The inside story on prison health.


The rate of imprisonment in England, Wales, and Scotland—at around 154 per 100 000 people—is one of the highest in western Europe. While dwarfed by that of the United States, the so called “land of the free,” where roughly one in 100 people is behind bars, the number of prisoners in England and Wales has nearly doubled in the past 20 years, even though recorded crime has fallen. In the final article of his five part series on prison health (BMJ 2013;346:f2216, doi:10.1136/bmj.f2216), Stephen Ginn asks whether prison is the right place for many offenders and whether earlier assistance in the community might prevent a prison sentence.

As Ginn writes, many of those held in British prisons “come from the most economically deprived and socially disadvantaged groups within society.” He adds: “Many prisoners have chaotic lifestyles and complex health and social problems. They may also have limited health aspirations and low expectations of health services, which may not have the flexibility to respond effectively to their needs.”

Prisons, meanwhile, are vulnerable to infectious disease because of overcrowding, poor ventilation, shared facilities, and a high turnover of prisoners, staff, and visitors. They have higher rates of tuberculosis, hepatitis B, and HIV infection than in the outside population, and very high levels of illegal drug use. Ginn says: “Prisons are not principally in the business of promoting health and some people argue that there is an inherent contradiction between the aims of care and control.” While prison has a role in meeting the health needs of marginalised people—for example, in 2009-10, 60 067 prisoners received clinical treatment for drug addiction in English and Welsh prisons—it is “ultimately not the best place to tackle poor health,” writes Ginn.

Moreover, the average cost of a prison place in England and Wales is about £40 000 (€47 000; $60 000), and in 2012, UK total prison spend was £4.1bn. While some people clearly need to be in prison, and society understandably demands a custodial sentence for certain—particularly violent—crimes, in most cases couldn’t the money be better spent? Ginn says that community based drug treatment, for example, was found to be particularly effective at saving costs “as offenders receiving treatment were 43% less likely to reoffend after release.” If crime were a disease (and indeed some in the public health community have seen it that way), wouldn’t the smart money be more on crime prevention rather than the so called cure?

Ginn points out that around 80% of prisoners in England and Wales smoke, which is four times the proportion of the general public. While there are no plans for British prisons to become smoke free, the switch to e-cigarettes, the topic of Douglas Kamerow’s Observations column this week (BMJ 2013;346:f3418, doi:10.1136/bmj.f3418), might at least improve the environment for non-smoking prisoners. However, as Kamerow writes, e-cigarettes are worrying the public health community. They appear to help maintain the smoking habit and reduce incentives to quit, and now Big Tobacco is moving into the e-cigarette market. “Now that the vapour is fully out of the cartridge, we’re not going to be able to get it back in,” says Kamerow. “We need to make the best of a bad situation before it gets worse.”

 

Source: BMJ.com

 

 

 

Is It Better to Walk or Run?.


29well_physed-tmagArticle

Walking and running are the most popular physical activities for American adults. But whether one is preferable to the other in terms of improving health has long been debated. Now a variety of new studies that pitted running directly against walking are providing some answers. Their conclusion? It depends almost completely on what you are hoping to accomplish.

If, for instance, you are looking to control your weight — and shallowly or not, I am — running wins, going away. In a study published last month in Medicine & Science in Sports & Exercise, and unambiguously titled “Greater Weight Loss From Running than Walking,” researchers combed survey data from 15,237 walkers and 32,215 runners enrolled in the National Runners and Walkers Health Study — a large survey being conducted at Lawrence Berkeley National Laboratory in Berkeley, Calif.

Participants were asked about their weight, waist circumference, diets and typical weekly walking or running mileage both when they joined the study, and then again up to six years later.

The runners almost uniformly were thinner than the walkers when each joined the study. And they stayed that way throughout. Over the years, the runners maintained their body mass and waistlines far better than the walkers.

The difference was particularly notable among participants over 55. Runners in this age group were not running a lot and generally were barely expending more calories per week during exercise than older walkers. But their body mass indexes and waist circumferences remained significantly lower than those of age-matched walkers.

Why running should better aid weight management than walking is not altogether clear. It might seem obvious that running, being more strenuous then walking, burns more calories per hour. And that’s true. But in the Berkeley study and others, when energy expenditure was approximately matched — when walkers head out for hours of rambling and burn the same number of calories over the course of a week as runners — the runners seem able to control their weight better over the long term.

