“Ice cream 'could be as addictive as cocaine',” reported the Daily Mail. In a bid to scoop its rivals, the newspaper claimed that new research had whipped up “concerns that the dessert could be genuinely addictive”.
It’s not clear who exactly had these chilling “concerns” over the possible addictive qualities of the frozen snack, but the study in question looked at measures of brain activity in 151 teenagers while they drank an ice cream milkshake. During the scans, teenagers who had frequently eaten ice cream over the past two weeks showed less activity in the “reward areas” of the brain that give pleasurable sensations. This reduced reward sensation was reported to be similar to what is seen in drug addiction as users become desensitised to drugs.
It should be noted that the study included only healthy teenagers of normal weight, and its results may not represent overweight or older people. It also only tested one food, so the results may not apply to other foods.
Unsurprisingly, the study did not directly compare brain responses to or cravings for ice cream with those for illegal drugs. Therefore, while some aspects of the brain’s response may be similar, it is not correct to say that this study has found that ice cream is “as addictive” as illegal drugs.
Where did the story come from?
The study was carried out by researchers from the Oregon Research Institute in the US. Sources of funding were not clear. The study was published in the peer-reviewed American Journal of Clinical Nutrition.
The newspapers focused on the suggestion that ice cream is “as addictive” as drugs. However, it is not possible to conclude this from the study.
What kind of research was this?
This experimental study looked at whether regularly eating ice cream reduces the brain’s pleasurable “reward” response. When we do things that support our survival, such as eating and drinking, the brain gives us a pleasurable reward sensation, reinforcing this behaviour and encouraging it in future. A similar process is also believed to occur in drug addiction, where a person’s reward response to the drug decreases with repeated exposure, leading to a need to take more of the drug.
The researchers reported that people who are obese experience less of a response to food in the reward centres of the brain, which may contribute to over-eating. Repeatedly eating foods with high levels of calories (called “energy dense” foods has also been shown to lead to brain changes that reduce reward response in rats. The researchers wanted to see if a similar thing happens in humans, by looking at whether regularly eating ice cream reduces the brain’s pleasurable reward response to an ice cream milkshake.
What did the research involve?
The researchers recruited 151 adolescent volunteers who were not overweight. They asked them how often they ate ice cream, and carried out brain scans while they drank either a tasteless solution or an ice cream milkshake. They then looked at whether the volunteers who ate ice cream frequently showed less brain activity in the reward centres of the brain when drinking the ice cream milkshake.
The study excluded any individuals who were overweight or had reported binge eating in the past three months, as well as any who had used illegal drugs, took certain medications, had a head injury or a mental health diagnosis in the last year. The volunteers completed standard food questionnaires about their eating habits over the past two weeks, including how often they ate ice cream. They also answered questions about food cravings and how much they liked certain foods, including ice cream. The volunteers also had their weight, height and body fat measured.
Volunteers were asked to eat their meals as usual but not to eat anything for five hours before the brain scan. The researchers then gave them either a sip of chocolate ice cream milkshake or a tasteless solution, and monitored the activity in their brain. Each participant received both drinks in a randomised order. The researchers then looked at what happened in the brain during each drink, and whether this varied depending on how much ice cream the volunteer usually ate. They also looked at whether body fat or energy intake from other foods influenced the response.
What were the basic results?
The researchers found that when the volunteers drank the ice cream milkshake, it activated the parts of the brain involved in giving a pleasurable “reward” feeling. Volunteers who ate ice cream frequently showed less activity in these pleasurable reward areas in response to the milkshake. Percentage of body fat, total energy intake, percentage of energy from fat and sugar, and intake of other energy-dense foods were not related to the level of reward response to the milkshake.
How did the researchers interpret the results?
The researchers concluded that their findings show that frequent consumption of ice cream reduces the “reward” response in the brain to eating the food. They reported that a similar process is seen in drug addiction.
The researchers also said that understanding these sorts of processes could help us understand how changes in the brain may contribute to, and help maintain, obesity.
