NSAID
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Dr. Rhonda Patrick makes her eighth appearance on the Joe Rogan Experience.
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Nutrition Alzheimer's Diet Microbiome Sleep Ketosis Omega-3 Fasting Micronutrients Multiple Sclerosis NSAID SaunaDr. Rhonda Patrick makes her eighth appearance on the Joe Rogan Experience.
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Inflammation and depression are often linked, particularly in older adults, who tend to experience chronic low-grade inflammation and elevated rates of depression. A recent study found that anti-inflammatory interventions may help reduce symptoms of depression and the risk of developing depression in older adults.
Researchers conducted a systematic review and meta-analysis of 31 randomized, placebo-controlled trials that assessed the effects of anti-inflammatory therapies on depression in older adults. The various anti-inflammatory agents included omega-3 fatty acids, nonsteroidal anti-inflammatory drugs, and plant-based compounds. The researchers included only trials with at least 20 participants.
The analysis revealed that anti-inflammatory treatments were more effective than placebos in reducing depression symptoms among older adults. On average, people receiving these treatments exhibited a moderate improvement in symptom severity compared to those taking a placebo. Omega-3 fatty acids and plant-based compounds, such as curcumin and soy protein, appeared particularly beneficial. There was also some evidence suggesting that these treatments might help prevent depression, although the results were not statistically conclusive.
These findings suggest that targeting inflammation is a promising strategy for managing depression in older adults, especially those with chronic inflammation. Learn more about links between inflammation and depression in Aliquot #36: Inflammation and Depression, part 2
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Can chronic use of anti-inflammatory agents paradoxically promote chronic inflammation through compensatory host response? pubmed.ncbi.nlm.nih.gov
NSAIDs may promote a paradoxical pro-inflammatory effect, increasing the risk of blood clots and cardiovascular events.
Non-steroidal anti-inflammatory drugs, or NSAIDs, are among the most widely used drugs worldwide, available in both prescription and over-the-counter forms, such as aspirin, ibuprofen, naproxen, and others. Despite the drugs' anti-inflammatory effects, their chronic use is associated with a higher risk of acute clot-related cardiovascular events, such as heart attack, stroke, or deep-vein thrombosis. Authors of a 2005 article posited that NSAIDs induce a rebound effect that promotes inflammation, driving the formation of blood clots and predisposing a person to acute cardiovascular events.
Inflammation is a protective response that involves immune cells, cell-signaling proteins, and pro-inflammatory factors. Acute inflammation occurs after minor injuries or infections and is characterized by local redness, swelling, or fever. Chronic inflammation occurs on the cellular level in response to toxins or other stressors and is often “invisible.” It plays a key role in the development of many chronic diseases, including cancer, cardiovascular disease, and diabetes. Inflammation initiates the clotting process and impairs the activity of natural anti-clotting mechanisms.
Most NSAIDs, with the exception of aspirin, dampen inflammation via the inhibition of cyclooxygenases, a family of pro-inflammatory enzymes. However, evidence from animal studies suggests that when these enzymes are inhibited, the body responds by producing more of the enzymes. The authors posited that by turning off the body’s natural inflammatory processes, NSAIDs might drive a compensatory response – ramping up the activity of pro-inflammatory pathways.
Lifestyle behaviors may reduce inflammation and the need for NSAIDs. For example, sauna use reduces levels of pro-inflammatory C-reactive protein and increases levels of anti-inflammatory protein interleukin (IL)-10. Similarly, cold exposure decreased the pro-inflammatory protein IL-2 and the inflammatory E2 series of prostaglandins while increasing the anti-inflammatory protein IL-10. Other lifestyle behaviors that may reduce inflammation include exercise, meditation, and dietary intake of polyphenols.
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New research may explain unexpected effects of common painkillers. www.sciencedaily.com
Some NSAIDs dampen inflammation by switching on the activity of Nrf2.
Non-steroidal anti-inflammatory drugs, or NSAIDs, are among the most widely used drugs worldwide, available in both prescription and over-the-counter forms. NSAIDs generally work by inhibiting the activity of cyclooxygenase, a type of enzyme that drives inflammatory processes. But because the drugs often elicit off-target effects, questions remain regarding other mechanisms that might be involved in their activities. A recent study demonstrates that some NSAIDs switch on the activity of Nrf2, a type of transcription factor.
Nrf2, or nuclear factor erythroid 2-related factor 2, is a cellular protein that regulates the expression of antioxidant and stress response proteins. It is an element of the Keap1-Nrf2-ARE biological pathway. Nrf2 activates the transcription of cytoprotective proteins that protect against oxidative stress due to injury and inflammation. Sulforaphane, a compound derived from broccoli and broccoli sprouts, is the most potent naturally occurring inducer of Nrf2.
Using cells from humans and mice, the investigators determined that various NSAIDs could induce the activity of GDF15 (a type of growth factor). This induction was dependent upon the activation of Nrf2. Then, using animal models of gout (an inflammatory disorder of the joints) and endotoxemia (a systemic inflammatory condition), they observed that the NSAIDs mediated the inflammation associated with the conditions and promoted Nrf2 gene expression. Deleting the Nrf2 gene in the cells canceled out the beneficial effects of the NSAIDs on gout and endotoxemia.
This study demonstrates a novel mechanism by which NSAIDs ameliorate inflammation and answers questions regarding some of their off-target effects. It also opens the door to future research on these commonly prescribed drugs.