One reason may be running’s effect on appetite, as another intriguing, if small, study suggests. In the study, published last year in the Journal of Obesity, nine experienced female runners and 10 committed female walkers reported to the exercise physiology lab at the University of Wyoming on two separate occasions. On one day, the groups ran or walked on a treadmill for an hour. On the second day, they all rested for an hour. Throughout each session, researchers monitored their total energy expenditure. They also drew blood from their volunteers to check for levels of certain hormones related to appetite.

After both sessions, the volunteers were set free in a room with a laden buffet and told to eat at will.

The walkers turned out to be hungry, consuming about 50 calories more than they had burned during their hourlong treadmill stroll.

The runners, on the other hand, picked at their food, taking in almost 200 calories less than they had burned while running.

The runners also proved after exercise to have significantly higher blood levels of a hormone called peptide YY, which has been shown to suppress appetite. The walkers did not have increased peptide YY levels; their appetites remained hearty.

So to eat less, run first.

But on other measures of health, new science shows that walking can be at least as valuable as running — and in some instances, more so. A study published this month that again plumbed data from the Runners and Walkers Health Study found that both runners and walkers had equally diminished risks of developing age-related cataracts compared to sedentary people, an unexpected but excellent benefit of exercise.

And in perhaps the most comforting of the new studies, published last month in Arteriosclerosis, Thrombosis and Vascular Biology and again using numbers from the versatile Runners and Walkers Health Study, runners had far less risk of high blood pressure, unhealthy cholesterol profiles, diabetes and heart disease than their sedentary peers. But the walkers were doing even better. Runners, for instance, reduced their risk of heart disease by about 4.5 percent if they ran an hour a day. Walkers who expended the same amount of energy per day reduced their risk of heart disease by more than 9 percent.

Of course, few walkers match the energy expenditure of runners. “It’s fair to say that, if you plan to expend the same energy walking as running, you have to walk about one and a half times as far and that it takes about twice as long,” said Paul T. Williams, a staff scientist at Lawrence Berkeley National Laboratories and the lead author of all of the studies involving the surveys of runners and walkers.

On the other hand, people who begin walking are often more unhealthy than those who start running, and so their health benefits from the exercise can be commensurately greater.

“It bears repeating that either walking or running is healthier than not doing either,” Dr. Williams said, whatever your health goals.

For confirmation, consider one additional aspect of the appetite study. The volunteers in that experiment had sat quietly for an hour during one session, not exercising in any fashion, neither running nor walking. And afterward they were famished, consuming about 300 calories more than the meager few they had just burned.

 

Source: NY Times

 

 

What’s the point in restaurant calorie counts?.


There are a lot of fat people in America. More than a third of US adults are obese according to data from the Centers for Disease Control and Prevention. In 2008, medical costs associated with obesity were estimated at $147bn (£97bn; 113bn); the medical costs for people who are obese were $1429 higher than those of normal weight. Between 1988-94 and 2007-8 the prevalence of obesity increased in adults at all income and education levels. It’s a big problem, no pun intended.

So it’s no surprise that measures are progressing to reverse this problem, and one of the more recent campaigns has been a push to require chain restaurants to list calorie counts on their menus. In the Patient Protection and Affordable Care Act, the US Food and Drug Administration (FDA) began the process of requiring calorie labeling for “restaurants and similar retail food establishments that are part of a chain with 20 or more locations doing business under the same name and offering for sale substantially the same menu items.” The guidelines have been a source of controversy ever since.

The evidence over the efficacy of such moves is mixed and an understandable reluctance from various quarters of the food industry probably doesn’t greatly help the cause.

This week the BMJ publishes research that will probably only add to the uneven picture rather than solve the conundrum. Investigators researching estimations of calorie content in consumers’ meals from fast food restaurants found a routine and sizable underestimation—so far so positive for calorie labeling (doi:10.1136/bmj.f2907). But despite the conclusion that labeling “might” reduce the underestimation it was hard for them to be more concrete as they also found that “noticing calorie information in the restaurant had no effect on the accuracy of calorie estimations.”

There’s no doubt that on an anecdotal level some people do find calorie labeling helpful, but if we’re tackling a public health problem and the population level data show questionable benefit, is this part of the Affordable Care Act worth the continuing controversy?

