Going on holiday really is good for your health... and the benefits last for months,' declares Mail Online, the website of the Daily Mail and Mail on Sunday.
Despite being listed in the "health" section of the website, the news is based on a report by Nuffield Health and Kuoni Travel Ltd. To more sceptical readers, the report may appear to be nothing more than an elaborate piece of marketing material.
If you were being hypercritical, this collaboration also arguably represents a financial conflict of interest so big you could see it from space.
The "healthy holiday" report bears little resemblance to a rigorous scientific study and has not undergone the peer review process, where independent experts scrutinise the methods and findings of a study. If the "research" had been subjected to peer review, it would almost certainly have been dismissed out of hand.
This small experiment involved just 12 people – half of whom were sent on exotic holidays, while half stayed at home – and tells us very little about the effect of holidays on our physical and mental health.
While its broad conclusion that holidays are generally good seems commonsense, we cannot read too much into this experiment because of a long list of methodological limitations.
Even if we do take the report's findings at face value, its results are less than impressive. In some cases, people actually experienced increased stress levels during their holiday and some gained weight.
What is depressing is Mail Online's willingness to take the report at face value, and its failure to inform readers about the extensive limitations of this "experiment".
Where did the story come from?
The experiment was carried out by staff from Nuffield Health (which runs gyms and hospitals) in collaboration with Kuoni Travel Ltd (a holiday company). While no funding source was explicitly stated, it appears to have been funded by one or both of the collaborating organisations.
The experiment was not published in a peer-reviewed journal and so has not undergone the scrutiny of independent experts in health or medicine. It was instead released as a brochure on the Nuffield Health website.
There is a substantial conflict of interest in a report like this, as both Nuffield Health and Kuoni stand to gain commercially from conclusions that support their respective core businesses of health and holidays.
While the Mail Online's reporting of the findings was accurate, what is worrying is what they failed to report – the significant conflicts of interest, the lack of a peer review process, and problems with the extremely small sample size. Although the story makes for a great feelgood headline, it could mislead many readers.
What kind of research was this?
This wasn't research in the way we would usually expect to see it: peer-reviewed, published in a journal and with clear methods. It is probably best to use the language of the authors and call it an "experiment", which is less scientifically rigorous.
As it has not been published in a peer-reviewed journal, this experiment has not been appraised by experts in the field. This crucial stage ensures that a study's conclusions are justified by the study design and findings, and allows for flaws in the research to be pointed out.
Without such a peer review process, the authors' conclusions may be mistaken and remain unchallenged.
What did the research involve?
The experiment recruited six couples and subjected them to a battery of clinical and psychological tests before sending three couples on a free holiday, while three couples stayed at home. It was unclear whether the stay-at-home controls had the equivalent time off work or if they continued working while the others jetted off.
Two weeks after the holidaymakers returned, more clinical and psychological tests were performed and participants wore heart monitors for several days. The Nuffield Health staff then reported differences in health and wellbeing measures between the couples who went on holiday and those who didn't.
Three holiday destinations involving different activities were selected to see if the impact of the type of holiday made any difference to health and wellbeing measures. One couple were sent to Thailand for an activity holiday, another couple were sent to Peru to volunteer, and the other couple went to the Maldives for a relaxing "fly and flop" holiday.
The six stay-at-home controls (three couples) were sought to match the lifestyles, age group, physical activity, and alcohol and caffeine intake of those sent on holiday. Controls underwent the same battery of physical and mental health assessments as the holidaymakers.
No randomisation or allocation concealment was reported in the study when assigning the couples to either the travellers group or those who stayed at home.
Statistical testing is also not reported, in order to compare the differences between the travellers and those who stayed at home. This is not a good approach, as it means that any reported differences may be due to chance.
What were the basic results?
The Nuffield Health brochure reported that having a vacation improved the holidaymakers' ability to recover from stress by 29%, while the ability of those who stayed at home deteriorated by 71%. Holidaymakers' sleep quality improved by 34 points, whereas stay-at-homers' sleep worsened by 27 points. Blood pressure was reduced in the holidaymakers by 6%, compared with an increase of 2% in those who didn't go on holiday.
Other reported improvements for holidaymakers included decreases in blood sugar levels, improved body shape, and improved energy and mood.
How did the researchers interpret the results?