Conclusion
This brain-scanning study suggests that the brain’s pleasurable reward response to ice cream decreases if it is eaten frequently. There are some points to note:
- The study only included healthy adolescents who were not overweight. Its results may not be representative of overweight or older individuals.
- The study only tested one food, so the results may not apply to other foods.
- Volunteers’ eating habits were only assessed for the past two weeks, and these may not be representative of their long-term eating habits.
- The study did not look at any other food with a discernable taste, only a “tasteless liquid”. It would have been interesting to see whether the reward response with tasting other foods, including less energy dense foods, also diminished over time.
- News reports of this research have claimed that this study shows that ice cream is “as addictive” as illegal drugs, but this is not the case. While the reduced brain reward seen with frequent ice cream eating was reportedly similar to that seen in the use of addictive drugs, the study unsurprisingly did not directly compare brain responses to ice cream and illegal drugs, or their addictive potential.
Analysis by Bazian
Links To The Headlines
Ice cream 'could be as addictive as cocaine', as researchers reveal cravings for the two are similar. Daily Mail, March 5 2012
Ice cream as 'addictive as drugs' says new study. The Daily Telegraph, March 5 2012
Links To Science
Burger KS and Stice E. Frequent ice cream consumption is associated with reduced striatal response to receipt of an ice cream–based milkshake. First published February 15 2012
“Babies born just a few weeks early have a higher risk of poor health,” The Guardian reported today. According to the newspaper, new research has found that being born just a few weeks early can raise their risk of conditions such as asthma.
It is already known that babies born prematurely (before 37 weeks of pregnancy may have a higher risk of immediate or longer-term health problems, and the earlier a baby is born, the higher the risk. To examine the issue, researchers followed over 14,000 children born between 2000 and 2002, and assessed their health at the ages of three and five years old. Outcomes including growth, hospital admissions, use of medication, asthma and long-standing illnesses were looked at particularly in relation to whether the children were moderately premature (32-36 weeks of pregnancy or born at what the researchers called “early” full term (37-38 weeks . Babies born moderately prematurely or at early term were more likely to have been re-admitted to hospital in the first few months of life than babies born at 39-41 weeks. Babies born moderately prematurely also had a higher risk of asthma symptoms than full-term babies.
These findings are broadly in line with what is already known about the effects of prematurity, and do not change the UK’s current definition of full-term pregnancy as 37 weeks and over. However, the study does show how different degrees of prematurity may affect health. Further study of the issue would be valuable, to explore longer-term health outcomes that may be caused by prematurity and the factors that may influence the likelihood of these poor health outcomes.
Where did the story come from?
The study was carried out by researchers from the University of Leicester and other UK institutions. It was funded by the Bupa Foundation and published in the peer-reviewed British Medical Journal.
The media generally covered this research in a balanced way.
What kind of research was this?
In the UK, the normal length of a pregnancy is classed as 37 weeks or above. It is already known that babies born prematurely (before 37 weeks may be at increased risk of immediate and longer-term health problems, and that the risks are higher the earlier a baby is born. However, the authors say that there has been minimal research into the longer-term health outcomes of infants specifically born moderately preterm (which this study defines as 32-36 weeks and at what the researchers termed as "early full term" (37-38 weeks .
To investigate this, the researchers used a cohort study. This is a good way to follow up and compare health outcomes in groups of people that have been exposed to different factors. In this case, the exposure was the number of weeks of pregnancy at which the babies were born. However, a cohort study that looks at a group’s health relies on the accuracy of reported health outcomes and diagnoses. For example, one condition this study looked at was asthma, and the researchers asked parents about whether their child had wheezing symptom or asthma. However, this does not necessarily equate to a medical diagnosis of asthma.
This type of study also needs to take into account potential factors that could be related to both risk of prematurity and risk of the health outcome ( confounding factors . For example, parental smoking is linked to an increase risk of prematurity, and also to an increased risk of asthma in the child.
What did the research involve?
