. It’s often possible to have reconstruction straight away – in the same operation as the mastectomy – though you can have it done later. Angelina Jolie had her breasts reconstructed with implants nine weeks after her double mastectomy. If your nipples have to be removed during the mastectomy, then they can be reconstructed with skin from another part of your body, and the areola created by tattooing.

Will the new breasts look and feel the same as before?

Reconstructed breasts won’t feel the same to you as your real ones did – the nerves have been cut, so they’ll always be numb, and there will be noticeable scars, but women generally report being happy with the cosmetic outcome. 

Edited by NHS Choices. Follow Behind the Headlines on twitter.

Links To The Headlines

My Medical Choice. New York Times, May 14 2013

'Redheads are at increased risk of skin cancer even if they don't spend time in the sun,' is the headline on the Mail Online website.

The story refers to a discussion piece in a journal that outlines theories about the results of some animal experiments. This research involved mice genetically engineered to have red fur and predisposed to develop melanoma.

Although exposure to ultraviolet (UV) light is known to be a major risk factor for melanomas, the researchers found that genetically engineered mice with red fur still had a high risk of developing melanomas even without UV exposure.

The article discusses potential explanations for why this could be the case, and these theories now need to be tested to see if they are correct.

It is not yet clear how well these animal studies represent what happens in people with red hair. It would be very difficult to test this directly, as keeping people completely away from sunlight would be impractical and potentially unethical.

UV light exposure is known to increase the risk of melanoma in redheads and non-redheads alike. It is important that people with red hair should continue to use sensible precautions to avoid excessive UV exposure and sunburn, despite this news.

Where did the story come from?

The article was written by researchers from the Cutaneous Biology Research Center at Massachusetts General Hospital in the US.

No sources of funding for the article were reported. It was published as an "Ideas and Speculations" article in the journal BioEssays. These pieces are described as "creative thinking and predictions on open questions and recent developments in biology".

The article has been peer-reviewed.

The news is based on an article by researchers that presents possible explanations for their previous finding that genetically engineered mice with red fur and a predisposition to melanoma develop this cancer even without UV exposure.

Some of the Mail Online reporting suggests that the findings of this research are more conclusive than is possible to say at this stage: "Scientists have discovered that the production of red hair pigment causes an increased risk of melanoma".

However, the BioEssays article was only presenting possible explanations for observations from animal experiments. It was not claiming to have definitive proof that these findings apply to humans.

What kind of article was this?

This was an article discussing the potential link between the red pigment in red hair and skin cancer.

People with red hair and fair skin are known to be at greater risk of getting melanoma, the least common but most serious form of skin cancer, which is responsible for around two thousand deaths a year in the UK.

In general, it is thought that redheads' pale skin makes them more susceptible to UV damage from the sun's rays.

However, the authors of the article say that a recent study from their lab suggests that the pigment that causes hair to turn red (pheomelanin) could itself be linked to the increased risk of cancer, even without UV exposure.

In their article, the authors discuss two possible ways in which the red pigment in red hair might increase the risk of cancer. These preliminary ideas – or hypotheses – are based on previous research and a general understanding of human and cancer biology.

A hypothesis is a possible explanation of why something that researchers have observed might happen. Researchers design experiments to test whether their hypothesis is correct. This process is fundamental to the scientific method.

What did the article say?

The researchers first describe how the red colour in red hair is made, and discuss the results of their recent study before going on to present their hypotheses.

Specific cells in the skin called melanocytes make two kinds of pigment – a brown pigment called eumelanin and a red-orange pigment called pheomelanin. A biochemical process within cells determines how much of each pigment is made.

This process involves a protein called MC1R, which influences the switch between the production of these pigments based on the strength of the signal it sends to the cell and whether the cell has enough of the amino acid cysteine.

In redheads, variations in the gene for the MC1R protein means that it sends weak signals. This means that the cells' stores of cysteine are usually enough for it to favour producing the red/orange pigment pheomelanin.

The researchers recently carried out a study where they introduced a genetic mutation commonly found in melanoma cells into the melanocytes of mice. When they also introduced a genetic mutation into these mice that inactivated the MC1R protein, the mice had red fur and developed melanoma, even without UV exposure. If they introduced another genetic mutation that stopped pigment being made altogether, the mice were albino but they did not develop melanoma.

This led the researchers to suspect that the red pigment pheomelanin could be itself increasing the risk of melanoma. Their research also found that the mice with red fur had more damage to their skin cell DNA caused by very reactive chemicals called free radicals. Free radicals can cause damage to cells at a molecular level.

The researchers do not yet know how the red pigment might be linked with the free radical DNA damage that can increase the risk of melanoma. However, they have presented two hypotheses:

The first hypothesis

The researchers' first hypothesis was that the red pigment itself might generate more free radicals, and that these cause DNA damage that could lead to melanoma. They say that the red pigment is already known to make free radicals when it is exposed to UVA light, but it may be able to do this without UVA light. These free radicals could potentially:

• damage DNA directly
• damage its building blocks, or
• use up the cell's stores of antioxidants, making it more vulnerable to damage by other free radicals

The researchers also discuss in detail the biochemical ways in which the red pigment might generate free radicals.

The second hypothesis

The second hypothesis was that the process of making the red pigment might use up the cell's stores of antioxidants, rather than the red pigment itself. This might make the cells more vulnerable to damage by other free radicals.

They say that the amino acid cysteine used in making the red pigment is also found in the most important antioxidant in the cell, glutathione. If cysteine is used to make the red pigment, this might reduce the cell's ability to make this antioxidant.

The researchers report that red-haired wild boars have been found to have less glutathione in their muscles. However, they acknowledge that it is not possible to say from this whether there is less glutathione due to free radicals from the red pigment itself or the making of the red pigment.

What were the researchers' conclusions?

The researchers presented two hypotheses that could explain how the red skin and hair pigment pheomelanin could increase the risk of the skin cancer melanoma.