The implementation of the Affordable Care Act is one of the big ongoing topics of 2013 and this week we also publish an international view on it from four visiting academics, currently researching in the US (doi:10.1136/bmj.f3261). Their conclusions on the challenges facing Medicaid expansion hardly make for a walk in the park either, but then, if health reform were straightforward, it would have been done already.

Source: BMJ

Which is better running on walking?.


According to the latest research it depends almost completely on what you are hoping to accomplish.

If, for instance, you are looking to control your weight —running wins, going away. In a study published last month in Medicine & Science in Sports & Exercise, and unambiguously titled “Greater Weight Loss From Running than Walking,” researchers combed survey data from 15,237 walkers and 32,215 runners enrolled in the National Runners and Walkers Health.

Participants were asked about their weight, waist circumference, diets and typical weekly walking or running mileage both when they joined the study, and then again up to six years later.

The runners almost uniformly were thinner than the walkers when each joined the study. And they stayed that way throughout. Over the years, the runners maintained their body mass and waistlines far better than the walkers.

The difference was particularly notable among participants over 55. Runners in this age group were not running a lot and generally were barely expending more calories per week during exercise than older walkers. But their body mass indexes and waist circumferences remained significantly lower than those of age-matched walkers.

Why running should better aid weight management than walking is not altogether clear. It might seem obvious that running, being more strenuous then walking, burns more calories per hour. And that’s true. But in the Berkeley study and others, when energy expenditure was approximately matched — when walkers head out for hours of rambling and burn the same number of calories over the course of a week as runners — the runners seem able to control their weight better over the long term.

One reason may be running’s effect on appetite, as another intriguing, if small, study suggests. In the study, published last year in the Journal of Obesity, nine experienced female runners and 10 committed female walkers reported to the exercise physiology lab at the University of Wyoming on two separate occasions. On one day, the groups ran or walked on a treadmill for an hour. On the second day, they all rested for an hour. After both sessions, the volunteers were set free in a room with a laden buffet and told to eat at will.

The walkers turned out to be hungry, consuming about 50 calories more than they had burned during their hour-long treadmill stroll.

The runners, on the other hand, picked at their food, taking in almost 200 calories less than they had burned while running.  So to eat less, run first.

In perhaps the most comforting of the new studies, published last month in Arteriosclerosis, Thrombosis and Vascular Biology and again using numbers from the versatile Runners and Walkers Health Study, runners had far less risk of high blood pressure, unhealthy cholesterol profiles, diabetes and heart disease than their sedentary peers. But the walkers were doing even better. Runners, for instance, reduced their risk of heart disease by about 4.5 percent if they ran an hour a day. Walkers who expended the same amount of energy per day reduced their risk of heart disease by more than 9 percent.

Of course, few walkers match the energy expenditure of runners. “It’s fair to say that, if you plan to expend the same energy walking as running, you have to walk about one and a half times as far and that it takes about twice as long,” said Paul T. Williams, a staff scientist at Lawrence Berkeley National Laboratories and the lead author of all of the studies involving the surveys of runners and walkers.

On the other hand, people who begin walking are often more unhealthy than those who start running, and so their health benefits from the exercise can be commensurately greater.

“It bears repeating that either walking or running is healthier than not doing either,” Dr. Williams said, whatever your health goals.

For confirmation, consider one additional aspect of the appetite study. The volunteers in that experiment had sat quietly for an hour during one session, not exercising in any fashion, neither running nor walking. And afterward they were famished, consuming about 300 calories more than the meager few they had just burned.

COMMENT:  While this column adds some interesting insights, the real take home message is that moving is good for your health whether it’s walking or running and from other studies also about any other exercise involving moving.

 

Source: BMJ

 

No magic answer for Achilles tendinopathy.


Although they are trendy money spinners, best evidence shows little effectiveness”—An attention grabbing subheading to an editorial by Nic Maffulli in the BMJ commenting on an intriguing randomised controlled trial (RCT) from New Zealand on the use of autologus blood injections in treating Achilles tendinopathy. It doesn’t work.

Evidence based sports medicine was radical new thinking when Tom Best and I first began to think about it. Care of the athlete had evolved empirically. Few asked questions. For example, when our university research group first began to study ice, perhaps the most commonly used treatment in soft tissue injury, there was little quality evidence to inform treatment; the duration of each application, over what period of time, the temperature of the ice (melting iced water is 0 degrees Celcius),  if it mattered if you were fat or thin etc. Clinicians then began to ask about the evidence for the tests used in clinical examination, the effectiveness of prevention, the appropriate management of common conditions. Where we thought there was certainty, there was little evidence. This RCT on Achilles tendinopathy is an important trial because it asked serious questions about a treatment that had become commonplace yet seemingly evidence free.

