Police are appealing for information after a parked Audi TT in Newmarket was damaged by a ‘sharp instrument’.
West Suffolk MP Matthew Hancock has officially opened the new Fiveways Service area at Barton Mills which has already created more than 120 jobs in the area.
The Met Office is warning of a blustery weekend ahead across the UK.
"Scientists warn smoking 'skunk' cannabis wrecks brains," The Sun reports, somewhat simplistically. A small study found some users of the high-strength skunk strain of cannabis had changes in nerve fibres in a specific part of the brain.
Researchers used MRI scanners to scan the brains of 99 adults – some with psychosis, some without – looking for any links between small changes in their brain structure and their cannabis habits.
The researchers looked specifically at the effect on the fine structure of the corpus callosum. This is a band of nerve fibres joining the left and right sides of the brain and is thought to help different parts of the brain "communicate" with each other.
They found users of skunk – as well as those who used any type of cannabis on a daily basis – had different structural changes in the corpus callosum, compared with those who smoked less or lower-strength strains.
What this study doesn't tell us is whether these structural changes do any harm or cause any negative mental health effects – which is why The Sun's headline is too strong. The study simply didn't look at this.
The effects of cannabis use – both in the short and longer term – are not firmly established. But cannabis is known to be one of many substances that can trigger a psychotic episode. Read more about psychosis.
The study adds new knowledge about the potential effect of cannabis smoking on the brain, which other researchers can build on. But this was exploratory research and cannot provide any concrete cause and effect conclusions.
Where did the story come from?
The study was carried out by researchers from King's College London and the Sapienza University of Rome.
It was funded by a King's College London Translational Research Grant, the National Institute for Health Research (NIHR) Mental Health Biomedical Research Centre at the South London and Maudsley NHS Foundation Trust, and King's College London.
Generally, the UK media covered the story accurately, but some of the headline writers overstepped the mark. The Sun's headline, "Scientists warn smoking 'skunk' cannabis wrecks brains", and the Daily Mail's, "Proof strong cannabis does harm your brain", were not based on any evidence.
This type of study cannot prove cause and effect, only suggest a possible link, so "proof" is too strong a term. Also, the study didn't look at how the small changes in the brain associated with skunk affected thoughts or other brain functioning, so it was not fair to say skunk "wrecks" the brain.
This study wasn't designed to look at the effect of skunk on mental health illnesses, only small changes in brain structure, so it tells us little about the link between cannabis use and the development of a mental health illness.What kind of research was this?
This cross-sectional study looked for differences in the structure of a specific area of the brain called the corpus callosum in people with psychosis and those without.
It also looked at how this was linked with their reported cannabis use. The researchers were most interested in the effect of cannabis potency and how regularly cannabis was used.
The research team says high-strength cannabis (skunk) has been associated with a greater risk and the earlier onset of psychosis – the experience of hallucinations or delusions, a characteristic feature of the mental health condition schizophrenia.
However, the possible effect of cannabis potency on brain structure has never been explored. The researchers set out to investigate this by studying the fine structure of the corpus callosum, a band of nerve fibres joining the left and right sides of the brain.
This type of study can't prove cannabis causes changes in brain structure or any associated mental health illness. A long-term cohort study would be needed for this – a randomised controlled trial wouldn't be appropriate for ethical and, in the UK, legal reasons. But this type of study can point to possible or probable links for further investigation, a useful exercise to guide the next round of studies.What did the research involve?
A group of 56 people with psychosis (37 cannabis users) and 43 people without psychosis (22 cannabis users) had their brains scanned. The scans were used to look for possible links between their cannabis habits and any differences in the structure of the corpus callosum area of their brains.
Those with psychosis had been medically diagnosed with first episode psychosis, which simply means someone who has experienced psychosis for the first time. Most of those with psychosis were taking antipsychotic medication (53 of 56), just three were not.
The brain scans used an MRI imaging technique – diffusion tensor imaging tractography – that maps how different parts of the brain are linked to each other and how easily information is transferred between both sides. This technique measures the efficiency by which signals in the brain travel (diffusivity), where low diffusivity scores indicate a healthy functioning brain and high diffusivity may indicate some form of damage.
The team looked at four common diffusion tensor imaging measures:
- fractional anisotropy (FA)
- mean diffusivity (MD)
- axial diffusivity (AD)
- radial diffusivity (RD)
FA is a sensitive way of picking up small brain structural changes and is relatively generic. MD, AD, and RD give more specific indications of where changes happen.
All participants filled in an illicit drugs questionnaire that included their cannabis smoking habits, when they first started, the strength they used, and how often they used it.
The statistical analysis took account of the following confounders:
- sociodemographic factors
- some lifestyle factors, such as alcohol intake
There were some interesting results, not all of which were picked up in the media reports. For example, those diagnosed with psychosis were more likely to have used cannabis at some stage in the past compared with those without psychosis.
But there were no differences between people with and without psychosis in terms of how long they had used cannabis, how old they were when they first used the drug, the type of cannabis used, how often it was used, and the strength.
