You’ve just sat down for dinner. Tonight, it’s a bag of Cheetos, a 3-liter of Coke, and a large pizza. You know it’s bad for you. You know it, and yet you don’t do anything about it.
You’re at the gym. You have no real performance goals; you’re only here to look better. Your diet today has been a few sticks of celery, an apple, and a salad. You know that you shouldn’t run on the treadmill for two hours. You know it, but you do it anyway.
Congratulations, you’ve just experienced the action of endocannabinoids. Most neurosci research focuses on dopamine and opioids as the key regulators of reward-chasing and hedonic (pleasure-seeking) behaviors in the brain. But there’s plenty of evidence that endocannabinoids play their own role in signaling slothful, gluttonous, greedy, and other delectably sinful behaviors.
As with all neuronal activity in the brain, the endocannabinoids work in pairs of receptors and neuromodulating chemicals that affect said receptors. CB1, as we call this receptor, is the same place that tetrahydrocannabanol — THC, the most chronic of goodness to be found in marijuana — does what it does. CB1 makes its home in the basal ganglia and limbic system. If you’re not up on your brain anatomy, those are fairly primitive regions responsible for appetite, mood, motivation, and reward-seeking behaviors, among other things. Action and the decision to want or not want a behavior filters through here. This will make more sense shortly.
Despite some claims to the contrary, neurochemistry plays a huge role in the regulation of energy intake, appetite, and overall bodyweight regulation. For an overview, Boguszewski, Paz-Filho and Velloso have an excellent review paper here (full text courtesy of Viamedica, PDF format) discussing the neuroendocrine regulation of body weight.
I like review papers. This one is especially interesting for detailing the interaction between the brain, the body, and various environmental signals in regulating appetite and energy intake (which aren’t always the same thing), and thus worth a read. There’s a detailed section on the action of endocannabinoids which relates to the topic at hand. As the authors state:
The endocannabinoid system participates in energy homeostasis by central and peripheral actions that influence appetite, motivation for consumption of palatable food, production and distribution of fat, energy expenditure, and glucose and insulin homeostasis.
Endocannabinoids, the CB1-binding chemicals native to the brain, play a major part in this bureaucratic regulatory cascade:
CB1 is widely and abundantly distributed in tissues involved with energy homeostasis, including brain areas such as the hypothalamus, brain-stem, and mesolimbic region, and peripheral tissues such as the GIT, fat, liver, muscle, thyroid, and pancreas. The binding of endocannabinoids to CB1 receptors results in increased appetite, weight gain, lipogenesis, and lower insulin sensitivity. In the hypothalamus, endocannabinoids increase the production of orexigenic neurotransmitters and reduce the anorexigenic signals. In the reward centre of the mesolimbic region, they promote motivation to seek and consume palatable food, while in the brainstem they block the signals of nausea and satiety transmitted by the vagus nerve. Peripherally, endocannabinoids facilitate the absorption of nutrients in the GIT, stimulate lipogenesis and im- pair glucose uptake in muscles. Accordingly, CB1 knock-out mice are hypophagic, lean, insulin sensitive, and resistant to diet-induced obesity.
Eating, feeling good, the regulation of appetite, and obesity (including overeating behavior) can all trace back to this beastie. Is it any wonder that people can’t control themselves while swimming in a calorie-rich environment?
You may find this old knowledge, but a startling number of people don’t. Failure to understand the central regulation of body mass, appetite, and energy intake leads to things like believing in Low Carb Magic.
Hilariously enough, the authors point out that insulin, long blamed for over-eating by Low Carb Magicians, diminishes appetite through these regulatory pathways:
Several studies have shown that the central action of insulin promotes anorexia, increases energy expenditure, and reduces body weight.
In humans, the central anorexigenic effects of insulin are potentially important for the future development of insulin analogues with higher and faster hypothalamic signalling compared to their peripheral actions, in order to avoid the weight gain commonly observed in the treatment of diabetes.
You want to be hungry, eat bad food, and get fat. There’s just no arguing it. The solution involves the brute-force Eat Less approach, and it helps to add that with the Move More term. Our bodies want to get fat, and if we don’t apply deliberate behavior interventions, that’s exactly what they’ll do. To most people, avoiding unwanted weight gain involves major lifestyle changes and commensurate procrastination and excuse-making, although there are certainly possibilities to smooth over the process.
I realize that it’s not as simple as saying ‘stop eating so much, fatty’. It really doesn’t work that way, as much as we’d love that to happen. These neurological and hormone signals are powerful stuff — the endocannabinoid system is how cocaine and opium make you feel good and how they turn addictive (more here). There’s a lot of evidence that other addictive or compulsive behaviors use the same neuro-circuitry:
“Remarkably, rewarding behaviours activate the same brain circuits that mediate the positive reinforcing effects of drugs of abuse and of other forms of addiction, such as gambling and food addiction.”
There’s will power, and then there’s built-in unconscious programming that takes more than conscious effort. Making a change rarely is so simple as knowing what you need to do. There have to be motivational changes and situational changes to help the process along. If there is a power to low-carb diets, this would be it. You make it easier to eat less by staying more full and by keeping binge-inducing foods out of sight and out of mind. You get into a habit of being a healthier person and sticking to the changes you want to make.
No insulin-induced dysfunction of adipose tissue need apply.
Big surprise, but this also affects exercise behavior, thus explaining runners that won’t quit running themselves into the ground, or figure girls that won’t get off the treadmill while eating 800 calorie diets and wonder why they feel burnt to cinders. Destructive exercise behavior leads right back to these reward-seeking pathways.
Endocannabinoids are good, but this mindset of constantly chasing what feels good can lead you down dangerous roads. Your body’s feel-good machinery isn’t tuned to your goals of being fit and lean. The clichéd ‘listen to your body’ slogan doesn’t account for the possibility of self-sabotage.
The lesson here is that your body doesn’t always want what you — conscious, analytical, rational you — want to happen. If you want to make changes, you have to realize this and not only fight for physical changes, but work to change your mental frame of reference as well. Your psychology is part of your physiology.
I think there’s something to be said for understanding the real basis of the problem and equipping yourself for the hard slog ahead, rather than cutting carbs and hoping for the best. The same goes for training; sometimes less really is better. One model offers you a real understanding and a mechanism for troubleshooting. The other might as well be a scared ostrich with its head in the ground. Honesty equips you for the process. Honesty allows you to cope, and to troubleshoot accurately.
Knowing what you want, consciously, and working towards those goals with deliberate, intentional steps — including whatever motivational and situational steps may be required — is the way to success.
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