“Smoking marijuana as a teenager lowers IQ for life, scientists warn,” the Mail Online reports. The headline is prompted by a critical review looking at the evidence about the potential harms associated with cannabis use.
This latest review was written by researchers from the US National Institute on Drug Abuse and provides an overview of the potential harms associated with cannabis use, ranging from increased risk of car accidents to an adverse effect on “life achievement”.
The Mail’s coverage of the story was an accurate representation of the research, although it took the review findings at face value and did not mention any of its limitations. The most important of which is that it does not appear to be a systematic review, where all available evidence on a particular topic is assessed.
It is unclear whether this study was prone to “cherry picking” – where evidence that supports the researchers’ arguments is included while evidence that opposes it is ignored. This has the potential to bias the findings and conclusions.
The timing of the study is also interesting. After the quasi-legalisation of cannabis in the states of Colorado and Washington there have been increasing calls to roll-out similar laws across America.
Many of the review's conclusions were tentative or indicated more research was needed. Based on this review alone, research into the effects of cannabis use in humans has not yet yielded any firm conclusions and often paints an unclear or inconsistent picture.
Pro-legalisation advocates argue that it is a much safer drug than cigarettes and alcohol in terms of damage to the person and wider society through crime and disorder. And while that may appear to be the case, we have far less evidence on the effects of cannabis than we do on the effects of alcohol and tobacco.
What is the basis for these current news reports about cannabis?
The authors state cannabis (marijuana) is the most commonly used illicit drug in the US with around 12% of people over the age of 12 reporting use in the past year, with particularly high rates among young people.
The regular use of cannabis in adolescence was of particular concern to the review group because of a higher chance of potential harm in younger groups.
The review highlighted a popular belief of cannabis as a harmless vice. Given the loosening of laws and regulation on recreational use in in some US states (Colorado and Washington), some may see this as giving legitimacy to this idea. And in response to the increase in the legalisation of cannabis for medical and recreational use in the US, patients may be more likely to ask their doctors about its potential benefits and risks to health.
The authors indicated many scientific studies report harmful effects associated with cannabis but others do not, which has led to heated debate about whether cannabis is harmful.
The review aimed to assess the current state of the science on the adverse health effects of recreational cannabis use, focusing on those areas for which the evidence is strongest.
What did the report find?
The review was broad, covering addiction, neurodevelopment, mental illness, risk of cancer and life chances.
Risk of addiction
The authors indicated that, “despite some contentious discussions regarding the addictiveness of marijuana, the evidence clearly indicates that long-term marijuana use can lead to addiction”. Around 9% of those who experiment with cannabis become addicted, and this figure rises to 50% of those who smoke it every day, the review said.
Effect on brain development and IQ
The negative effects of cannabis use on the brain were said to be particularly prominent if use starts in adolescence or young adulthood. The review flagged up one study that found an association between frequent use of cannabis from adolescence into adulthood with significant declines in IQ.
Role as a gateway drug
There is a theory that using cannabis in early adulthood could encourage the use of other addictive drugs such as nicotine or alcohol. The review found animal studies that were consistent with this theory. However, they also acknowledged they didn’t know whether people with more addictive tendencies are more likely to try cannabis, alcohol and nicotine, or whether cannabis use itself directly increased the chances of them trying these things.
Regular cannabis use was reported to be associated with an increased risk of anxiety and depression, but causality has not been established.
It has also been linked to psychosis (including those associated with schizophrenia), especially among people with a pre-existing genetic vulnerability, and worsens illness in people with schizophrenia.
The authors say it is difficult to establish causality in these types of studies, because factors other than cannabis use may be directly associated with the risk of mental illness. Other factors could also predispose a person to both cannabis use and mental illness. This makes it difficult to confidently attribute the increased risk of mental illness to cannabis use.
Effect on school performance and lifetime achievement
The review indicated that cannabis use impairs critical cognitive functions, both during acute intoxication and for days after use. For this reason, students who smoke cannabis could be functioning at a cognitive level that is below their natural capability for considerable periods of time. However, the results from studies included in the review were inconsistent.