Three of the four measures of corpus callosum function were no different in people with psychosis compared with those without (MD, RD, AD). FA was found to be different, but was borderline statistically significant, meaning there is a reasonable probability the result is down to chance – specifically, a 1 in 25 chance, p=0.04.
As the corpus callosum structure wasn't that different between those with and without psychosis, the researchers pooled the groups to study the effect of cannabis on the brain. Overall, they found the corpus callosum structure was negatively affected in people using high-potency cannabis, compared with those using a lower-potency strain or not using cannabis at all, across MD, AD and RD diffusion measures, but not the more generic FA.
These alterations were similar in users with and without psychosis. A similar mixed pattern was found for frequency of use, with daily users having the most changes compared with occasional or never users. No link was found between those first using cannabis before the age of 15 and those starting after in terms of changes in the corpus callosum structure.How did the researchers interpret the results?
The researchers concluded: "Frequent use of high-potency cannabis is associated with disturbed callosal microstructural organisation in individuals with and without psychosis.
"Since high-potency preparations are now replacing traditional herbal drugs in many European countries, raising awareness about the risks of high-potency cannabis is crucial."Conclusion
This research studied the brains of 99 people – some with psychosis and some without – looking for any links between small changes in their brain structure and their cannabis habits. The researchers looked specifically at the effect on the fine structure of the corpus callosum, a band of nerve fibres joining the left and right sides of the brain.
They found the corpus callosum wasn't very different in those with or without psychosis. But smoking high-strength cannabis (skunk) and using any type of cannabis daily was linked to structural changes in the corpus callosum, compared with those who smoked less or lower-strength cannabis.
What this study doesn't tell us is whether these structural changes do any harm or cause any negative mental health effects. The study simply didn't look at this, a subtlety much of the news reporting failed to recognise.
The study also can't tell us whether cannabis use is the direct cause of these observed differences, or whether other factors could be having an influence. Cohort studies following people over time, examining their cannabis use and carrying out follow-up brain scans, would be beneficial to look at this.
The researchers made the best of what they had in terms of collecting a sample of almost 100 people and analysing the results appropriately.
However, as with all research, this study has its limitations. For example, 100 people isn't enough if you are splitting people into many groups, such as those with and without psychosis and different levels of cannabis use.
Some of the group numbers start to become quite small, which increases the chances you won't have enough people to find statistically significant differences, even if they exist. It can also throw up some unusual findings that wouldn't be the case in a larger group. This study carries these risks.
Similarly, the findings themselves weren't entirely consistent. There is a mix of significant and non-significant findings for the four measures taken (FA, MD, RD and AD). This lack of consistency muddies the picture somewhat and reduces our confidence in the findings a little.
The effects of cannabis use – both in the short and long term – are not firmly established. This study adds new knowledge about the potential effect of cannabis smoking on the brain that other researchers can build on. But it was exploratory research and so cannot provide concrete cause and effect conclusions.
Cannabis is a class B drug that is illegal to possess (up to five years in prison) or supply (up to 14 years in prison). And while it may not trigger mental health problems in everyone, it may make pre-existing symptoms such as depression and paranoia more severe. If you think you may be using cannabis to cope with mental health problems, contact your GP for advice.
Links To The Headlines
Scientists warn smoking 'skunk' cannabis wrecks brains. The Sun, November 27 2015
Smoking high-strength cannabis may damage nerve fibres in brain. The Guardian, November 27 2015
Skunk 'causes damage to vital nerve fibres'. The Daily Telegraph, November 27 2015
Smoking skunk may damage brain junction. The Times, November 27 2015
Links To Science
Rigucci S, Marques TR, Di Forti M, et al. Effect of high-potency cannabis on corpus callosum microstructure. Psychological Medicine. Published online November 27 2015
Police are warning members of the public to be vigilant after Hadleigh residents were telephoned by scammers, with one resident handing over a large sum of money.
"The drug Ritalin should be prescribed with caution as the quality of evidence available about its benefits and risks is poor," the Mail Online reports. A review of available evidence found no high-quality evidence about both the benefits and risks.
Researchers aimed to assess the beneficial and harmful effects of the attention deficit hyperactivity disorder (ADHD) drug methylphenidate for children and adolescents – Ritalin is the most commonly known brand name.
The review identified a large number of trials including more than 12,000 children and adolescents. It found a slight improvement in symptoms of ADHD in children treated with methylphenidate compared to placebo (dummy drug) or no treatment.
There was no increase in risk of serious adverse effects, but there was also a 29% increase in non-serious side effects, such as sleep problems and decreased appetite. However, the findings were based on very low-quality evidence, so we can't be sure of these effects, and better-quality studies would be required to look at this further.
The researchers conclude: "Better designed trials are needed to assess the benefits of methylphenidate".
Alternative treatments for ADHD include behavioural therapy and cognitive behavioural therapy. Read more about treatment options for ADHD.
Where did the story come from?
The study was carried out by researchers from a number of institutions, including the Region Zealand, University of Southern Denmark and Copenhagen University Hospital, all in Denmark.
Funding for the study was provided by the Psychiatric Research Unit, Region Zealand Psychiatry, Roskilde; Region Zealand Research Foundation; and the Copenhagen Trial Unit, Centre for Clinical Intervention Research, Copenhagen University Hospital, Copenhagen.
