“A hormone patch may protect women with schizophrenia or other severe mental illnesses from psychotic feelings”, BBC News reported. It said that scientists had found that giving women oestrogen made them less likely to report suffering hallucinations or delusions.

The story is based on a study in 102 women with schizophrenia, half of whom wore a daily patch of estradiol, the most common form of oestrogen, for four weeks. As the researchers acknowledge, this is a small study and much further research in a greater number of women, and over a longer period of time, is needed to look at the effectiveness of this treatment alongside other standard treatments. Most importantly, future studies will need to consider the long-term safety implications of giving women a high concentration of unopposed oestrogen (i.e. not combined with a progestogen hormone, as in the contraceptive pill) for long periods of time.

Dr J Kulkarni and colleagues from The Alfred Hospital, Monash University’s School of Psychology, Psychiatry and Psychological Medicine and Monash Medical Centre, Melbourne, Australia, carried out the research. Funding was provided by the Stanley Medical Research Institute and the National Health and Medical Research Council of Australia. The study was published in the peer-reviewed medical journal: Archives of General Psychiatry.

This was a double blind randomised controlled trial designed to look at the effects on psychotic symptoms in women with schizophrenia of applying either an oestrogen patch or placebo patch to the skin, alongside standard treatment.

The researchers recruited 102 women to the study from inpatient and outpatient units of two hospitals in Melbourne. All women had verified diagnoses of schizophrenia or a related schizophrenia type condition and all were diagnosed to have severe illness, including some who had not responded to previous treatments. The researchers excluded those women with a bipolar subtype of illness (although they included those with a depressive subtype), those currently receiving hormone treatment such as the pill, those pregnant or breastfeeding, those around the time of menopause, those with overactive thyroid and any with an unstable medical condition.

The women were randomly assigned to receiving either a 100 microgram per day oestrogen patch (56 women) or a placebo patch (46 women) for four weeks. Neither the women or the research team were aware of which treatment they were receiving. Other antipsychotic medications were continued. The researchers used a recognised assessment scale (Positive and Negative Syndrome Scale; PANSS) to look at psychotic symptoms at the start of the study and then once weekly for four weeks. On this scale, positive symptoms include such things as hallucinations, delusions, disorganised thinking, negative symptoms include things such as reduced emotional response, emotional and social withdrawal; and general symptoms are things like anxiety, depression, and poor control of impulses. Side effects of treatment were assessed at each follow up, and blood samples were taken to look at hormone levels at the beginning and end of the study. Statistical tests were used to look at differences in symptoms and side effects between the groups.

In all, after some dropouts and exclusions, 85.3% of the 102 women were analysed at the end of the study (91% of the treatment group and 78% of the placebo). There were no differences between the women in either group in terms of age, severity or duration of illness, medication used, or menstrual cycle phase at the beginning of the study. Compared to the placebo group, women who received oestrogen had significantly greater improvement over time in overall symptoms, and also in positive symptoms (as measured with the PANSS total score, positive symptom score and general psychotic symptom score). There was no difference between the groups in negative symptoms as measured on the PANSS. There was no difference in rate of adverse side effects between the groups.

The researchers concluded that the addition of 100 micrograms of oestrogen, delivered via a patch to standard treatment, significantly reduced positive and general psychotic symptoms during the four-week trial compared to standard treatment alone.

This is a well-designed and carefully conducted randomised controlled trial into the effects of adding oestrogen to standard treatment for schizophrenia. However, the results must be considered in context:

• This was a small trial of only 102 women with schizophrenia disorders who fulfilled specific criteria. Further research will be needed in much larger groups of women and in those with different severities of condition and comorbidity (other conditions that they have as well as schizophrenia), to get a clearer indication of whether treatment does significantly improve symptoms.
• The duration of the trial, at four weeks, is very short. Much longer trials will be needed to look at longer-term effects and, most importantly, to consider the long term safety implications of daily giving women a high concentration of oestrogen. The oestrogen used in this patch was at a much higher concentration that that given in standard contraceptive treatment. It is also not combined with the protective effects of a progesterone hormone as in the contraceptive pill. Higher concentrations of such unopposed oestrogen are likely to make the risk of known complications of oestrogen treatment (e.g. deep vein thrombosis, high blood pressure) greater. Also in this context, there are a number of women for whom oestrogen treatment may not be suitable at all, such as those with risk factors or family history of blood vessel disease, those with migraine or liver conditions, and those who are  overweight or smoke heavily.
• Hormone treatment does carry the risk of known side effects, such as depression, nervousness or irritability symptoms, and these must be considered given the context of this disease. The implications upon the reproductive cycle and personal relationships must also be considered (for example the possibility of women assuming this as contraception and therefore engaging in unsafe sexual activity).
• No assumptions can be made from this study about the effects of isolated hormone treatment, without standard treatment being given alongside.

Further research is awaited.

“Eating broccoli could reverse the damage caused by diabetes to heart blood vessels”, BBC News reported. It said that researchers have found that the compound sulforaphane, found in the vegetable, encourages the production of enzymes which protect blood vessels and cause a reduction in the number of molecules that can damage cells.

This story is based on a complex laboratory study in which sulforaphane was directly applied to blood vessels that had been damaged by high blood sugar levels. It found that the compound reduced the production of potentially damaging molecules called reactive oxygen species. However, the results have been overinterpreted by the news; applying the compound in broccoli to cells in the laboratory is not comparable to eating broccoli. The blood vessel cells were not taken from a person with diabetes but had been incubated with sugar. It is unclear what effects sulforaphane would have on the blood vessels of a person with diabetes, and whether it would protect them from damage or have any effect upon the disease process. Optimal blood sugar control through diet and medication remains the best option for people with diabetes.