Some studies suggested the long term negative effects of cannabis use on learning may be reversible, whereas others indicated memory and attention got significantly worse the more years someone had been using cannabis regularly.
Some studies suggested early cannabis use is associated with impaired school performance and an increased risk of dropping out of school, but there were other factors that could explain this link. For example, shared environmental factors like growing up in a neighbourhood where drug use is high and academic achievement low.
Risk of motor-vehicle accidents
There were studies indicating that both immediate exposure and long-term exposure to cannabis impair driving ability. According to a meta-analysis, the overall risk of involvement in an accident increases by a factor of about two when a person drives soon after using cannabis. The risk associated with the use of alcohol in combination with cannabis was reported to be greater than that associated with the use of either drug alone.
Risk of lung cancer
The effects of long-term cannabis smoking on the risk of lung cancer are unclear and often complicated by the fact many cannabis smokers also smoke tobacco – which is known to cause cancer. Separating the health effects of the two types of smoking remains a challenge. The researchers warned that the strength of cannabis in circulation is increasing and so any potential risks may also be increasing.
Can we believe the review’s findings?
The review’s main weakness is that it didn’t describe how it searched and reviewed the evidence on this subject and whether this was systematic. This means that key evidence may have been missed, leading the authors to potentially draw biased conclusions. It is not possible to say that the results were biased; only that without the methods, there remains a risk that they are.
A second limitation is that the evidence behind the review’s conclusions was drawn largely from early animal studies, or from observational studies that couldn’t establish cause and effect. This means we can’t really make clear cut, definitive statements about the health effects of cannabis use as the evidence, at least the evidence identified in this review, was not strong in most areas. The long term effects of cannabis use, for example, remain in the authors’ words “poorly understood”.
The review generally highlighted a scarcity or lack of knowledge on the beneficial or harmful effects of cannabis. This may be a true reflection of the evidence base, or may be in part because the review has not included all the relevant evidence.
One of the biggest challenges in studying the effects of cannabis is that due to its legal status in much of the world, researchers could not legally use cannabis in the “gold standard” of studies – a randomised controlled trial. There could also be ethical problems in randomly assigning people to use cannabis who don’t already, given its potentially damaging effects.
As more and more parts of the world are now legalising (or at least partially decriminalising) cannabis, research of this type could potentially be carried out and may allow us to learn more about the benefits and risks of this widely used drug.
“New obesity jab could be available within two years,” the Mail Online reports. The headline comes following news that scientists have identified a protein that may help stimulate the production of brown fat.
Brown fat helps keep mammals warm. In humans, it is mostly found in newborn babies, who are particularly vulnerable to cold. As we age, we do not need brown fat as much, and in adulthood we have mostly white fat. Excess white fat (obesity) can damage your health, whereas brown fat has been linked to protection against obesity and type II diabetes; as such, it has attracted increasing interest and research.
Brown fat also helps to burn calories when the body is exercising (or, less pleasantly, when you are cold enough to shiver). Unlike white fat, it acts like muscle, keeping the body firm and toned.
The study, which involved mice rather than people, found that the new protein helped stimulate the production of brown fat.
The optimism surrounding these findings is based on the hope that researchers could potentially harness the effects of this molecule to develop an obesity treatment in the future.
However, claims that an “obesity jab could be available within two years” seem overly optimistic.
Studies on people are needed before any claims of this kind can be made.
Where did the story come from?
The study was carried out by researchers from Harvard Medical School and the Dana-Farber Cancer Institute, in the U.S., and was funded by grants from the US National Institutes of Health and JPB Foundation.
The study was published in the peer-reviewed science journal Cell.
The Mail Online’s headline that “a new obesity job could be available within two years” is not supported by the publication, although the authors did state that the “therapeutic potential in metabolic diseases is obvious”.
There was a related study, performed by the same research team, in which the effects of the hormone irisin were studied, also in mice. Evidence suggests that irisin can also help stimulate production, by turning white fat into brown fat.
Somewhat confusingly, the Mail Online and the Daily Express seem to have reported on the findings of both studies as if they were a single piece of research.
What kind of research was this?
This was a laboratory study that used mice to identify and investigate the function of hormones released in muscles in response to exercise and cold.