The Nuffield report, called 'Revealed: how holidays help you live longer', stated that "taking the right kind of holiday for you may lower your stress levels, improve your resilience to stress, and therefore improve your mental and physical health".
This small experiment involving just 12 people (six couples) tells us very little about the effect of having a holiday on physical or mental health. While its conclusions seem commonsense, we cannot read much into this experiment for the following reasons:
Small study sample
Only 12 people took part in this study. Basing conclusions on the experiences of so few people is risky and unreliable. Studies on larger groups of people may reach different conclusions. Similarly, it is not clear how representative the 12 people in the study were in relation to the general UK population, as physical and mental health can vary with age, ethnicity and social background.
No statistical testing
There was no statistical testing performed in this experiment. This is a huge limitation. It means that we don't know whether any observed differences between the holidaymakers and those who stayed at home were actually likely to be real, or whether they are simply chance findings.
No allocation concealment
It is unclear whether the people who stayed at home knew they were taking part in an experiment on the effect of going on holiday. The knowledge that they weren't lucky enough to be sent on a free holiday, and were instead in the stay-at-home group, may have adversely affected their short-term health and physical measures.
Conflict of interest
Both parties in this report have financial interests in promoting the advice that holidays are good for your health, and that leading a healthy lifestyle helps you live longer. This may have biased the experiment design and reporting of the findings.
As discussed above, without being published in a peer-reviewed journal and appraised by other leading experts, the authors are free to report and conclude what they wish. The peer review and publication process can add an extra layer of reliability and believability to research findings that are absent in this report.
The definite claim of the report's title – that holidays "help you live longer" – is completely unsubstantiated, based on the evidence the authors present.
The bottom line is that this experiment contributes very little to scientific research, but does reinforce the commonsense view that a holiday is generally a good thing, whether you are whisked away to a luxury hotel in exotic climes or a seaside chalet in Skeggy.
Shows Obesity by class, county. More than 6 out of 10 men are obese or overweight whilst more than 5 out of 10 women are obese or overweight. Obesity has increased from 15% in 1993-5 to 25% in 2009-11.
Much of the media are reporting the news that a new meningitis B vaccine called Bexsero has been licensed by the European Commission. This means the vaccine should soon be available for use in the UK.
What is meningitis B?
Meningitis B is a highly aggressive strain of bacterial meningitis which infects the protective membranes surronding the brain and spinal cord. It is very serious and should be treated as a medical emergency. If the infection is left untreated, it can cause severe brain damage and infect the blood (septicaemia). In some cases bacterial meningitis can be fatal.
How common is meningitis B?
The charity Meningitis UK, estimates that there are 1,870 cases of meningitis B each year in the UK. Meningitis B is most common in children under five years old, and in particular in babies under the age of one.
Initial signs and symptoms of meningitis B in babies include:
While there are effective vaccines against the other common strains of bacterial meningitis (A, C, W-135, Y3), until now, there has been no vaccine against the B strain.
The development of a safe and effective meningitis B vaccine is the culmination of over 20 years of research and represents a significant breakthrough in disease prevention.
What do we know about the vaccine?
The vaccine, Bexsero, is thought to provide 73% protection against meningitis B, which should significantly reduce the number of cases. The vaccine can be administered to infants aged two months or older – either by itself, or in combination with other childhood vaccines.
The vaccine has been tested in clinical trials involving over 8,000 people.
In infants, it was found to have similar levels of safety and tolerability as other routine childhood vaccines. The most commonly reported side effects were:
redness and swelling at the site of the injection
Will the NHS provide the vaccine free-of-charge?
At the moment that is uncertain. The body that advises on vaccination policy – the Joint Committee on Vaccination and Immunisation (JCVI) – has not yet made any announcement.
The JCVI is due to meet in June 2013, although they are unlikely to make a decision until they have had time to consider the evidence of cost-effectiveness and safety in greater detail. However, they may decide to ‘fast-track’ the decision.
The Bexsero vaccine is likely to be expensive and there is certainly no guarantee that the JCVI will rubber-stamp a positive decision.
There are currently three possibilities:
the vaccine could be added to the routine NHS childhood vaccination schedule
the vaccine may only be provided by the NHS to high-risk groups, such as people with a weakened immune system, in the same way as the seasonal flu jab
the vaccine may only be available on a private basis
Macular degeneration is the UK's leading cause of visual impairment
The Daily Telegraph reports that using aspirin regularly could triple the risk of developing one of the commonest forms of blindness; “wet” age-related macular degeneration (AMD) – which causes progressive loss of central vision.