They say that their two proposed methods could both be occurring, and that more research could help identify how redheads can reduce their risk of melanoma.

Conclusion

The researchers' article discusses potential ways in which the red pigment found in the cells of people with red hair might increase the risk of melanoma, the most serious form of skin cancer. It is not a standard report of a research study, but the authors put forward potential explanations for their previous research findings. These now need to be tested to see if they are correct.

The researchers' previous research found that mice genetically engineered to be predisposed to melanoma and red fur developed melanomas even without UV exposure. It is not clear to what extent these genetically engineered mice represent what happens in humans.

It would be very challenging to test this – keeping people completely away from UV light would not be feasible or ethical, as we need some sun exposure to make vitamin D, which is needed to make and maintain strong bones. For this reason, research in mice can be very helpful.

It is important that redheads do not take this news as a reason not to protect themselves from the effects of the sun. We already know that UV light exposure increases the risk of melanoma in people regardless of hair colour. People with red hair should continue to use sensible precautions to avoid excessive UV exposure and sunburn.

Read more about reducing your melanoma risk. 

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Redheads are at increased risk of skin cancer even if they don't spend time in the sun. Mail Online, May 10 2013

Links To Science

Morgan AM, Lo J, Fisher DE. How does pheomelanin synthesis contribute to melanomagenesis? BioEssays. Published online May 7 2013

Much of the UK media are covering the release of data that indicates breast cancer rates in the under-50s are now at a record high. Changes in childbirth patterns and alcohol consumption could be to blame, according to a leading charity.

The news follows new data released by Cancer Research UK. Its data shows that breast cancer diagnoses among women aged under 50 have now reached an all-time high, breaking the 10,000 mark for the first time in 2010. One in five diagnosed breast cancer cases are now in women under the age of 50.

Possible explanations for the increases are speculated to be due to known hormonal risk factors for cancer – such as having children later in life. Increased alcohol intake, another risk factor for breast cancer, could also be involved.

The rise in the number of new cases is not restricted to the under-50s: there has been a steady increase in the number of cases diagnosed for women of all ages since the 1970s.

But the rise isn’t necessarily as bad as it sounds. For example it could reflect better breast awareness and improved diagnosis and screening, which in turn might lead to early treatment and improved chances of survival.

The good news is that – despite the increase in breast cancer diagnoses – breast cancer deaths are actually falling. An increasing number of women are now survivors of breast cancer.

What does the data show?

Breast cancer is the most common cancer among women, accounting for almost a third of all new cancer cases in women. Cancer Research UK reports how their latest statistics revealed that in 2010, there were 10,000 new cases diagnosed among women aged under 50. This is an 11% increase from 15 years previously in 1995 when there were 7,700 cases of breast cancer diagnosed among women in this age group.

One in five breast cancers (20%) are now diagnosed in women aged under 50. Nearly half of breast cancers (48%) are diagnosed in women aged between 50 and 69 – the age group currently invited for breast cancer screening.

However, the rise in the number of breast cancer cases is not restricted to the under-50s. Since the 1970s there has been a gradual and steady increase in the number of breast cancer cases. Overall there was an 18% increase in rates between 1995 and 2010.

What are the possible reasons behind the increased rates among younger women?

Cancer Research UK says that, though it is not clear why cases of breast cancer are increasing among younger women, alcohol intake and hormonal factors may play a role.

Alcohol

Alcohol is an established risk factor for breast cancer. Cancer Research UK reports that the combined results of two large systematic reviews of the published evidence, in addition to findings from the UK Million Women Study, suggest that each additional unit of alcohol per day can increase a woman’s risk of the disease by between 7% and 12%. The research suggests that by the age of 80, roughly the following number of women will have developed breast cancer:

• 9 out of 100 if they don't drink at all
• 10 out of 100 if they have two drinks a day
• 13 out of 100 if they have six drinks a day

However, as Cancer Research UK does say, the possible risk increase from alcohol is less compared to the greater influence of other factors – particularly hormonal factors.

Hormonal factors

Very generally, increased exposure to the hormone oestrogen is associated with increased risk of breast cancer because it can stimulate breast cancer cells to grow. Higher lifetime oestrogen exposure is associated with:

• starting periods at a younger age
• going through the menopause at a later age
• use of the combined oral contraceptive pill (which contains oestrogen)
• fewer (or no) pregnancies
• shorter duration of (or no) breastfeeding
• use of HRT (which contains oestrogen)

Both having children and breastfeeding are known to be protective against breast cancer. In theory the younger a woman is when she has her first pregnancy, and the more pregnancies she has in her lifetime, further decreases her risk. Similarly, the more a woman breastfeeds will decrease her risk. Therefore, modern western lifestyles (that include women generally starting families later and having smaller families) may give some possible explanation to the increase in breast cancer rates among younger women.

Are there any positive signs?

Despite the increased rates among women overall and specifically among women aged under 50, Cancer Research UK does report some good news: that fewer women than ever before are now dying from breast cancer. This due to better treatment, the charity says.

The rate of women aged under 50 who are dying from breast cancer has fallen by 40% since the early 1990s. Twenty years ago, the death rate from breast cancer in the under-50s was 9 per 100,000 women in the UK.  By late 2000, this had fallen to 5 per 100,000 women. More than 8 in 10 women diagnosed with breast cancer before the age of 50 are now reported to survive the disease for at least five years.

Although not discussed by the Cancer Research UK report, the rise in cases could be a reflection of increased awareness of breast cancer and increased rates of diagnosis and improvement in screening techniques.

As a concluding message, Sara Hiom, Cancer Research UK’s director of health information, says: “Breast cancer is more common in older women, but these figures show that younger women are also at risk of developing the disease. Women of all ages who notice anything different about their breasts, including changes in size, shape or feel; a lump or thickening; nipple discharge or rash; dimpling, puckering or redness of the skin, should see their GP straight away, even if they have attended breast cancer screening.