Obesity levels in middle- and high-income countries is high and continuing to rise, with associated diseases including type 2 diabetes, cardiovascular disease and cancer.
As a result, the authors state there is increasing interest in brown fat – which uses energy to create heat and stops mammals becoming overly cold. In humans, brown fat is mostly found in newborn babies, who are particularly vulnerable to cold (as they have a large surface area to body volume ratio and are unable to shiver). As we age, we do not need as much brown fat to keep us warm, and have mostly white fat. However, brown fat has also been linked to protection against obesity and type II diabetes. Some hope that finding a way to make the body produce more brown fat, or convert white fat into brown fat, may help prevent obesity.
Exercising is a simple way to increase energy expenditure, and helps prevent obesity and associated metabolic disorders. It also increases the circulating levels of certain hormones released from muscle, which are known to mediate some of the beneficial effects of exercise.
The researchers wanted to see if there was the potential to harness some of these hormones to artificially mimic the beneficial effects of exercise, and investigated the role of brown fat in this process.
What did the research involve?
The research involved numerous genetic and protein studies involving mice. They were looking for molecules that were released during exercise and in response to cold, which would give them clues as to how exercise and brown fat activity were generating health benefits. By screening numerous molecules, they sought to identify those that were having the most important effects.
What were the basic results?
The experiments identified a molecule called meteorin-like (Metrnl) (Genecards), which was present in muscle and fat.
Circulating levels of Metrnl rose after mice exercised and when they were exposed to the cold.
Metrnl was found to stimulate energy expenditure and converted regular fat into heat-producing brown fat. Metrnl also improved glucose tolerance – a sign of metabolic health – in mice fed a high-fat diet. It was doing this by interacting with many aspects of the body’s immune system and its temperature regulation systems.
Blocking Metrnl action stopped these beneficial effects – confirmation that it was heavily involved in this process.
Metrnl levels increased as a result of repeated bouts of prolonged exercise, but not during short-term muscle activity.
How did the researchers interpret the results?
The researchers concluded that Metrnl’s “therapeutic potential in metabolic diseases is obvious. The recombinant Metrnl protein used here hints at that potential, but other proteins with better pharmacological properties will be required”.
This study identified a molecule that is induced by exercise and exposure to cold. It has been implicated in stimulating brown fat development and improving glucose tolerance – both of which have been linked to a lower risk of obesity and type II diabetes, giving hope that harnessing the effects of this molecule could create obesity treatments.
However, this optimism appears premature, as the research was conducted solely in mice. It will need to be reproduced and validated in humans to see if it is safe and effective at stimulating weight loss or other benefits. These remain unproven at this stage.
Other promised potential “anti-obesity jabs” include leptin and irisin, neither of which have delivered convincing results in human trials. This serves to highlight that when a new compound shows promise in mice, these don’t necessarily translate into effective medicines for humans.
On this basis, the Mail’s headline that a “new obesity jab could be available within two years” appears unjustified.
Rather than holding out hope of some magic medical bullet to beat or treat obesity, it’s best to try and lose weight through healthy eating and exercise. Our free 12-week NHS Weight Loss plan can help you achieve sustainable weight loss.
Proposals to extend the use of statins should be scrapped, a group of leading doctors and academics says.
The National Institute for Health and Care Excellence published draft guidance in February calling for their use to be extended to save more lives.
It could mean another five million people in England and Wales using them on top of seven million who already do.
But in a letter to NICE and ministers, the experts expressed concern about the medicalisation of healthy people.
The letter said the draft advice was overly reliant on industry-sponsored trials, which "grossly underestimate adverse effects".
And it added: "The benefits in a low-risk population do not justify putting approximately five million more people on drugs that will then have to be taken lifelong."
The drugs reduce levels of cholesterol in the blood, lowering the risk of a heart attack or stroke.
The signatories include Royal College of Physicians president Sir Richard Thompson and former Royal College of GPs chairwoman Clare Gerada as well as cardiologists and leading academics.
Prof Simon Capewell, an expert in clinical epidemiology at Liverpool University and one of the signatories, said: "The recent statin recommendations are deeply worrying, effectively condemning all middle-aged adults to lifelong medications of questionable value.