Dr Mingzhan Xue and colleagues from the University of Warwick and University of Essex carried out the research. It was supported by Juvenile Diabetes Research Foundation International, the Wellcome Trust, and the Biotechnology and Biosciences Research Council. The study was published in the peer-reviewed medical journal: Diabetes.

The aim of this laboratory study was to look at whether sulforaphane, a compound found in broccoli, could prevent metabolic damage to small blood vessels caused by high blood sugar. Sulforaphane activates a protein called nrf2, which initiates the production of a number of enzymes that protect cells from potentially damaging chemicals, including a type of free radical called reactive oxygen species (ROS).

The researchers incubated cells taken from the lining of human small blood vessels with two different concentrations of sugar – low and high. They then used laboratory methods to see what effects incubation with sulforaphane had on a range of complex metabolic and biochemical pathways. The researchers used concentrations of sulforaphane that they said were representative of the levels that have been reported to be found in the blood stream after eating broccoli.

The researchers found that activation of the protein nrf2 by sulforaphane, caused increased expression of various protective and metabolic enzymes, including three to five fold increases in the enzymes transketolase and glutathione reductase.

Incubating blood vessel cells in high sugar concentrations resulted in a three-fold increase of the potentially harmful free radical ROS, but adding sulforaphane reduced ROS levels by 73%. The enzyme transketolase played a role in this reduction. Sulforaphane also prevented the production of other chemicals that may potentially cause blood cell dysfunction in high blood sugar conditions.

The researchers concluded that activation of nrf2 may prevent the biochemical dysfunction of cells that line the inside of blood vessels caused by high levels of blood sugar.

The news report overinterpreted the results of this complex laboratory study.

• Although the researchers say that the concentrations of sulforaphane used were limited to those ‘found in plasma after consumption of broccoli’ it is unclear how these laboratory effects would be comparable to the real life situation of eating broccoli or what frequency or quantity of consumption of broccoli would be required to mimic these effects.
• The blood vessel cells were not taken from a person with diabetes, but had instead been incubated with sugar. Short-term incubation of cells in high sugar concentrations cannot be directly related to the situation in a person with diabetes.
• It is unclear whether any of the biochemical and metabolic changes seen in the blood vessels would relate to functional change in the blood vessels of a person with diabetes and whether it would protect them from damage or have any effect upon the disease process.
• The news article suggests that ‘eating broccoli could reverse damage caused by diabetes to heart blood vessels’. It is unclear from the journal article where in the body the blood vessel cells were taken from, but they were from small blood vessels – microvessels. Although poor blood sugar control can cause significant small vessel damage in the body (for example to the retina, kidney and nerve cells), heart disease as a complication of diabetes is considered to be a large vessel – macrovascular – complication.
• There is no indication from this study how the biochemical changes could reverse damage that had already been caused.

Optimal blood sugar control through diet and medication remains the best option for people with diabetes, and broccoli should be considered only as part of a healthy diet.

“A painful womb condition that affects around two million British women may be triggered by an out-of-control enzyme”, the Daily Mail reported. It said that scientists claim the findings of a study could be used to diagnose and treat endometriosis, a condition which causes pain, menstrual problems and can affect fertility. The enzyme, telomerase, aids the replication of DNA sequences, and is found in cells that divide frequently. The scientists said the telomerase-generating cells that line the uterus of women with endometriosis act like cancer cells, ‘dividing uncontrollably’ causing the cells to survive for longer and migrate outside of the uterus to other locations.

Although the newspapers said the findings may be used in the diagnosis and treatment of endometriosis, at the current time this is too early to say. The findings have shed some light on the possible pathological development of the condition, but this is preliminary research using laboratory samples from a few women. Whether this could lead to any diagnostic or treatment options is far from clear and has yet to be investigated.

Dr D.K. Hapangama and colleagues from the School of Reproductive and Developmental Medicine at the University of Liverpool, and the Crucible Laboratory and Henry Wellcome Laboratory for Biogerontology Research at the University of Newcastle carried out the research. Funding was provided by the University of Liverpool and a Royal College of Obstetrics and Gynaecology grant to Dr Hapangama. The study was published in the peer-reviewed medical journal: Human Reproduction.

This was a case control study designed to investigate the theory that endometriosis is associated with abnormal expression of telomerase and telomere lengthening in the endometrium (lining of the uterus).

The researchers recruited a sample of 29 women with surgically diagnosed endometriosis (group one) and 27 women who were found not to have the condition during a routine surgical sterilisation procedure (group two). All women were between 18 and 46 years of age and had regular periods and were not taking any hormonal supplements, such as the contraceptive pill.

All women had biopsies taken of their endometrium (the lining of the uterus) during the second half of their menstrual cycle (the luteal phase). The biopsies were taken during the ‘window of implantation [of a fertilised egg]’ phase (between days 19 and 23) in 17 women from group one and 15 women from group two. The remaining 12 women in each group had biopsies in the last days of their cycle (days 24 to 28). Blood samples were also taken to assess levels of oestrogen and telomerase circulating in the blood.

In the laboratory, the tissue samples were examined for expression of telomerase and oestrogen receptor (ERß) using an antibody that would bind to telomerase and then be highlighted during staining. As positive controls (and so should show telomerase activity), the researchers also compared several different tissue types to the biopsies, including cancerous endometrial tissue, cancerous breast tissue, tonsillar tissue, and endometrial tissue taken during the early proliferative phase of the menstrual cycle.  An antibody that would not bind to telomerase was used as a negative control. It is unclear where the comparison tissues came from, but presumably not from the same women. It was a blind study, so the researchers examining the samples were unaware of which samples they were examining.

Using another technique, the tissue and blood samples were used to examine the average length of the telomeres during cell division. Statistical tests were used to look at the differences in telomere length depending on when the biopsy was taken and whether or not the woman had endometriosis.