“It’s more likely not to be cancer, but if it is, detecting it early gives the best chance of successful treatment,” she added.

What can I do to reduce my risk of breast cancer?

Unlike some other cancers, the body of evidence about proven methods of reducing risk is relatively small. Though most experts would recommend that:

• you stick to the recommended alcohol consumption rates for women
• you take plenty of exercise
• you maintain a healthy weight
• avoid smoking

It is also important that you attend breast cancer screening appointments when invited. Women aged 50 to 70, who are registered with a GP, are automatically invited for screening every three years.

Read more about the NHS Breast Screening Programme.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Breast cancer cases in UK under-50s top 10,000 a year. BBC News. May 3 2013

Breast cancer rates increase among younger women. The Guardian, May 3 2013

Breast cancer cases soar to 27 a day among the under-50s... and experts fear modern lifestyles are to blame. Daily Mail, May 3 2013

Under-50s with breast cancer at record high. The Daily Telegraph, May 3 2013

Breast cancer on the rise in under 50s who now account for 1 in 5 cases. Daily Mirror, May 3 2013

Links To Science

Cancer Research UK. Breast cancer in women under 50 tops 10,000 cases for first time. May 3 2013

BBC News has revealed that, "Women who smoke have a higher risk of cancer than men," reporting the results of a new study examining the relationship between gender and bowel cancer caused by smoking. 

The large-scale study found that smoking increased the risk of bowel cancer in women by 19% compared with women who had never smoked. This was much larger than the (non-significant) 8% risk increase seen in male smokers.

Smoking is a recognised risk factor for bowel (colon) cancer and several other life-threatening diseases in both men and women. It is important to bear in mind that this research only looked at colon cancer. Whether there are gender differences in other smoking-related cancers, such as lung cancer, is uncertain based on the findings of this study alone.

The authors point out that their study did not take into account important risk factors known to be linked to bowel cancer, such as family history, diet, and alcohol consumption. If these had been accounted for the results may well have been different.

The study also didn't produce any firm evidence to explain why there may be a difference in risk between women and men. Future research will need to address these limitations to see if the gender differences in risk still apply and, if so, why.

Where did the story come from?

The study was carried out by researchers from the University of Tromsø, Norway in collaboration with researchers from institutions in Hawaii and Finland, and was funded by the Norwegian Cancer Society.

It was published in the peer-reviewed journal Cancer Epidemiology, Biomarkers and Prevention.

The BBC's coverage was generally accurate, although it wasn't initially obvious that the study only related to bowel cancer rather than all cancers, which readers may have assumed from the headline.

The BBC also discussed a second recent study (also covered by the Mail Online website) that reportedly showed how teenage girls exposed to passive smoking had lower levels of the "good" form of cholesterol that reduces heart disease risk. This, the BBC reported, gave a possible explanation as to why women who start smoking increase their risk of a heart attack.

What kind of research was this?

The researchers reported how smoking is a recently established risk factor for what medical professionals refer to as colon cancer, or cancer of the large bowel. They explained that the levels of colon cancer in Norwegian women are unusually high when compared with similar countries.

In men, smoking levels peaked during the late 1950s, while in women levels did not peak until the 1970s. The fact that historically women smoked less but still had high levels of colon cancer could mean they were more vulnerable to the harmful effects of smoking in terms of colon cancer risk.

To test this, the researchers carried out a cohort study to see if women may be more susceptible to smoking-related colon cancer than men.

What did the research involve?

The researchers recruited 602,242 Norwegians who were aged 19 to 67 at enrolment between 1972 and 2003.

They combined the information gathered from four separate cohort studies into one larger study. The researchers linked unique IDs assigned to each of the study participants to National Cancer Registry databases so they could establish whether any of the study group developed cancer.

At enrolment, and at various other points throughout the study period, participants filled out multiple questionnaires about a wide range of health and lifestyle behaviours, such as smoking, diet and physical activity levels, as well as demographic information.

Smoking levels were categorised into two main groups for analysis:

• those who had never smoked (never-smokers)
• a pooled group of current smokers and ex-smokers (ever-smokers)

The main analysis looked at how the two levels of smoking influenced the risk of developing colon cancer overall, as well as specific subgroups of colon cancer. That is, whether the cancer was located in the first part of the colon (proximal colon cancer) or lower parts of the colon (distal colon cancer).

The main analysis took account of age at enrolment, level of physical activity, body mass index (BMI) and years of education. These represented factors known to influence the risk of developing colon cancer (confounders).

What were the basic results?

The study followed people for an average of 14 years, during which time 3,998 people (46% women) developed colon cancer.

Female ever-smokers had a 19% increased risk of colon cancer compared with female never-smokers (hazard ratio [HR] 1.19, 95% confidence interval [CI] 1.09 to 1.32). This was much larger than the non-significant 8% increased risk found between male ever-smokers compared with male never-smokers (HR 1.08, CI 0.97 to 1.19).

Women categorised in the groups who started smoking the earliest, smoked for longest, or smoked the most cigarettes per day were at more than 20% higher risk of colon cancer (range 28-48%) than women never-smokers.

The increase in risk was much larger for proximal colon cancer, with female ever-smokers more than 40% more at risk of developing the disease compared with female never-smokers.

The researchers also tested for differences in the findings between men and women. They found this was only the case for the association between female ever-smokers and the risk of proximal colon cancer.

How did the researchers interpret the results?

The researchers concluded that their findings meant that, "Female smokers may be more susceptible to colon cancer, and especially to proximal colon cancer, than male smokers."

Conclusion

In this study, the researchers suggest that smoking played a role in increasing the risk of colon cancer in both sexes, but it seemed to play more of a role in women smokers. This particularly increased the risk of cancer of the first part of the large bowel (proximal colon cancer).

