We've all bitten into a jalapeno and experienced the slow burning pain that is associated with it. And whether you love it or hate it you've probably wondered why some people have a higher tolerance for spicy foods than others. The answer to that is two-fold.
To understand why we must first understand the mechanism through which capsaicin (the oily substance found in peppers which gives them their signature 'kick') works. Capsaicin targets a subgroup of sensory neurons called nociceptors. Prior research has shown that capsaicin excites these neurons by increasing the permeability of the plasma membrane to cations (K+, Na+ and Ca++ in particular) although it was unknown whether this was through direct disruption of the plasma membrane (capsaicin is hydrophobic and could thus perturb the phospholipids of the membrane)or though a ligand-system in which the molecule binds to specific receptors on the surface of the cell. The latter possibility was ruled more likely as capsaicin derivatives operate in dose-dependent manners highly characteristic of receptor activation via ligand binding. This was further supported through the use of resiniferatoxin, an extremely potent capsaicin analog derived from the plant genus Eurphorbia. This neurotoxin's extreme potency, eliciting responses at nanomolar concentrations, allowed scientists to assume that it bound with great affinity to the proposed capsaicin receptor. Using this, the molecule was radio labeled and researchers were able to visualize its binding to cell-surface receptors.
This provides the first the leg of the answer. The density of these receptors on an individual's nociceptors can influence the affect spicy food has. More receptors, more binding, greater response evoked.
An interesting side note...why do spicy foods produce a burning sensation? The specific receptors that capsaicin binds to are heat-gated receptors. These are analogous to our very well known voltage-gated channels but open is response to changes in ambient temperature and apparently capsaicin binding. This produces pain and the burning sensation that I for one love.
The second leg to our answer comes with a remarkably interesting point of immense pharmacological importance. Exposure to capsaicin initially excites a neuron leading to the pain response. However prolonged exposure (in this paper just a few hours) can cause cell death. Examination of dead cells revealed no evidence of DNA fragmentation meaning that no apoptotic events occurred. The actual cause of death was cytotoxicity caused by excessive ion influx, similar to the excitiotoxicity observed in TBI.
So as you can imagine eating spicy foods can actually kill these neurons, desensitizing your mouth to the pain a jalapeno can produce.
I did mention a pharmacological importance that is briefly covered by the authors, although they do not go into any sort of detail about it. In the opening paragraph they say that this nociceptor desensitization has lead to use of capsaicin as an analgesic agent in the treatment of n analgesic agent in the treatment of disorders ranging from viral and diabetic neuropathies to rheumatoid arthritis. While they do not elaborate on the mechanisms of this we can assume that these diseases cause pain through stimulation of these same nociceptors.