This study involved participants of the Millennium Cohort Study (MCS , a piece of research in which the subjects were gathered by random sampling of child benefit registers. It featured 18,818 infants born in the UK between 2000 and 2002. The number of weeks of pregnancy at birth was calculated from the mother’s report of her expected due date. Births were grouped into:
- very preterm (defined by the authors as 23-31 weeks
- moderate preterm (32-33 weeks
- late preterm (34-36 weeks
- early term (37-38 weeks
- full term (39-41 weeks
These are not the standard accepted definitions. For example, the charity BLISS, for “babies born too soon”, defines full-term pregnancy as 37 weeks or more, moderately premature as 35-37 weeks, very premature as 29-34 weeks, and extremely premature as birth before 29 weeks.
Child health outcomes were monitored over five years of follow-up. Outcomes assessed included:
- child height, weight and body mass index at three and five years
- parental reports of the number of hospital admissions (not related to accidents since birth or the previous interview, collected at nine months and at three and five years.
- parental reports of any longstanding illness or disability of more than three months’ duration and diagnosed by a health professional, collected at three and five years (a limiting longstanding illness was defined as one which limited activities that are normal for the child’s age group
- parental reports of wheezing within the previous 12 months, and parental reports of asthma collected at three and five years
- parental reports of the use of prescribed drugs, collected at five years
- parents’ ratings of child health, defined as excellent, very good, good, fair or poor, collected at five years
The researchers used statistical methods to look at the outcomes in groups born at different stages of pregnancy and compared them to (their definition of full-term babies. Analyses were adjusted to account for various potential confounding factors, principally numerous social and demographic factors. The researchers also estimated “population attributable fractions” (PAFs associated with preterm and early term birth. This is an estimate of the contribution that a particular risk factor has to a health outcome. PAF represents the reduction in the proportion of people in the population with a particular health problem that could be expected if the exposure to a risk factor were reduced to the ideal exposure. In this case, it would represent the proportion of children that would no longer have a particular health problem if all babies were born at full term rather than preterm.
What were the basic results?
After the researchers excluded participants in the MCS study with incomplete data on time in the womb at birth, they interviewed the parents of 14,273 children at 3 years of age and 14,056 at 5 years. They found certain sociodemographic factors, such as lower maternal educational status and maternal smoking, to be associated with prematurity, as is already known.
The researchers generally found a “dose response” effect of prematurity, meaning that the more premature a baby was, the higher the likelihood of general health problems, hospital admissions and longstanding illnesses. They calculated the odds of each outcome compared to children born at 39-41 weeks. The full details of these outcomes are as follows:
The odds for three or more hospital admissions by five years of age were:
- 6.0 times higher for children born at 23-31 weeks
- 3.0 times higher for children born at 32-33 weeks
- 1.9 times higher for children born at 34-36 weeks
- 1.4 times higher for children born at 37-38 weeks
The odds for any longstanding illness at five years of age were:
- 2.4 times higher for children born at 23-31 weeks
- 2.0 times higher for children born at 32-33 weeks
- 1.5 times higher for children born at 34-36 weeks
- 1.1 times higher for children born at 37-38 weeks
The odds for the child’s health being rated as only fair or poor by parents at five years of age were:
- 2.3 times higher for children born at 23-31 weeks
- 2.8 times higher for children born at 32-33 weeks
- 1.5 times higher for children born at 34-36 weeks
- 1.3 times higher for children born at 37-38 weeks
The odds for asthma and wheezing at five years of age were:
- 2.9 times higher for children born at 23-31 weeks
- 1.7 times higher for children born at 32-33 weeks
- 1.5 times higher for children born at 34-36 weeks
- 1.2 times higher for children born at 37-38 weeks
The greatest contribution to the burden of disease at three and five years was among children born at late/moderate preterm or early term. The calculated PAFs for being admitted to hospital at least three times between the ages of 9 months and 5 years were:
- 5.7% for children born at 32-36 weeks (i.e. you would expect a 5.7% reduction in the number of young children admitted three or more times if babies were born at full term rather than moderate preterm
- 7.2% for children born at 37-38 weeks (you would expect a 7.2% reduction in the number of young children being admitted if babies were born at full term rather than early term
- 3.8% for children born before 37 weeks (you would expect a 3.8% reduction in the number of young children being admitted if babies were born at full term rather than very preterm
Similarly, PAFs for longstanding illnesses were:
- 5.4% for early term births
- 5.4% for moderate or late preterm births
- 2.7% for very preterm births
How did the researchers interpret the results?
