It is well known that lifestyle changes can alter several physiological functions in the human body. For exercise and diet, these effects are used sensibly in basic therapies, as in cardiovascular diseases. However, the physiological changes induced by exercise and a modified diet also have the capacity to influence the efficacy and toxicity of several drugs, mainly by affecting different pharmacokinetic mechanisms. This pharmacological plasticity is not clinically relevant in all cases but might play an important role in altering the effects of very common drugs, particularly drugs with a narrow therapeutic window. Therefore, with this review, we provide insights into possible food–drug and exercise–drug interactions to sharpen awareness of the potential occurrence of such effects.

Introduction: Non-steroidal anti-inflammatory drugs (NSAID) are the most commonly used drugs for the treatment of pain, inflammation and fever. Although they are effective for a huge number of users, their analgesic properties are not sufficient for several patients and the occurrence of side effects still constitutes a big challenge during long term therapy. Areas covered: This review gives an overview about the first and second generations of NSAIDs (COX1/2 non-selective, COX-2 selective), and their main side effects which gave still an urgent need for safer drugs and for the establishment of novel treatment strategies (improved safety, tolerability, patient convenience). The current developments of a possible third generation NSAID class comprise changes in the formulation of already approved drugs, combination therapies, dual cyclooxygenase-lipoxygenase inhibitors, NO- and H₂S-releasing NSAIDs, prostaglandin synthase inhibitors and EP receptor modulators, respectively. Literature search has been done with PubMed NCBI. Expert opinion: Currently, there is no newly developed drug that is superior to the already approved selective and non-selective NSAIDs. Several novel approaches show promising analgesic efficacy but side effects are still an important problem. Solutions might be constituted by combination therapies allowing administration of lower drug doses or by individualized therapies targeting molecules apart from COX, respectively.

NEUROPATHIC pain is defined as pain initiated or caused by a primary lesion or dysfunction in the nervous system. It can arise from a wide variety of injuries to peripheral or central nerves, including metabolic disorders, traumatic injury, inflammation, and neurotoxicity, and is characterized by spontaneous pain, hyperalgesia (increased pain response to a noxious stimulus), and allodynia (pain elicited by a nonnoxious stimulus), which can persist long after the initial injury is resolved.1 Common causes of neuropathy are diabetes, herpes zoster infections, chronic or acute trauma, and neurotoxins. Furthermore, neuropathic pain occurs frequently in cancer as a direct result of peripheral nerve damage (e.g. , compression by a tumor) or as a side effect of many chemotherapeutic drugs.