Much of what we think is fact in sport is hype, based often on weak science, but mostly on extrapolation from observation. People in sport are forever looking for that extra added magic ingredient to set them apart. Complicit and gullible because they want to believe.  They follow the training programme, wear the headband, chase the logo the champions wear. It is no surprise that they take the drink, buy the supplement, wear the shoe, or do the exercise endorsed by champions. Ever susceptible, suggestible—looking for an easy way, its human nature.  So, it was no surprise to see the hype surrounding yet another product on the margin. This was the next big thing—an injection to cure one of the most common and troublesome injuries.

Its great to see good quality research and more is needed. But, research is expensive and its almost impossible to justify research in sports medicine when competing for funds with cancer, cardiology, and other core medical topics.  There is an evidence vacuum and in sports medicine there is huge pressure to do something. And, always someone looking for the magic answer.

Sourc: BMJ

 

 

Pneumonia and pneumonia related mortality in patients with COPD treated with fixed combinations of inhaled corticosteroid and long acting β2 agonist: observational matched cohort study (PATHOS).


 

Abstract

Objective To investigate the occurrence of pneumonia and pneumonia related events in patients with chronic obstructive pulmonary disease (COPD) treated with two different fixed combinations of inhaled corticosteroid/long acting β2 agonist.

Design Observational retrospective pairwise cohort study matched (1:1) for propensity score.

Setting Primary care medical records data linked to Swedish hospital, drug, and cause of death registry data for years 1999-2009.

Participants Patients with COPD diagnosed by a physician and prescriptions of either budesonide/formoterol or fluticasone/salmeterol.

Main outcome measures Yearly pneumonia event rates, admission to hospital related to pneumonia, and mortality.

Results 9893 patients were eligible for matching (2738 in the fluticasone/salmeterol group; 7155 in the budesonide/formoterol group), yielding two matched cohorts of 2734 patients each. In these patients, 2115 (39%) had at least one recorded episode of pneumonia during the study period, with 2746 episodes recorded during 19 170 patient years of follow up. Compared with budesonide/formoterol, rate of pneumonia and admission to hospital were higher in patients treated with fluticasone/salmeterol: rate ratio 1.73 (95% confidence interval 1.57 to 1.90; P<0.001) and 1.74 (1.56 to 1.94; P<0.001), respectively. The pneumonia event rate per 100 patient years for fluticasone/salmeterol versus budesonide/formoterol was 11.0 (10.4 to 11.8) versus 6.4 (6.0 to 6.9) and the rate of admission to hospital was 7.4 (6.9 to 8.0) versus 4.3 (3.9 to 4.6). The mean duration of admissions related to pneumonia was similar for both groups, but mortality related to pneumonia was higher in the fluticasone/salmeterol group (97 deaths) than in the budesonide/formoterol group (52 deaths) (hazard ratio 1.76, 1.22 to 2.53; P=0.003). All cause mortality did not differ between the treatments (1.08, 0.93 to 1.14; P=0.59).

Conclusions There is an intra-class difference between fixed combinations of inhaled corticosteroid/long acting β2 agonist with regard to the risk of pneumonia and pneumonia related events in the treatment of patients with COPD.

Conclusions and future research

This observational matched cohort study indicated that there is an intraclass difference between inhaled corticosteroid/long acting β2 agonist regarding the risk of pneumonia and pneumonia related mortality in the treatment of patients with COPD. The higher risk of pneumonia in patients treated with fluticasone/salmeterol might be related to differences in immunosuppressant potency and pharmacokinetic and pharmacodynamic properties between budesonide and fluticasone. Whether other unknown risks of pneumonia that were not adequately controlled for in this matched cohort study contributed to our findings remains uncertain. The magnitude of the intraclass difference in pneumonia needs to be put in context with the benefits of each regimen in preventing exacerbations. Long term randomised controlled trials comparing fixed combinations of inhaled corticosteroid/long acting β2 agonist in COPD with respect to occurrence of pneumonia and exacerbations are, therefore, warranted.

