Is back pain and muscle soreness an inevitable consequence of intense physical activity and getting older?
I don’t believe so. The conclusion of my recent research and personal experience is that back and muscle pain can largely be prevented and reversed. (Caveat: This article is about pain that originates in muscles and connective tissue — I will not address pain due to disc herniation, spinal stenosis, degeneration, infection or cancer).
By implementing a few key strategies over the past year, I’ve almost eliminated the sore muscles or back pain that I used to experience after a long run or heavy workout. I’m able to quickly recover with little downtime. And I do it without resorting to anti-inflammatory medicines, icing, massage, stretching or many techniques that are commonly recommended to reduce or prevent pain and soreness. As I’ll show, a combination of specific exercises and dietary interventions can great help reduce and immunize you against back pain and muscle soreness.
This article is one of my longer ones, because I had to synthesize a broad spectrum of information into a coherent perspective on muscle pain and its prevention. I hope you can stick with me or read it in bite sized pieces. I will break it into four parts. If you just want my recommendations, skip to Part 4. For those who want to understand the science, read on…
Part 1. The biology of pain
Part 2. Exercise for pain prevention
Part 3. Diet for pain prevention
Part 4. Recommendations
PART 1. THE BIOLOGY OF PAIN
What is pain? A closer consideration of the biological mechanisms underlying pain, soreness and stiffness reveals some unexpected but very effective ways to prevent, reduce and more quickly recover, without relying on pain killers or anti-inflammatory medications.
Let’s start by considering what causes pain in the first place. Some types of chronic pain occur in the central nervous system, but most back and muscle pain is sensed by nociceptors — pain receptors — that are widely distributed in muscle tissue, fascia (connective tissue), joints and the spine. The nociceptors nerve endings are exquisitely evolved to sense chemicals that signify one thing: tissue damage. As unpleasant as pain is, it serves an important biological function. People with impaired nociception (pain detection) are vulnerable to continued injury that can quickly become life-threatening.
Here is a diagram of a muscle nociceptor from an anatomy text by Mense. You’ll notice that there are numerous receptors on the surface that respond to the binding of a diverse range of sensitizing biochemical signals that either activate or inhibit pain signaling. A number of the pain activators are specifically released or derived from damaged muscle cells (such as the prostaglandin PGE-2, the inflammatory cytokines IL-6 and TNF-alpha, the energy molecule ATP, the neurotransmitter serotonin, sodium or potassium ions, or receptors that respond to low pH) or damaged blood vessels (such as bradykinin (BKN). Likewise, there are receptors for pain inhibitors that dial down the pain or increase pain tolerance, such as opioids:
For the purposes of this blog post, it’s not important to understand the details of the biochemistry. The key point to remember is that pain receptors respond to chemical signals that stem from tissue damage.
The basic unit of a muscle, the sarcomere, is composed of cells known as myocytes. Injury or overstressing of muscles or other tissue is actually a cellular event: The myocytes literally burst. At the biochemical level, the bursting of cells means rupturing of the thin phospholipid bilayer membranes that surround the outside of the cell, separating the internal cytoplasm from the outside environment. There are also similar membranes inside the cell that isolate the mitochondria, the cell’s energy furnace, from the cytoplasm When muscle cells are damaged by being physically or chemically taxed beyond their limits, membranes are breached and the damaged cells spill their guts. This is a traumatic event!
Bursting of muscle cells is directly detected by the outpouring of the energy molecule ATP, as well as sodium potassium and acidic components — all of which are sensed directly by the nociceptor you see in the above diagram.
The inflammatory response. But the detection of tissue damage doesn’t stop with the direct detection of the molecules released from damaged cells. The body responds to pain by activating the process of inflammation. While the word “inflammation” has acquired a negative connotation, it may surprise you that it is actually an important and necessary process! Inflammation is nothing other than the body’s way of responding to tissue damage. Think of inflammation as the the fire alarm and the fire department that shows up to put out the fires. With regard to pain, inflammation is the process that sounds the alert that something needs to be done. Being against inflammation is like killing the messenger who brings you unpleasant news, or disabling fire alarms and fire engines because you don’t like the noise.