This story is based on a relatively large, long-term study which looked at whether and how often middle-aged and elderly people took aspirin, and their subsequent vision or sight loss. The study found that about 4% of occasional or non-users of aspirin developed wet AMD, compared with about 9% regular users of aspirin.
However, the study method used means that the groups of people being compared may differ in ways other than their aspirin use, and these other factors may be influencing the results. For example, cardiovascular disease (CVD) and wet AMD share some common risk factors, such as smoking. So it is not possible to say for certain – based on a single study of this type – whether aspirin definitely increases risk of wet AMD.
Two very large randomised controlled trials (RCTs) – one reported in Behind the Headlines in 2009, found that taking aspirin for seven to ten years did not increase risk of AMD. Evidence from RCTs is likely to carry more weight than evidence from the type of study used in this latest research. However, these older RCTs have their own limitations, such as relying mainly on participants to self-report whether they had AMD.
Ideally, a systematic review would be needed to summarise all of the available research evidence to determine whether it looks like aspirin could be contributing to AMD risk.
Macular degeneration – warning signs
All older people, whether or not they are taking aspirin, should be vigilant for changes in their eyesight that could be the initialsymptoms of wet AMD. In general, it is thought the sooner macular degeneration is treated, the better the prognosis.
If you notice problems with your vision, such as blurring, see your GP or optometrist. If your vision suddenly gets worse or you notice blind spots in your field of vision, seek advice immediately. Either book an emergency appointment with an optometrist or visit your local hospital's accident and emergency (A&E) department.
Where did the story come from?
The study was carried out by researchers from the Universities of Sydney and Melbourne and the National University of Singapore.
It was funded by the National Health and Medical Research Council, Australia.
The study was published in the peer-reviewed Journal of the American Medical Association – Internal Medicine.
In general, the BBC, The Daily Telegraph, and the Daily Mail covered the story well – emphasising the important point that the potential risk of aspirin-associated AMD had to be balanced against the drug’s protective effect against heart disease and stroke.
However, the Mail and the Telegraph could not agree whether there was a two-fold or three-fold increase in risk detected by the study – the precise figure from the main analysis was 2.46, so it’s a case whether you choose to round up or down.
What kind of research was this?
This was a prospective cohort study looking at whether aspirin use was linked with risk of developing age-related macular degeneration (AMD). AMD is a common cause of blindness in older people, and comes in two forms – “wet” AMD and “dry” AMD.
The macula is the area of the light sensitive covering on the inside of the eye that is responsible for the central part of our vision. In dry AMD, the cells of the macula gradually become damaged, affecting vision. In wet AMD, new blood vessels grow underneath the macula in the eye and disrupt vision. In some cases, symptoms of dry AMD (which tend to be less severe) are then followed by symptoms of wet AMD (which usually causes a greater disruption to normal vision). The only known preventable risk factor for AMD is smoking. Some studies have suggested that aspirin use may be a risk factor for AMD, while others not have found a link.
A cohort study is a good way to look at links between a long-term real-life exposure (in this case aspirin use) and a particular outcome (in this case AMD), particularly if a randomised controlled trial would not be feasible.
However, as people in this study were deciding for themselves whether to take aspirin, they may have characteristics that differ from those who take aspirin less frequently, and this could affect results (known as confounding).
Long-term RCTs of aspirin have been carried out, and the results of these trials should not be affected by confounding, so from this perspective their results would be seen as more robust. However, the RCTs would not have set out to look specifically at AMD, and this means they would not have done specific examinations of people’s eyes as part of the study. Therefore, researchers would have to rely on people reporting their condition or it being recorded in their medical notes. So, the current study has the advantage of setting out to assess the effect of aspirin on AMD, and therefore included thorough eye examinations to look specifically for the condition.
What did the research involve?
The study recruited Australians aged 49 and over, living in urban areas, between 1992 and 1994, following them up for 15 years. The participants were assessed four times during this period, initially filling out questionnaires assessing their aspirin use, whether they had cardiovascular disease, or risk factors for AMD. Participants also provided a list of all the medications they had taken in the last month, and were asked to show the researchers all the medicine bottles of the medicines they used.