"They steal huge funds from a cash-strapped NHS and they steal attention from the major responsibilities that government and food industry have to promote healthier life choices for ourselves and our children."
Currently, doctors are meant to offer statin tablets to the estimated seven million people who have a 20% chance of developing cardiovascular disease over 10 years, based on risk factors such as their age, sex, whether they smoke and what they weigh.
Statins and risk
• Statins are a group of medicines that can help lower rates of so-called "bad cholesterol" in the blood
• They do this by curbing the production of low-density lipoprotein cholesterol in the liver
• High rates of LDL are potentially dangerous as they can lead to hardening and narrowing of the arteries, known as atherosclerosis, which increases the risks of strokes and heart attacks
• Doctors use a risk calculator called QRisk2 to work out a person's chance of having a stroke or heart attack to decide if they should be given statins
• The calculation factors include age, weight and smoking
• If someone has a 10-year QRisk2 score of 20%, then in a crowd of 100 people like them, on average, 20 people would get cardiovascular disease over the next 10 years
But the draft guidance suggested that people with as low as a 10% risk should be offered the treatment.
The NHS currently spends about £450m a year on statins. If the draft recommendations went ahead, this bill would increase substantially, although the drugs have become significantly cheaper over the years.
Cardiovascular disease develops when fatty substances build up in the arteries and narrow them, which can lead to heart attacks and stroke.
Too much cholesterol in the blood can lead to these fatty deposits. Statin drugs work by lowering cholesterol.
Eating a healthy diet, doing regular exercise and keeping slim will also help lower cholesterol.
Like all medicines, statins have potential side-effects. They have been linked to muscle, liver and kidney problems, but just how common these are is a contentious issue.
One of the signatories to the letter is London cardiologist Dr Aseem Malhotra, who last month had to withdraw claims he made in a British Medical Journal article that a fifth of people who use statins experience side-effects.
Mike Knapton, of the British Heart Foundation, said NICE was right to want to extend the use of statins.
"Evidence shows that statins are a safe, effective, cholesterol-lowering drug and proven to lower the risk of heart disease."
He added that, if anything, NICE should go further by looking at the lifetime risk rather than 10-year timeframe being proposed.
NICE has consulted on its draft proposals and is expected to publish final guidance at the end of July.
Prof Mark Baker, from NICE, said as well as the consultation the recommendations are being peer-reviewed.
He also pointed out that the guidance did not say patients had to go on these drugs - as GPs and patients can also discuss lifestyle changes to reduce risk - but just gave them the option of using them.
"This guidance does not medicalise millions of healthy people. On the contrary, it will help prevent many from becoming ill and dying prematurely," he added.
"One in three adults in England 'on cusp' of diabetes," BBC News and others report. The media reports are based on a study that estimated that 35.3% of adults in the UK now have prediabetes (also known as borderline diabetes).
Prediabetes is where blood sugar levels are abnormally high, but lower than the threshold for diagnosing diabetes. It is estimated that around 5-10% of people with prediabetes will go on to progress to "full-blown" type 2 diabetes in any given years.
Researchers analysed information from the Health Survey for England (HSE). This is a survey that combines questionnaire-based answers with physical measurements and the analysis of blood samples from a representative sample of the English population.
This study found that there has been a significant increase between 2003 and 2011 in the proportion of people aged 16 or older with prediabetes, from 11.6% in 2003 to 35.3% in 2013.
Known risk factors, confirmed in this study, include age (40 and above), body mass index (25 and above), being of south Asian ethnicity, and having high blood pressure.
If you think you may be at high risk of prediabetes, you can ask your GP for a blood test. It is often possible to prevent the condition progressing into diabetes proper through lifestyle changes, such as improving your diet and exercising more.
Where did the story come from?
The study was carried out by researchers from the University of Florida and the University of Leicester, and was somewhat surprisingly funded by the US Department of Defense.
This study was accurately reported in the UK media, with many articles also helpfully outlining the complications of diabetes, its impact on public health, and some relevant contextual information.