There are numerous parallel inflammatory responses. One of the best studied and exploited is prostaglandin signaling. It’s quite an elegant process. The cell’s phosopholipid membrane is made up of phospholipids — a polar phosphate “head” group linked to two hydrophobic fatty acids. One of the predominant fatty acids of muscle membranes is arachidonic acid (abbreviated AA), an essential omega-6 fatty acid. Even people eating an “anti-inflammatory” diet rich in fish and grass-fed beef need and have AA in their muscle cell membranes, albeit at slightly lower levels. You can’t live without it. When muscle tissue is damaged or stressed, arachidonic acid is released and rapidly converted by the cyclo-oxygenase pathways (COX-1 and COX-2) into the inflammatory signaling molecule, prostaglandin PGE-2. PGE-2 is an eicosanoid with multiple inflammatory effects, including the production of pain. Pain intensity is directly proportional to the amount of PGE-2 released.
Anti-inflammatory medicine. The conventional “Western” approach to stopping or blunting pain is to interfere with the COX-1 and COX-2 pathways. This is what non-steroidal anti-inflammatory (NSAID) agents like aspirin, ibuprofen (Advil) and acetaminophen (Tylenol) are designed to do: block the conversion of AA released from busted cell membranes into the pain mediator PGE-2. The prevalence of NSAIDS in pain treatment is testament to the fact that these products work — at least in the short term.
But it that really what we really want to be doing long term to address pain? Blocking the cyclo-oxgenase pathways blunts pain in the short term, but can lead to serious side effects and long term complications. Prolonged use of NSAIDS that block the COX-1 pathway can lead to gastric upset, ulcers and renal toxicity. And COX-2 inhibitors, while avoiding these particular side effects, can lead to even more serious cardiovascular risks. This lesson was learned the hard way through the numerous deaths caused by the COX-2 inhibitor VIOXX, before it eventually had to be withdrawn from the market. Although COX-1 and COX-2 inhibitors block AA from being converted to PGE-2, they don’t stop it from following other cycloxygenase and lipoxygenase pathways, eventually turning into other inflammatory eicosanoids: thromboxanes and leukotrienes. As with other inflammatory signalling compounds, these eicosanoids help marshal the resources needed to repair injuty. But when sustained, elevated levels of thromboxanes and leukotrienes can cause cardiovascular damage and induce heightened asthma, allergy and autoimmune responses.
An even more powerful anti-inflammatory effect is exerted by corticosteroids such as cortisone. Injections of cortisone into injured muscles and joints provides immediate and long-lasting relief of pain. Yet, as with the milder NSAIDs, corticosteroids don’t treat the root injury, they merely silence the messenger. Steroids like cortisone suppress inflammatory signals like histamine and serotonin. But is that a good thing? A 2010 meta-analysis in The Lancet found that, while cortisone injections for shoulder and elbow injuries provide rapid pain relief, the picture was quite different after 6-12 months. Compared with a control group that received no steroids, recovery was significantly slowed, and relapse increased. While inflammation was controlled initially, tendons actually continued to degenerate unabated.
Many turn to traditional or alternative medicine, advocating “natural” anti-inflammatory compounds that block the conversion of arachidonate to inflammatory eicosanoids. For example, fish oil supplements and certain herbs are touted as a natural alternatives to NSAIDs. On the surface, these are effective approaches to reducing inflammation and pain. And there are many good reasons besides pain relief to get adequate essential omega-3 fatty acids in the diet; deficiencies of omega-3 are linked to brain and heart health, among other thinks. But natural anti-inflammatories are targeting the same pathways as the NSAIDs! Studies show that supplementation with fish oil doesn’t come free of risk. It can inhibit platelet aggregation in the same manner as aspirin — which can be either a good or a bad thing. A recent study by Brasky et al. in JAMA of 2000 men found that those with the highest blood levels of EPA and DHA had 71% higher risk of aggressive prostate cancer and 44% higher risk of low-grade prostate cancer than their cohorts. This replicated an earlier 2011 study, so it is unlikely to be a fluke. A closer analysis of the data by Bailey showed that the increased risk was associated with higher levels of the more easily peroxidized DHA, not EPA. Elevated levels of lipid peroxides are implicated in numerous diseases, including cancer, and cardiovascular disease. A recent review in The Scientist by Anderson and Taylor suggests that — somewhat paradoxically– the beneficial effects of these easily oxidized lipids may actually result from a hormetic effect they have, when consumed in moderation, in stimulating the body’s endogenous anti-oxidant defenses.