Women in groups one and two were similar in age, height, weight, and usual menstrual cycle length; however, of the women biopsied in the late cycle days, those in group one were younger than those in group two. Half of the women with endometriosis had mild/moderate disease, and the other half had severe disease.

In the group two women without endometriosis, telomerase activity was weak or not apparent throughout the luteal phase of the menstrual cycle. In the women with endometriosis, staining for telomerase was significantly increased compared to the group two women at both the window of implantation and late, premenstrual phases. In healthy group two women, expression of telomerase and oestrogen receptor (ERß) was seen in the connective tissue (stroma) and cells surrounding the blood vessels during the luteal phase, but was significantly less in group one women. The researchers also found that the average telomere length was significantly longer during the window of implantation phase in women with endometriosis compared to those without it.

Telomere length was not affected by age, height, weight, or BMI. In the peripheral blood samples, oestrogen levels rose with increases in telomere length. There was no difference between the groups in circulating progesterone levels. The positive control samples showed telomerase activity, as expected.

The researchers suggest that abnormal expression of telomerase in the endometrium enhances proliferation of the cells and may contribute to the pathogenesis (origin and development) of endometriosis.

This carefully designed study has shed light on some cellular processes that might be responsible for the excess proliferation of endometrial tissue in endometriosis. However, as the researchers openly acknowledge, this is preliminary research. Tissue samples from only a small sample of women were studied and much larger numbers would be needed to confirm these results. Also, a case control study such as this cannot prove causation. As such, it is too early to suggest that this could lead to any diagnostic or treatment options for the conditions.

This study is a valuable first step in the further understanding of endometriosis, a condition which can be treated symptomatically but currently has no cure. More research is anticipated.

‘Three oily fish meals a week can cut memory loss by 25%’, reported the Daily Mail. It said researchers found that eating oily fish (baked or steamed, not fried) can reduce the harmful brain lesions that can cause Alzheimer’s disease. The research involved looking at brain scans of over 2,000 people, and seeing how changes in the brain were associated with eating oily fish in the diet.

Although this is a study of a large group of people, it has several limitations, including how fish consumption was assessed, and by its design cannot provide conclusive evidence that eating oily fish prevents brain changes. In addition, the links found between risk of areas of infarct in the brain (areas starved of oxygen) and fish consumption were not statistically significant. This study did not assess how the changes seen on brain imaging relate to any memory change or to cognitive brain function in the person. Although Omega-3 or ‘essential fatty acids’ as found in oily fish are known to be an important part of a healthy balanced diet, this study does not bear out the claim that they protect memory or brain function.

Dr Jyrki Virtanen and colleagues from the University of Kuopio, Finland, carried out the research. Funding was provided by the National Heart, Lung and Blood Institute, the National Institute of Neurological Disorders and Stroke, the Finnish Cultural Foundation, and several other Finnish foundations. The study was published in the peer-reviewed medical journal: Neurology.

The aim of this cohort study was to investigate the association between fish consumption and brain abnormalities. The researchers used participants who were already involved in the ongoing Cardiovascular Health Study (CHS), a prospective cohort study of 5,888 adults in the United States. All participants were aged 65 or older when they enrolled between 1989 and 1990.

At the beginning of the study, the participants had all undergone extensive clinical assessments and completed questionnaires, with diagnoses of coronary heart disease, stroke, high blood pressure, or diabetes being noted. Their diets were assessed using a pictorial version of the food frequency questionnaire, which asked how frequently they had consumed certain foods during the past year. At their first assessment when they enrolled, they were asked how much tuna fish, ‘other broiled or baked fish’ or ‘fried fish or fish sandwiches’ they ate. When diets were assessed again in 1995-1996, they were asked how much canned tuna fish, dark-meat fish (mackerel, salmon, sardines, bluefish, swordfish) or other white fish they consumed. At this assessment, they were not asked about fried fish. The researchers estimated the participants’ nutrient intake and omega 3 fatty acid intake from the questionnaire responses.

The CHS participants were invited to have MRI brain scans between 1991 and 1994. A total of 3,660 (62%) agreed. Those who agreed tended to be slightly younger and healthier than those who did not. All the participants were again invited to have a scan five years later, at which point 2,313 were scanned. There was a total of 2,116 participants who received both scans (36% of total cohort) and these people were reported to be healthier than those who only received the first scan, with lower prevalence of chronic diseases and smoking. When the scans were analysed, attention was given to areas of brain infarct (areas that have been starved of oxygen). People who have had a stroke have these, but in this study the infarcts were termed “subclinical”, as they were not associated with any known clinical effects in the person. Other structures in the brain were also examined, including the ventricles (brain cavities continuous with the spinal cord), brain sulci (brain folds) and white matter (nerve fibres). These latter three structures were given a grade (details of the grading system not provided in the report).

The researchers carried out cross-sectional statistical analyses to see how dietary intake affected the risk of brain infarcts or ventricular, sulcal or white matter grades seen on brain imaging. This considered the timing of the food questionnaires to roughly correspond to the timing of the MRI scans. After confirming that results were similar, they then compared diet intake at the first questionnaire to the second brain scan. They excluded from their evaluations those people who had a history of stroke or mini-stroke (TIA), those with prior brain haemorrhage and those with incomplete information on fish consumption. Analyses were adjusted for other potential medical and lifestyle confounders.

After exclusions, 2,465 subjects were left at the first scan, 1,663 left at the second scan, and 1,124 were left with both scans available for analysis. Of the participants who had the first scan, 23% had evident subclinical infarcts. The researchers also found that 23% of the participants who had the second scan had infarcts.

After taking into account various confounding factors, there were no significant associations between fish consumption of any type or frequency and risk of subclinical infarcts on brain scan. The 26% reduction in risk reported by the study from eating ‘tuna or other fish’ three times per week (compared to eating it less than once a month), was not significant (95% CI 0.54 to 1.01). There was no link between ventricular and sulcal grade and fish consumption, but there was correlation seen between lower white matter grade and higher tuna and other fish consumption.

