Hunger and Pain

Hunger and pain are intimately intertwined. As discussed in last week’s post, weight has a significant impact on pain levels– just 10 pounds of extra weight increases the force on our knees by 30-40 pounds with every step. On ground level the force on our knees is 1.5x our body weight. And it’s worse on an incline. Losing those 10 pounds can decrease progression of osteoarthritis in the knees by 50%.

That makes sense. The bigger we are the more our joints have to carry. Of course part of the significant increase is due to the mechanics of carrying excess pounds and the inflammation caused by fatty tissue.

Amazing studies show that the perception of hunger and how we choose the foods we eat is also affected by chronic pain. In one study, structural changes in the nucleus accumbens within the brain’s limbic system was documented in participants whose pain had became chronic, possibly explaining the increased risk for obesity. In studies that followed acute, subacute and those progressing to chronic pain, values were assigned to different food groups. The value placed on high sugar and fat rich foods was only altered in the latter group. Meaning chronic pain itself impacts our desire to eat those specific foods and ultimately gain weight.

The limbic system is buried below the cerebral cortex above the brain stem. It comprises the:
* Thalamus and hypothalamus that produce hormones regulating thirst, hunger, mood.
* Basal ganglia that regulates the reward center, habit formation, movement and learning.
* Hippocampus is the center where all episodic memories are formed and catalogued for long term storage elsewhere, as well as giving us spatial orientation in order to navigate the world.
* Amygdala plays a pivotal role in our emotional responses, such as pleasure, anger, fear, and anxiety, and determines how strongly our memories are stored, especially those related to fear.

MRI scans showed that the area signaling the brain we’ve had enough food or caloric intake – the satiety center- uses the exact same pathways as those that stimulate chronic pain sensations. It’s postulated that once pain becomes chronic it actually changes how we see pleasure and alters our normal reward pathways.

Since the limbic system is also associated with emotions and motivation those struggling with chronic pain showed loss of motivation and decreased ability to feel pleasure- anhedonia. Brain scans consistently show altered activity within the limbic system as well as dopaminergic transmission- a significant neurochemical associated with motivation. A healthy accumbens is critically important in how we decide which foods to eat, assigning a value to the foods we choose. When pain becomes chronic and the accumbens is altered, we seek out higher fat, sugar and caloric contents to satisfy our hunger and continue eating far past survival needs because normal signals to stop are lost.

Another breakthrough study pinpointed that just 300 cells in the brain are responsible for prioritizing hunger over chronic pain sensations. They found that the need for nourishment and the sensation of pain reside within the same brain pathway. It makes intuitive sense that hunger and pain should be linked. We all need a steady nutritional diet to survive but knowing we are acutely injured is also imperative, so the brain prioritizes depending on the type of pain involved.

Acute injury is always allowed through to our consciousness but chronic inflammatory pain is not. At this point finding sustenance is the priority but knowing we’ve been injured and need immediate help is a close second. They were shocked to learn that turning on neurons that mediate hunger actually suppressed long term pain while still allowing immediate threats through.

In one experiment, mice who hadn’t been fed in 24 hours did not avoid a place where they had been exposed to inflammatory pain. Well fed mice and those that had been given an anti-inflammatory pain medication did. When researchers turned on neurons known to get activated by hunger, chronic inflammatory pain responses were minimized at the same time acute pain was not affected. They then found the exact neurotransmitter responsible for selectively blocking inflammatory pain- NPY.

When receptors for this molecule were blocked, hunger was reversed and pain returned.
This implies everything we feel isn’t sent routinely up to the brain for processing, but rather it is a part of a hierarchy that competes for attention. The possibilities for targeting this area for the treatment of chronic pain without impacting the crucial responses for acute injury are exciting.