Absent fathers linked to depression risk in girls

Posted on May 17th, 2013

“Study shows girls with absent fathers more likely to develop depression,” the Mail Online has revealed.

It reports on a large UK study that found that girls whose biological fathers were absent during the first five years of their childhood had an increased risk of symptoms of depression. No increase in risk was found for girls whose fathers were absent later in childhood, and no increase in risk was found for boys with absent fathers.

Researchers collected information regarding the physical absence of the biological father during childhood, as well as information on depression symptoms when the child was 14. They assessed whether there was any association between these factors.

During their analysis, the researchers took into account several factors that may influence the link, such as family characteristics. However, despite the researchers’ efforts to take these variables into account, the reasons why a father may be absent from the family home can be incredibly complicated. This means we can’t be sure whether other factors have produced the association between absent fathers and depression in girls.

Where did the story come from?

The study was carried out by researchers from the University of Bristol and was funded by the UK Medical Research Council, the Wellcome Trust and the University of Bristol.

The study was published in the peer-reviewed journal Psychological Medicine.

Media coverage of this research was broadly accurate, though neither ITV nor Mail Online outlined any of the study’s limitations.

What kind of research was this?

This was an analysis of data from a prospective cohort study called the Avon Longitudinal Study of Parents and Children. This is a study that has been ongoing since the 1990s that assesses influences on the health and development of children.

The researchers were interested in the potential link between the absence of the biological father in early childhood and the risk of mental health problems. They were specifically interested in symptoms of depression that were not necessarily severe enough to be considered clinical depression.

As a prospective cohort study, this research is less likely to be affected by certain types of bias, especially recall bias. It was important that the researchers collected data on the effect of family factors on the children’s mental health at the time, rather than at a later date, to help ensure the information was accurate. Prospective studies allow for this.

What did the research involve?

The researchers measured two main factors:

  • absence of the biological father during childhood
  • experience of depressive symptoms during the teenage years

To measure parental absence, the researchers used questionnaires, filled out by the children’s mothers regularly throughout the children’s lives. These questionnaires asked whether the ‘present live-in father-figure is the natural father of the child and, if not, how old the child was when the natural father stopped living with the family’. This information was used to divide the children into three groups:

  • biological father present
  • biological father not present during the first five years of life (during early childhood)
  • biological father not present from age 5 to 10 (during middle childhood)

To assess the teenagers’ experiences of depressive symptoms, the researchers asked the study participants to complete a 13-item questionnaire when they were approximately 14 years old. This asked about the presence of certain symptoms over the previous two weeks. The questionnaire is reported to be a reliable and valid measure of depression in children. Children scoring 11 or higher on this questionnaire were considered to have high levels of depressive symptoms. This is not the same as being diagnosed with depression, however.

The researchers then analysed the data, comparing the risk of having high levels of depressive symptoms among children whose biological father left during early or middle childhood to the risk in children whose fathers were still living with them. These analyses were adjusted for several factors (confounders) that could be linked to both the absence of the father and depressive symptoms, including:

  • socioeconomic status (including home or car ownership, major financial problems, family size and parents’ jobs)
  • mother’s characteristics (including having a child before the age of 20, experiencing depression during pregnancy), and
  • any parental conflict between the mother and her current partner

Separate analyses were carried out for boys and girls, to determine whether the child’s gender had any impact on the relationship between father’s absence and depressive risk.

What were the basic results?

There were approximately 14,500 children in the original cohort study, approximately 11,000 of whom had data available on the presence or absence of their biological father. Among these children, approximately 6,000 had available data regarding depressive symptoms at age 14.

Overall, girls reported higher levels of depressive symptoms than boys, regardless of whether their father lived with them or not – a trend that has also been found in previous studies.