The researchers also found that other social and lifestyle factors, such as sex, education and fruit and vegetable intake, was associated with type of fish intake (i.e. frequency of tuna or other fish consumption, and frequency of fried fish consumption).

The researchers concluded that modest consumption of tuna and other fish, but not fried fish, is linked with a lower prevalence of subclinical infarcts and white matter abnormalities on brain imaging.

This is a study of a very large cohort of people; however, it has been over interpreted by the newspapers and does not demonstrate that oily fish, or any other type of fish, protects against memory loss, risk of Alzheimer’s dementia, or risk of any other type of dementia. This is borne out by the following points:

• None of the links between risk of subclinical infarct and fish consumption of any type were statistically significant.
• The presence of ‘subclinical infarcts’ does not necessarily relate to any change in memory or cognitive function in the person, and these were not tested by the study.
• Subclinical infarcts are also not a feature of Alzheimer’s disease (a condition characterised by having unknown cause). The brain ventricles are known to become enlarged in people with Alzheimer’s, but there was no link seen between ventricular grade and oily fish in this study. Other changes known to be associated with Alzheimer’s, such as neurofibrillary tangles and brain plaques, were not examined.
• Fish consumption was assessed by a person’s recall of how much fish they had eaten over the past year. There are several limitations to this. Although this was assessed at two separate time periods, it cannot be assumed that consumption remained the same. There is also likely to be some errors in the participants estimations of their normal consumption, and portion sizes are subjective and the method of assessing this is not specifically reported in this study. Finally, although examples are given of the fish groupings asked about, the method of grouping used in the analyses of ‘tuna and other fish’ or ‘fried fish’ are extremely broad and cannot be assumed to relate to oily fish or any other particular type of fish without further information.
• There are likely to be a large number of confounders that will affect brain change, and although the researchers have considered many, there may be others.
• Only a small proportion of the total participants received both scans (36%), and the researchers reported that these people were younger and healthier than those receiving only first scans or not scanned at all. The results may have been different again if all the participants could have been scanned.
• There may be some difference in detection of infarcts and grading of ventricular, sulcal and white matter abnormalities, between different observers.

Omega-3 or ‘essential fatty acids’, such as those found in oily fish, are known to be an important part of a healthy balanced diet. However, this particular study does not prove that they protect memory or brain function.

“Vaccinating children against flu may be an effective way of protecting the rest of the population”, The Independent reported. Many newspapers covered the same story, with The Daily Telegraph saying that, “flu could be virtually wiped out if all under 16s were vaccinated against the disease”, and the Daily Mail saying that vaccinating children under five could cut infection rates by 70%. Most newspapers also said that the Joint Committee on Vaccinations and Immunisation (JCVI), considered and rejected the idea in 2006, but was keeping the issue under review.

These reports are based on a study that used mathematical techniques to model the potential effects of vaccinating children of different ages in England and Wales against flu. Although this model provides a useful forecasting tool to look at the possible effects of vaccination, further real-life studies on efficacy and safety, and modelling of cost-effectiveness of a flu vaccination programme in children, would be needed before being considered to become national policy. Carrying out a vaccination programme of all children in the UK on an annual basis would be a massive undertaking and there are also ethical issues to be considered.

Dr Emilia Vynnycky and colleagues from the Health Protection Agency Centre for Infections carried out the research. One of the authors was funded by a grant from the UK Department of Health; the Department did not have a vested interest in the study’s outcome. No other sources of funding are reported. The study that was appraised was a pre-publication version awaiting publication in the peer-reviewed medical journal: Vaccine.

In this mathematical modelling study, the researchers used complex mathematical techniques to predict the long-term effects of vaccinating children of different ages in England and Wales against flu. As it had not been modelled before, the researchers were particularly interested in the effects of only vaccinating preschool children, and looking at how the children’s contact patterns (i.e. who they came into contact with) affected transmission rates.

The researchers based their model on existing models of the effects of global flu epidemics. To develop the model for the UK population, they had to make assumptions about major contributing factors in the occurrence of influenza. These assumptions were based on real life observations as much as possible. Their model was adapted to take three main factors into account. First, that there are annual flu epidemics in the winter in the UK, with influenza type A epidemics occurring annually, and type B epidemics occurring every 2-3 years. Second, that children have a higher rate of infection than adults as they have not been exposed to as many flu viruses in the past. And third, that re-infection with the same strain of flu can occur, because the virus gradually changes (mutates).

The model took into account the various flu strains and their reoccurrence over time, based on what has been observed in the past. The model also took into account: percentage of people covered by vaccination, efficacy of the vaccine, immunity based on previous exposure, mutation in the influenza virus, period of infectiousness (set at an average of two days), and the percentage of people who would show symptoms if they were infected (64%). The study assumed that asymptomatic individuals would not be infectious.

The model’s birth and mortality rates from flu were taken from England and Wales in 2003. Children were assumed to have different levels of contact with people of different ages. Five different sets of probabilities of contact by age were used; these were based on assumptions used in previous models and have been shown to give good estimates of what happens in real life. These were adjusted further to better fit observed UK data. The definition of an effective contact was given as contact between an infected and an uninfected susceptible person that was sufficient for transmission of infection. Efficiency of contact was presumed to be greatest in the winter, when flu epidemics occur. Vaccination was assumed to be finished before the influenza season began. Vaccinations were assumed not to be given to children aged under six months. The model assumed that 60% of children within the targeted age groups could be effectively vaccinated (i.e. would receive the vaccination, and would develop immunity against flu).