The researchers concluded that “the health outcomes of moderate/late preterm and early term babies are worse than those of full term babies.” They say that it would be useful for further research to look into how much of the effect is due to prematurity itself, and how much is due to other factors such as maternal or foetal complications.
Conclusion
This valuable research examined childhood health outcomes in a large group of children born at different stages of pregnancy.
Important points to consider when interpreting this research include:
- The authors generally found that the likelihood of poorer health outcomes was higher with increasing prematurity (a dose response effect . This is in line with what is already known about the generally poor immediate and longer-term health outcomes among babies born increasingly prematurely.
- The greatest contribution to overall burden of disease at ages three and five years was calculated to be among children born at 32-36 weeks or at 37-38 weeks. Though a gestation of less than 32 weeks might be expected to have a greater influence on the burden of disease, it must be remembered that many more babies are born above 32 weeks of gestation than below it. Therefore, in the population as a whole, the greater number of babies born within the 32-38 week range would have a greater effect than the small number of babies born extremely early.
- The definitions that the authors used for the purposes of this study are not standard definitions. For example, the standard definition of full-term pregnancy is birth at 37 weeks or more, and it is not split into “early term” at 37-38 weeks and “full term” only at 39-41 weeks. Similarly, definitions of prematurity differ from those used by other UK health organisations.
- There is a possibility of inaccuracy as both age at birth and health outcomes were reported by parents, rather than assessed through medical records. For example, a parental report of wheezing or asthma does not necessarily constitute a confirmed medical diagnosis of asthma.
Overall, the study found that the more premature a baby is, the greater the likelihood of health problems in childhood, and that some effect of prematurity may even be seen in pregnancies approaching full term. Further study in this area would be valuable, both to explore the wider range of longer-term health outcomes that may be caused by prematurity, and to look into associated factors (medical or sociodemographic, for example that may influence the likelihood of these outcomes.
Analysis by Bazian
Links To The Headlines
Infancy health risk linked to early birth by research. BBC News, March 2 2012
Babies born a few weeks early 'suffer health risks'. The Guardian, March 2 2012
Links To Science
Boyle EM, Poulsen G, Field DJ et al. Effects of gestational age at birth on health outcomes at 3 and 5 years of age: population based cohort study. British Medical Journal 2012; 344
Press release: Population-based cohort study of the effects of gestational age at birth on health outcomes at three and five years of age. British Medical Journal, March 1 2012
Hackers demonstrate new wireless attacks against insulin pumps, GE and Masimo ink a new OEM deal and Cardiac Science and Flight Medical launch Class I recalls.
Say hello to MassDevice +3, a bite-sized view of the top three med-tech stories of the day. This feature of MassDevice.com's coverage highlights our 3 biggest and most influential stories from the day's news to make sure you're up to date on the headlines that continue to shape the medical device industry.
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The Swedish-American actor is now confirmed to play the cyborg-cop in Jose Padilha's new version of the Paul Verhoeven science-fiction thriller
Joel Kinnaman, star of the
US remake of Danish crime series The Killing, has been cast as the new
Robocop in Jose Padilha's remake of Paul Verhoeven's 1987 science-fiction film, reports
Deadline.
Kinnaman had been tipped to take on the role made famous by Peter Weller in Verhoeven's dystopian tale of a Detroit police officer who is returned to duty as a cyborg enforcer following his death in the line of duty. Weller also starred in a poorly received sequel in 1990 but did not return for
Robocop 3 in 1993.