This allowed researchers to check their aspirin use, although the dose was not recorded.
At the start of the study, participants also had pictures taken of the retinas in both eyes to ensure they did not have any signs of AMD. These pictures were taken every five years during the 15-year study, and each time the researchers looked for signs of wet or dry AMD (defined by an international standard).
The researchers had complete data for 2,389 people for their analyses. Aspirin use was classified as:
regular – one or more per week in the last year
occasional – less than once per week in the last year
They compared the risk of AMD in aspirin users with non-users. In some analyses occasional and non-users were grouped into “non-regular users”.
The researchers took into account potential confounding factors that could affect outcomes, including:
history of cardiovascular disease
body mass index (BMI)
markers of inflammation in blood tests
What were the basic results?
The researchers found that 10.8% of participants regularly used aspirin (257 people), this group were older, more likely to have high blood pressure, cardiovascular disease and diabetes than non-regular users.
Almost a quarter of participants (24.5%, 63 people) developed wet AMD during the study. When classified by aspirin use, 9.3% of aspirin users developed wet AMD during the 15-year study, compared with 3.7% of people who did not regularly use aspirin.
The researchers took into account the age, BMI, systolic blood pressure, gender, smoking, and cardiovascular disease of the participants when analysing their results. They found that those who used aspirin had about two and a half times the odds of developing wet AMD as those who did not take aspirin (odds ratio [OR] 2.46, 95% confidence interval [CI] 1.25 to 4.83).
Taking into account additional cardiovascular risk factors (blood total cholesterol level, diabetes mellitus, fish consumption, and markers of inflammation in blood tests) made the results become just non-statistically significant (OR 2.05, 95% CI 0.96 to 4.40).
There was no difference between aspirin users and non-users in the risk of developing dry AMD.
How did the researchers interpret the results?
The researchers concluded that “regular aspirin use is associated with increased risk of [developing wet] AMD, independent of a history of cardiovascular disease and smoking”.
This cohort study has suggested that there may be a link between aspirin use and risk of developing wet AMD. The main strengths of this study are that it followed people up over a long time, collected data prospectively and carried out thorough eye examinations for AMD. This means that cases of AMD were not likely to be missed. However, it should be noted that:
The study’s main weakness was that, as a cohort study, its results may be affected by confounding, although the researchers did try to take into account factors that could be having an effect. Confounding ‘by indication’ is a possibility; this is where the reason for taking the aspirin may be influencing the results, rather than the aspirin itself. The researchers controlled for this by taking into account cardiovascular disease, and this led to a reduction in the association. This suggests that cardiovascular disease could be contributing to the increased AMD risk.
The authors note that two large RCTs (which should not be affected by confounding) found no increase in risk of AMD in people taking aspirin for seven to 10 years. However, they note that these RCTs mainly relied on self-reported AMD diagnosis or used definitions of AMD that have been criticised, and did not analyse the wet and dry forms of AMD separately.
Aspirin use in the past year was assessed only at the start of the study, and may have differed either before or after this.
Overall, the inherent limitations to this type of study, the fact that RCTs have not found a link with AMD as a whole, and that taking into account certain factors makes the link non-significant, mean that it is not possible to conclusively say whether aspirin increases wet AMD risk.
If your doctor has prescribed you aspirin for a specific purpose, for example to reduce your risk of blood clots, it is likely that the benefits of taking it will outweigh the unconfirmed potential increase in risk of developing wet AMD in the long term.
In general, you, you should always see your GP or your optometrist as soon as possible if you notice any deterioration to your vision.
Hormesis (wikipedia) involves a biphasic response in which a small amount of a toxin has a beneficial effect whilst increasing quantities are toxic.
An example of a hormetic product is selenium which is a micronutrient and improves health at low doses but is toxic at high doses. Plants and vegetables (5 a day) and Exercise have a hormetic effect too.
A very low dose of a chemical agent may trigger from an organism the opposite response to a very high dose.
Klempel MC, Kroeger CM, Varady KA.
Department of Kinesiology and Nutrition, University of Illinois at Chicago, 1919 West Taylor Street, Room 506F, Chicago, IL, 60612.
Alternate day fasting (ADF) with a low-fat (LF) diet is effective for weight loss and cardio-protection. However, the applicability of these findings is questionable as the majority of Americans consume a high-fat (HF) diet.