The researchers found that the effect of a vaccination programme depended on the age of children vaccinated. Vaccinating children aged under one year had little effect on overall cases of flu in the entire population. Vaccination in other age groups led to reduction of clinical flu cases not only in their own age group but also in the overall population. Vaccination in these groups led to an initial reduction in cases of flu (a “honeymoon” period), followed by an increase, and finally settling at a rate lower than the pre-vaccination rate.

The effect on influenza B was greater than the effect on influenza A. Vaccinating children aged under two years could reduce clinical cases of influenza A by 11-22% in the overall population, and influenza B by 25-35%. Vaccination in children under five years of age was estimated to reduce clinical cases of influenza A by 22-38%, and influenza B by 44-69%, and in children aged under 16 years the estimates were 65-97% and 85-96% respectively.

These predictions were sensitive to certain assumptions used to make the model, mainly the patterns of contact the children had; this means the results change if you change these assumptions.

The researchers concluded that achieving a high level of effective flu vaccination among preschool children could bring benefits both to the children themselves, and to the wider community. They suggest that further population based studies on the effects of child vaccination programmes are needed to confirm their results.

This modelling study provides predictions for the effects of flu vaccines in different age groups of children. As with any model, the accuracy of the predictions depends on how accurate the assumptions are. The authors note that although some of their assumptions may be overly simplistic compared with real life, they are based on real data where possible. They say the model improves on other existing models by including the indirect effects of vaccination (known as “herd immunity” – where immunity at a certain level in the community protects other, non-immune members of the community).

As the authors suggest, actual population based studies will be needed to confirm the accuracy of their model, and to refine it if necessary. Also needed are further studies that assess the costs of different vaccination programmes, and balance them against the costs saved by avoiding illnesses, to see which strategy is most likely to be cost effective. These studies would need to be carried out before any nationwide programmes were considered.

As there are different strains of influenza virus circulating during different seasons, the vaccinations are prepared before the flu season starts and are designed to protect against the strains that are expected to be predominant. Even then, it is not always possible to get this 100% correct and the vaccination is more effective in seasons where it matches well with the strains of virus that are causing infection. Carrying out a vaccination programme of all children in the UK on an annual basis would be a massive undertaking. Even if immunisation reduced transmission rates to vulnerable and elderly population groups, the ethical issues of giving yearly injections to children who would normally suffer only an uncomplicated and self-limiting illness, must be considered.

“Vitamin C injections can destroy cancer”, the Daily Express reported. Widespread media attention was given to a study that found that high dose injections of vitamin C could slow the growth of cancers. The newspapers said that tests in mice showed that this treatment could halve the size of pancreatic, brain, and ovarian tumours. Most reports mentioned that the concentrations of vitamin C used in the study could not be achieved simply by eating vitamin C-rich foods or by taking supplements. In addition, Dr Alison Ross from Cancer Research UK called for more research, and cautioned, “there is currently no evidence from clinical trials in humans that injecting or consuming vitamin C is an effective way to treat cancer. Some research even suggests that high doses of antioxidants can make cancer treatment less effective, reducing the benefits of radiotherapy and chemotherapy.”

Although this research may prompt other studies into the potential anticancer effects of vitamin C, it should not be taken as proof that vitamin C injections will necessarily have the same effects in humans. More research is needed before it is possible to be certain what the effects of this treatment might be.

Dr Qi Chen and colleagues from the National Institute of Diabetes and Digestive and Kidney Diseases, and other research institutions in the USA, carried out the research. The study was funded in part by the National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health. The study was published in the peer-reviewed medical journal: Proceedings of the National Academy of Sciences.

This experimental laboratory study looked at the effects of high doses of ascorbic acid (vitamin C) on tumour cells grown in the laboratory, and on transplanted tumours in mice. Ascorbic acid is an essential part of the diet, and is considered to be an antioxidant, thought to protect cells from free radicals which have been linked to cell damage and cancer. In this study, the researchers considered the possibility that in high concentrations, ascorbate is in fact a pro-oxidant, and generates the chemical hydrogen peroxide, which can kill tumour cells.

The researchers took 43 different cancer cell types (including rat, mouse, and human cancers) and five different normal cell types grown in the laboratory, called cell lines. After exposing these cell lines to varying concentrations of ascorbic acid for up to two hours, they looked at whether the cells died, what concentration of ascorbic acid was needed to kill half the cells, and whether this was different for cancer and normal cells. To ascertain whether hydrogen peroxide was involved, they tested whether the cells would still die if they added an enzyme that breaks down hydrogen peroxide.

The researchers then took a selection of the cell lines that were most susceptible to ascorbic acid and transplanted them into mice and allowed them to grow. Once the mice had developed tumours that were 5-7mm in diameter, some of them (between 9 and 18 mice) received daily injections of high concentration ascorbic acid into their abdominal cavity for 30 days. The remaining mice were injected with salt water (the control groups, which included between 10 and 18 mice). The researchers compared tumour growth in these two groups of mice.

Finally, the researchers looked at whether they could achieve the concentrations of ascorbate seen in mice in humans, using intravenous injections of ascorbic acid.

The researchers found that ascorbic acid killed most of the different mouse, rat and human cancer cells at a lower concentration than that which killed normal cells. Some human cancer cells also survived these lower concentrations. Experiments showed that hydrogen peroxide was involved in killing the cells.

In the second phase of the experiment, the researchers injected mice with cancer cell lines that were susceptible to ascorbic acid in their first set of experiments - a human ovarian cancer cell line, a rat brain tumour cell line, and a mouse pancreatic cancer cell line. They found that injecting these mice with ascorbic acid reduced tumour growth and weight compared to controls. They found that about a third of the control mice injected with the brain tumour cells had metastases (tumours spread from the original tumour), but none of the ascorbic acid treated mice had metastases.

The mice did not seem to experience adverse effects from the ascorbic acid injections. The researchers found that they could achieve similar concentrations to those seen in mice in humans by using intravenous injections.