 

What is already known on this topic

  • Pneumonia is a common complication of COPD, which is associated with considerable morbidity, mortality, and health costs
  • Treatment with inhaled corticosteroids and long acting β2 agonists (fixed dose combinations) can increase the risk of pneumonia in these patients, though it is not known if there is a variation in risk between different combinations
  • This observational matched cohort study indicated that there is an intraclass difference between fixed combinations of inhaled corticosteroid/long acting β2 agonist with regard to risk of pneumonia and pneumonia related events in patients with COPD

What this study adds

 

Sourc: BMJ

Dynamic spread of happiness in a large social network: longitudinal analysis over 20 years in the Framingham Heart Study.


Abstract

Objectives To evaluate whether happiness can spread from person to person and whether niches of happiness form within social networks.

Design Longitudinal social network analysis.

Setting Framingham Heart Study social network.

Participants 4739 individuals followed from 1983 to 2003.

Main outcome measures Happiness measured with validated four item scale; broad array of attributes of social networks and diverse social ties.

Results Clusters of happy and unhappy people are visible in the network, and the relationship between people’s happiness extends up to three degrees of separation (for example, to the friends of one’s friends’ friends). People who are surrounded by many happy people and those who are central in the network are more likely to become happy in the future. Longitudinal statistical models suggest that clusters of happiness result from the spread of happiness and not just a tendency for people to associate with similar individuals. A friend who lives within a mile (about 1.6 km) and who becomes happy increases the probability that a person is happy by 25% (95% confidence interval 1% to 57%). Similar effects are seen in coresident spouses (8%, 0.2% to 16%), siblings who live within a mile (14%, 1% to 28%), and next door neighbours (34%, 7% to 70%). Effects are not seen between coworkers. The effect decays with time and with geographical separation.

Conclusions People’s happiness depends on the happiness of others with whom they are connected. This provides further justification for seeing happiness, like health, as a collective phenomenon.

 

What is already known on this topic

  • Previous work on happiness and wellbeing has focused on socioeconomic and genetic factors
  • Research on emotional contagion has shown that one person’s mood might fleetingly determine the mood of others
  • Whether happiness spreads broadly and more permanently across social networks is unknown
  • Happiness is a network phenomenon, clustering in groups of people that extend up to three degrees of separation (for example, to one’s friends’ friends’ friends)
  • Happiness spreads across a diverse array of social ties
  • Network characteristics independently predict which individuals will be happy years into the future

What this study adds

 

 

Source: BMJ

 

Coca-Cola’s bid to teach the world to slim is not on.


coca cola can

Coca-Cola wants to join the global fight against obesity. No, really. CEO Muhtar Kent announced: “We want to be part of the solution” and spoke of plans to place calorie counts more visibly, stop targeting the under-12s with advertising and promote exercise and active lifestyles.

That last one sounds intriguing – I expect to see virals in real time, showing an obese character (Mr Fizz?) jogging for entire days. Along the bottom, a tickertape could read: “If, like this man, you can’t be bothered to read our labels, drink Diet Coke, Coke Zero, or any of our other delicious artificially sweetened drinks. Or Sprite, now sweetened in the UK, not with aspartame, but with a ‘natural sweetener’ derived from the plant stevia. Did you hear us say ‘natural’? Did we mention that stevia is a plant – a real plant, green, with leaves, and everything? Great isn’t it! (Disclaimer: don’t worry too much about the ‘derived’ bit or that our other diet products use aspartame).”

Mr Fizz could bump into his friends, Miss Insulin Spikes and Mr Pre-Diabetic, and they could snack on giant doughnuts, thus illustrating Coca-Cola’s point (made in its recent “Coming Together” advert) that it is overall calories that count, not just fizzy drinks. In the spirit of public service, I’m going to offer up Mr Fizz and friends for free, in the hope that Coca-Cola can achieve its aims. Hats in the air! Job done! Though sadly not really. Where global obesity is concerned, how can a company peddling one of the most significant contributory factors ever be part of the solution?

Why do companies such as Coca-Cola bother trying to be health-conscious? Clearly, it is trying (let’s admit that). Let’s also acknowledge that Coca-Cola is not the only sugary drinks manufacturer out there, just the most successful. However, the game’s up. It’s now extensively documented that these drinks, even some “healthy fruit juices”, can have devastating effects on people’s weight. Many people are shown to have more problems with such drinks than with food, sometimes without other factors involved. Add to this the fact that sweeteners in diet drinks are increasingly controversial, and sales of bottled water (relatively non-profitable) are rising, and it’s a brand nightmare.