Kinnaman plays Stephen Holder, partner of homicide detective Sarah Linden in the US version of The Killing. He is also known in Sweden as the star of the critically acclaimed 2010 thriller Easy Money and appeared in six films in the Johan Falk series as Frank Wagner. The actor has joint Swedish-American citizenship through his Swedish mother and US-born father, and made his Hollywood debut in the Timur Bekmambetov alien-invasion film
The Darkest Hour last year. He also appeared in
Safe House opposite Denzel Washington and Ryan Reynolds, released in the UK last month.
The new Robocop film may have special resonance in the UK, as the original film depicts the takeover of the city's police force – with disastrous consequences – by a private corporation. The Guardian disclosed last week that the
West Midlands and Surrey police authorities have invited private security companies to bid for a wide range of services, including criminal investigations, patrolling neighbourhoods and detaining suspects.
Brazilian film-maker Padilha is best known for the two films in his
Elite Squad series about a special police unit operating within the drug-ravaged favelas of Rio de Janeiro.
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Mo Costandi writes in the
Guardian:
My latest
news story for
Nature
describes
a new study which explains how marijuana causes impairments in working memory, or the ability to retain information for short periods of time. This is a well known side effect of marijuana, which is unwanted with respect to medicinal use of the drug, but until now the underlying neurobiology was unknown.
The research shows that tetrahydrocanabinol (THC, the psychoactive ingredient in marijuana impairs working memory by inducing a form of synaptic plasticity that weakens neuronal connections. This could lead to new THC-related drugs that have therapeutic value but do not cause this unwanted effect. More interestingly, though, the findings provide compelling evidence that hitherto neglected brain cells called astrocytes are critical for brain function and play a direct role in cognitive processes.
There are two different types of synapitc plasticity. One of these, called
long-term potentiation, strengthens the connections between neurons so…
Not so long ago, this year's must-see action hero was sleeping in his car. Now, after saving the world in John Carter, he's starring alongside Rihanna
"Oh fuck off!" The words are out of my mouth before I have a chance to think about the ramifications of saying them to a Hollywood actor, especially one whose star is about to turn supernova. As soon as I do, I think I might throw up. And then, after the briefest of pauses, Taylor Kitsch's perfect eyes wrinkle up and his perfect mouth emits a perfect laugh, all manly and throaty and sounding of a thousand cigarettes.
The incident occurs just after Kitsch has finished telling me about the house he's building by a lake in Austin, Texas, and the boat, which he sails upon said lake. It comes after he's said how much he loves England ("I love the dry, wry humour" , and doesn't like LA ("It's too one-sided" ; all punctuated with swearing, jokes and the confidence of a man who can wear cowboy boots, bootcut jeans (well, he does live in Texas and
still
look absurdly attractive.
I don't mean to curse at him, but it is almost too much to take, all of this, and the vision of him building a house just doesn't seem fair to the rest of the population, neither male nor female. If there was a real-life, modern-day Adam, or if Gosling in The Notebook really did exist, it would be in the form of the man sitting in front of me. Which is probably why he's saving the planet in two films this spring. First up is John Carter, a Disney action behemoth based on the 1964 book by Tarzan creator Edgar Rice Burroughs; then comes the guns-blazing Battleship, in which he stars alongside Liam Neeson and
Rihanna. As if that isn't enough, Kitsch will follow with
Oliver Stone's Savages, in which he plays a pot grower taking on a Mexican drug cartel to rescue his girlfriend (Blake Lively .
It might seem a brazen burst on to the scene but Kitsch, 30, has done his time in the waiting room. There was the almost career as a hockey player in his native Canada, until injury got the better of him, then a move to New York and a brief stint as a model. During that time he studied acting on the side and won small roles in forgettable films such as
Snakes On A Plane and John Tucker Must Die. There was a stint in LA, living – literally – out of his $1,100 car, in between auditioning for parts. But it was not until getting cast as Tim Riggins in American football TV drama,
Friday Night Lights – a spin off from the 2004 film – that his career kick-started his career in earnest.