The researchers concluded that ascorbic acid “may have benefits in cancers with poor prognosis and limited therapeutic options.”

This is a very preliminary study looking at the effects of high levels of vitamin C on tumour cells grown in the lab, or in small numbers of mice. It is worth noting that not all of the tumour cells grown in the laboratory were susceptible to ascorbic acid, and only one of the cancer cell lines that was tested in mice was a human cell line.

Although this study may lead to further research into the anticancer effects of vitamin C, it cannot prove that vitamin C injections will necessarily have the same effects in humans. The authors report that the concentrations of vitamin C used could not be achieved orally; therefore it certainly should not be assumed that taking vitamin C orally would have similar effects.

“One of the main benefits of flu jabs for the elderly - protection against pneumonia - may not exist”, BBC News reported. It said that a study in thousands of vaccinated and unvaccinated people found that healthy, older people who had the jab had the same risk of pneumonia as those who had not.

This study found that flu vaccination appears to offer little protection from community acquired pneumonia (CAP), a common complication of flu, for relatively healthy, elderly people who do not live in institutions. Other studies have provided evidence to suggest that it is beneficial for vulnerable groups, such as those who are immunocompromised (from current treatments or chronic illness) and those in nursing homes.

Although the study was well-conducted, and the researchers used robust analyses to adjust for other factors that could explain the results, they admit that they might not have measured all of these. Also, it is unclear what type of CAP the participants had - viral or bacterial. Bacterial CAP is more common both as a complication of flu and as an isolated infection. Their episodes of CAP may be unrelated to flu episodes. Further research is needed; the researchers themselves call for this.

Dr Michael L. Jackson and colleagues from the Group Health Center for Health Studies, the Fred Hutchinson Cancer Research Centre, PATH and the University of Washington carried out this study. The research was funded by the Group Health Center for Health Studies and by a fellowship grant from the Group Health Community Foundation. The study was published in the peer-reviewed medical journal: The Lancet.

The study was a nested case-control study in healthy (immunocompetent) elderly males and females between 65 and 94 years of age. The participants were enrolled with a health management organisation called Group Health (an organisation that provides medical coverage and healthcare services) in the western Washington state. They were healthy adults with no history of serious cancer, chronic renal failure, prescriptions for immunosuppressive medications during the previous two years, and no history of treatment for cancer in the previous three months. Each had also made more than two visits to Group Health in the previous two years.

For each year of the study (2000, 2001 and 2002), the researchers were interested in whether or not the participants who contracted pneumonia had been given that year's influenza vaccine. The cases in the study were those people who had an episode of CAP (either as outpatients or inpatients) during that year. Their illness was validated through assessment of their chest radiographs and medical records; the researchers who performed this task were unaware which people had been vaccinated. Each case subject was randomly matched to two control subjects from the source population for age (within one year of the case’s birth date) and gender. The controls had not had an episode of CAP before their matched case fell ill.

Researchers reviewed the participant’s medical records for the two years preceding the study start date, with particular attention to the following details: asthma, chronic obstructive pulmonary disease, congestive heart failure, alcoholism, diabetes, dementia, and stroke. The researchers also collected information on the functional status of participants; whether they needed assistance bathing, walking or eating, and whether they smoked. Other prescription data from the General Health records were also collected as indicators of other diseases. People who were living in a nursing home or another institution or who were immunocompromised (according to their records) were excluded from the study.

For each year of the study, the researchers compared the likelihood of an episode of CAP in relation to vaccination while taking into account other health factors. Their overall sample included 1,173 validated cases of CAP and 2,346 matched controls.

Overall, people who had CAP were more likely to have chronic diseases, functional impairments, and prescriptions for lung medications and antipsychotics. The cases and controls were equally likely to have received the flu vaccination.

When the researchers took into account all the factors they believed may have influenced the outcome including age, sex, asthma, smoking, antibiotics for lung conditions and previous pneumonia, they found that there was no significant effect of vaccination on the risk of CAP in the participants. This means that people who got pneumonia were as likely to have been vaccinated as those who did not get pneumonia. Further analysis of subgroups found no effect of vaccination on infection during the peak season, on risk of hospitalisation, or on risk of infection in one of the flu seasons included in the study (2000, 2001 or 2002).

The researchers concluded that their ‘large, population-based, nested case-control study’ found no effect of flu vaccination on the risk of community-acquired pneumonia in the elderly.

In this well-conducted study, the researchers took into account as many additional factors as possible. They repeated their analyses using different statistical techniques and found that their overall conclusions did not change. In addition, they chose to analyse data from three flu seasons in which the flu vaccination was shown retrospectively to be well matched to the flu virus that ended up circulating in the population. The researchers also did what they could to validate the diagnoses of pneumonia by independently reviewing records or chest X-rays.

The main problem with studies of this design is the adjustment for, or taking into account of, other factors that might be responsible for the association between the exposure (vaccination) and the outcome (pneumonia). The efforts the researchers made in order to account for these factors increases confidence in the results.

In this study, the researchers were interested in the effect that the flu vaccination had on pneumonia in the elderly. Pneumonia is a common and serious complication of the flu virus and arises either from the influenza virus directly infecting the lungs or from a secondary bacterial infection. The researchers say that their results could mean one of two things:

• First, that pneumonia is not an important complication of influenza in this age group, i.e. the flu vaccine may be highly effective at reducing flu in the participants, but if pneumonia is not usually associated with flu then there wouldn’t be a parallel reduction in pneumonia cases.
• Second, that the flu vaccination is ineffective at reducing influenza in people at risk of pneumonia.

They say that these two possibilities have quite different implications for vaccine policy and development and that further research is needed to clarify the results.