You could almost feel sorry for them. It’s reminiscent of the aftermath of Morgan Spurlock‘s Super Size Me when McDonald’s went into a health-conscious frenzy, painting restaurants green and inserting salads on to its menus. Few people wanting a salad would go to McDonalds, but never mind – at least it was trying, “responding”, whatever companies call it, when they realise that a public mea culpa (sort of) is their best option, as they wait for another brand to get Spurlocked and divert the attention away from them.

Which is what seems to be happening to Coca-Cola. In recent times, the company, and similar brands, has been Spurlocked. This time, it’s not by just one man scarfing meal-deals, but people becoming concerned about sugary drinks generally. What’s more, with Coca-Cola, it is the core product that’s the problem. It’s not labelling (they already have labelling), and it’s not encouraging active lifestyles (who looks to a drinks company for exercise tips?). Nor could Coca-Cola hurriedly shove some salad into the can to make it “healthier”.

To engage properly with the obesity debate, Coca-Cola would have to slag off the vast majority of its own products. Instead, it talks about diet ranges, exercise, overall calorie counts et al. It could be seen as its version of the McDonald’s green-painted restaurants – responsibly “responding” to public concern, while it waits for something else to get Spurlocked. The more sceptical might say that Coca-Cola can want all it likes, when it comes to being part of the solution. While it was opportune for the company to join the fight against global obesity, it’s also thoroughly farcical.

It’s not Glasto‘s prices that suck, it’s the glampers

Ah, British music festivals. You wade around in mud, watching bands you can’t see or hear, taking fake drugs, drinking beer that smells of roadie wee, surrounded by people who think “wild” is wearing wet socks a couple of days in a row, and shouting “Gerrof!’ at Mumford & Sons.Music festivals suck, and always have done, but don’t worry, because you probably can’t afford to go anyway.

A survey by the moneysaving website Watch My Wallet says British music festivals such as Glastonbury or Isle of Wight have nearly doubled in price in the past decade, and that some people now prefer festivals in such countries as Poland or Croatia. British high prices particularly exclude teenagers, as well as “seasoned festivalgoers” (translation: prancing loser-hippies in jester hats).

Good riddance, prancing loser-hippies! Unfortunately, they’ve been replaced by the repellent glampers, those hedge-fund, high-roller types who “glamp” in five-star teepees, “slumming it” in Hunter wellies – barbecuing prawns, drinking prosecco and probably still wearing moronic jester hats (“Oh Xavier, you’re so ironic!”) No wonder people are decamping to far-flung festivals. It’s their best chance of avoiding the glampers.

Take me down that street of shame

Piers Morgan, former Daily Mirror editor, now CNN chatshow host, is executive-producing a new US television series about British tabloid journalism. The pilot episode will be written by Danny Brocklehurst (Shameless) and set in the 1970s. Which is handy – all safely tucked away in the past, away from all the phone-hacking/Leveson unpleasantness. Like your thinking, Piers (wink).

A drama about us beauteous (inside and out) journalists – what a rare treat. How often does the media get to be navel-gazing and self-referential to an absurd and nauseating degree? “All the time!” you cry? Silence, haters!

I’m picturing a journo Life on Mars vibe, with squalid lunchtime piss-ups that last for weeks and ballooning expense accounts that could make a Russian oligarch weep. Perhaps with some debonair editor character, mysteriously also called “Piers”, who’s initially sneered at for his big girl’s blouse name, and for starting on the showbiz pages, but ends up winning over the hardened hacks with his gritty charisma, offset by a gentle self-deprecating charm…

It’s going to be a difficult wait. Less happily, there’s some “artistic confusion” that needs urgent clarification. Morgan says that it would be about “ruthless, amoral” 1970s journalists “drinking, brawling, fornicating, night-clubbing and cocaine-snorting”. Which, from what I’ve heard, sounds a bit like journalism in the 1990s, or, for that matter, journalism in the Noughties, or indeed… journalism.

Hence the artistic confusion. I’m still looking forward to Fleet Street, but perhaps Morgan could explain why I’m feeling this strange sense of over-identification with the journalists of the 1970s, particularly as he has specifically selected them as the most appalling disreputable hacks ever.