The study had many strengths, including its large size and long follow-up time. However, the research suffers from some limitations, meaning that we can't be sure that women smokers really do have a higher risk of colon cancer based on this study alone.

These limitations include:

• The study did not take account of many factors known to increase the risk of colon cancer, such as higher alcohol and red meat consumption. Had it done so, the results may have been different. The researchers point out that, generally, alcohol and red meat consumption is higher in men, putting them at an increased risk of colon cancer. Not taking these factors into account means it was less likely to find the results they did.
• The study only looked at colon cancer. This tells us nothing about whether women smokers are more susceptible than men to other types of cancers. This would need direct investigation.
• Smoking was categorised into only two groups rather than a more detailed breakdown, and did not account for passive smoking levels. There will therefore have been some error in using this simple categorisation method.

Overall, the study suggests the effect of smoking on the risk of developing colon cancer may differ by gender, but it cannot confirm this is definitely the case, or explain why this may be. Further research is required to confirm both of these questions.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Smoking 'poses bigger risk to women'. BBC News, May 1 2013

Links To Science

Parajuli R, Bjerkaas E, Tverdal A, et al. The Increased Risk of Colon Cancer Due to Cigarette Smoking May Be Greater in Women than Men. Cancer Epidemiology Biomarkers Prevention. Published online April 30 2013. 

“Breast implants may harm breast cancer survival chances,” The Guardian warns, along with other media sources reporting on the same subject.

It is important to stress that the research the media has reported does not suggest that breast implants cause breast cancer.

Instead, the research suggests that breast implants may cause a delay in diagnosis in women who have breast cancer, which may increase their risk of dying from the condition.

The researchers suggest that the implants could hide cancerous tissue that would otherwise be detected during screening.

To test this, the researchers reviewed several small studies looking at whether having cosmetic breast implants was associated with (no causal association) a delay in diagnosis, and whether women with breast cancer who had implants were at increased risk of dying from the disease.

They found some evidence of an association. Women with breast implants had a 26% increased risk of being diagnosed at a later stage of breast cancer than those without implants. Women with implants also had a 38% greater risk of dying from breast cancer than women without implants.

However, as the authors rightly point out, the results of these analyses should be viewed with caution. This is because they couldn’t find previous research of high enough quality to draw firm conclusions, and better quality studies would be needed to confirm the association.

Where did the story come from?

Links To The Headlines

Breast implants may harm breast cancer survival chances, study finds. The Guardian, May 1 2013

Do breast implants raise cancer danger? They make tumours harder to spot, says report. Daily Mail, May 1 2013

Boob jobs ‘increase risk of cancer death by 40%’. Metro, May 1 2013

Breast implants 'increase cancer death risk,' say scientists. The Independent, May 1 2013

Breast Implants 'Raise Cancer Death Risk'. Sky News, May 1 2013

Links To Science

Lavigne E, Holowaty EJ, Pan SY, et al. Breast cancer detection and survival among women with cosmetic breast implants: systematic review and meta-analysis of observational studies. BMJ. Published online April 30 2013

“Hormone treatments can cut breast cancer rates in at-risk women by 38%,” reports the Daily Mirror.

The news, covered by much of the media, is based on research into selective oestrogen receptor modulators (SERMs), a class of drug that binds to oestrogen receptors in breast cells and elsewhere.

The study making today’s news suggests that SERMs could be effective for preventing breast cancer. Researchers combined the results of several studies that had compared SERMs with other drugs in women without breast cancer.

Most of the trials recruited women who were either at high risk of breast cancer or who had osteoporosis.

Researchers found that SERMs reduced the incidence of breast cancer during 10 years of follow-up.

Links To The Headlines

500,000 to be offered daily breast cancer pill. The Times, April 30 2013

Breast cancer drug 'benefits at-risk patients'. The Daily Telegraph, April 30 2013

Drug that PREVENTS breast cancer could soon be given to half a million women on the NHS. Daily Mail, April 30 2013

Four drugs 'can reduce chance of breast cancer in at-risk women'. The Guardian, April 30 2013

Hormone treatments can cut breast cancer rates in at-risk women by 38%. Daily Mirror, April 30 2013

Links To Science

Cuzick J, Sestak I, Bonanni B, et al. Selective oestrogen receptor modulators in prevention of breast cancer: an updated meta-analysis of individual participant data. The Lancet. Published online April 30 2013

"Smoking just a few cigarettes a day more than doubles a woman's risk of developing rheumatoid arthritis," the Mail Online website reveals. The website reports on a Swedish study that found women who only smoke a small number of cigarettes a day significantly increase their risk of developing the condition.

This large study followed more than 30,000 women over a seven-year period to look at whether smoking increased their risk of developing rheumatoid arthritis. Smoking is already recognised as a possible risk factor for developing the condition. 

But this study showed that the risk increased even at relatively low levels of smoking. It found that even smoking as many as between one and seven cigarettes per day more than doubled a woman's chance (2.31 times) of developing rheumatoid arthritis compared with a woman who had never smoked.

Although this study provides further evidence about the dangers of smoking, it does have a number of limitations. For example, it is not clear how many women dropped out of the study, which could have biased the results. It is also unclear whether similar risk patterns would be seen in men (the condition is more common in women) or a more ethnically diverse group.

Nonetheless, this study provides evidence of yet another disease that smokers may be at significantly increased risk of developing, even if they are considered to be 'light' smokers.

Where did the story come from?

The study was carried out by researchers from the Karolinska Institutet in Sweden and was funded by research grants from the Swedish Research Council's Committee for Medicine, Committee for Research Infrastructure for maintenance of the Swedish Mammography Cohort, and the Swedish COMBINE inflammation research consortium.

It was published in the peer-reviewed science journal Arthritis Research and Therapy.

The Mail Online's coverage of the study was generally accurate, and included information about the study sample size and an idea of the prevalence of the condition.

What kind of research was this?