Flu vaccinations are prepared before the flu season starts and are designed to protect against the strains that are expected to be predominant. They do not protect against bacterial infection. Bacterial pneumonia is common in the elderly either as a complication of flu or as an isolated infection. The results would have been clearer if the infecting cause of the pneumonia was known, e.g. from microbial reports in the laboratory, and also if it were known whether there had been an epidemic of a particular bacterial pneumonia in those seasons. Although the majority of the participants appear to have had the pneumococcal vaccine, these factors could explain in part the differences seen here.

Importantly, this study only included relatively healthy individuals (who were immunocompetent and not living in nursing homes or other institutions). The flu vaccination is recommended for a number of different groups who are considered vulnerable, such as people living in institutions, those with a chronic illness, and those who are immunocompromised for some reason (such as receiving steroid treatment or treatment for cancer). These people should continue to receive vaccinations as recommended, as there is good evidence that pneumonia, hospitalisations and possibly even death may be reduced.

“Heart attack victims ‘should not give up taking statins’” reported The Times saying that people who have a heart attack and who give up taking statins afterwards double their risk of dying in the following year. The newspaper goes on to say that “even though the pills may appear to have failed to prevent a heart attack, it is much better to go on taking them anyway”.

This study used data on patients enrolled with GPs across the UK to investigate the effect of continuing or discontinuing statins in people who survived heart attacks and who were still alive three months later. These are potentially important findings, but they are based on a small subgroup of people (only 137 out of nearly 10,000) who stopped taking statins after their heart attack. The researchers themselves call for more research given the potential clinically important implications of this study.

Dr Stella S. Daskalopoulou and colleagues from McGill University and the University of Washington carried out this study. Some of the researchers and their work were funded by Les Fonds de la Recherche en Sante du Quebec. Another researcher received the CIHR Distinguished Scientist Award. The study was published in the peer-reviewed medical journal: the European Heart Journal.

The study was a retrospective cohort study that followed up people in the UK who had survived a myocardial infarction (heart attack) between January 01 2002 and December 31 2004. They were identified using the General Practice Research Database (GPRD), which collects information on the health of more than three million people through 400 GP practices across the UK. The GPRD also collects information on demographics and lifestyle (height, weight, smoking, alcohol). This database is representative of the UK population and has been shown to be of high quality and is often used to study the population of the UK. Participants in this study were those who had survived at least 90 days after their first heart attack, were at least 20 years old, and had a minimum of three consecutive years of records in the database.

The participants were divided into four groups depending on their statin use around the time of their heart attack. These groups were: those who did not use statins 90 days before or after their heart attack; those who used statins before and after their heart attack; those who did not use statins before their heart attack but used them after; and those who used statins before their heart attack but did not use them afterwards.

The researchers compared the survival of the four groups (all causes of mortality) between 90 days and one year after the heart attack. In this way, they could investigate what effects different patterns of statin use around the time of a heart attack have on survival. They also took into account other factors that might have had an effect such as age, sex, smoking, alcohol, obesity, and number of hospitalisations. In total, 9,939 survivors were included in this study.

Of the 9,930 survivors of their first heart attack, 2,124 had not used statins for 90 days before or after the event, 137 had been taking statins before but did not take them afterwards, 5,652 did not take statins before their event but took them afterwards, and 2,026 were taking statins both before and after.

Compared to people who never took statins, those who started taking them after their heart attack were less likely to die after one year. However, those who stopped statins after their heart attack were at increased risk of dying after one year. Those who took statins before and after their event were not statistically different from those who never took statins.

The researchers say that their study suggests there is a strong harmful effect of stopping statins, and that those people who did not continue to take them after their heart attack were 88% more likely to die during the one year follow up (95% CI 1.13 to 3.07). This effect was not just due to stopping using a drug, as the same effect was not observed in people who stopped taking aspirin, beta blockers or PPIs.

This large, population-based cohort study suggests that stopping statins in the 90 days after a heart attack increases the risk of death. This is potentially a very important finding.

However, only 137 out of 9,939 patients had been taking statins and then stopped. The fact that the main conclusions of this study are based on results from such a small sample suggests some caution in interpreting these results. The researchers have taken into account some of the factors that may be responsible for this relationship, although they add that they cannot rule out the possibility that there are some other factors involved that were not measured. There are other weaknesses with this study, some of which the researchers discuss:

• As they acknowledge, they were unable to look at the contribution of different types of statins to the outcomes (they only looked at whether people took any type of statin or not, as opposed to individual types of statins).
• They did not have any information on how serious the heart attack was or what treatment was received in hospital.
• It was assumed that if people did or did not take statins in the 90 days after their heart attack, they continued to do this during the entire follow up period (i.e. that if people discontinued statins in that time, they did not start taking them again and vice versa. This may not have been the case for all people.
• The researchers do not look at why statin use may have stopped. The people who stopped taking statins may have been at a higher risk of death for some other reason.
• In recent years, statins have become available over the counter. This study only analyses data from before they were available (2002 and 2004) and the results may be somewhat different if the current general population was studied.

As the researchers suggest, more population-based studies are needed to confirm their findings that statins should be continued after a heart attack given the potential clinical importance. The editorial that accompanies this study suggests that given the small sample size and the observational nature of this data, the study is ‘inherently more hypothesis-generating rather than hypothesis-proving’. Despite this, the editorial’s authors conclude that these findings are important and that ‘continuation of statin therapy following onset of acute coronary syndromes is crucial and is probably most important in patients at high cardiovascular risk’.

“California has become the first US state to ban restaurants and food retailers from using trans-fats”, BBC News reported. Arnold Schwarzenegger, the governor of California, has pledged to phase out the use of trans-fats in Californian restaurants by 2010 and trans-fats in baked goods will be removed by 2011.

What are trans-fats? Trans-fats are artificially created fats used in the manufacture of foods. They increase shelf life and the flavour-stability of foods. They are also often found in fast food, cakes and biscuits.

