인스턴트식품 ‘중독’ 사실이다
인스턴트 식품이 “중독성”이 강하다는 사실을 입증하는 새로운 연구결과가 나왔다.
미국 스크립스 연구소(Scripps Research Institute)의 폴 케니(Paul Kenny) 박사는 베이컨, 소시지, 치즈케이크 등 지방과 칼로리가 높은 인스턴트 식품이 마약처럼 뇌의 핵심 보상중추를 지나치게 자극, 쾌감을 유발함으로써 먹지 않고는 못 견디는 강박섭식장애(compulsive earing disorder)를 일으킬 수 있다고 밝힌 것으로 AFP 통신 등이 28일 보도했다.
케니 박사는 쥐실험에서 이 같은 사실이 밝혀졌다면서 인스턴트 식품에 중독된 쥐들은 기분나쁜 전기충격을 가해도 인스턴트 식품을 뿌리치지 못했다고 밝혔다.
그의 연구팀은 정상적인 먹이로 길러진 쥐들에 인스턴트 식품을 주기 시작하자 입맛이 바뀌면서 하루 종일 주는대로 인스턴트 식품을 먹어댔으며 몸무게는 점점 불어났다.
이들은 다리에 전기충격을 가해도 아랑곳없이 먹어댔다. 균형된 먹이만 주고 인스턴트 식품은 거의 주지 않은 다른 쥐들은 전기충격을 가하자 먹이를 포기했다.
더욱 놀라운 것은 인스턴트 식품을 끊고 정상적인 먹이를 주자 단식투쟁이라도 하듯 2주 동안이나 먹기를 거부했다.
연구팀은 인스턴트 식품으로 뚱뚱해진 쥐들의 뇌를 살펴 본 결과 코카인, 헤로인 중독과 관련이 있는 것으로 알려진 도파민2 수용체(D2R)가 줄어 있었다.
코카인 사용자는 처음엔 도파민2 수용체의 과도한 자극으로 쾌감을 유발하는 신경전달물질 도파민이 과다분비되지만 시간이 가면서 우리 몸은 이에 적응하기 위해 도파민2 수용체의 활동을 줄이게 된다.
이처럼 뇌의 “보상반응”이 줄어들면 코카인 사용자는 더 자주 코카인을 투여하고 투여량도 늘리게 돼 결국 중독상태에 빠져든다.
비만도 마약중독과 마찬가지 메커니즘에 의해 비만상태가 오래 계속되면 도파민2 수용체가 줄어들면서 점점 더 많이 먹게되는 강박섭식장애로 이어지게 되는 것으로 보인다고 케니 박사는 설명했다.
도파민2 수용체는 신경세포 표면에서 도파민과 결합하는 곳이다. 도파민은 섹스, 음식, 마약에 의해 분비되는 쾌감유발 신경전달물질이다.
이 연구결과는 영국의 과학전문지 ‘네이처 신경과학(Nature Neuroscience)’ 온라인판(3월28일자)에 실렸다. (서울=연합뉴스)
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Junkies and junk-food addicts share craving mechanism
출처 : AFP Mar 28 2010
PARIS (AFP) – The same molecular pathways that steer people into drug addiction also lie behind the craving to overeat, driving individuals into obesity, a new study suggests.
The research, based on lab animals, bolsters long-standing suspicions that addiction to pleasure stems from overstimulus of a key reward mechanism in the brain, its authors say.
Publishing online in the journal Nature Neuroscience, scientists at the Scripps Research Institute in Florida fed rats high-fat, high-calorie treats — bacon, sausage, cheesecake and so on — and watched the rodents bulk out dramatically.
The junk-food rats gobbled down twice as many calories as “control” rodents fed on a more balanced diet.
“When we removed the junk food and tried to put them on a nutritious diet — what we called the ‘salad bar option’ — they simply refused to eat,” said Paul Kenny, an associate professor.
“The change in their diet preference was so great that they basically starved themselves for two weeks after they were cut off from junk food.”
Even when the scientists threatened the rats with an electric shock, the animals continued to overeat, a clear sign of uncontrolled behaviour.
Having shown that obese rats were addicted, the next step was to explore how this happened in the brain.
Kenny and graduate student Paul Johnson focussed on a docking point, or receptor, on the surface of neurons that binds to a “feel-good” brain chemical called dopamine.
Dopamine is released by pleasurable experiences such as sex, food and narcotics.
Previous research found that among cocaine users, the brain becomes flooded with dopamine and overstimulates the so-called dopamine 2 receptors (D2Rs).
The overstimulation causes the body to adapt by decreasing the activity of the D2Rs.
As a result, there is a progressively worsening “reward response,” or uptake of the pleasure-giving chemical in brain cells.
The cocaine user needs more and more frequent stimulation from the drug to avoid entering into a persistent state of negative reward — in other words, he quickly goes on the slippery slope from casual to compulsive drug-taking.
Similar changes in the D2Rs occur in the food-addicted lab rats, the study found.
“These findings confirm what we and many others have suspected, that overconsumption of highly pleasurable food triggers addiction-like, neuroadaptive responses in brain reward circuitries, driving the development of compulsive eating,” says Kenny.
“Common mechanisms may therefore underlie obesity and drug addiction.”
The research has yet to be conducted among humans, but when it was unveiled in its early stages at a conference last October, it prompted nods of agreement from obese people who said they had always argued that bingeing on sweet or fatty foods was an addiction.
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Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats
Paul M Johnson, Paul J Kenny
출처 : Nature Neuroscience (28 March 2010) doi:10.1038/nn.2519 Article
http://www.nature.com/neuro/journal/vaop/ncurrent/abs/nn.2519.html
We found that development of obesity was coupled with emergence of a progressively worsening deficit in neural reward responses. Similar changes in reward homeostasis induced by cocaine or heroin are considered to be crucial in triggering the transition from casual to compulsive drug-taking. Accordingly, we detected compulsive-like feeding behavior in obese but not lean rats, measured as palatable food consumption that was resistant to disruption by an aversive conditioned stimulus. Striatal dopamine D2 receptors (D2Rs) were downregulated in obese rats, as has been reported in humans addicted to drugs. Moreover, lentivirus-mediated knockdown of striatal D2Rs rapidly accelerated the development of addiction-like reward deficits and the onset of compulsive-like food seeking in rats with extended access to palatable high-fat food. These data demonstrate that overconsumption of palatable food triggers addiction-like neuroadaptive responses in brain reward circuits and drives the development of compulsive eating. Common hedonic mechanisms may therefore underlie obesity and drug addiction.