By the way, Piers, when it comes to casting, Hugh Grant says he’s busy.

Source: http://www.guardian.co.uk

Cancer risk in 680 000 people exposed to computed tomography scans in childhood or adolescence: data linkage study of 11 million Australians.


This study highlights one of the main dilemmas of modern medicine; namely, the threshold at which a clinician performs an investigation, particularly where this involves receiving a radiation dose such as computed tomography scan. The dilemma lies between not missing significant pathology and not utilising resources unnecessarily plus potentially increasing the patient’s future risk of cancer. In most specialities there are guidelines, from a variety of bodies including the national institute of clinical excellence and national specialty societies, which help determine the investigative pathway of patients. However, individual patients often present with a constellation of signs, symptoms and risk factors which may not fit within the guidelines. An example would be the young patient with a strong family history of coronary disease and first degree relatives presenting with myocardial infarction or death below the age of 40, with very atypical chest pain which is clearly non-cardiac in nature. A further example would be the patient who is in complete remission from cancer but notices vague intermittent bloating in the abdomen despite being very well with a normal clinical examination, ultrasound abdomen and blood profile. Some clinicians may just re-assure the patient whilst others may perform a coronary CT angiogram in the former case and CT abdomen in the latter case. Often the real-world decision making is based partly on clinical judgement of the physician but also increasingly on managing expectations and re-assuring patients. Patients should be made aware of the dose of radiation they receive and what implications this has on their future risk of cancer so they can be fully informed about the risks and benefits of their chosen pathway.

Source: BMJ

 

 

Risk of incident diabetes among patients treated with statins: population based study.


Abstract

Objective To examine the risk of new onset diabetes among patients treated with different HMG-CoA reductase inhibitors (statins).

Design Population based cohort study with time to event analyses to estimate the relation between use of particular statins and incident diabetes. Hazard ratios were calculated to determine the effect of dose and type of statin on the risk of incident diabetes.

Setting Ontario, Canada.

Participants All patients aged 66 or older without diabetes who started treatment with statins from 1 August 1997 to 31 March 2010. The analysis was restricted to new users who had not been prescribed a statin in at least the preceding year. Patients with established diabetes before the start of treatment were excluded.

Interventions Treatment with statins.

Main outcome measure Incident diabetes.

Results Compared with pravastatin (the reference drug in all analyses), there was an increased risk of incident diabetes with atorvastatin (adjusted hazard ratio 1.22, 95% confidence interval 1.15 to 1.29), rosuvastatin (1.18, 1.10 to 1.26), and simvastatin (1.10, 1.04 to 1.17). There was no significantly increased risk among people who received fluvastatin (0.95, 0.81 to 1.11) or lovastatin (0.99, 0.86 to 1.14). The absolute risk for incident diabetes was about 31 and 34 events per 1000 person years for atorvastatin and rosuvastatin, respectively. There was a slightly lower absolute risk with simvastatin (26 outcomes per 1000 person years) compared with pravastatin (23 outcomes per 1000 person years). Our findings were consistent regardless of whether statins were used for primary or secondary prevention of cardiovascular disease. Although similar results were observed when statins were grouped by potency, the risk of incident diabetes associated with use of rosuvastatin became non-significant (adjusted hazard ratio 1.01, 0.94 to 1.09) when dose was taken into account.

Conclusions Compared with pravastatin, treatment with higher potency statins, especially atorvastatin and simvastatin, might be associated with an increased risk of new onset diabetes.

Discussion

In this population based study, we found that patients treated with atorvastatin, rosuvastatin, or simvastatin were at increased risk of new onset diabetes compared with those treated with pravastatin. No such risk was evident with fluvastatin or lovastatin. The risk associated with rosuvastatin could depend on dose and duration of treatment. The risk of incident diabetes was similar whether statins were being used for primary or secondary prevention.