"I played a high school kid at 26, 27; I still never use a razor, maybe to spite him," grins Kitsch, reclining back into his sofa. "But I love that role, man. I was told it was to be supporting at the beginning: you're going to be used incrementally, you could be gone by the first season. But it turned out to be quite the opposite. They gave me the empowerment to be really free. No rehearsals and the most important thing to me was to be able to improv. I love to throw curveballs; all those quotes people come up to me and say about Riggins, I'd say 90% are from the improv. I'd be like, 'Hey, this paragraph here? Literally not going to do it. Just going to do a look right here.' And they'd be like, 'Let's try it!'"
The confidence the role gave him obviously worked. It led to meatier parts, playing war photographer Kevin Carter in 2010's The Bang Bang Club and Gambit in X-Men Origins: Wolverine. And FNL also saw Kitsch forge a friendship with the show's director, Peter Berg, who hand-picked him for the lead role of Alex Hopper in Battleship.
"Pete and I go way back," says Kitsch, grinning, and extolling his pal in language you might expect from a veteran of a US sports drama. "He came to pitch Battleship to me and that alone is incredible; we're friends first and foremost and we've gone through a lot together personally, so it's a big risk to ask a close friend to get in the trenches with you on a different level. Because making movies is fucking tough and you're going to bat heads and you're going to challenge each other. But I think that was why I signed on, to go to battle with Pete."
'For 11 months, I was on a regimen of training and dieting. I was working six-day weeks. I would get my wake-up call at 4.33am'
Before Battleship, however, is John Carter – or "JC" as Kitsch likes to call him – an American civil war veteran transported from Earth to Mars. Not the easiest of premises to sell, but with the help of giant billboards featuring a long-haired Kitsch half-naked save for a loin cloth, one that has the potential to sell itself. It's his first lead role, and the pressure is on.
"I don't think anyone is going to put more on it than me," he says, ruffling that hair underneath his oversized beanie hat. "Of course it's the grandeur of it all, and the effects. I don't have any power over that but the character is something you just dive into. For 11 months, I was on a regimen of training and dieting. I stayed four months at the Metropolitan hotel in Mayfair, right by Hyde Park, but I was working six-day weeks, so I literally went out once. I would get my wake-up call at 4.33am to train. But it's worth it; the aesthetic of John Carter … you can't fuck around with that."
Was there a pie or two at the end of filming, then? "Oh my god, if I even fucking
told
you how hard I partied after that …" he starts, going almost misty eyed. "I rented an over-the-top house on the lake where I live in Austin, that I would never live in, like
ridiculous
; it was a joke. I flew in 11 of my friends, and my brother; friends that I grew up with and a few that I met through work. Eleven guys for five days, on the lake and going into the town. I fucking was a different person."
He is a confident fellow, Taylor Kitsch. We are used to a more falsely humble Hollywood these days – "Oh I'm so lucky, oh it just happened, oh I'm so blessed" and so forth – but perhaps because he doesn't live there, Kitsch doesn't seem to suffer from that syndrome. He will happily tell you how hard he worked to get a role. He will sing praises of those he has learned from – Willem Defoe,
Dominic West, or Benicio Del Toro – and cast shadows upon those he hasn't, dismissing their methods without naming names. It may sound over-bearing but with Kitsch, such self-belief seems to come from a genuine place of simply wanting to make things happen. You sense he's used to being the best. But it's not every ex-model pretty boy who manages to land two lead roles in a year, convincing studios to take a risk on a relative unknown. How did he manage to pull it off?
"Oh I threatened them quite often," he says, grinning. "I would love to ask them that, too. I had a call from my manager saying the director, Andrew Stanton (Wall-E , wanted to meet me. The screen test was quite heavy; John Carter has quite a burden. I think getting that part of it was a big thing [for Stanton]. But he was so emphatic and his energy was so infectious, that I left the audition thinking, 'If he gives me a good kick at it, I'm going to fight for it, I'm going to throw my hat in the ring for sure.'"
'John Carter tested me quite intensely. I literally suffered from exhaustion, passed out a couple of times. It took everything I had'
For all his fighting talk, Kitsch is the first to admit that it was not an easy ride, and not only for the training that left him physically battered and bruised.