Anti-inflammatory medicines and foods may have a role in the the short-term treatment of pain, particularly in the urgent treatment of unrelenting or disabling pain. But it’s really not the way to go. It’s basically a form of “shooting the messenger”. Back or muscle pain is nature’s way of telling us that something is wrong with our muscle or connective tissue – blunting the pain with anti-inflammatories does nothing to correct the damage or prevent further injury. In fact, there is considerable evidence that anti-inflammatories may actually slow down and impair the healing process. As Prisk and Howard note, by blocking prostaglandin synthesis, anti-inflammatory medicines inhibit the activatation and proliferation of myocytes, slow down muscle protein synthesis and promote excessive formation of fibrotic scar tissue that can interfere with normal muscle repair.
The root cause of pain. A major theme of this blog is that best strategy for sustained health is to address underlying causes rather than treating symptoms. So let’s go to the source of pain: tissue damage. Of course, we can’t absolutely prevent tissue damage; humans are always vulnerable to cuts, bruises, burns and other forms of physical trauma that are just part of life. But outside of this kind of direct physical damage to human flesh, I think we can question whether muscle and back pain are an unavoidable consequence of normal and even vigorous activity. We can also ask whether back and muscle pain are a normal part of getting older.
At the cellular level, the initial event in muscle or back pain is loss of integrity of the cell membrane. As we’ve seen, once the cell is damaged, a key component of the membrane — arachidonic acid — is released and then converted to the pain messenger, PGE-2. Other key components of the now disrupted cytoplasm — ATP, sodium, potassium, acids — also bind to channels and receptors on the surface of nociceptors.
Membrane integrity can be compromised either by physical or biochemical means. Accordingly, I will lay the foundation for my two recommended approaches to reversing and preventing back pain: targeted exercise and dietary hormesis.
PART 2. EXERCISE FOR PAIN PREVENTION
Physical insult to the membrane can be sudden and acute, or the result of extended and repeated mechanical stress. Professional and amateur athletes are familiar with both of these. In both acute and chronic or repetitive stress injury, physical stress to whole muscles translates down to the level of individual muscle fibers and cells, and ultimately to failure of individual cell membranes.
People vary widely in their resistance to muscle injury by physical activities such as sports or lifting heavy objects. Resilience to injury is to some degree genetic, but resilience largely reflects conditioning. Interestingly, there is a very strong correlation between those who experience lower back pain and those with weak back muscles.
Does poor physical hygiene cause pain? Somehow, the connection between pain and muscle strength has been missed. The more common view is that pain is caused by poor habits. There is a popular notion that back pain results primarily from poor physical hygiene — errors in posture or lifting. Ester Gokhale is a forceful advocate for the “Paleo” view that primitive and non-Western populations such as the Ubong from Borneo and Indonesia, or water chestnut gatherers in Burkino Faso, have low prevalence of lower back pain because their postural and walking habits. She advocates changes to a more “primal” posture as a means of reversing and preventing back pain. As evidence for this view, Gokhale uses photographs of people from non-Western cultures exhibiting proper poster and bending, arguing that “tucked pelvis” and slouched posture puts undue stress on the the lower vertebrae, compressing nerves. To prevent back pain, she teaches students to properly “stack” and elongate their vertebrae by adopting new hunched “relaxed” postures that are somewhat unfamiliar and require hours of training to learn.
Gokhale’s portrayal of the pain-free primitive has been challenged by James Steele. In his survey of back pain in different cultures, Steele found that back pain is actually prevalent in non-industrialized cultures such as Thai rice farmers. And he found that the agrarian rice farmers were inconsistent in their posture, as illustrated in the photo at right, reproduced here from Steele’s blog post. Contrary to Gokhale, as many stiffen their backs and bend from the knee as adopt a relaxed primal arc and hinged hip bend. Most interestingly, Steele found no correlation between habits of bending and posture and the incidence of back pain among the Thai farmers.
