| Feds: Don't tip off miners on surprise inspections By SAM HANANEL 2010-08-26T20:47:53ZWASHINGTON (AP) -- Some mine companies are tipping off their underground workers before federal officials make surprise inspections, an illegal practice that has become more prevalent since a West Virginia explosion killed 29 miners, the nation's top mine official said Thursday.... hosted.ap.org |
Why do we eat chilli? Chillies burn our tongues, make our eyes water and bring us out in a sweat. Jason Goldman looks at a peculiarly human form of masochismJason is a developmental psychologist and blogs at The Thoughtful AnimalDave's Red Hot. Mother Puckers. Green Bandit. Scorned Woman. Pain is Good. Blair's Death. No, they're not rock bands. These names represent just a small selection of the brands of hot sauce available at my local supermarket.Humans, apparently, enjoy torturing themselves. Spiciness, after all, is not a flavour, not like sweet or salty or sour. Spicy means pain. The sensation of spiciness is the result of the activation of pain receptors in the tongue. According to psychologist Paul Rozin of the University of Pennsylvania, about a third of the people around the world eat hot peppers every single day. Why? Because they "love the burn". At a symposium on gastro-psychology during this year's Association for Psychological Science convention, Rozin pointed out that humans are the only species – we know about – that specifically seek out what would otherwise be considered negative events.Healthy, sane humans do not stab themselves in the thighs, or bathe their eyes in lemon juice. So why do we so love to assault one of the most sensitive organs in the human body, the tongue, with what amounts to chemical warfare? Chillies are unique among foods that we should otherwise not enjoy. For example, humans also have natural aversions to the bitterness of coffee or the harshness of tobacco, but those substances have some addictive qualities, which might make them desirable. Capsaicin, the compound that provides the mouth-watering punch of chillies, does not seem to have any addictive qualities whatsoever. And yet the preference for capsaicin is almost universal; nearly every culture has incorporated it into their cuisine in some way, for milllennia.Rozin writes:"There are records suggesting use of chilli pepper dating back to 7000BC in Mesoamerica; they were domesticated some thousands of years after this. These fiery foods made their debut in the Old World when they were brought back by Columbus and other early explorers. In spite of their initial unpalatability, they became accepted as a basic part of the diet in many parts of the world: west and east Africa, India, south-east Asia, parts of China, Indonesia, Korea, and other smaller geographic regions, such as Hungary."Most young children, even from cultures known for their spicy recipes, are averse to capsaicin. So maybe, then, instead of actually liking the pain, we're merely desensitising ourselves: what used to be really painful is now just sort of painful.Since capsaicin is a member of the vanilloid family of molecules, it binds to a receptor on the tongue called the vanilloid receptor subtype 1. Upon binding to the VR1 receptor, the sensation produced by the capsaicin molecule is the same sensation that heat would cause, which explains capsaicin's burn. When scientists discovered that the VR1 receptor was a member of the larger family of TRP ion channels, the VR1 receptor was renamed TRPV1. TRP receptors are known to be sensitive to changes in temperature and are likely responsible for temperature sensation. When chilli peppers are the source of the capsaicin, there isn't any actual tissue damage; but because it binds to the TRPV1 receptor, the brain is tricked into believing that the tongue truly is on fire.In 1980, Rozin and a colleague, Deborah Schiller, reported a study in which they compared the pepper preferences of Mexicans and Americans. Mexicans generally eat chillies several times per day, while Americans only eat chillies a few times a week. If desensitisation could explain our preference for oral pain, then Mexicans should show higher tolerance for capsaicin than Americans, and Americans should more easily detect capsaicin, even in small amounts, than Mexicans.The data only weakly supported these predictions: the differences were seen, but were not statistically significant. Another prediction made by the desensitisation hypothesis is that individual tolerance should increase with exposure, and therefore with age. Rozin and Schiller found no correlation between age and tolerance though. Experiments conducted to try to induce a preference for capsaicin in rats, using traditional reinforcement techniques, proved futile.In the late 1970s, Frito-Lay tried to market a brand of corn chips in Mexico that had the flavour of chilli peppers, but without any capsaicin. As would be expected in a culture that actually enjoys the burn, the product was a failure. Likewise, bell peppers, which have some pepper flavour but no capsaicin, are not at all popular in Mexico.While most scientists still do not quite have a handle on the human preference for spicy foods, the best explanation comes from a mechanism called "hedonic reversal", or "benign masochism". Something happens, in millions of humans each year, which changes a negative evaluation into a positive evaluation, like flipping a light switch.Rozin writes: "If the oral receptors are sending the same message to the brain in the chilli liker and the chilli hater, then the chilli liker must have come to like the very same sensation that the chilli hater, the infant, and nonhuman animals find aversive. One gets to like the burn." Only humans seem to be able to derive pleasure from the negative sensation itself. Animals have been trained to endure self-harm, but only within the context of positive reinforcement.Perhaps we seek out the painful experience of snacking on chillies while consciously maintaining awareness that there is no real danger to ourselves. After all, people seem to enjoy – and actively seek out – many other sensations that are otherwise undesirable but are ostensibly safe: the sensation of falling provided by rollercoasters or skydiving, the feelings of fear and anxiety while watching horror movies, the physical pain experienced upon jumping into icy water, or even the feelings of sadness that come while watching a tear-jerker. Perhaps it is this cognitive mismatch itself that provides the thrill: like strapping into a rollercoaster or popping Hostel into your DVD player over and over again, the burn of capsaicin only seems to be threatening.Want a thrill? Go out and buy yourself a bottle of One Fuckin' Drop At A Time Hot Sauce. It comes with an eye-dropper for portion control. Benign masochism, indeed.Jason Goldman is a developmental psychologist and blogs at The Thoughtful AnimalFood sciencePsychologyFood & drinkNeuroscienceguardian.co.uk © Guardian News & Media Limited 2010 | Use of this content is subject to our Terms & Conditions | More Feeds guardian.co.uk |