"John Carter tested me quite intensely," he says in a southern drawl that belies the fact he's actually from a tiny Canadian town called Kelowna. "I literally suffered from exhaustion on John Carter, passed out a couple of times from it, so it took everything I had on that level. But also, emotionally. We shot the scene where his family are taken away from him, and that's 14 hours of Carter in mourning; that's intense. If it's Friday Night Lights, you can do it because you need two takes of raw emotion. You do it for literally about 30 minutes, if that, and then you're done. This was rough, but rewarding because when you see it cut in at certain spots, fuck it can hit ya, and I love that."
He may be owning the action hero this year, but Kitsch is determined to be taken seriously as an actor. "I love the story part of acting," he says. "I love bringing people into the emotional part of it. My favourite scenes in John Carter are the emotional ones, especially when you can collaborate with Stanton, who can rip your heart out and make you cry laughing in the same breath."
It's quite rare for an action picture to have a heart, I suggest; mostly it's just brawn and battles. "It is, but if it was one of those movies, I wouldn't have done it." He pauses, then with the confidence dipping a notch, says, "I was scared shitless with Bang Bang Club. Kevin Carter was a South African, drug-addicted, suicidal war photographer, and it was a true story that his family and best friend would see. Doing that justice is way more pressure … Then shooting Savages with Oliver Stone. I think that role will turn some heads in the sense of how unapologetic the character is. ThHe just doesn't give a fuck. But that's fun."
It is an exciting time for Taylor Kitsch and if he plays things right, he could have just what he wants. Is he happy with where he is going? "You work for years on end," he says, "and it's not theatre where you can have that validation right away. You hope people love it, and you're proud of the work. I remember driving around Sunset Boulevard in the car that I was living in. Now you drive down Sunset and there is a huge John Carter billboard. I had probably about 25 people texting me about it, and that is a pretty cool feeling. But what I
really
love is how different these guys are. And that's the beauty of it, hopefully."
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Our understanding of misery has changed less than we think
In the middle of the 12th century
Hildegard of Bingen explained the aetiology of melancholia. The clue was in the name. Black bile, too much of it: "It causes the veins in the heart to overflow; it causes depression and doubt in every consolation so that the person can find no joy in heavenly life and no consolation in his earthly existence." It was the result of an imbalance of
the four humours that circulate in the body. A physician as well as a nun and composer, she is very specific about the biology and anatomy of the humours: "Each of the dominating humours is covered with a quarter of the one coming after and a half of the third. The weaker humour regulates the two parts and the remaining part of the third, to make sure it doesn't exceed its limits."
Today, we believe we know better. Depression is largely considered to be an imbalance of the neurochemistry in the brain, and is treated accordingly. Clark Lawlor explains the contemporary view: "An early model was
norepinephrine, one of the amine family …too little meant depression, too much meant elation. Serotonin deficiency is possibly the most well-known of the contenders for causing depression." Selective serotonin reuptake inhibitors (SSRIs such as Prozac increase the amount of serotonin in the brain, and are now the most widely prescribed response to a modern diagnosis of depression and even the newer, milder condition of
dysthymia – chronic low mood and sadness, perhaps equally well described as "melancholia".
People on SSRIs often feel better. Which is odd, because the number of people whose mood is improved is only very slightly above that of control groups taking placebos, and some drugs that actually reduce serotonin levels are statistically as effective as antidepressants which increase those levels.
The fact is that, as a non-neurologist and non-biochemist, I have no more real understanding about the functioning of genes, the resulting brain chemistry and the effect on mood than Hildegard of Bingen had about the proportion and action of the humours on the veins in the heart. It seems, too, that psychiatrists aren't entirely sure about the chemical mechanisms of depression. Even so, I pop a prophylactic Prozac every morning, because if I don't think too hard about what I don't know, like the early moderns, the notion of chemical imbalance makes some sense to me (in conjunction with other causes of my life-long tendency to sink into debilitating depression.
