Inflammation and Low Back Pain: What's Really Happening? | Podcast Ep. 256

They were looking previously at herniated discs or discogenic pain. There's an imbalance that seems to push forward the presence, I guess you could say, or expression, as they say, of inflammatory mediators. An imbalance in the inflammatory cytokine network has been suggested for one of the processes in degenerative joint disease and a shift towards pain. Perceptible inflammatory cytokine profiles have been reported in people with painful neuropathies. So what does that mean? Well, that imbalance, right, between catabolic and anabolic processes leads to a greater expression of inflammatory mediators. What they're seeing is that there's the potential for these cytokine imbalances, these networks, as a potential cause for degenerative joint disease. It starts to get really, really interesting when we start to be able to peel back. I know we look at degenerative joint disease. We say, well, how does that happen? It happens due to, influenced by previous injuries, influenced by aging, influenced by inflammation, chronic inflammation. These are influenced by genetics. Right. There's a lot that goes in to influence the advancement of degenerative joint pain. In the show notes, you can get access to where this paper lives on PubMed and it was published by Clinical Pain in October 2019. So what were they looking at? They were looking at the inflammatory profiles of patients with acute and chronic low back pain. And basically they were saying, is there a profile number one? And then number two, is there a difference in profiles between acute pain and between chronic pain? So this is a really interesting study, really novel, and the first time anybody's really taken a look at it. So previously, several studies have reported on the possible involvement of inflammatory cytokines in cohorts of low back pain pain patients. Now, systematic levels of inflammatory markers, including interleukin 6, tumor necrosis factor TNF or C reactive protein were found to be elevated in diverse groups of low back pain patients. So basically, previous studies, take a look, they said what's going on with cytokines and specifically what's going on with interleukin 6, what's going on with this TNF, the tumor necrosis factor alpha and what's going on with C reactive protein. And they found all of these to be elevated in different groups of low back pain patients. So that's interesting to begin with because we're talking about mechanical low back pain. So the interactions of pro inflammatory and anti inflammatory molecules within the inflammatory MILU are pretty complex. And this is where, when we start really geeking out and diving in to these specific chemical markers, sometimes almost Paradoxes tend to show themselves. So we'll look at more of that as we continue to dive in. But investigations into pain mechanisms and spinal pain patients with herniated discs and those with discogenic pain have suggested an imbalance of catabolic and anabolic processes leading to an increased expression and inflammatory mediators. So it's this imbalance between these catabolic processes and these anabolic processes. When somebody's in pain, specifically in this case, they were looking previously at herniated discs or discogenic pain, there's an imbalance that seems to push forward the presence, I guess you could say, or expression, as they say, of inflammatory mediators. An imbalance in the inflammatory cytokine network has been suggested for one of the processes in degenerative joint disease and a shift towards pain. Perceptible inflammatory cytokine profiles have been reported in people with painful neuropathies. So what does that mean? Well, that imbalance, right, between catabolic and anabolic processes leads to a greater expression of inflammatory mediators. Now, what they're seeing is that there's the potential for these cytokine imbalances, these networks, and as a potential cause for degenerative joint disease, then it starts to get really, really interesting. We start to be able to peel back. I know we look at degenerative joint disease. We say, well, how does that happen? It happens due to, influenced by previous injuries, influenced by aging, influenced by chronic inflammation. These are influenced by genetics. Right. There's a lot that goes in to influence the advancement of degenerative joint disease. And they're saying, hey, this cytokine network and the balance between catabolic and anabolic process processes and inflammatory mediators might have a major role to play with that. More to come on that with future research, but super, super interesting to start. Now, this research paper took cohorts or people with low back pain and they split them up. Acute back pain and chronic low back pain. And they looked at these inflammatory mediators. So compared with asymptomatic controls, baseline levels of TNF, tumor necrosis factor and interleukin 1 and 6 were all significantly increased in both groups of low back pain patients. So they found, hey, interleukin tnf, if you have back pain, these are probably elevated. However, in patients with acute low back pain, IL2 production was noticeably augmented by over 30%. So again, Interleukin 1 and Interleukin 6 raised for everybody. Interleukin 2 only raised for those acute low back pain patients. And when compared with both the asymptomatic control and patients with acute low back pain. Production of Interleukin 1 RA was significantly increased in patients with chronic low back pain. So interleukin 2 elevated. Acute low back pain. Interleukin 1 RA significantly increase in patients with chronic low back pain. TNF, IL 1, IL 6 raised with everybody. So we're getting into the nitty gritty of a lot of technical data here, but I think it's important to know and understand the differences in how a patient expresses how their body's expressing at a, you know, a chemical level, the pain that they're experiencing. Now, in both low back patient groups, the production of Pro inflammatory cytokines, TNF, IL1, IL6 was significantly elevated. We just went over that and that of an anti inflammatory cytokine, IL10 significantly reduced when compared with the asymptomatic control. So there's an anti inflammatory cytokine which is IL10. If this is not confusing enough. So there's an interleukin that's anti inflammatory and that was down when compared with asymptomatic, which makes sense, right? There is inflammation going on. So the anti inflammation cytokines, that is down, that's that imbalance. As we spoke of earlier, some of these ILS are way up, the pro inflammatory ones, some of them are weighed down. The anti inflammatory, that's the imbalance that leads to the expression of pain potential for degenerative joint disease further down the road. So the principal differences between acute and chronic low back pain cohorts were basically these three things. Number one, the production of TNF and two anti inflammatory mediators, IL1 and TNFR2 were significantly augmented in the chronic low back pain group relative to the acute low back pain group. So that's number one. Number two, let me find number two here. Make sure I get this straight. In the acute low back pain cohort, the production of CD4 derived anti inflammatory cytokines, IL2 in INF were altered. Relative to the chronic low back pain group, the production of IL2 increased markedly by over 30% resulting in a significant increase in the ratio of IL2 to IL10. Again, IL2, excuse me, pro inflammatory, IL10, anti inflammatory. And then number three, possible positive correlation between self assessed pain level. VAs and IFN levels were found in patients with acute low back pain where TNF and IL1 production levels correlated positively with VAS scores in patients with chronic low back pain. So this is where it gets interesting as well. So we just went through a lot of pretty good geeky stuff. On ILS 1, IL 10, IL 2, TNF, et cetera, you can get lost in that stuff. But the takeaway message is that these things have been correlated to pain levels, so it matters. And furthermore, you could almost reverse engineer, so to speak, or think about, hey, if I have a patient with acute pain, acute low back pain, or if I have a patient with chronic low back pain, I can make an inference that they might have these type of things going on. Increase in IL, decrease in, you know, an IL 10. You can infer what's going on based upon the pain levels of the individual. So how do we bring this to clinical practice? That's a good question, right? I think there's a lot to be said in terms of supplementation, there's a lot to be said in terms of the food we eat. There's a lot to be said in terms of the mind body connection and how we think influencing how our body expresses inflammation and how we express inflammatory mediators. There's a lot to be said for all of that. But before we get there, we have to start with what we know today, which is exactly what we just went over by identifying the inflammatory profiles, those individuals who have chronic pain and those individuals who have acute pain and the commonality between the two. Because as we saw at the beginning of this episode, there are some common things that happen, whether it's acute pain or whether it's chronic pain. There are some inflammatory profiles, inflammatory mediators that go up or go down, anti inflammatory mediators go down, pro inflammatory mediators go up when somebody is dealing with pain. So a lot of geeked out biochemical type stuff going on on this episode. But keep in mind, when you're seeing patients in pain, there is a lot that is going on. And even in this age of quote unquote non specific low back pain, and we can't find the etiology of nonspecific low back pain. Every time I see that, I almost question it to a certain degree because I start to think to myself, I see a ton of research around non specific low back pain. Now what is the exact cause that can be varied. But there is no question at this point in time that research over the last 5, 10, 15 years has advanced our understanding of what happens when somebody's deep dealing with nonspecific low back pain to a level that's never been seen before. We can now understand what are the potential challenges that showcase themselves as nonspecific low back pain. Could be a facet challenge, could be a disc challenge that hasn't reached a certain point to be qualified or quantified as a disc bulge or disc herniation, it could be degenerative changes and modic changes that are early on, as we talked about on last week's episode with the MRI findings, there's almost that bell shaped curve right where people very, very early on, quote, unquote, totally normal, not at skeletal maturity. No injuries. Things are looking good, but when changes just start to happen, you might even be imperceptible on some imaging, but they're just starting to happen. That's actually the time that we see the most, the highest likelihood of pain. If somebody's dealing with pain, they're dealing with these inflammatory profiles, inflammatory changes that we talked about today. And then of course we see the bell shaped curve slide down the other side where we see crazy advanced changes on an mri and it almost self stabilizes due to bridging osteophytes or whatever the case may be, and pain tends to decrease. So keep in mind all of these things are going on with your patient at all times. Our bodies are dynamic. That's the beauty of it. But that's also the challenge of it. When we're going about taking care of individuals, sometimes it seems like there is no rhyme or reason. And that I think is because our bodies are so dynamic. Our pain perceptions are different, our expression of pain is different. Our expression and I guess experience of degenerative changes of aging is just so varied person to person. But when we look at inflammatory mediators, I think back to inflammation, chronic inflammation, what we do, how we eat, the lifestyle factors that we go through each and every day, I have a feeling we're going to see continue to play more and more of a role. How are you moving your body? How are you thinking? What are you putting in there for fuel, AKA food? And how are you going about the proactive steps you need to be healthy? These are the things that matter. And small changes, small habits early on in life can pay big dividends later on down the road. And unfortunately, the same thing happens on the opposite end where bad habits, bad eating, chronic inflammation. This can lead to challenges and I think we're gonna continue to learn more about as time goes on. So that's a lot on inflammatory profiles and inflammatory mediators. If you have any questions, feel free to shoot me an email, Jeff, the evidencebasedchiropractor.com, i'll do my best to answer, so check out next week's episode of the podcast. Be sure you are subscribed if you're just tuning in for a one off. Subscribe to this podcast. We deliver research and marketing and the time it takes to get to your office each and every week. 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