If low serotonin levels aren't responsible for depression, what is? By studying the other effects that antidepressants have in the brain, we may arrive at more effective ways to treat depressionScicurious blogs at Neurotic PhysiologyWe've all seen the commercials. There's a sad little white marshmallow, a person in a darkened room unable to attend the party, or unable to enjoy a beautiful day. And then a voice shouts out that here is hope. That depression of yours is a result of imbalances in chemicals in your brain and, if you can correct those chemicals, you will feel better. Easy!It's not that these commercials sell you a pack of lies. Most antidepressants do increase the levels of chemical messengers in the brain called neurotransmitters. A specific type of neurotransmitter, the monoamines, appear to be the chemicals of choice for these drugs. Scientists once thought that simply increasing the amount of monoamines in the brain would treat the symptoms of depression. And that meant, of course, that depression itself must be caused by low levels of monoamines, particularly serotonin. For years, scientists have tried to find drugs that increase these serotonin levels in the brain safely, and tried to find evidence that decreases in monoamines are responsible for depression itself. Well, after much searching, we did find a lot of very interesting things. But some things just didn't add up.The first problem was one of time. If low serotonin levels were really what made you feel depressed, then increasing levels of serotonin should alleviate the symptoms right away. But antidepressants don't work immediately, and in fact can take more than a month to alleviate symptoms. Strike one.The second problem was one of whether the drugs actually worked. Serotonin-specific antidepressant drugs don't work on everyone. In fact, new estimates show that the current antidepressants on the market only work in about 60% of patients. If low serotonin levels were really responsible for depression, then increasing serotonin should have worked on more than 60% of patients. Strike two.The final problem is one of evidence. If low serotonin levels were responsible for depressed mood, then we should be able to induce depression in people by decreasing serotonin, and we should find low levels of serotonin in patients with depression. But neither of those things exist. Decreasing serotonin in humans can lower your mood, but it doesn't always work. And studies looking for low serotonin in depressed patients have been inconclusive. It appears that even though antidepressants increase serotonin, a lack of serotonin doesn't cause depression (kind of like aspirin treats a headache, but headaches are not caused by a lack of aspirin). Strike three. Serotonin is out.So what's in? After all, antidepressants do work in some patients. It's instructive to look at other things these drugs are doing in the brain.Antidepressants increase levels of neurotransmitters in the brain, but they also increase neurogenesis, the birth of new cells in the brain. Throughout your life, you will grow new neurons in an area of the brain called the hippocampus. And if you take antidepressants for several weeks, you will get increased neurogenesis. These new neurons correspond to changes in animal behaviours that are associated with long-term antidepressant treatment. The behaviours are novelty-induced hypophagia, which measures how much of a tasty food an animal will eat in a novel environment and reflects aspects of anxiety and anhedonia (the inability to experience pleasure); and the tail suspension test, which measures behavioural despair. Animals show improvement in both of these tests (eating more, or moving more) after long-term treatment with antidepressants, and these improvements correlate with neurogenesis in the brain.Not only that, if you make animals display signs of depression, you can reduce this neurogenesis, and you can reverse both the behaviour and the neurogenesis by treating them with antidepressants. Antidepressants may increase serotonin in your brain, but the alleviation of depression may be due to the long-term effects of the drugs on neurogenesis.The neurogenesis theory of depression fulfils many of the criteria that the serotonin theory did not. It takes the right amount of time to develop, the three to fours weeks that matches up with long-term treatment with antidepressants. We find reduced neurogenesis in animals and patients that display signs of depression. So far, we're two-thirds of the way towards an explanation. Many scientists are now examining the role of neurogenesis in depression, and looking for new targets to increase neurogenesis directly, rather than increasing neurotransmitters as the current drugs do.The role of neurogenesis in the potential treatment of depression is an exciting idea. But it is not flawless. Many studies cannot discern whether there are real changes in neurogenesis in humans with depression. Some studies show changes, but others do not.While traditional antidepressants do increase neurogenesis and relieve depression symptoms in some animal models, others show that neurogenesis and antidepressant behaviours are unrelated. Much of this debate comes down to the fact that we don't yet have a real understanding of neurogenesis, how it works, and how it is controlled both in normal brains and in the presence of antidepressants. Until we know, finding a truly effective antidepressant may remain out of reach. So while the monoamine/serotonin hypothesis for depression may be out, neurogenesis needs to step it up a little to make it in.Scicurious blogs at Neurotic PhysiologyPsychologyNeuroscienceDepressionMental healthHealthHealth & wellbeingguardian.co.uk © Guardian News & Media Limited 2010 | Use of this content is subject to our Terms & Conditions | More Feeds guardian.co.uk |
A Global Warming 'Work Party' Climate campaigners organize thousands of events aimed at limiting warming. feeds.nytimes.com |
Astronomers say they've found oldest galaxy so far By SETH BORENSTEIN 2010-10-20T21:17:28ZWASHINGTON (AP) -- Astronomers believe they've found the oldest thing they've ever seen in the universe: It's a galaxy far, far away from a time long, long ago.... hosted.ap.org |