This was a cohort study that aimed to discover how much a woman needs to smoke in order to increase her risk of developing rheumatoid arthritis.

The authors pointed out that previous studies have shown that cigarette smoking was directly associated with a higher risk of developing rheumatoid arthritis. What was unclear was whether this risk was associated with so-called 'light' smoking and whether quitting smoking reduced the risk.

The focus of this study was therefore on examining how much the risk of developing rheumatoid arthritis increased depending on how much a woman smoked and how long they had smoked for, and whether it was possible to reduce this risk if a woman quit smoking.

Rheumatoid arthritis is what is known as an autoimmune condition, where the body's own immune system starts to attack the cells that line the joints, causing pain and swelling. Hands, feet and wrists are commonly affected, but it can also damage other parts of the body.

The condition is estimated to affect more than 580,000 people in England and Wales, and occurs more frequently in women than men. It is most common between the ages of 40 and 70, but can affect people of any age.

Exactly how smoking can increase the risk of a person developing rheumatoid arthritis is still uncertain. One theory is that that it can disrupt the normal workings of the immune system, leading to the type of abnormal immune response associated with the condition.

What did the research involve?

The researchers used an existing cohort of women called the Swedish Mammography Cohort, which included 34,101 women aged 54 to 89 years. For the current study, the group were followed from January 1 2003 to December 31 2010, in which time 219 cases of rheumatoid arthritis occurred.

Women were asked about various aspects of their diet and lifestyle via questionnaire, as well as additional questions about their smoking habits and history, physical activity, and their use of some medications and dietary supplements.

The current study population of 34,101 excluded women from the mammography cohort who had missing data on their smoking status (797), as well as women with non-rheumatoid arthritis joint conditions (2,052). Women already diagnosed with rheumatoid arthritis were also excluded.

Cases of rheumatoid arthritis were identified by linking the records of women in the cohort to medical databases. The researchers also had access to a national rheumatology register so they would be notified if a diagnosis of rheumatoid arthritis was made.

The analysis estimated the relative risk (RR) between various aspects of smoking behaviour – such as intensity, duration and time since quitting – and the risk of developing rheumatoid arthritis. The analysis took into account a variety of potentially modifying factors (confounders), including alcohol consumption, menopausal status, educational level and body mass index.

What were the basic results?

Over the seven-year study period, 219 cases of rheumatoid arthritis occurred from within the group of 34,101 (0.6% of the cohort). There was a statistically significant association between smoking intensity and the risk of developing rheumatoid arthritis.

Women who smoked between one and seven cigarettes per day were 2.31 times more likely to develop the condition compared with never smokers (RR 2.31 95% confidence interval (CI) 1.59 to 3.36) over the course of the seven-year study.

There was also a statistically significant association between how long a woman had smoked for and the risk of developing rheumatoid arthritis. Women who had been smoking for between one and 25 years were 1.60 times more likely to develop the condition compared with never smokers (RR 1.60, 95% CI 1.07 to 2.38).

Compared with never smokers, the risk for these smokers was still significantly elevated (to about twice the risk of never smokers) 15 years after the women had quit smoking (RR 1.99, 95% CI 1.23 to 3.20).

Among former smokers, there was a suggested trend that the risk of rheumatoid arthritis decreased over time since stopping smoking. For example, women who stopped smoking 15 years before the start of the study had a non-significant 30% lower risk of rheumatoid arthritis compared with those who had stopped only a year before the start of the study (RR 0.7, 95% CI 0.24 to 2.02).

How did the researchers interpret the results?

The researchers concluded that, "even light smoking is associated with increased risk of rheumatoid arthritis in women and that smoking cessation [stopping smoking] may reduce, though not remove, this risk".

Conclusion

This research indicates that a relatively low level of smoking (one to seven cigarettes per day) is associated with an increased risk of developing rheumatoid arthritis compared with women who had never smoked. This adds further knowledge to previous research that has suggested that cigarette smoking is directly linked to a higher risk of developing rheumatoid arthritis.

While this study is relatively robust and its results believable, it does have limitations that should be considered. It was not clear how many women dropped out of the study. If this was a large proportion of the women who started, it could significantly bias the results of the study.

The study also only recruited women. The same risk pattern may not have been seen if the study had recruited men, who are at lower risk of developing the condition than women. Similarly, the size of the risk differences between different smoking behaviours may be slightly different in men than women. Further research is needed to establish whether this is the case.

Another drawback is that women were recruited from just two Swedish counties. While no ethnicity data was reported, it is likely they were fairly similar ethnically, and it could be that different ethnicities may have different risk profiles for developing rheumatoid arthritis. This means that the results may differ if the study was repeated in a more ethnically diverse population.

This relatively robust study suggests that smoking can significantly increase a woman's risk of developing rheumatoid arthritis compared with women who never smoked, even if a woman only smokes relatively low levels of between one and seven cigarettes per day.

It adds to a growing body of evidence that there is no such thing as a safe level of smoking. Aside from the risk of rheumatoid arthritis, 'light' smoking can significantly increase your risk of developing lung cancer, heart disease and stroke.

Read more about how the NHS can help you quit smoking.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Smoking just a few cigarettes a day can double a woman's risk of arthritis. Mail Online, April 22 2013

Links To Science

Giusueppe DD, Orsini N, Alfredsson L, et al. Cigarette smoking and smoking cessation in relation to risk of rheumatoid arthritis in women. Arthritis Research and Therapy. Published online April 22 2013

There is wide coverage of new research that argues that routine screening could reduce deaths from prostate cancer, with BBC News, The Daily Telegraph and the Daily Mail all reporting the story. This controversial study is likely to reignite the debate about whether routine screening for prostate cancer does more harm than good.

The large long-term study involved prostate-specific antigen (PSA) blood tests on a group of men aged between 30 and 55. PSA tests can be used to help doctors diagnose prostate cancer, which raises the level of PSA in the blood. The men were followed-up over a period of 20 to 25 years to see if they developed or died from advanced prostate cancer.