Muscle weakness and back pain. What Steele did find was something else: a strong correlation between back pain and weak back muscles. Regardless of postural habits. According to a study at the University of Florida, people with weak and atrophied lumbar extensor muscles are precisely those who are vulnerable to back pain. Strong lumbar extensor muscles protect against pain.
While Steele and Gokhale can agree that the modern sedentary lifestyle is a primary cause of back pain, their explanations are fundamentally different: For Gokhale, it’s the bad posture associated with sitting that is the culprit. For Steele, it is the deconditioning and atrophy of the lumbar back muscles that are the root cause of back pain.
According to Steele, our tree-dwelling primate ancestors had much stronger and developed lower back muscles than do modern humans. As our species became bipedal and terrestial, the spine lengthened, and the glutes and hamstrings became more powerful. Reliance on the lower body for locomotion lessened the need for strong backs, but left us with an evolutionary vulnerability to injured and weak backs muscles.
If you’ve ever had sudden back pain from doing “nothing” but bending over to pick up something light, you may have wondered why something so insignificant can produce more pain than straining to pick up a heavy object or exercising vigorously. The fact is that muscle atrophy from underuse or a sedentary lifestyle can be just as deleterious as overuse in weakening the membrane integrity of muscles.
Steele’s research focuses on a comparative study of different back exercises to find the most effective way of strengthening the lower back. He has found that free weight exercises like the deadlift and standard lumbar extension machines fail to strengthen the lumbar extensors because those exercises fail to focus the force stimulus in those muscles; the stronger “dominant” leg and large back muscles bear the brunt of the work. Steele and other researchers have found that a modified version of a lumbar extension machine that restrain movement of the pelvis and hips is effective in training the extensors. This type of pelvic restraint lumbar extension machine, sold by MedX, is depicted at right. Individual who train with this approach experience significant reductions in lower back pain.
Targeted strengthening of the back. Steele’s view is that the antidote to back pain is targeted strengthening. The key word here is “targeted”. The reason that strength training so commonly fails to alleviate back pain is that certain muscles — like the lumbar extensors — are buried in the musculature in a way that make them hard to target with conventional exercise or physical therapy, because other, larger muscles take over the job.
I think Steele is really onto something here. The key to rehabilitation is focusing the work onto the weakest link of a system, stimulating it to adapt. I’ve written about this in my blog page on Rehabilitation. Constraint Induced Motion Therapy is a type of physical therapy designed to help stroke patients strengthen atrophied muscles by immobilizing the stronger hand or leg in order to prevent it from taking over and sparing the weak side from doing the hard work necessary to recover. I’ve advocated a similar approach to reversing myopia by forcing eyes, atrophied by close work and glasses, to remodel in response to the deliberate application of incremental defocus stress.
Combating muscle soreness. While Steele has concentrated his work specifically on chronic lower back pain, I think his model is generalizable to other types of muscle pain. Stronger leg, ankle and foot muscles reduce the risk of pain from running and related sports; stronger arm and shoulder muscles are protective against injuries and pain that result from actions like throwing, swinging and climbing. The key thing to keep in mind in any of these exercises is to follow a protocol that to the greatest extent possible forces the weaker or atrophied muscles to pick up the lion’s share of the work. Only then will those muscle become more resistant to injury-induced pain and inflammation.
One of the most common forms of muscle pain is known as DOMS — Delayed Onset Muscle Soreness. This is what you often experience when running or lifting weights at a higher level of exertion or after a period of inactivity. It occurs in under-adapted muscles, and typically is worse a day or two after the event. Research shows that it is caused primarily by exercises with an eccentric or lengthening motion, as opposed to a concentric or shortening motion. In weight lifting, for example, squats will produce more DOMS soreness than a power clean, in which a weight is lifted and dropped without an active lowering component. And running downhill will produce more soreness than running uphill because of the way that downhill running forces your leg muscles to absorb impact forces. By contrast, cycling has relatively little concentric component and thus produces much less DOMS,
Eccentric exercise appears to cause much more soreness of unconditioned muscles by elevating intracellular calcium levels, causing contraction-induced muscle damage. As we’ll see below, the release of calcium activates the enzyme phosophipase A2, causing release of AA the initial step in the cycle-oxygenases prostaglandin cascade that produces pain-mediator PGE-2.
Recent research suggest that DOMS is not due primarily to micro-trauma or inflammation within the muscle body but rather occurs where the muscle interfaces with fascia or connective tissue, in the extracellular matrix. In any case, the origin of the pain is in tissue damage.
An effective strategy for combating DOMS is to continue to use the sore muscles to the degree it can be tolerated. This is known as the “repeated bout” effect; continued use promotes adaptive healing, and pain subsides. An ineffective strategy is inactivity.
Biochemical foundations. If muscular strengthening is in fact the best way to prevent and recover from injury and associated pain, why is that the case? What is the biochemical basis for muscular strength? While the muscle size or hypertrophy results from certain types of exercise, size is not the same as strength. Strength is fundamentally related to cellular energetics — the ability of the cell to efficiently and rapidly convert fuel into energy — specifically to convert glucose or fatty acids into the universal energy currency, known as ATP (adenosine triphosphate). This conversion can be carried out rather inefficiently by glycolysis, within the cell’s cytoplasm, producing 2 ATP molecules per glucose molecule. However the conversion is carried out almost 20 times as efficiently by the process of oxidative phosphorylation that is carried out inside the mitochondria — the cell’s energy powerhouse. With well-functioning mitochondria, a cell can can generate 38 ATP per glucose molecule! And it’s not just a matter of efficient conversion: the more mitochondria per cell, the faster the conversion of fuel to energy.
Mighty mitochondria. The greatest benefit of exercise is not muscle size, but rather strength. Exercise induces muscle cells to grow more mitochondria. Mitochondrial biosynthesis occurs only in response to imposed demand. Use it or lose it. But not all exercise is equal. Biosynthesis only occurs near the point of exhaustion and failure. Hence, high intensity is required. And it occurs only in the particular muscles that experience the demand for increased performance. While light aerobic activity has its benefits, only intense effort that goes into the anaerobic zone has the power to force the massive growth of new mitochondria.
Mitochondria protect muscles against membrane damage. Muscle cells rich in mitochondria are one of your best defenses against muscle soreness and back pain in particular.In the process of converting glucose to useful energy in the form of ATP, the mitochondria generate reactive oxygen species (ROS). This is not a bad thing in and of itself, but rather a necessary consequence of energy production. When you exercise, you inevitably generate a high level of ROS. These ROS play important cell signaling roles that enable channeling of energy into action. A healthy cell will control ROS levels using its built-in antioxidant machinery. The cell’s mitochondria protect themselves via the Nrf2 pathway, producing the endogenous antioxidants such as superoxide dismutase (SOD) and glutathione (GSH) — to ward off and repair ROS damage. Cells or organisms deficient in these antioxidant systems will accumulate damage beyond their repair capacity, as happens with aging, disease, excessive fatigue or atrophy. On the other hand, excess levels of antioxidants can impair the cell signaling crucial to muscular action. Studies show that supplementation with high levels of Vitamin C can impair athletic performance by downregulating your body’s production of it’s own antioxidant enzymes. For a more in-depth discussion of this effect, see my post, The case against antioxidants.
In fact, to strengthen mitochondrial defenses, it is good idea to subject yourself to intermittently elevated levels of oxidative stress, through intense exercise. It may seem paradoxical to increase oxidative stress in order to reduce oxidative stress. But there is no real paradox if this is thought of in terms of hormesis. Moderate or intermittently elevated oxidative stress enhances mitochodrial function according to a 2012 review by Kolb and Eizirik in Nature:
Increased mitochondrial activity leads to enhanced ROS production from the mitochondrial electron transfer chain. In healthy states, a hormetic response….ensues, whereby increased ROS generation upregulates the production of ROS-neutralizing enzymes, such as SOD2 and glutathione peroxidase, as well as the transcription factors PGC-1α and NRF-1, which promote mitochondrial biogenesis. These transcription factors are also induced as a consequence of muscle fiber contraction and the subsequent influx of calcium ions and consumption of ATP. As a consequence of these changes, cells deal more efficiently with the influx of fatty acids through oxidative phosphorylation, which reduces the amount of lipid metabolism intermediates produced (such as ceramides, DAG and acyl carnitine) and decreases the release of ROS. These effects prevent the induction of insulin resistance. Transient heat stress also induces a protective hormetic response.