Where have they been banned? In Europe, Denmark has banned all but trace amounts of trans-fats in food since 2003. The use of trans-fats has also been banned in restaurants in New York City since July 1 2008. California will phase out their use completely by 2011.

Why have they been banned in the US? Schwarzenegger is quoted as saying: "Consuming trans-fat is linked to coronary heart disease”. Trans-fats have been shown in many studies to increase the risk of coronary heart disease (CHD) by increasing levels of “bad” cholesterol (low-density lipoprotein – LDL)  and decreasing levels of “good” cholesterol (high-density lipoprotein – HDL) in the blood.

In light of the US restrictions, in December 2007, Alan Johnson, the health secretary, asked the Food Standards Agency to look at:

• the health impacts of current UK intakes of trans-fats, 
• activities by the UK food industry to reduce levels of artificial trans-fats in food, and 
• actions against trans-fats taken in other countries.

The report concluded that there was evidence to show that trans-fats increase the risk of coronary heart disease (CHD), but that evidence linking trans-fats to obesity and cancers was lacking.

Based on evidence of the adverse effects of these fatty acids on risk of CHD, it is recommended that trans-fats should contribute no more than 2% food energy. In the most recent survey of UK food trends, trans-fats made up 1.2% of food energy (according to the National Diet and Nutrition Survey in 2000/1). This is well below the current recommended intakes of trans-fats and is almost half the US average dietary intake (estimated to be 2.6% of food energy).

Does food in the UK contain trans-fats? Since January 2008, members of the British Retail Consortium, which include the major UK supermarkets and fast food chains, have stopped using trans-fats as an ingredient in foods. However, food manufactured outside of the UK, such as in Europe or the US, could still contain trans-fats.

What can I do about trans-fats in my diet? The Food Standards Agency has proposed changes to food labelling in the UK which will mean that consumers will be able to see the amount of trans-fats in the foods they consume. People can also look at the list of ingredients in their food, if "partially hydrogenated fat/oil" or "hydrogenated fat/oil," is listed, the food contains trans-fat.

Until any new labelling is implemented, the Food Standards Agency recommends that people should be aware of their fat intake in general. It is well-known that trans-fats are linked to an increased risk of CHD and, as part of a healthy diet, consumption should be reduced.

“Scientists have invented a drug that keeps you as fit as an athlete without having to flex a muscle,” the Daily Express reported. Mice that had never exercised could run for 44% longer when given the drug, while another drug enabled them to run 76% further when they also exercised. In addition to being a “couch potato’s dream” (Daily Mail), The Independent called it “a new threat to the Beijing Olympics” as the drugs could “potentially boost the performance of endurance athletes”.

It is important to point out that these chemicals have only been tested on mice, and their effects in humans may not be the same, and may have serious side effects. The chemicals are not readily available to the public. If athletes do manage to get hold of them, they should realise that they are risking not just their reputation, but also their health. It is also misleading to suggest that couch potatoes can take a pill that gives them the full benefits of exercise. Although the chemicals enhanced athletic ability in mice, they have not been shown to have the other beneficial effects of exercise, such as weight loss and reduction of the risk of various diseases.

Dr Vihang Narkar and colleagues from the Salk Institute and other research institutes in the US and South Korea carried out the research. The study was funded by the Howard Hughes Medical Institute, Hilblom Foundation, and National Institutes of Health. The study was published in the peer-reviewed scientific journalCell.

This was an experimental laboratory study looking at the effects of two different chemicals, AICAR and GW1516, on exercise endurance in mice. Both these compounds target related chemical pathways in cells, and the researchers wanted to know if these pathways were involved in exercise endurance.

The researchers first took a group of 36 male mice and randomly divided them into four groups. The first group was not exercised (was sedentary) and was not given any drugs. The second group was also sedentary, but was given GW1516 by mouth. The third group was exercised (on a treadmill) and not given any drugs, and the fourth group was exercised and given GW1516.

Before treatment started and after four weeks of these treatments, six mice from each group had a treadmill test to see how far they could run, and for how long. The muscles in the remaining mice in each group were examined for changes in which genes were expressed or for changes in muscle structure.

The researchers carried out a similar experiment, where they injected sedentary mice with the chemical AICAR or a control substance and tested their performance before and after four weeks of treatment. They also carried out experiments where they gave mice GW1516, AICAR or both for six days, and then looked at which genes were switched on in the mice’s muscles.

The researchers found that treating sedentary mice with GW1516 switched on genes which are involved in metabolism, but that it did not alter their muscle fibres or improve their endurance in the treadmill test. However, when the mice received both GW1516 and exercise training, it caused changes in gene expression, as well as in their muscle fibres, and increased their treadmill running time by 68% and running distance by 70% compared with mice who had exercise training but no GW1516.

Treating sedentary mice with AICAR switched on similar genes to those activated with GW1516 and exercise, and reduced the mice’s body fat without changing their weight. In addition, AICAR-treated sedentary mice ran 23% longer and 44% further than untreated sedentary mice on the treadmill test.

The researchers conclude that they have identified chemical pathways that can be targeted by drugs taken orally. The drugs can improve the effects of exercise and can increase endurance without exercise. They say that drugs which mimic the effects of exercise have potential for use in treating muscle diseases and obesity.

These complex experiments further the understanding of the biochemical pathways involved in developing endurance. Developing drugs that target these pathways may well provide treatments for human diseases in the future, but this is still a long way off. This study did not assess the safety of the compounds tested, and they may not prove to be safe for testing in humans, or to have the same effects on endurance.

Although these drugs improved endurance, they may not have the other benefits of exercise, such as weight loss and reduction in risk of various diseases. In particular, the authors specifically noted that the drugs did not affect the mice’s weight. Therefore, it is premature to suggest that these drugs could be the antidote to a couch potato lifestyle.