The study aimed to see if researchers could identify a PSA cut-off level for different age groups. If men had PSA levels above the cut-off, this would indicate a 'red flag' for developing advanced prostate cancer, and would warrant long-term follow-up and re-testing.

Researchers found small high-risk subgroups with the highest PSA levels had a moderately significant higher risk of developing or dying from advanced prostate cancer. They found that most men in the study who developed or died from advanced prostate cancer during follow-up tended to have the highest PSA levels in their 40s and 50s.

From this, they concluded that potentially incurable prostate cancers could be detected by careful surveillance of small subgroups of men with the highest PSA levels, while longer re-testing intervals could be considered for those with lower levels.

However, this was not a study designed to evaluate whether or not population-wide screening using the PSA test should be offered. A more reliable test than the PSA test alone is needed before routine prostate cancer screening can be introduced. 

Where did the story come from?

The study was carried out by researchers from Memorial Sloan-Kettering Cancer Centre in New York and other institutions in the US, Sweden and the UK. Funding was provided by various sources, including the National Cancer Institute and the Swedish Cancer Society.

It was published in the peer-reviewed British Medical Journal.

Overall, the news coverage accurately reflects the results, with the BBC, The Daily Telegraph and the Daily Mail all pointing out that the issue of routine screening for prostate cancer remains controversial.

Any evaluation of screening programmes for prostate cancer would need in-depth consideration of the full body of research as well as the risks and benefits of such a programme.

The BBC quotes Dr Anne Mackie, director of NHS screening programmes at Public Health England, who says that the organisation is considering the results of the study and that, "We are currently in the process of a scheduled review for a screening programme for prostate cancer and will make a recommendation towards the end of 2013".

What kind of research was this?

This was a nested case-control study. It aimed to see whether there is a link between the level of prostate-specific antigen (PSA) measured in the blood of men aged 40-55, and their subsequent risk of developing advanced prostate cancer or dying from prostate cancer.

PSA is a protein produced by the male prostate gland. PSA levels are usually raised in men with prostate cancer and, when considered alongside other signs or symptoms on examination, a raised PSA level may indicate that a man could have prostate cancer.

PSA levels are also usually monitored in people who have diagnosed prostate cancer to see how they are responding to treatment.

However, prostate cancer screening looking at PSA level alone is not currently done in the UK as it is often not a very reliable indicator of prostate cancer. PSA levels can be raised by many other non-cancerous conditions, including benign enlargement of the prostate gland (which is common with increasing age), inflammation of the prostate, or a urine infection. It has been very difficult to find an accurate cut-off PSA level that could reliably indicate whether a man has prostate cancer or not.

Overall, considering PSA as a routine screening test for prostate cancer would need to involve many important considerations. It could also lead to potential risks, including:

• the possibility of incorrectly indicating that a man with a non-cancerous condition has cancer, leading to unnecessary tests and anxiety
• failing to diagnose a man with prostate cancer whose PSA is not above the cut-off level
• diagnosing prostate cancer in a man whose cancer would not have actually caused him significant problems in his lifetime or affected his life expectancy, leading to unneeded treatment that can have serious side effects, such as erectile dysfunction and urinary incontinence

The current study aimed to look at some new evidence about whether there is a particular screening approach, where the benefits of screening outweigh the risks.

What did the research involve?

The researchers used members of the Malmö Preventive Project, an ongoing cohort study that began in 1974.

This study included a subset taken from the cohort study of 21,277 Swedish men from the general population who had a single blood test between 1974 and 1984, when they were between the ages of 27 and 52. The blood sample was then frozen and stored.

About six years later, subsets of men from particular age brackets were asked to give a second blood sample. A total of 4,922 men gave these second blood samples (72% of those who had been invited).

The researchers then linked these men's records to the cancer registry at the National Board of Health and Welfare in Sweden to identify men diagnosed with prostate cancer up to the end of 2006. They reviewed medical records to identify any prostate cancers that were metastatic, where the cancer was advanced and had spread to other parts of the body. The researchers also reviewed death certificates from those who had died to identify the cause of death.

The researchers then measured concentrations of PSA in the blood samples frozen more than 20 years previously. This is a method which researchers say has been shown to be compatible with measuring PSA in freshly obtained blood.

They focused their research questions around the men's age at the time the blood samples were taken to see at what age PSA testing could reduce the risk of advanced prostate cancer or death from prostate cancer. The age groups they focused on tested PSA at:

• around age 40 (37.5 to 42.5 years – 3,979 men)
• mid to late 40s (45 to 49 years – 10,357 men)
• early to mid 50s (51 to 55 – 4,063 men)

For their analyses, the researchers used a nested case-control study design within the cohort. This means that for each man with metastatic prostate cancer or who had died from prostate cancer (the cases), they randomly selected three controls who were alive and free from either of these outcomes during the same time period. The PSA tests between the control and the cases were then compared.

What were the basic results?

The researchers identified 1,369 cases of prostate cancer, of which 241 cases were metastatic prostate cancer. They identified that 162 men had died from prostate cancer.

As would probably be expected, higher levels of PSA concentration were significantly associated with metastatic prostate cancer and death from prostate cancer in the cohort as a whole. The researchers then looked at the association within specific age groups.

Around age 40

At around age 40 (37.5 to 42.5 years) the researchers found that, even for men with PSA in the highest 10th of values for this age group (above 1.3 micrograms per litre), their risk of having metastatic prostate cancer during follow-up (about 15 years) was very low at around 0.6%. They concluded that this would make it difficult to justify PSA screening for all men around the age of 40.

Mid to late 40s

When looking at the men in the next age bracket (45 to 49 years), the researchers found that for men with PSA levels in the highest 10th of PSA levels (above 1.6 micrograms per litre) now had a 1.6% risk of developing metastatic prostate cancer during 15 years of follow-up. Although a higher figure, an incidence rate of 1.6% (around one in 63) would still be hard to justify routine PSA screening.