The review has been reported in much of the media as a warning to be cautious about over-prescribing such drugs. However, the Mail Online explained that the research team could not be confident about the results.
What kind of research was this?
This study was a systematic review and meta-analysis which aimed to assess the beneficial and harmful effects of methylphenidate for children and adolescents with ADHD. This is a good way to gather and combine the findings from trials that have been conducted to date, to draw firmer conclusions; however, a systematic review can only be as good as the included studies.
What did the research involve?
This systematic review searched numerous literature databases and two trials registers to identify all randomised controlled trials (RCTs) comparing methylphenidate to inactive ("dummy") placebo, or no treatment in children and adolescents with ADHD aged 18 years or younger. At least 75% of participants in each study were required to have normal intellectual functioning.
Data was extracted from the studies for the following outcomes:
- ADHD symptoms (attention, hyperactivity and impulsivity), short-term (within six months) or long-term (longer than six months)
- serious adverse events
- non-serious adverse events
- general behaviour in school and at home
- quality of life
Numerous study authors were responsible for data extraction and quality appraisal of the studies, which included an assessment of bias and differences in the results of the individual studies (heterogeneity).
Where appropriate, data from the different studies was pooled using meta-analysis to give an overall result.
What were the basic results?
The systematic review included 38 RCTs (5,111 participants) and 147 crossover trials (7,134 participants – crossover being where participants act as their own control, receiving treatment and no treatment).
The average age of participants across all studies was 9.7 years, but ranged from three to 18 years. As is frequently the case with ADHD, a larger number of boys were represented in the sample, with a boy-to-girl ratio of 5:1.
The length of methylphenidate treatment time ranged from one to 425 days, with an average of 75 days. All included trials were considered to be at high risk of bias.
In a pooled analysis of 19 trials, the researchers found that methylphenidate gave a slight improvement in teacher-rated ADHD symptoms when compared to placebo or no intervention. Those treated with methylphenidate had an average of 9.6 fewer points (95% confidence interval [CI] -13.75 to -6.38) on the ADHD Rating Scale (ADHD-RS).
The ADHD-RS is a scoring system, based on the variety and severity of symptoms, which has a range of 0 to 72 points. A change of 6.6 points is considered to represent the minimal relevant or clinically meaningful difference.
There was no evidence to suggest methylphenidate was associated with an increase in serious adverse events.
The number of non-serious adverse events was, however, higher in the methylphenidate group, with a 29% increase in the overall risk of any non-serious adverse events (relative risk [RR] 1.29, 95% CI 1.10 to 1.51). The most common non-serious adverse events were sleep problems and decreased appetite.
These side effects are acknowledged by the manufacturers of methylphenidate and are described as common in the patient information leaflets that come with the medication.
How did the researchers interpret the results?
The authors conclude: "At the moment, the quality of the available evidence means that we cannot say for sure whether taking methylphenidate will improve the lives of children and adolescents with ADHD. Methylphenidate is associated with a number of non-serious adverse events, such as problems with sleeping and decreased appetite.
"Although we did not find evidence that there is an increased risk of serious adverse events, we need trials with longer follow-up to better assess the risk of serious adverse events in people who take methylphenidate over a long period of time."
This is a well-conducted systematic review that aimed to assess the beneficial and harmful effects of methylphenidate (Ritalin being the most commonly known brand name) for children and adolescents with ADHD.
The review found that methylphenidate was associated with a slight improvement in the symptoms of ADHD, compared to placebo or no treatment – just on the borderline of what would be considered clinically meaningful. However, the researchers state this improvement should be weighed up against the increased risk of adverse events, such as sleeping problems and decreased appetite.
The review identified a large number of trials and included 12,245 children and adolescents, representing the gathering of extensive research into the effects of this drug. However, a major limitation is the poor-quality evidence that was available, with most trials being assessed as being of very low quality.
As the review authors suggest, more research with well-designed trials is needed to better assess the benefits and harms of the treatment, preferably with some subgroup analyses to see if it is possible to identify those who might have better or worse outcomes.
There is no cure for ADHD, but support and advice, and sometimes treatment in the form of medication or "talking" therapies can be useful, to make day-to-day life easier. Sometimes links may be noticed between symptoms and certain foods, such as sugar or additives. However, the most important thing is for the child to follow a balanced diet and not to make drastic changes or add supplements (e.g. omega 3 or 6 fatty acids) without first discussing with a GP.
Read more about living with ADHD.
Links To The Headlines
Experts call for cautionover Ritalin. BBC News, November 25 2015
Links To Science
Storebø OJ, Ramstad E. Krogh HB, et al. Methylphenidate for children and adolescents with attention deficit hyperactivity disorder (ADHD). Cochrane Database of Systematic Reviews. Published online November 25 2015
Police say net is closing on killers of six year-old Rikki Neave as fresh appeal launched on 21st anniversary of his death
The net is closing on the killers of six year-old Rikki Neave, police revealed today.
New rules to help crack down on large-scale tipping of waste that blights the countryside and threatens the future of rural businesses have been welcomed.