For example, this included information about the NHS Health Check programme, which invites people between the ages of 40 and 74 to have a check to assess their risk of heart disease, stroke, kidney disease and diabetes, and to give support and advice to help people reduce or manage their risk.
But as the NHS Health Check programme is in its infancy, it is hard to estimate what the likely take-up will be in the future and what impact it will have on public health.
What kind of research was this?
This was a cross-sectional study that aimed to report trends in the prevalence of prediabetes among people aged 16 or older in England.
Cross-sectional studies are the ideal way of determining how many people have a condition.
What did the research involve?
The research used information collected by the Health Survey for England (HSE) in the years 2003, 2006, 2009 and 2011.
The HSE is an annual population-based survey that combines questionnaire-based answers with physical measurements and the analysis of blood samples from a random sample of participants.
People were classified as having prediabetes if they had glycated haemoglobin (an indicator of blood sugar levels) between 5.7% and 6.4% and had not previously been diagnosed with diabetes.
Glycated haemoglobin is formed when haemoglobin is exposed to glucose in the blood. As the amount of glucose in the blood increases, the fraction of haemoglobin that is glycated increases.
Diabetes is diagnosed when the level is 6.5% or above. However, there is no internationally agreed lower level for prediabetes.
The prevalence of prediabetes increased over the study period. It was:
11.6% in 2003
20.4% in 2006
32.6% in 2009
35.3% in 2011
Age, being overweight, obesity, blood pressure level and cholesterol level exhibited significant relationships with prediabetes in all years that these were measured.
People with greater socioeconomic deprivation were more likely to have prediabetes in 2003 and 2006, but the relationship was no longer significant in 2009 and 2011.
The researchers found that predictors of prediabetes in 2003 and 2011 included:
being 40 years or older
being of south Asian ethnicity
having a high body mass index (BMI) of 25 or over
having been diagnosed with high blood pressure
being socioeconomically deprived (being in the second most deprived quintile)
How did the researchers interpret the results?
The researchers concluded that, "There has been a marked increase in the proportion of adults in England with prediabetes. The socioeconomically deprived are at substantial risk.
"In the absence of concerted and effective efforts to reduce risk, the number of people with diabetes is likely to increase steeply in coming years."
This study indicates that there had been an increase between 2003 and 2011 in the proportion of people aged 16 or older with prediabetes, with more than a third of adults in 2011 having prediabetes.
The study is useful because it is based on information from the Health Survey for England (HSE), which sampled a representative sample of the English population.
However, the researchers defined prediabetes using cut-offs used by the American Diabetes Association (5.7-6.4%), but in the UKNICE recommends higher cut-offs to identify people at high risk of diabetes (6.0-6.4%).
“Fasting for at least two days regenerates immune systems damaged by ageing or cancer treatment, research has shown,” the Daily Express reports. However, the study that is being reported on only involved mice, not humans.
Prolonged or intermittent fasting has become an increasingly popular strategy to achieve weight loss. This has been demonstrated through the incredibly popular 5:2 diet, where participants eat normally for five days a week and then fast for the remaining two.
There have been reports that the 5:2 diet can lead to weight loss for some people, with others claiming that fasting can boost immune function and prevent chronic diseases.
In this study, which used only mice, the researchers aimed to see whether prolonged fasting could reverse the toxic effects of chemotherapy– specifically, damage to white blood cells and bone marrow activity, which leaves the body weakened and vulnerable to infection.
Researchers found that mice fasting for two to five days before being given chemotherapy showed a faster recovery in terms of their white blood cell count. A later-stage clinical trial in humans is reported to be underway.
It is extremely important to stress that if you are undergoing chemotherapy treatment, you should not make any kind of radical changes to your diet unless advised to by your doctor. Doing so could make you vulnerable to complications.
Where did the story come from?
The study was carried out by researchers from the University of Southern California, Ohio University and the University of Palermo, in Italy. The study was supported by the National Institutes of Health and Aging and was published in the peer-reviewed science journal Cell. It has been published on an open-access basis, so it is free to read online.