The goal of this study was to determine if these beneficial changes in body weight and coronary heart disease (CHD) risk can be reproduced if an HF background diet is used in place of an LF diet during ADF.
Thirty-two obese subjects were randomized to an ADF-HF (45% fat) or ADF-LF diet (25% fat), which consisted of two phases: 1) a 2-week baseline weight maintenance period, and 2) an 8-week ADF weight loss period. All food was provided during the study.
Body weight was reduced (P<0.0001) by ADF-HF (4.8%±1.1%) and by ADF-LF (4.2%±0.8%). Fat mass decreased (P<0.0001) by ADF-HF (5.4±1.5kg) and ADF-LF (4.2±0.6kg). Fat free mass remained unchanged. Waist circumference decreased (P<0.001) by ADF-HF (7.2±1.5cm) and ADF-LF (7.3±0.9cm). LDL cholesterol and triacylglycerol concentrations were reduced (P<0.001) by both interventions (ADF-HF: 18.3%±4.6%, 13.7%±4.8%; and ADF-LF: 24.8%±2.6%, 14.3%±4.4%). HDL cholesterol, blood pressure, and heart rate remained unchanged. There were no between-group differences for any parameter.
These findings suggest that an ADF-HF diet is equally as effective as an ADF-LF diet in helping obese subjects lose weight and improve CHD risk factors.
"One million people who have non-body odour gene still use deodorant," is the headline from The Daily Telegraph, with a similar Daily Mail report saying many people use deodorant needlessly because their sweat doesn’t smell.
The stories are based on research on a particular DNA sequence variation within the ABCC11 gene. This variation has previously been associated with both earwax production and armpit sweat production, with one variation (genotype) linked with both dry earwax and less smelly sweat, and another genotype linked with wet earwax and more odorous sweat.
In the current study, the researchers looked at a group of parents and children from a birth cohort and looked at which gene variant the mothers had and how often they used deodorant. They also looked at the partner’s (usually the father’s) deodorant use and whether it was linked to which form of gene their child had.
The researchers found a link between which variant mothers had and their deodorant usage. There was also a link between the partner’s use of deodorant and which variant their child had. However, around 80% of people with the dry earwax, “non-odorous” sweat variant still reported using deodorant.
After extrapolating these figures in order to take into account both the UK population and deodorant sales figures, the researchers estimated that around £9 million is wasted annually on deodorant by people who don’t need it. Ultimately, rather than judging by earwax type, whether people use deodorant or not will remain a personal choice.
Where did the story come from?
The study was carried out by researchers from the University of Bristol and Brunel University, London, and was funded by the UK Medical Research Council (MRC), the Wellcome Trust and the University of Bristol.
The study was published in the open access peer-reviewed medical journal Journal of Investigative Dermatology.
Both the Daily Mail and The Daily Telegraph reported the findings of this study accurately.
The research focused on examining a single letter variation in the DNA (called a single-nucleotide polymorphism, or SNP) in the ABCC11 gene, which has previously been found to be associated with earwax type and armpit odour. Most SNPs have no noticeable effect on health and development, but a minority of them can have, in some cases, profound effects.
One variant of this SNP is reported to lead to a dry earwax type while another variant leads to a wet earwax type. The researchers say that there is a link between the glands that produce earwax and the glands that produce sweat, and people with the gene variant that produces dry earwax also produce less odorous sweat.
In this study the researchers wanted to see whether people with the dry earwax and less odorous variant may be using deodorant less, or using it when they may not need to.
What did the research involve?
The ALSPAC cohort recruited 14,541 pregnant women living in Avon and who were due to deliver their baby in 1991-92. There were 14,062 live-born children. This long-running study has collected a lot of data on health, genetics and environmental factors in these participants, which has been used in many research studies.
Eight months after the child’s birth the mother had been asked about deodorant use on a section of a questionnaire entitled “Chemicals in your environment”. The question asked was: “In the last few months, how often have you used the following (whether at home or at work)?” This was followed by a list of chemicals, including “deodorants”. The mother’s partner had been asked similar questions while the woman was pregnant about their deodorant use.
Of the mothers who answered questions on deodorant use, they were able to examine the DNA of 6,495 mothers and 7,132 of their children in the cohort to see which variant of the SNP (rs17822931) in the ABCC11 gene they had. They also had deodorant information available for 5,047 partners (most of whom were the father of the child).