Early to mid 50s

When looking at men who had PSA levels in the highest 10th at age 51-55 (above 2.4 micrograms per litre), there was a 5.2% risk of developing metastatic prostate cancer during follow-up.

From this, the researchers argued that not starting prostate cancer screening until the early to mid 50s "would leave an important proportion of men at a considerably increased risk of later being diagnosed with an incurable cancer".

Follow-up testing

The researchers then looked at whether below-average PSA test results at an earlier age could justify follow-up testing in later life.

Men with below-average PSA at age 45-49 had a 0.09% risk of developing prostate cancer over 15 years, and 0.85% risk over the slightly longer follow-up time of 25 years. Meanwhile, men with below-average PSA in the 51-55 age bracket had a 0.28% risk over 15 years and 1.63% risk over 25 years.

However, given that a substantial number of men who developed metastatic cancer did in fact have have below-average PSA levels at these ages, this led the researchers to argue it may be unsafe to conclude that subsequent testing is unnecessary for men with below-average PSA levels before the age of 55.

Re-testing interval

The researchers' next step was to consider what the appropriate re-testing interval would be. They found that with a low cut-off PSA level below 1.0 micrograms per litre, the risk of metastatic cancer is no higher than 0.4% in any group. So, for men below this level, a re-testing interval of "less than five years would be unnecessary".

Looking at deaths, 44% of men who died within 25-30 years had concentrations in the highest 10th at ages 45-49, and 44% had concentrations in the highest 10th at ages 51-55. The researchers considered that, "This suggests that close to half of all prostate cancers destined to lead to death would be detected early by careful surveillance of a small high-risk subgroup."

How did the researchers interpret the results?

Overall, the researchers conclude that PSA concentration can be used to predict long-term risk of metastatic prostate cancer or death from prostate cancer, and "can identify a small group of men at greatly increased risk compared with a much larger group highly unlikely to develop advanced cancer if [further] screening is delayed for seven or eight years".

They say that, "Given existing data on the risk of death by PSA concentration at age 60, these results suggest that three lifetime PSA tests (mid to late 40s, early 50s, and 60) are probably sufficient for at least half of men."

Conclusion

Overall this is well-conducted research, but screening is a complex issue for consideration.

In the UK there is currently no general population PSA level prostate cancer screening programme. PSA level alone is often not a very reliable indicator of prostate cancer and could lead to further unnecessary and invasive diagnostic tests and treatments.

The current study tried to find out whether a more targeted approach, using different PSA cut-off levels for different age groups and different re-screening intervals according to level, would be more effective.

However, overall the results were not very conclusive, and this research did not intend to offer guidance as to whether and how screening should or should not be offered.

The current study is likely to be added to the breadth of research informing the issue of prostate cancer screening. It is not possible to conclude from this research whether or not men of a certain age should be screened. It is also not possible to say whether PSA testing might one day be considered as a prostate cancer screening test in the UK.

Currently in the UK, doctors perform PSA testing on an individual basis, taking the results into account alongside a man's symptoms, signs on examination, and other test results to aid in the diagnosis and monitoring of prostate cancer.

For more information, read Know your prostate.

 

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

Prostate cancer: Call to test men in their 40s. BBC News, April 17 2013

Prostate screening 'could detect half of potentially fatal cases'. The Daily Telegraph, April 16 2013

Links To Science

Vickers AJ, Ulmert D, Sjoberg DD, et al. Strategy for detection of prostate cancer based on relation between prostate specific antigen at age 40-55 and long term risk of metastasis: case-control study. BMJ. Published online April 16 2013

“A glass of wine a day will not affect a woman’s chance of beating breast cancer,” reports the Mail Online website.

It has long been known that higher alcohol intake is associated with increased risk of developing breast cancer. It is less clear whether the amount a woman drinks before or after a breast cancer diagnosis has any effect on her chances of survival.

The news is based on a new study that found that moderate alcohol consumption before breast cancer diagnosis is associated with a reduced risk of death due to breast cancer compared to never drinking. Similarly, alcohol intake after a breast cancer diagnosis was not associated with increased risk of death from breast cancer.

These findings suggest that although drinking alcohol increases your risk of getting breast cancer, it might not increase your risk of actually dying from breast cancer. For this reason, it’s best to stick with the NHS guidelines on alcohol consumption.

The researchers also found that moderate consumption of alcohol before diagnosis (one to nine drinks per week) was associated with a reduced risk of dying from heart disease and with reduced risk of death from any cause compared to never drinking at all. Women who consumed higher levels of alcohol after diagnosis were also less likely to die from cardiovascular disease or from any cause than women who never drank.

The findings do not change current alcohol recommendations – women should not drink more than two to three units a day.

Where did the story come from?

The study was carried out by researchers from the Fred Hutchinson Cancer Research Centre and the Harvard Medical School and Brigham and Women’s Hospital in the US in collaboration with an international team of researchers. It was funded by the US National Cancer Institute and the charity Komen for the Cure.

The study was published in the peer-reviewed Journal of Clinical Oncology.

This story was covered by the Mail Online website. The Mail concentrated on the link between wine intake and the reduction in risk of dying from heart disease (drinking beer and spirits did not have the same effect). The study did reach this conclusion (prior to diagnosis), but as it was based on a limited sample size the researchers did not attach the same level of significance to the findings as the Mail chose to.

The main focus of the study was the effect of alcohol on breast cancer deaths.

What kind of research was this?

This was a cohort study that aimed to analyse the relationship between alcohol consumption and breast cancer survival.

This is the ideal study design. However, like all cohort studies it can only show associations between alcohol consumption and changes in risk, and not direct cause and effect. This is because there may be other factors responsible for the association seen (confounders).

What did the research involve?

