Fatty food may cause addictive behaviour by affecting the dopamine system in the brain
Researchers at The Scripps Research Institute in Florida have found that fatty food may act on the brain in a similar fashion to cocaine and heroin, affecting the dopamine receptors and causing addition, albeit in a milder manner than those drugs.
In experiments with obese rats (which behave quite similarly to humans when it comes to food intake and obesity) the researchers have discovered compulsive feeding behaviour in obese rats (but not in lean rats) due to the down-regulation (desensitization) of their dopamine D2 receptors. Dopamine is the brain chemical responsible for reward, pleasure and excitement, and down-regulation of dopamine receptors in the brain has been reported in humans addicted to drugs.
In fact, total desensitization of the dopamine D2 receptors rapidly accelerated the development of addiction-like behaviour and the onset of compulsive food seeking in rats who had free access to high-fat food.
The researchers concluded that over-consumption of palatable food triggers addiction-like adaptive responses in the brain reward system and drives the development of compulsive eating. Common pleasure-seeking mechanisms may therefore underlie obesity, just as in drug addiction.
Boost your natural dopamine production by changing your priorities in life
Similar effects have been demonstrated a few months ago in relation to the also highly palatable sugary foods. The notion that palatable food causes addiction by affecting the pleasure-reward system in the brain means that to fight obesity (and consequently cellulite) you need to ensure that there are aspects in your life other than fattening food (or other sources of instant yet temporary gratification, such as smoking, drinking etc.) that provide you with enough satisfaction so that you do not become addicted to sugar, fat, smoking, alcohol or drugs.
This is understandably quite difficult today, as we are forced to seek even more instant gratification due to our unrewarding, artificial and stressful lifestyle, but it is not impossible. All that is needed is a little re-prioritisation. Having meaningful personal, social and community relationships, being in contact with nature, exercising regularly, developing a healthy interest in music, culture or other interests, practising meditation, and setting achievable, rewarding goals are some strategies to increase life satisfaction (and dopamine production), so that you do not need to resort to fat and sugar for temporary satisfaction and behave like those laboratory rats. Keeping fat gain (and cellulite) at bay will then become an effortless task that does not require discipline and hard work.
Boost the palatability of low-calorie food to enjoy it without weight gain and cellulite
Boosting the palatability of food with herbs and spices offers you double benefits: it makes the food more tasty without the addition of fat, sugar and salt, and helps improve your health and beat cellulite thanks to the health-boosting and anti-cellulite effects that most herbs and spices possess.
Consuming high-fat oily fish such as salmon, sardines, mackerel, halibut and trout, not only satisfies your fat-seeking urges in a healthy way but also helps you reduce fat and cellulite. Highly unsaturated fatty acts (HUFA) found in fish oil/oily fish have been proven to help you lose weight.
Finally, exercise not only boosts your dopamine levels but also helps you spend excess calories, improves your overall health, raises your energy levels and provides you with valuable mechanical stimulation that keeps cellulite at bay. Interval training is the most rewarding type of exercise and ideal for cellulite reduction and prevention.
- Paper: Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats.
- Abstract: 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.