The researchers used statistical models to look at weekly deodorant usage and variant type in the mother. They also looked at associations between deodorant usage by the partner and variant type of their child. As they did not have DNA information from the partner, they were using the child’s DNA as an indicator of which variant the partner may have. However, we don’t know for certain the father and child would share the same SNP variant within the ABCC11 gene. In fact, we are not even certain the partner is the child’s biological father in all cases. Therefore, information on deodorant use according to genotype will be less reliable for men than it will be for the women (where they looked at the woman’s own genotype).
What were the basic results?
The researchers found that which variant of the rs17822931 SNP people had was associated with how often they used deodorant. Women who had the variant associated with dry earwax and less odorous sweat were almost five times more likely to have reported never using deodorant or using it infrequently. However, 78% of women with this “non-odorous” variant, and 80% of fathers of children with the “non-odorous” variant, still used deodorants at least once a week.
Comparatively, only 5% of women with the gene variant associated with wet earwax (and more odorous sweat) did not use deodorant. A slightly higher percentage of fathers (13%) of children with this “odorous” gene type did not use deodorant.
These results were for people whose ethnicity was reported as white. The results were broadly similar for non-white people, although there were fewer non-white people in the study, which makes it harder to give reliable results for non-white people.
How did the researchers interpret the results?
The researchers conclude that they have shown that which variant of the rs17822931 SNP people have is a strong predictor of their deodorant usage. However, despite this, around 80% of genetically “non-odorous” white European mothers still use deodorant, and the findings may be true for men as well.
The researchers say that this is likely to be caused by sociocultural factors, but people with the dry earwax type could choose to abandon the chemical exposures and costs of deodorant use.
This is intriguing research following up on the previous finding that a particular DNA sequence variation in the ABCC11 gene is associated with both earwax and armpit sweat odour. One form of the variant is linked with dry earwax and less odorous sweat, while another is linked with wet earwax and more odorous sweat.
The researchers did find that there was a link between which variant mothers had and their deodorant usage. However, almost 80% of women with the dry earwax, “non-odorous” variant still reported using deodorant around once a week. The researchers’ results indicate the same may be true for men, but this would ideally need confirmation. This is because it is not certain whether the variant of the child was the same as the partner’s own or, indeed, whether in all cases he was the biological father.
The researchers suggest these people with the “non-odorous” variant could choose not to use deodorant. The study doesn’t appear to have asked people whether they find they experience body odour themselves, or why they do or don’t choose to use deodorant.
These results may prompt people to reassess whether they need a deodorant. However, it seems unlikely that you could persuade most people who usually use deodorant that they can abandon its use, simply by pointing out that they have dry earwax. Instead, it seems likely that whether people use deodorant (or not) will remain a personal choice depending on what they feel most comfortable with.
In mice on Intermittent Fasting (IF), Mark P. Mattson found that 'sporadic bouts of hunger trigger new neurons to grow'. 'Why should a brain cell generate new cells when you stop feeding it?' asked Michael Mosley of Mark Mattson (5.30s) :- In evolutionary terms, if when you are hungry, it is good to increase your cognitive ability as this could give a survival advantage eg food, predator and hazard locations. In mice, Mattson found that new brain cells [in the hippocampus] grow more than on restricted calorie diet.
But this is just one researcher with trials on mice. Was this research published in a peer reviewed journal? Has his research been repeated in other labs? We do not know whether this growth of brain cells will happen in humans.
Mark P Mattson said (4.10s) that the evidence was 'very good' to 'excellent' that 'Intermittent Fasting IF could reduce the risk of brain diseases in people like Michael Mosley.'
Brain-derived neurotrophic factor
In human terms, putting genetically modified, Alzheimers susceptible mice, on IF means that they develop Alzheimers at 80 rather than at 50 years. Mice on IF diet have increased production of Brain Derived Neurotrophic Factor (BDNF - wikipedia) which stimulates stem cells to turn into new nerve cells in the hippocampus, a part of the brain essential for learning and memory. Research on humans on IF diets, may show, using MRI, that hippocampi size changes. When people exercise (eg walking) the hippocampus size can increase (1). Regular walkers have brains that in MRI scans look, on average, two years younger than the brains of those who are sedentary. (Ref: Michael Mosley & Mimi Spencer, 'The fast diet, The simple secret of Intermittent Fasting: Lose weight, stay healthy, live longer', pub. January 2013 by Short books, pages 44-48)
Michael Mosley (pg 49 in above book) took the cognitive test http://cognitivefun.net/test/2 - the Stroop Test before and after starting the IF and found, purely anecdotally, that his memory had improved.