The Daily Telegraph’s reporting of the study was accurate and included discussion from experts, who said that while the findings may have relevance for people receiving cancer treatment, further study is needed, and prolonged fasting should only be considered under the guidance of a doctor. As the Professor of Regenerative Medicine at UCL, Chris Mason, suggests: “The most sensible way forward would be to synthesise this effect with drugs. I am not sure fasting is the best idea. People are better eating on a regular basis.”
The Daily Express’s coverage, while not inaccurate, was not as clear as it should be. It is not until the last part of the article that you realise the study involved mice, not humans.
What kind of research was this?
This was a scientific study using mice, which aimed to look at the effect prolonged fasting might have on reversing the toxic effects of chemotherapy.
This included how it affected bone marrow regeneration and circulating white blood cells – key components of the body’s immune system.
The researchers explain how immune system defects are central to the ageing process and are associated with a range of diseases. One of the effects of chemotherapy is DNA damage and cell death, to both circulating blood cells and to stem cells of the bone marrow, which are responsible for producing new blood cells.
This leads to reduced numbers of red blood cells (which carry oxygen), platelets (which help blood to clot) and white blood cells (which make up the body’s immune system), leaving the body weakened and vulnerable to infection.
The authors state that prolonged fasting for two to five days activates cellular pathways in mice and humans, which enhance the resistance of cells to toxins, such as chemotherapy. Previous studies in mice have found that prolonged fasting leads to this protective effect, by reducing levels of insulin-like growth factor-1 (IGF-1) – a protein involved in growth and development, with a similar function to insulin.
The theory is that the reduction of IGF-1 resulting from prolonged fasting may allow regeneration of stem cells in the bone marrow, and so help to reverse the toxic effects of chemotherapy.
What did the research involve?
Mice were divided into two groups who were either fed or fasted prior to being injected with chemotherapy drugs for two weeks. The researchers looked at white blood cell counts during and after chemotherapy treatment, and also assessed DNA damage in circulating blood cells and bone marrow cells.
As their previous study had shown that prolonged fasting leads to a reduction in IGF-1 levels, and they believed that this was responsible for the protection against chemotherapy, they also looked at what would happen when mice genetically engineered to have IGF-1 deficiency were given chemotherapy without having fasted.
What were the basic results?
The researchers found that multiple cycles of prolonged fasting protected mice from some of the toxic effects of chemotherapy, reducing DNA damage to both circulating white blood cells and bone marrow stem cells. It also led to the regeneration of bone marrow stem cells. Mice who were given chemotherapy but fed as normal showed prolonged white blood cell depletion, while mice who had fasted beforehand saw their white blood cell count return to normal levels at a faster rate.
As expected, they found that using mice genetically engineered to have IGF-1 deficiency – replicating the effects of prolonged fasting – also showed faster recovery of their bone marrow stem cells. This confirmed that the effect on bone marrow stem cells was probably being mediated by a reduction in IGF-1 levels. Reduction of IGF-1 signalling seemed to promote the renewal of bone marrow stem cells.
How did the researchers interpret the results?
The study authors concluded that their results “indicate that cycles of an extreme dietary intervention represent a powerful mean[s] to modulate key regulators of cellular protection and tissue regeneration, but also provide a potential therapy to reverse or alleviate the immunosuppression caused by chemotherapy treatment and ageing”.
This scientific study suggests that multiple cycles of prolonged fasting may be able to reverse some of the toxic effects of chemotherapy in mice, by causing the regeneration of stem cells in bone marrow.
This allowed white blood cell counts to return to normal much faster after chemotherapy, compared to mice that were allowed to eat normally.
The study researchers indicated very early-stage study in humans (not appraised here), which found that fasting for 72 hours, rather than 24 hours, in combination with chemotherapy reduced some of the toxic effects of chemotherapy, in line with the findings in mice.
However, the study’s authors acknowledge that these results are very tentative and will need to be confirmed in larger, more robust, human studies.
Based on this study alone, it can be stated that people receiving cancer treatment, including chemotherapy, should not fast for extended periods of time without fully consulting a health professional, as this could be damaging to their health in other ways. Appropriate nutrition is very important for people with cancer, during treatment and when recovering from treatment. You should not make any significant changes to your diet without first seeking the advice and guidance of the health professionals treating you.