Mammals have an adaptive advantage in seeking fat-rich foods, which are nutritionally essential but scarce in most natural habitats. This innate preference can become maladaptive, however, when it is not limited by environmental constraints. The unrestricted availability of fatty foods, in diets of industrialized societies is a factor for obesity, diabetes, and cardiovascular disease.

Why is fat so rewarding? How is it that fat consumption is rewarded? What reward system can we identify?

In short, it was scarce during evolutionary times, though not now. Within the constraints of reproduction, a biological system will always act to reduce oxidative stress and conserve energy. However, acquisition of energy, growth, repair, movement and resistance to infection are all associated with oxidative stress; this is why redox (reduction oxidation state) must have evolved as part of the normal signalling process.

It seems that there is a positive feedback reward system that involves endocannabinoids (endogenous opioids) as signals that makes one like fatty foods.  The taste or presence of fat stimulates the endocannabinoids 2-AG and anandamide in the rat small intestine. The sensory properties of fat stimulate oral sensors that stimulate further intake once fat is tasted. The rat even develops a preference for the place it found the fat. Oral intake of fat stimulates release of dopamine, which is a reward signal in a part of the brain called the ventral striatum.

Small-intestinal levels of endocannabinoids 2-AG and anandamide rise during food deprivation and fall upon refeeding, which suggests they may signal energy imbalance and promote caloric intake. A fat-rich diet modifies intestinal endocannabinoid levels.

When the food environment contains scarce sources of fat, a positive feedback control system seems to have developed to encourage fat consumption in order to maintain life. For humans, the drive may be strong because of the needs of the nervous system for energy and fatty acids. The endocannabinoid uses oxidative stress to ensure survival by functioning as a driver of energy acquisition. It also has anti-inflammatory properties. It is this dual role of oxidative stress that is the issue; one insures food acquisition through movement, the other promotes inflammation. The brain is both a heavy energy user and highly susceptible to oxidation.

Fat stimulates reactive oxygen species (ROS) that signal through out the body. In turn, fat shifts metabolism toward fat oxidation in the mitochondria, which reduces ROS production.

The endocannabinoid system (ECS) was only ‘discovered’ in the 1990s. The ECS is a homeostatic system, which integrates energy seeking and storage with resistance to oxidative stress. The ECS may induce our evolutionarily conserved form of mild insulin resistance to become an inflammation-driven insulin resistance when fat becomes readily available. Lipotoxicity from excessive fat consumption promoted by our ECS reward system can overcome our ROS protections and that can tip us from mild insulin resistance to a pathological form inflammation-driven insulin resistance and metabolic syndrome.

So, inflammatory insulin resistance may be an adaptation to resist oxidative stress when we consume so much fat that we develop lipotoxicity. The tipping point into the metabolic syndrome may result from a chronic lack of physical activity, which results in reduced mitochondrial function and a reduced capacity to clear lipids. This will result in increased visceral adipose tissue volume, abnormal ectopic fat content and systemic inflammation.

I am sorry it has been so difficult to distill this hypothesis from the poorly written, but novel, paper I drew some of this from. Let me try to relate the essence of the hypothesis.

The reward system for fat consumption is an evolutionary adaptation the promoted survival during time of fat scarcity. It rewards fat intake with a positive feed back loop that involves ROS signalling, endogenous opioid signalling and by releasing dopamine. The ECS system also signals a system that up regulates systems that protect against ROS. Excessive fat consumption can become so rewarding that it overwhelms oxidative protection through lipotoxicity. The systemic inflammation that results can tip the protective, evolutionarily acquired mild insulin resistance into a pathological, inflammatory form of insulin resistance.

So long as you consume adequate fruits and vegetables on you high-fat Paleo diet and remain active, you may not develop an inflammatory lipotoxicity that leads to the pathological form of inflammatory insulin resistance. The fruits and vegetables consumed in a Paleo diet may limit the inflammation that a high-fat diet tends to promote. Your activity will also protect you because it increases mitochondrial density and function so the mitochondria can clear the fats you consume. The problem that may occur is in your ability to resist fats because you may develop a powerful positive feedback loop in your ECS that rewards fat intake powerfully.

The power of the reward system and limits in antioxidant capacity may lead some high-fat consumers to develop an inflammatory form of insulin resistance.

I tend to limit my fat intake and to promote my anti-inflammatory defenses by taking Guardian. Its Ultra-thione is the ultimate balancer of your ReDox state.