For a NHS Choice update published May 2013 see here.
NHS Choices undertook a non-systematic review of IF. What is the evidence intermittent fasting increases life-span? "There is quite a wide range of work on the effects of IF on combating the effects of aging, but almost all of these studies involved either rats, mice or monkeys." Only one piece of 1957 IF evidence in humans. So don't rely on IF to increase your life-span! What is the evidence intermittent fasting prevents cognitive decline? All of the studies on the supposed protective effects of IF against conditions that can cause a decline in cognitive function (such as dementia or Alzheimer’s disease) involve animals. So don't rely on IF to prevent cognitive decline! What is the evidence intermittent fasting prevent diseases? Much of the published research into the potential preventative effects of IF involve measuring biological markers associated with chronic disease, such as insulin-like growth factor-I (IGF-I) – known to be associated with cancer, do not guarantee successful real-world outcomes. A 2007 clinical review looking at the effects of IF in humans in terms of ‘real-world’ health outcomes concluded that IF (specifically, alternative day fasting) may have a protective effect against heart disease, type 2 diabetes and cancer. However, it concluded ‘more research is required to establish definitively the consequences of ADF (alternative day fasting)’. So don't rely on IF to prevent diseases!
Replicated in full from the above NHS Choices review.
Monday January 14 2013
The 5:2 diet is an increasingly popular diet plan with a flurry of newspaper articles and books being published on it in the run up to Christmas 2012 and in January 2013.
The diet first reached the mainstream via a BBC Horizon documentary called Eat, Fast and Live Longer, broadcast in August 2012.
The 5:2 diet is based on a principle known as intermittent fasting (IF) – where you eat normally at certain times and then fast during other times.
The 5:2 diet is relatively straightforward – you eat normally five days a week, and fast on the other two days.
What does a daily 500-calorie diet look like?
A 500 calorie a day diet could consist of one bowl of cornflakes for breakfast, a single sausage for lunch and just one slice of pizza for dinner. And of course, nothing but water to drink all day.
Champions of the 5:2 diet claim that other than helping people lose weight, 5:2 diet can bring other significant health benefits, including:
improved cognitive function and protection against conditions such as dementia and Alzheimer’s disease
protection from disease
However there is no peer-reviewed evidence that the 5:2 diet can bring these benefits, and only a very limited evidence base for IF in general.
What we don’t know about intermittent fasting
Despite its increasing popularity, there is a great deal of uncertainty about IF with significant gaps in the evidence.
For example, it is unclear:
what pattern of IF is the most effective in improving health outcomes – 5:2, alternative day fasting, or something else entirely different
what is the optimal calorie consumption during the fasting days – the 5:2 diet recommends 500 calories for women and 600 for men, but these recommendations seem arbitrary without clear evidence to support them
how IF compares to conventional calorie-controlled diets in terms of leading to weight-loss and improving health
how sustainable is IF in the long-term – would most people be willing to stick with the plan for the rest of their lives?
Are there any side-effects from intermittent fasting?
Little is known about possible side-effects as no systematic attempt has been made to study this issue. Anecdotal reports of effects include:
bad breath (a known problem with low carbohydrate diets)
However, more research would be needed to confirm these side-effects and their severity.
If you are fasting, you may want to think about how fasting will impact on your life during your fasting days. You are likely to be very hungry and have less energy and this could affect your ability to function (such as at work), in particular it may affect your ability to exercise which is an important part of maintaining a healthy weight.
Also, IF may not be suitable for pregnant women and people with specific health conditions, such as diabetes, or a history of eating disorders.
Because it is a fairly radical approach to weight loss, if you are considering trying IF for yourself, it is wise to speak to your GP first to see if it is safe to do so.
What do we know?
There does not appear to be any research evidence that looks directly at the 5:2 diet.
There is some degree of evidence about the potential benefits of other forms of IF – albeit with some significant limitations.