Lawlor's history of the journey from Aristotle and Galen on melancholia, to
Aaron Beck's and
Martin Seligman's cognitive behavioural approach to depression is notably not a story of progress and increased understanding, but of changes in culture, language and technology about a particular common human condition. It is most valuable as a history of thought about the varying degrees of sadness and despair that have been consistently experienced from antiquity to the present day. Timothie Bright's 1613 description of the effect of excessive black bile – "which shut up the hart as it were in a dungeon of obscurity, causeth manie fearfull fancies … whereby we are in heaviness, sit comfortless, feare distrust, doubt dispaire, and lament, when no cause requireth it" – is as good a picture of depression as I know it as any I've heard or read.
It's surprising, then, when Lawlor says that the early moderns' understanding of what seemed to them like an epidemic of melancholia as a result of the imbalance of bodily humours is "alien to our contemporary world view, even if we can discern similarities with modern symptoms". He uses the phrase "profound strangeness" about their treatment of melancholia with both religious and physical cures. Call the religious spiritual or psychological, and the physical purgings an attempt to rebalance the system, and neither their descriptions nor their fundamental ignorance seem all that different from our own flailing attempts to deal with what again looks like an epidemic of depression.
The Elizabethan picture is confusing, with melancholia being recognised as a fashionable pose, a disorder of the mind, a sign of genius and a precursor of psychosis, but it was hardly more diversely understood than it has been since modernity offered us psychoanalytical, physicalist and cognitive versions of the experience of what is now officially called "major depressive disorder". MRI scans and biochemistry are our new tools, but they are as subject to interpretation as the possibility of the spleen overheating and tipping the system into a hot, dry, burnt condition of melancholia.
Galen's assumption was that the perfect balance is rare, and that most people were in flux, tipping more or less away from balance according to their own behaviours, the environment and their humoral predispositions. This is hardly alien to our understanding of how the body, mind and external circumstances work inextricibly together, and how difficult it is to discern any single cause of mental functioning, positive or negative, no matter how much we yearn for a simple, certain explanation. Perhaps the ancients and early moderns were better at living with uncertainty than we are.
The main theme running through the second half of Lawlor's book is the way in which our present understanding of depression has been increasingly simplified in the
Diagnostic and Statistical Manual of Mental Disorders
(
DSM
, and the power that drug companies seem to have had in the creation of some of those definitions. Checklists appear there which assist doctors (or anyone with the list to diagnose depression via elementary symptom spotting. Causes become irrelevant because they are so much harder and more expensive to know about and to treat. Humoral imbalance, a rackety childhood, who cares? If you have five of the designated symptoms every day over a two-week period, a doctor can confidently diagnose depression and medicate it.
Some people claim (as Freud would that this has resulted in the pathologising of normal sadness. Even grief is now subject to a time-limit.
DSM-V
, due out in 2013, will have a new condition called "complicated grief disorder", which allows doctors to treat excessive mourning (designated by a symptom list as depression within a few weeks of a bereavement, and puts a limit on normal mourning at six months. It isn't just that we want certainty, we seem to have come to the conclusion that feelings of sadness or a low mood are not just intolerable but actually abnormal.
Unfortunately, rather as if he were trying to make more simple sense of the subject than there was and is to be made, Lawlor's book is an overly brisk addition to the history of and thinking about melancholia and depression. It reads like a series of notes for a longer and more considered book and is broken into sub-headings in which major topics such as romantic melancholy and Christianity's influence on depression are wrapped up in little more than a page and a half of text.
There's a good bibliography, so I suppose anyone particularly interested can find more substance than is on offer here, but it isn't clear who the intended reader is who urgently wants these more considerable books boiled down. The long inquiry into melancholia and depression is so full of extraordinary writing – Ficino, Burton, Shakespeare, Donne, Milton, Keats and Coleridge, Freud, Styron, Kristeva – that this exiguous "what comes next" approach feels meagre.
• Jenny Diski's
What I Don't Know about Animals
is published by Virago.
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