The researchers recruited to their study 22,890 women aged between 20 and 79 years old who were diagnosed with breast cancer between 1985 and 2006.

The women were asked to report their alcohol consumption prior to their diagnosis, and a sub-sample also reported on their drinking habits after their diagnosis (4,881 women, alcohol consumption reported on average 5.7 years after diagnosis) via telephone interview.

Separate questions were asked on the amount and frequency of beer, wine and spirits intake. Alcohol intake was classified as:

• never drinking
• one to two drinks per week
• three to six drinks per week
• seven to nine drinks per week
• 10 or more drinks per week

Women were also asked about other breast cancer risk factors, including:

• reproductive and menstrual history
• physical activity
• height
• weight
• family history of cancer
• use of oral contraceptives
• hormone replacement therapy

Information about their breast cancer was also collected (such as the stage that the disease had progressed to).

The women were followed up for a median of 11.3 years after their diagnosis. Deaths during follow-up were monitored using the National Death Index.

The researchers looked at the association between alcohol consumption and death from breast cancer, cardiovascular disease (diseases that affect the heart and blood vessels, such as heart disease) or from any cause, after adjusting for a number of potential factors that could explain any association seen (confounders).

What were the basic results?

During the 11.3 years of follow-up 7,780 deaths occurred, 3,484 of which were due to breast cancer. The researchers found that moderate alcohol consumption before diagnosis was associated with breast cancer survival.

Compared to non-drinkers, women who consumed three to six drinks per week had a significantly reduced risk of dying from breast cancer (hazard ratio (HR) 0.85, 95% confidence interval (CI) 0.75 to 0.95).

The results were not statistically significant for other levels of alcohol intakes – one or two drinks, or more than six.

Women who drank spirits one or twice per week (compared to never drinking spirits) had a borderline significant reduced risk of death from breast cancer (HR 0.92, 95% CI 0.85 to 1.00), but in general results did not vary much by type of alcohol (beer, wine or spirits) consumed.

Consuming between one and nine drinks per week was associated with a reduced risk of death from cardiovascular disease, and of death from any cause, compared to never drinking.  

Looking at a sub-cohort of women who provided information about alcohol consumption after their breast cancer diagnosis (4,881 women), alcohol consumption at any level after diagnosis was not significantly associated with a reduced risk of death from breast cancer (after adjusting for how much they drank before their diagnosis). No type of alcohol was associated with any change in risk. However, women who consumed high levels of alcohol after diagnosis (10 or more drinks per week) were less likely to die from cardiovascular disease, and women who drank more than three drinks per week were less likely to die from any cause.

The researchers also looked to see if changing alcohol intake after diagnosis was associated with death from breast cancer, cardiovascular disease or any cause.

Increasing or decreasing alcohol intake was not associated with an increased risk of death from breast cancer.

However, women who increased alcohol consumption by more than one drink per week after diagnosis were at decreased risk of death from cardiovascular disease or death from any cause.

How did the researchers interpret the results?

The researchers conclude that, “overall alcohol consumption before diagnosis was not associated with disease-specific survival, but we found a suggestion favouring moderate consumption. There was no evidence for an association with post-diagnosis alcohol intake and breast cancer survival. This study, however, does provide support for a benefit of limited alcohol intake for cardiovascular and overall survival in women with breast cancer”.

The researchers also state that, “although women may alter their habits after breast cancer diagnosis, our results do not support a meaningful effect of changing consumption patterns on breast cancer survival”.

Conclusion

This large cohort study with a long follow-up has found that moderate alcohol consumption before breast cancer diagnosis (three to six drinks per week) is associated with a reduced risk of death due to breast cancer, but that alcohol intake after diagnosis did not have any benefit, but also did not cause any harm.

The study also found that consuming between one and nine drinks per week before a diagnosis of breast cancer is associated with a reduced risk of death from cardiovascular disease, and of death from any cause, compared to never drinking.

The study also suggested that women who consumed higher levels of alcohol after diagnosis (10 or more drinks per week) were less likely to die from cardiovascular disease. However, this group of women represented a much smaller sample, so these risk figures are less reliable.

Women who drank more than three drinks per week after diagnosis were less likely to die from any cause than women who never drank.

Women who increased their level of alcohol consumption after breast cancer diagnosis had better survival from cardiovascular disease and other causes, and did not affect their survival from breast cancer.

This research has the strengths of being a large cohort study with long-follow-up and it collected information on and adjusted for a number of potential confounding factors. However, it suffers from the inherent limitation of all cohort studies in that it can only show association and not cause and effect due to the possibility of confounding factors.

In addition, alcohol consumption was based on self-reported values for the previous two years, and may be subject to recall bias as well as possibly not being representative of alcohol consumption during the women’s lifetime.

Also, post-diagnosis alcohol consumption was collected on average 5.7 years after diagnosis, meaning that the results for post-diagnosis alcohol intake may only be applicable to women who survive several years after diagnosis.

Overall, this study suggests that moderate alcohol consumption prior to breast cancer diagnosis may be associated with improved breast cancer survival, but it found no link between any level of alcohol consumption after cancer diagnosis and breast cancer survival.

However, the study also suggests that alcohol intake is associated with improved cardiovascular and overall survival.

Taking into account the other health risks associated with alcohol consumption, this study would suggest that women living with or recovering from breast cancer should not worry about the occasional drink. But like all women, they should not regularly exceed the recommended consumption levels for women (two to three units a day, or 14-21 units per week).

Analysis by NHS Choices. Follow Behind the Headlines on Twitter.

Links To The Headlines

A glass of wine a day will not affect a woman's chance of beating breast cancer. Mail Online, April 8 2013

Links To Science

Newcomb PA, Kampman E, Trentham-Dietz A, et al. Alcohol Consumption Before and After Breast Cancer Diagnosis: Associations With Survival From Breast Cancer, Cardiovascular Disease, and Other Causes. Journal of Clinical Oncology. Published online April 8 2013