It should be stressed that our assessment of the evidence was confined to entering a number of keywords into Google Scholar and then looking at a small number of studies which we felt would be useful to explore further.
We did not carry out a systematic review (though arguably, it would be useful for researchers to do so). So the information provided below should be taken in the spirit of us trying to provide an introduction to some of the evidence and science of IF – not an exhaustive 'last word' on the topic.
Is there any evidence that intermittent fasting aids weight-loss?
One of the most recent pieces of research on intermittent fasting is a 2012 study (PDF, 291.4Kb) which recruited 30 obese women known to have pre-existing risk factors for heart disease.
After an initial two week period they were then given a combination diet of low calorie liquid meals for six days of a week (similar to Slim Fast diet products) and then asked to fast for one day a week (comsuming no more than 120 calories).
After eight weeks, on average, the women lost around 4kg (8.8lb) in weight and around 6cm (2.3 inches) off their waist circumference.
However, there are a number of limitations to consider when looking at this as evidence that it might be a generally beneficial thing to do for most ordinary people, including that:
These women may have had increased motivation to stick with the diet because they knew their weight would be monitored (this is a psychological effect that slimming clubs make use of).
The women had been told that they were at risk of heart disease. It is uncertain how well most of us would cope with such as extreme diet.
The follow-up period was short – just two months. It is not clear whether this diet would be sustainable in the long-term or whether it could cause any side effects.
30 people is quite a small sample size. A much larger sample – including men – is required to see if intermittent fasting would be effective in most overweight or obese people.
Is there any evidence intermittent fasting increases life-span?
There is quite a wide range of work on the effects of IF on combating the effects of aging, but almost all of these studies involved either rats, mice or monkeys. One big problem with studies in animals – particularly rodents – is that they are only expected to live for a few years, this makes them ideal subjects for longevity studies. However, to carry out similar, more useful experiments in humans, requires decades-long research to gain credible results.
In an unsystematic look at the evidence, we find only one study involving humans: a 2006 review (PDF, 64.7Kb) of an experiment actually carried out in 1957 in Spain.
In this 1957 study, 120 residents of an old people’s home were split into two groups (it is unclear from the study whether this was done at random). The first group (the control group) ate a normal diet. The second group (the IF group) ate a normal diet one day and then a restricted diet (estimated to be around 900 calories) the next.
After three years there were 13 deaths in the control group and only six deaths in the IF group.
This study is again limited by the small sample size meaning that the differences in death are more likely to be the results of a statistical fluke. Also, many experts would feel uneasy about issuing dietary guidelines based on a study over half a century old with unclear methods. It is unlikely that this experiment could be repeated today – denying food to elderly people in residential care is unlikely to be looked at kindly by an ethics committee.
Is there any evidence intermittent fasting prevents cognitive decline?
It seems that all of the studies on the supposed protective effects of IF against conditions that can cause a decline in cognitive function (such as dementia or Alzheimer’s disease) involve animals.
For example, a 2006 study (PDF, 843.1Kb) involved mice that had been genetically engineered to develop changes in brain tissue similar to those seen in people with Alzheimer’s disease.
Mice on an IF diet appeared to experience a slower rate of cognitive decline than mice on a normal diet (cognitive function was assessed using a water maze test).
While the results of these animals tests are certainly intriguing,animal studies have inherent limitations. We can never be sure that the results will be applicable in humans.
Is there any evidence intermittent fasting prevent diseases?
Much of the published research into the potential preventative effects of IF involve measuring biological markers associated with chronic disease, such as insulin-like growth factor-I (IGF-I) – known to be associated with cancer.
Using these kinds of biological surrogates is a legitimate way to carry out research, but they do not guarantee successful real-world outcomes.
For example, some medications that were found to lower blood-pressure readings taken in laboratory conditions failed to prevent strokes once they had been introduced for use in the healthcare of patients in the world.
A 2007 clinical review (PDF, 118.6Kb) looking at the effects of IF in humans in terms of ‘real-world’ health outcomes concluded that IF (specifically, alternative day fasting) may have a protective effect against heart disease, type 2 diabetes and cancer. However, it concluded ‘more research is required to establish definitively the consequences of ADF (alternative day fasting)’.
Due to the very real uncertainties about the 5:2, especially as little is known about whether it could be harmful to health in the long-term, most health professionals would recommend you stick to the tried and trusted methods for weight loss and disease prevention: