I’ve written many times about the outside factors that can influence movement (musculoskeletal) pain. How sleep directly correlates with pain, how our thoughts can change how we physically feel, and how social interactions can influence our bodies (let alone other variables). One outside factor that comes up again and again, and seems consistent with my patients, is diet.
Diet is a huge factor for overall health. Specifically, an inflammatory diet can lead to all sorts of musculoskeletal problems such as tendinopathy and osteoarthritis (among other things).
I recently shared a study that showed it was the biomarkers of inflammation and poor diet that correlated with osteoarthritis, not weight..
James Crownover, MD has written a 3 part article series that wonderfully summaries the research and theory on how a high carb diet can increase our body’s inflammation and lead to osteoarthritis and tendinopathy. I would recommend spending some time reading these articles, but for those that aren’t comfortable reading medical articles or don’t have the time, I’ll summarize them below.
The overall take home point in all the articles is that we need to reduce our carbohydrate intake and exercise (strengthening) more.
High body-fat (specifically abdominal) and high blood glucose are associated with increased risk of tendon pathologies.
“Tendons of diabetics are thicker, have more disorganized ECM, and more aberrant calcification which increases the risk of tears [11-14]. The tendons are mechanically different with increased stiffness and decreased elasticity [13, 15, 16].
“...[hyperglycemia] leads to an accelerated accumulation of advanced glycation endproducts (AGE’s), collagen cross links and elevated systemic inflammation with oxidative stress [17, 18]. The heightened inflammatory state further accelerates collagen cross linking in a feed forward cycle of damage .”
“Reducing simple processed sugar and acellular carbohydrate intake will likely reduce the accumulation of AGE’s and therefore reduce the associated collagen cross linking, inflammation and oxidative damage”
Improving diet with low glycemic index food and a lower carbohydrate diet may improve tendon health
Green tea, tumeric, and glycine-rich foods may also help
High body-fat (specifically abdominal), systemic inflammation, and metabolic syndrome are associated with increased risk of arthritis/osteoarthritis
Poor diet and high fat content is associated with low-grade systemic inflammation
“Chronic systemic low grade inflammation plays an important role in OA pathophysiology [17, 18]. Fat tissue can be considered to be an endocrine organ that secretes pro-inflammatory cytokines such as TNFα and IL-1β as well as hormones called adipokines, all of which are implicated in OA pathophysiology [19-21].”
“The disruption of leptin signaling appears to be a major link between metabolic dysfunction and osteoarthritis.”
Sarcopenia (loss of muscle mass due to aging) is prevelant in the aging population and further increases the risk of osteoarthritis. But not just because of aberrant forces and less shock absporption. Muscles too have an endocrine role. Thus body composition (muscle mass to fat mass ratio) plays an important role, not just overall weight.
“ Muscle tissue (especially type II fibers) is highly metabolically active. It helps maintain insulin sensitivity, lower blood glucose, and increase one’s metabolic rate. It is also known to release some anti-inflammatory proteins called myokines.”
“It has been suggested that the myokines released from healthy muscle interact with your joints, and there are multiple studies demonstrating anti-inflammatory effects. Other studies suggest that certain myokines promote cartilage cell growth. Overall, it appears that myokines released by healthy muscles are joint protective .”
Insulin resistance (part of metabolic syndrome) is a problem for the joints
“It is important to understand that there are insulin receptors on the synovial lining of our joints...In the presence of [insulin] resistance, Insulin loses the ability to block these destructive TNFα pathways, suggesting that its protective role is diminished .”
NLPR3, when over-active, is a main driver for arthritis, osteoarthritis, and degenerative disk disease, rheumatoid arthritis, and gout
“In arthritis, over-activation of [NLRP3] results in over-production of inflammatory cytokines  and cartilage degrading proteins, leading to rapid chondrocyte (cartilage cell) death, breakdown of Type II Collagen, and the development of osteophytes (bone spurs) [6-9].”
“ It has been shown that NLRP3 expression was increased 5.4 fold in the synovial membrane of patients with knee OA . It appears that inflammation of the synovium is associated with dysregulated NLRP3 resulting in elevated inflammatory mediators within the joint and cartilage [3, 11]. This may suggest that synovitis has a causal role for cartilage degeneration. “
“In a 2016 study, patients with chronic lower back pain and degeneration of vertebral endplates seen on MRI’s, had significant up-regulation of NLRP3, caspase-1, and IL-1B within the cartilaginous endplate of the vertebrae compared to those with acute injuries .”
Ketones (released from being in a state of ketosis) block the NLRP3 pathway
“The ketone body, beta-hydroxybutyrate (BHB), strongly inhibits the NLRP3 infammasome pathway ! BHB was shown to reduce NLRP3 mediated inflammatory cytokine (IL-1B and IL-18) production in HUMAN monocytes .”
Metabolic syndrome increases pain sensitivity. Fasting, calorie restriction, and ketosis may decrease pain by modulating adenosine and NLRP3.
“Like anticonvulsant medications, it is well established that the ketogenic diet is effective at reducing seizures. Also similar to anticonvulsants, the ketogenic diet partly works by decreasing neuron excitability [8, 9]. Since there are some similarities in their mechanism-of-action, it is reasonable to hypothesize that the ketogenic diet may also be effective at reducing pain; especially neuropathic pain.”
“Fasting and caloric restriction have been shown in animal studies to result in significant reduction in pain sensitivity regardless of the pain source (thermal, chemical, cutaneous, or visceral). This appears to act via activation of endogenous K-Opioid pathways which block pain signals centrally in the spinal cord [10, 11].”
“The neuromodulator, adenosine, has been shown to decrease pain levels [12, 13] and appears to be involved in acupuncture’s beneficial effects [14, 15]. High-intensity exercise in an animal model has been shown to significantly reduce neuropathic pain by activating the adenosine pathways . Fasting and the ketogenic diet both increase adenosine levels, presenting another potential pathway for improved pain control with these tools [17-21].”
“The ketone body, beta-hydroxybutyrate (BHB), strongly inhibits the NLRP3 infammasome pathway ! BHB was shown to reduce NLRP3 mediated inflammatory cytokine (IL-1B and IL-18) production in HUMAN monocytes ...In a rodent model for gout, Rats fed a Ketogenic Diet were significantly protected from IL-1B elevation, knee swelling, synovial inflammation, and joint necrosis when compared to the control group, and this was by direct NLRP3 and IL-1B inhibition .”
And finally, no one ever died from carbohydrate withdrawal or ketone overdose, but many are dying from opioid overdoses...
These topics need to be studied further, but there is enough studies to show a strong correlation. Thus, altering diet should be a strong consideration for those who have musculoskeletal pain. Especially those who have not found any relief from traditional pharmaceutical and medical interventions.
However, don’t do any drastic changes. Starting with simply reducing added sugars, simple carbohydrates, and processed carbohydrates may be a good start. It’s best to speak to your primary care physician or licenced dietician first.
For more information check out Dr. Crownover’s website.