Overall, we observed a 10-22% increased risk of diabetes for some statins that is consistent with findings from previously published meta-analyses of clinical trials. The increased risk with rosuvastatin significantly decreased after covariate adjustment and became non-significant once dose was taken into consideration. This could possibly represent greater use of rosuvastatin in patients with lower cardiovascular risk.3 In 2009, an analysis of five placebo controlled trials (n=57 593) found a 13% (relative risk 1.13, 95% confidence interval 1.03 to 1.23) increased incidence of diabetes in people taking statins compared with placebo over an average 3.9 years of follow-up,9 with a subsequent analysis of 13 placebo controlled trials (n=91 140) showing a 9% (odds ratio 1.09, 95% confidence interval 1.02 to 1.17) increased incidence of diabetes over four years of follow-up.10 More recently, two meta-analyses have suggested a dose dependent effect for patients receiving high dose atorvastatin or simvastatin treatment versus moderate dose treatment (odds ratio 1.12, 95% confidence interval 1.04 to 1.22) and when considering only atorvastatin trials.11 12 Our results differ from those of the Women’s Health Initiative study, which showed a nearly 50% increase in new onset diabetes with statins compared with placebo (hazard ratio 1.48, 95% confidence interval 1.38 to 1.59), with no differential risk among low potency (fluvastatin, lovastatin, pravastatin) and high potency (simvastatin, atorvastatin) statins.14 Our findings, however, are consistent with the findings of Zaharan and colleagues in 2012, who found an increased risk with atorvastatin (hazard ratio 1.25, 1.21 to 1.28), rosuvastatin (1.42, 1.33 to 1.52), and simvastatin (1.14, 1.06 to 1.23).30 Our population based assessment adds to the discussion of risk when doctors are considering starting statin treatment in a patient for primary versus secondary prevention.

Possible mechanisms

Several factors could explain the increased risk of new onset diabetes among patients receiving certain statins.2 7 15 The increased production of plasma derived low density lipoprotein (LDL) cholesterol as a compensatory response to de novo cholesterol synthesis inhibition might result in direct inflammation and oxidation within the β cell. Consequently, the functional and structural integrity of β cells is compromized, impairing insulin secretion as a result of cellular apoptosis.15Additionally, metabolic receptor effects interfere with cellular glucose uptake, energy production, and insulin secretion.2 7 15 16 Statins can also inhibit calcium mediated pancreatic insulin release and decrease expression of the β cell glucose transporters GLUT-2 and GLUT-4.15 Finally, statins are also known to interfere with the synthesis of ubiquinone (CoQ10), which could independently alter insulin secretion.15 16 The degree to which statins are involved in these respective mechanisms of diabetes onset is variable and supports why some statins pose a higher risk than pravastatin.7 As shown in our dose and potency analyses, the risk could be greater for atorvastatin and simvastatin, regardless of the dose prescribed.

Limitations and strengths

Some limitations of our study merit emphasis. We could not identify and account for potentially important risk factors for diabetes such as weight, ethnicity, and family history. Newer statins might be preferentially used in patients at higher risk of diabetes, though the characteristics of patients in our study were highly similar across study groups. Secondly, data on blood lipids, hemoglobin A1C concentration, or triglyceride concentrations were unavailable, and therefore we could not use these measures for risk stratification or diagnostic purposes. The ODD, however, has been shown to be both sensitive (86-90%) and specific (92-97%).19 Furthermore, we had no data on marketing or promotional efforts nor did we have data on physicians’ preferences for particular statins. Although the statin groups were well balanced with respect to a wide variety of demographic and clinical variables, we cannot exclude the possibility of residual confounding.

Our study also had several strengths including a large sample size, use of pravastatin as an active comparator reference group, and a population based design. Our findings suggest that older patients treated with certain statins are at increased risk for incident diabetes, regardless of dose or whether treatment is used for primary or secondary prevention. The risk seems to be greatest with atorvastatin, rosuvastatin, and simvastatin. After adjustment for dose, however, the risk did not seem to persist among rosuvastatin users. Clinicians should consider this risk when they are contemplating statin treatment for individual patients. Preferential use of pravastatin, and potentially fluvastatin or lovastatin, while recognizing the limited efficacy data and increased risk of drug interactions with these two agents, might be warranted. Pravastatin might have a preferential benefit among primary prevention patients at high risk of diabetes.

What is already known on this topic

  • Given the widespread use of statins to manage hypercholesterolemia, small effects in their efficacy and safety profiles can have important population impact.
  • Statins have previously been associated with an increased risk of incident diabetes, though there is controversy around whether this risk differs among drugs
  • When compared with pravastatin, atorvastatin, rosuvastatin, and simvastatin are associated with a greater risk of new onset diabetes, regardless of their use for primary or secondary prevention of cardiovascular events
  • The risk for rosuvastatin users might depend on the dose prescribed

What this study adds

 

 

Source: BMJ