Girls

The study included:

  • 374 girls whose father left during early childhood, 87 (23.3%) of whom had high depressive symptoms at age 14
  • 193 girls whose father left during middle childhood, 27 (14.0%) of whom had high depressive symptoms at age 14
  • 2,295 girls whose father was present throughout childhood, 332 (14.5%) of whom had high depressive symptoms at age 14

Boys

The study included:

  • 357 boys whose father left during early childhood, 30 (8.4%) of whom had high depressive symptoms at age 14
  • 185 boys whose father left during middle childhood, 17 (9.2%) of whom had high depressive symptoms at age 14
  • 2,227 boys whose father was present throughout childhood, 166 (7.4%) of whom had high depressive symptoms at age 14

When assessing the association between the absence of the father in early childhood and teenage depressive symptoms, researchers found that:

  • Girls with absent fathers during early childhood had a 53% greater chance of experiencing high levels of depressive symptoms compared with girls with fathers present during this time (odds ratio  [OR] 1.53, 95% confidence interval [CI] 1.07 to 2.21).
  • Boys with absent fathers were no more likely to report high levels of depressive symptoms at age 14 than boys whose fathers were present during early childhood (OR 1.08, 95% CI 0.65 to 1.79).

There was no significant association between middle childhood father absence and teenage depressive symptoms.

How did the researchers interpret the results?

The researchers concluded that “father absence in early childhood increases risk for adolescent depressive symptoms, particularly in girls”.

Conclusion

This large prospective cohort study suggests that there is a link between a father’s absence during the first few years of life and a girl’s risk of experiencing depressive symptoms.

This study has several strengths, including its large sample size, its long-term follow-up and prospective collection of data for the analyses. It also attempted to consider confounding variables during the analysis and was based in the UK, which helps to ensure that the results are applicable here.

There are some limitations, however, that should be taken into account, including the following.

  • Only a third of the original cohort was analysed due to missing data on key factors. It is unclear to what extent those included differed from the entire population-based cohort. The researchers report that drop-outs were more likely among participants in lower socioeconomic groups. This factor is linked to both parental absence and depressive symptoms, so it could reduce the validity of the results and how much we can infer from them.
  • The adjusted analyses further reduced the available sample size due to missing data on confounding factors, and the researchers suggest that this may have resulted in loss of statistical power to detect an effect.
  • Several potential confounders were not included in the analysis, and could have influenced the results. The study authors report some of these potential confounders (quality of parent-child relationship, the father’s involvement in the child’s life regardless of whether he lived in the same house).
  • The questionnaire used to assess depressive symptoms is not a measure of clinical depression. A high score on this questionnaire does not indicate that the child has or will develop a diagnosable depressive disorder.

Overall, this study suggests that early childhood family environments may play an important role in the mental health of children. At this stage we don’t know what accounts for the study’s results, and the researchers say that this should inspire future research into the possible biological and psychological mechanisms underpinning this relationship.

Depression is one of the most common mental health conditions, yet there is very little good quality evidence about how to prevent people developing depression. Research that gives us insight into the factors that increase children’s likelihood of developing depression would be invaluable.

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No proof that red hair raises skin cancer risk

Posted on May 17th, 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.

Reproduced with the permission of NHS Choices

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Angelina Jolie’s surgery to ‘reduce breast cancer risk’

Posted on May 16th, 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.

Reproduced with the permission of NHS Choices

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Drug combination offers hope for osteoporosis

Posted on May 16th, 2013

Double drug hope for brittle bone sufferers”, reports the Daily Mail.

This headline follows a small but well-designed trial of treatments for postmenopausal osteoporosis. As women go through the menopause, levels of the hormone oestrogen begin to fall. This drop in oestrogen can lead to a thinning and weakening of the bones, increasing the risk of broken bones (fractures).

While current treatments can help prevent further weakening of the bones, they are not particularly effective at restoring bone strength – known as bone mineral density (BMD). In this study, researchers found that using a combination of teriparatide (Forsteo) and denosumab (Prolia) led to a significant improvement in BMD, when compared to using either medicine on its own.

While this research is encouraging, there are still questions that need answering. For instance, it isn’t clear whether this combination treatment is effective at preventing fractures (more participants would be required) or safe past 12 months (the length of this study).

Similarly, the research was mainly in white, city-dwelling postmenopausal women, so the effectiveness may differ in women from different places and ethnic backgrounds. Similarly, it is not clear whether it would benefit men with osteoporosis (which is less common, but still accounts for roughly 20% of cases).

Aside from these limitations, this research is a positive step forward in the search for new treatment options for osteoporosis. The encouraging results are likely to lead to further, larger studies.

Where did the story come from?

The study was carried out by researchers from at the Massachusetts General Hospital, Boston (US) and was funded by the National Center for Research Resources as well as the pharmaceutical manufactures Amgen and Eli Lilly.

Amgen manufactures denosumab and Eli Lilly manufactures teriparatide.

However, the publication states that the funders of the study had no role in study design, data collection, data analysis, data interpretation, or the writing of the report.

The corresponding author had full access to all the data in the study and had final responsibility for the decision to submit for publication.

The study was published in the peer-reviewed medical journal The Lancet.

The media reporting generally described the research findings accurately although discussion about the limitations of the research was minimal.

What kind of research was this?

This research used a randomised control trial (RCT) to test whether combining two approved osteoporosis medicines (teriparatide and denosumab) would improve bone mineral density in postmenopausal women.

Osteoporosis is a condition that affects the bones, causing them to become weak and fragile and more likely to break (fracture). These fractures most commonly occur in the spine, wrist and hips, but can affect other bones such as the arm or pelvis. Approximately 3 million people in the UK are thought to have osteoporosis. Although commonly associated with postmenopausal women, osteoporosis can also affect men, younger women and children.

The two drugs, teriparatide and denosumab, are already used individually to treat osteoporosis but they work in slightly different ways. So the researchers wanted to test whether there was any added benefit of using the two drugs together.

Despite drugs being available for osteoporosis, the researchers’ say no currently approved treatment actually restores normal bone density in most patients with osteoporosis – they merely halt the decline. And options for those with severe osteoporosis are limited; the resulting risk of fracture, aside from affecting people’s quality of life, puts a considerable strain on the NHS. It is estimated that there are around a quarter of a million fractures each year in the UK. This means there is a continual need for new or improved treatments.

An RCT is one of the most reliable ways of testing whether a new drug, or in this case combination of drugs, is effective.

What did the research involve?

Between September 2009 and January 2011 the researchers enrolled 100 postmenopausal women (aged 45 years or older, with at least 36 months since last period) with osteoporosis who were at high risk of bone fracture. Women were enrolled through a mailing advertisement and on referral to Massachusetts General Hospital in Boston (US).

Bone mineral density is measured by ‘T-score’ and is simply the number of units, known as standard deviations, above or below the expected average for a healthy 30-year-old adult of the same sex and ethnicity as the patient. Only about 2.5% of women would have a T-score less than -2.0, for example.

The researchers defined high fracture risk as either:

  • T-score –2.5 or less at the spine, hip, or femoral neck
  • T-score –2.0 or less with at least one risk factor; fracture after age 50 years, parental hip fracture after age 50 years, previous overactive thyroid, inability to get up from a chair with arms raised, or current smoking
  • T-score –1.0 or less already with history of a fracture from osteoporosis

Women were split into three equal groups to receive 20 microgram teriparatide daily, or 60 milligram denosumab every six months, or both.

Bone mineral density was measured at 0, 3, 6, and 12 months. This included measuring bone density at the lumbar spine, hip bone and neck of the femur using low-dose x-rays and bone biomarkers. Calcium intake (which can influence bone strength) was also recorded at the start of the study through a food frequency questionnaire.

Women who completed at least one study visit after baseline were assessed in a modified intention-to-treat analysis. Physicians interpreting bone mineral density assessments and the laboratory staff doing bone-marker assays were unaware of patients’ treatment groups.

The analysis compared changes in bone density from baseline (the start of the study) to the different time points (3, 6, and 12 months) for each of the different locations (spine, hip bone, and neck of femur).

What were the basic results?

Of the 100 eligible women, 94 completed the 12 month study. At 12 months, the main findings were that:

  • Lumbar spine bone density had increased significantly more in the combination group (9.1%, standard deviation (SD) 3.9) than in the teriparatide (6.2%, SD 4.6) or denosumab (5.5%, SD 3.3) groups.
  • Femoral-neck bone density also increased more in the combination group (4.2%, SD 3.0) than in the teriparatide (0.8%, SD 4.1) and denosumab (2.1%, SD 3.8) groups.
  • Total hip bone density also increased more in the combination group (4.9%, SD 2.9; teriparatide, 0.7% SD 2.7; denosumab 2.5%, SD 2.6).

All these results were statistically significant.

How did the researchers interpret the results?

The researchers concluded that, “combined teriparatide and denosumab increased bone mineral density more than either agent alone and more than has been reported with approved therapies.” Furthermore, “combination treatment might, therefore, be useful to treat patients at high risk of fracture.”

Conclusion

This small but well-conducted RCT showed that combining licensed osteoporosis medicines teriparatide and denosumab may increase bone density more than either medicine used on their own, in postmenopausal women at high risk of bone fracture.

The researchers highlighted that their results were not consistent with previous trials looking at combination therapies for osteoporosis, which found no benefit of combining them.

However, previous research did not use the same combination of medicines in the same dose as the present trial. It could be the case that the dosages used in previous research were not given at the optimal level.

And while the study showed statistically significant differences in bone density at 12 months, this does not necessarily mean the treatment lead to a reduced rate of fractures – which is the ultimate aim of treating osteoporosis. Larger, longer-term studies are required to see what impact this combination treatment has on fracture risk, as well as assessing how safe and effective both drugs are in the longer-term.

This is particularly relevant because teriparatide is only licensed to be used for a maximum of 24 months (a point the Daily Mail usefully highlighted). It remains to be seen what would happen when this combination of therapies were stopped – would the benefits be reversed, and would it be safe to continue using the medicine longer than recommended?

These issues would need to be thoroughly addressed before this potentially useful combination could feasibly be routinely used in the NHS.

Reproduced with the permission of NHS Choices

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‘Broken’ body clock may be linked to depression

Posted on May 16th, 2013

“Depressed people are out of sync with the rest of the world because their body clocks are broken,” reports the Mail Online website, while The Independent claims that depressed people live in a “different time zone”.

The story comes from a study that looked at the activity of genes thought to be involved in regulating the body’s internal clock – the innate sense that most people have of the changes over a 24-hour day to night cycle (circadian rhythms).

Researchers did a detailed study of gene expression, the effect that certain proteins contained inside individual genes have on genetic activities inside the body.

The study involved examining brain tissue taken from people who donated their brains to science after their deaths. Of the sample, 55 people had no history of psychiatric illness, while 34 patients had a history of severe depression (major depressive disorder, or MDD).

Researchers found that the gene activity associated with regulating circadian rhythms was much weaker, and often disrupted, in the brains of patients who had MDD.

These results possibly present, as philosophers put it, a “causality dilemma” (a chicken and egg problem) – does depression lead to a disrupted body clock, or does a disrupted body clock make people vulnerable to depression?

It is too early to say what help these findings may be in the understanding and treatment of MDD.

Where did the story come from?

The study was carried out by researchers from the University of Michigan, the University of California, Weill Cornell Medical College, Stanford University and the HudsonAlpha Institute for Biotechnology, and was supported by the Pritzker Neuropsychiatric Disorders Research Fund.

It was published in the peer-reviewed Proceedings of the National Academy of Sciences.

Both the Mail Online and The Independent covered the research uncritically. Given the specialised nature of this research, it’s not surprising that both of the news stories appeared to be strongly based on an accompanying press release and were not a critical appraisal of the study itself.

What kind of research was this?

This was laboratory research using donated post-mortem brains. In it, researchers analysed in detail the gene expression of certain genes thought to be associated with circadian rhythm regulation at the time of death.

The authors point out that a common symptom of major depressive disorder is the disruption of circadian patterns, which can trigger symptoms of insomnia as well as excessive daytime sleepiness and fatigue (feeling tired all the time). However, to date there is no direct evidence of “circadian clock dysregulation” in the brains of patients with major depressive disorder.

What did the research involve?

Researchers used human brain tissue taken from a US donor programme with the consent of next of kin. They also took information from medical records, medical examiners and interviews with relatives to record the donors’ previous physical health, medication use, psychiatric problems, substance use and details of death.

This was done in order to assess whether donors had a major depressive disorder, a severe form of depression that has a significant impact on day-to-day living.

They also assessed whether physiological stress at the time of death would have had an effect on gene expression, and took account of this potential confounding factor.

Researchers analysed the brain tissue of 55 donors with no history of psychiatric or neurological illness and 34 patients with major depressive disorder. Using specialist techniques called DNA microarray, they measured the expression of genes thought to be associated with regulating circadian rhythms in different areas of the brain.

They used the control group to build a detailed picture of circadian gene expression in brain tissue and compared the results with those found in the brains of people with MDD. They also used the rise and fall of the top 100 “cyclic” genes in 60 of the donors to predict the time of death in all the others, both cases and controls.

What were the basic results?

In the brain tissue from donors without major depressive disorder, they found that the activity of “circadian” genes at certain times of the day and night was consistent with data derived from other diurnal (day-active) mammals. More than 100 genes showed “consistent cyclic patterns” over six brain regions.

However, in the brains of patients with MDD gene expression of cyclic patterns was far weaker and more disrupted, with the patients’ day pattern of gene activity often resembling a night pattern.

They found that predictions of time of death were more accurate among controls than for those with MDD.

How did the researchers interpret the results?

The researchers say the results provide convincing evidence that there is a “rhythmic rise and fall” in the activity of hundreds of genes in the human brain associated with regulating the day/night cycle. There is also evidence that the activity of genes associated with circadian rhythms is abnormal in people with MDD.

The study identifies hundreds of genes in the human brain that are likely to be involved in the sleep/wake cycle. The researchers conclude that daily rhythms in these genes are “profoundly dysregulated” in MDD. They say the results pave the way for the identification of new biomarkers and treatments for mood disorders.

Conclusion

This study is of interest, but at the moment it has little bearing on our understanding and treatment of depression. It could lead to new insights and treatments in the future, but there is no guarantee that this will be the case.

Also, as the authors point out, gene activity can result from many factors, including disease and drug history. In particular, it should be pointed out that:

  • the researchers relied on only 55 patients to build a “normal” picture of genetic expression associated with the sleep/wake cycle
  • it is not clear whether those in the MDD group had all been formally diagnosed with MDD or how long they had had depression, and it is possible there were errors in the classification of patients either with or without MDD

In conclusion, it is too early to say whether this study’s findings might help in the understanding and treatment of major depressive disorders.

Reproduced with the permission of NHS Choices

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US guidelines recommend CT scans for smokers

Posted on May 15th, 2013

Older people with a history of smoking heavily should be offered annual low-dose CT scans to screen for lung cancer according to new US guidelines reported by the Reuters news agency.

These guidelines recommend that annual CT (computerised tomography) scans should be offered to current or former smokers aged 55-74 who have smoked 20 cigarettes a day for 30 years or more. However, screening should only be offered in facilities that can provide high standards of clinical care, the guidelines say.

Screening means testing everyone in a particular population for early stages of a disease before they have any symptoms. In the UK, screening is already in place for some cancers, such as bowel and breast cancer, but lung cancer is not currently screened for.

Mass-population screening, such as that carried out for bowel and breast cancer, is unfeasible for lung cancer because of the cost. One study has estimated that to save one lung cancer death would cost around $250,000. However, focusing resources on high-risk groups, as recommended in the US guidelines, is a more cost-efficient approach.

Heavy smokers are particularly at risk of developing lung cancer because cigarettes contain a number of cancer-causing substances (carcinogens).

Screening could be of particular use in heavy smokers because the symptoms of lung cancer often do not develop until the cancer is at an advanced stage. This makes treatment of the condition challenging.

The US guidelines point to research that suggests that these recommendations could cut rates of lung cancer deaths in smokers or ex-smokers by around 20%.

Low-dose CT scanning

CT scans use X-rays and a computer to create detailed images of the inside of the body. They can be particularly useful for spotting abnormalities and injuries to internal organs. The advantages of the new ‘low-dose’ CT scanning are that:

  • it can provide images with a greater degree of contrast, so it can often spot problems that would be missed by a traditional CT scanner
  • it exposes patients to a lower level of radiation, making it safer

Who produced the guidelines?

The guidelines on screening have been produced by the American College of Chest Physicians.

They form part of comprehensive guidance for US doctors on the diagnosis and management of lung cancer.

What are the pros and cons of CT screening for lung cancer?

An obvious pro of CT screening for lung cancer is that it could cut lung cancer deaths. Lung cancer is one of the leading preventable causes of death in the UK and around the world.

However, no screening technique is without risk.

One risk, often overlooked, is the danger of false positives. This is where the screening test detects a sign that turns out to be harmless. In cases of lung cancer this would usually be when a lesion (abnormality in tissue) is detected, but the lesion turns out to be non-cancerous (benign).

In the general population, the rates of false positives for screening could be unacceptably high. For example, the authors say that more than 90% of nodules found by CT in the studies they looked at turned out to be benign.

This figure drops dramatically for high-risk groups, such as smokers, but one study quoted in the guidelines estimated that the false positive rate in high-risk groups could still be around one in four.

While CT scans themselves have a very low risk of causing complications, other more invasive procedures used to confirm or discount a diagnosis of lung cancer do not.

Screening could subject people to unnecessary tests that turn out to cause them harm, and there is still the possibility of false negatives. No matter how good a test is, it is likely that some cancers will be missed, leading to false reassurance.

There is also risk from radiation exposure. Although one low-dose CT scan involves only a small amount of radiation, if further imaging is required it can rapidly drive up the radiation dose patients receive.

What evidence did the guidelines look at?

The guidelines looked at evidence on the effectiveness of different methods of screening for lung cancer. These were:

  • chest X-ray
  • examining mucus from the airways for abnormal cells (sputum cytology)
  • low-dose CT screening

The guidelines’ authors conducted a systematic review of randomised controlled trials (RCTs) and observational studies looking at the effectiveness of the different methods of screening. Most of the studies focused on middle-aged or older people with a history of smoking and, therefore, at high risk of lung cancer. In particular, they examined the death rates from lung cancer among people at high risk who were screened by low-dose CT, X-ray or sputum analysis.

The review also looked at the potential downsides of screening, including:

  • the death rates, or complications resulting from further investigations of any suspected cancers, in people who had been screened
  • the death rates from radiation exposure of people who had low-dose CT screening
  • the rate of surgery for benign disease

What were the results?

The main finding came from one large RCT (the National Lung Screening Trial), involving more than 53,000 participants who had three annual rounds of screening. This trial showed a 20% reduction in the rate of death from lung cancer in people who were screened with low-dose CT, compared with those screened using a chest X-ray (relative risk 0.80, 95% confidence interval 0.73 to 0.93).

This trial also found that low-dose CT posed “few harms” when carried out in the context of a structured programme of care. The risk of death or major complications from further investigations into harmless conditions was between 4.1 and 4.5 per 10,000.

Other research found that using chest X-rays or sputum analysis did not reduce lung cancer deaths.

What recommendations on screening did the guidelines make?

The guidelines recommend that:

  • Smokers and former smokers aged 55-74 who have smoked for 30 pack-years or more and who either continue to smoke or have quit within the past 15 years should be offered annual screening with low-dose CT.
  • This should only be done in settings that can deliver the same standard of care provided to participants in the big lung cancer screening trial.
  • CT screening should not be offered to people who do not meet the above criteria, say the guidelines. For example, if they are younger or older or have smoked less, since benefits outside the high-risk group are uncertain.
  • Screening for lung cancer using X-rays or sputum analysis is not recommended.

What else did the lung cancer guidelines say?

The guidelines also make several other suggestions:

  • Patients at risk of lung cancer should be counselled in detail about the potential benefits and risks or harms of CT screening, to help them make an informed decision.
  • Screening should be conducted in centres with multidisciplinary, co-ordinated care and a comprehensive process for screening, management of findings and evaluation and treatment of potential cancers.
  • Screening for lung cancer is not a substitute for stopping smoking. The guidance says “the most important thing patients can do to prevent lung cancer is not smoke”.

What is the current NHS policy regarding screening for lung cancer?

At the moment there is no national screening programme for lung cancer in the UK for the reasons outlined above.

Currently, testing for lung cancer is normally only offered to people with symptoms associated with lung cancer, such as coughing up blood or persistent unexplained weight loss. It is likely that these American guidelines will be read with interest by relevant authorities in the UK and across Europe.

The guidelines also mention additional RCTs involving 25,000 people that are underway and due to report results in 2015. These results may (or may not) provide further evidence to support the advice set out in these guidelines.

It is likely that the debate on the pros and cons of CT screening for lung cancer in high-risk groups will be discussed widely in the months to come.

Reproduced with the permission of NHS Choices

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Rugby star Ollie Phillips becomes one of Alzheimer’s Society’s Dementia Friends

Posted on May 15th, 2013

Ollie Phillips with a Dementia Friends banner

Rugby Sevens star and Alzheimer’s Society supporter Ollie Phillips has become a Dementia Friend.

The England winger ‘tackled’ an awareness session with other members of the public wishing to learn more about the condition at the NHS Healthcare Innovation Expo.

After speaking to health and social care professionals about his Nan Audrey, who passed away with dementia in January, Ollie decided to attend one of the hourly Dementia Friends sessions being run at the event by Alzheimer’s Society.

Talking about the session, Ollie said:

‘I know how dementia affected my Nan but the condition is different for everyone. The Dementia Friends session I attended today really put me in the shoes of someone with dementia, and made me think about what it’s really like to live with it on a day-to-day basis.

‘The condition affects 800,000 people across the UK so it’s really important that as a society we improve our understanding. It was a real privilege to take part in the session and be amongst others who also want to improve their knowledge and be part of making life better for people with dementia.’

Ollie recently swapped his rugby scrumcap for a cycling helmet and signed up for Alzheimer’s Society’s London to Brussels cycle ride challenge in September, to help raise money in the fight against the condition. To sign up to join Ollie visit alzheimers.org.uk/events

Press Release from Alzheimer’s Society

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A Healthy Start

Posted on May 15th, 2013

Free vitamin supplements for children, pregnant women and new mothers on low incomes will now be more widely available to encourage greater uptake.

The Healthy Start scheme provides vitamin supplements to low income families, in addition to vouchers towards the cost of milk, fruit and vegetables.

Previously, vitamins were distributed through NHS Boards.  However, the average uptake of the scheme as a whole across Scotland was only 71 per cent, with the uptake of vitamin supplements being significantly lower.

In a drive to ensure that everyone who needs these vitamins receives them, community pharmacies will now be able to give eligible women and children Healthy Start vitamins directly.

The 1,246 community pharmacies and around 120 dispensing practices across Scotland have been asked to join the one year pilot.

Minister for Public Health Michael Matheson said:

“There is a strong link between low income and poor nutrition in pregnant women, mothers and children.  As part of our work to address health inequalities in Scotland, we must make sure that everyone has access to all that is available.

“Vitamins are essential nutrients that help our bodies work properly. Even though we can get lots of vitamins from a healthy balanced diet, certain people still might not get everything they need at certain times in their life – such as pregnant women, a new mum or a small child.

“We know that some families have had difficulty accessing these vitamins in the past.  That is why we worked to identify a better way for these to be distributed, and I’m pleased to say that indications suggest the pilot using community pharmacies in NHS Greater Glasgow and Clyde was a success.

“By using community pharmacies, we will ensure a consistent, easily understood and sustainable method of distribution across Scotland for those in most need of these vitamins.”

Healthy Start women’s vitamin tablets contain:

  • Folic acid: reduces the chance of your baby having spina bifida, a birth defect where the spine doesn’t form properly
  • Vitamin C: helps maintain healthy tissue in the body
  • Vitamin D: helps your body to absorb calcium and so supports your baby’s bones to develop properly.

Healthy Start children’s vitamin drops contain:

  • Vitamin A: for growth, vision in dim light and healthy skin
  • Vitamin C: helps maintain healthy tissue in the body
  • Vitamin D: for strong bones and teeth.

The Healthy Start Scheme provides eligible families with vouchers that can be used in shops to help pay towards milk, formula milk, fresh and frozen fruit and vegetables.  The scheme also provides coupons to exchange for vitamin supplements.

Healthy Start vouchers and coupons are provided to pregnant women, breastfeeding mothers and families and children up to their fourth birthday on income related benefits.  All young women who are under eighteen and pregnant are also eligible, regardless of income.

At a meeting with Healthy Start NHS Board leads, it was agreed that the preferred option for ensuring an effective distribution system was to agree a national remuneration scheme for community pharmacies.  This also ensures that community pharmacies are able to access Health Start vitamins from their own suppliers, rather than go through the NHS supply chain process.

Data on the uptake of the vitamins by community pharmacy/Board area will be analysed looking at the impact of the trial.  The Scottish Government will then use this data to look at whether it can become part of a more formal on-going agreement with community pharmacies.

Reproduced with the permission of The Scottish Government

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Fears grow over new Sars-like virus

Posted on May 14th, 2013

Patient on a drip in hospital (Fotolia)

Health officials have said a deadly virus which has killed 18 people worldwide appears to be able to spread from person-to-person.

There have been 34 reported cases of the Sars-like novel coronavirus, known as hCoV-EMC, which causes severe pneumonia in victims and sometimes kidney failure.

It is most closely related to a bat virus and scientists are considering whether bats, camels or goats are a possible source of infection.

Read Full Press Release at YAHOO

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South Shields sprint could be Savage for Robbie

Posted on May 14th, 2013

Football legend turned popular pundit Robbie Savage is swapping his football boots for his running shoes when he takes on the Bupa Great North Run to raise money for Azheimer’s Society.

Robbie’s father, Colin, had Pick’s disease, one of the less common forms of dementia and sadly passed away aged 64 in March last year. Robbie, who has just started his training, has already taken part in a 5k run as part of his rigorous regime. Speaking about the upcoming half marathon on Sunday 15 September 2013, Robbie said:

‘I’ve faced a lot of challenges on the pitch but watching my father and my hero battle against dementia was the biggest of my life.

‘Now I’m ready to take on a new challenge and hopefully raise lots of money in the process. The aches, pains and inevitable blisters will be worth it knowing that the money I raise will be helping in the fight against dementia.

‘As a proud ambassador of Alzheimer’s Society, I can’t speak highly enough of the work they do to support people living with dementia, their carers and families.’

The Bupa Great North Run is the UK’s most iconic half marathon, from Newcastle to South Shields. Robbie will be leading a team of over 1200 Alzheimer’s Society runners. Those with a place in this year’s run who would like to join the Alzheimer’s Society charity team can do so by visiting alzheimers.org.uk/greatnorthrun

Liz Monks, Director of Fundraising at Alzheimer’s Society said:

‘Robbie, like many of our runners, has faced dementia in his family and understands the impact of the condition which currently affects 800,000 people across the UK. We’re so proud to have Robbie leading Team Alzheimer’s Society at the Bupa Great North Run.

‘As a charity, we rely on the generosity of people like Robbie to help us continue our vital work. Please back him in his fundraising efforts so that Alzheimer’s Society can continue leading the fight against dementia.’

Press Release from Alzheimer’s Society

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