Interestingly, mitochondrial health is important not just to ensure muscle strength, but also to prevent intervertebral disc degeneration, another major cause of lower back pain. Futhermore, disuse and inactivity of muscles rapidly lead to atrophy, also known as “sarcopenia”, associated with loss of mitochondria and the accumulation of myostatin, a regulatory protein. And it may surprise many people to learn that inactivity and immobilization actually increases ROS! Exercise reverses atrophy and normalizes ROS levels. Based on this newer understanding, it should be apparent that bed rest is not the best remedy for back pain or muscle soreness. As soon as one can tolerate movement, and increasing intensity as one is able, active use of the muscles is the best way to promote mitochondrial biogenesis, heal membranes, and reverse the pain. The more that the exercise can be targeted to the pain-prone muscles, the better.
In short, healthy and abundant mitochondria are able to keep up with normal and even elevated levels of ROS, minimize lipid peroxidation of muscle membrane phosopholipids, and thereby halt the cellular damage that initiates the entire process of inflammation and pain.
Thus muscular strengthening prevents pain in two mutually reinforcing ways
- Growth and proliferation of stronger muscle tissue is better able to absorb physical insults by distributing the stress across more muscle mass, thereby preventing or limiting cellular damage
- Great density and abundance of muscle mitochondria, in response to specifically imposed demand, increases resistance against muscle cell membrane damage at the level of the individual muscle cell
PART 3. DIET FOR PAIN PREVENTION
Biochemistry of membrane integrity. Targeted exercise is only half the story when it comes to strengthening the integrity of the cell against membrane damage and release of pro-inflammatory and pain-mediating chemicals. What you eat, and how much of the time you eat, also can have a significant impact on membrane integrity, and thus on how much pain you experience.
To see why this is so, let’s take a closer look at the process by which the cell membrane disintegrates and release arachidonic acid (AA), the fatty acid that is converted to the pain-producing eicosanoid PGE2, by way of the COX-1 and COX-2 pathways. In the cell membrane, the arachidonic acid is esterified (chemically linked) to a phosphate head group. The enzyme that allows AA to come free of the membrane is called phospholipase A2. To give you an idea of the its power, phosopholipase A2 is the key ingredient in snake venom , bee venom and wasp venom that destroys muscle tissue, causing inflammation and pain by breaking down the muscle cell membranes, releasing AA. In our bodies, it is normally sequestered in the cell as is released during injury, when the balance of intracellular calcium ions is disturbed. Phosopholipase A2 is activated only when intracellular calcium levels rise.
On the flip side, natural and artificial corticosteroids (like cortisone and prednisone) work by activating enzymes called lipocortins that directly inhibiting phosopholipase A2. This is a powerful and often desirable effect, shutting down inflammation and pain at the source, so cortisone shots are frequently used to alleviate back and muscle pain. However, corticosteroids can also inhibit the COX-2 pathway directly. leading to some of the undesirable effects we’ve already mentioned for other anti-inflammatory medications.
Insulin, calcium and membrane integrity. The important thing to note in this context is that phosopholipase A2 (PLA2) is tightly regulated by intracellular calcium levels. And intracellular calcium levels are regulated by an important metabolic hormone. That hormone is insulin. As shown by Baldi and Zemil, insulin attentuates build-up of intracellular calcium in insulin-sensitive individuals, but for those with insulin resistance, levels of both insulin and intracellular calcium become elevated. Studies linked here show that people with hyperinsulinemia or metabolic syndrome have elevated levels of intracellular calcium. Conversely, when basal insulin levels are low, intracellular calcium in low, so PLA2 activation is inhibited. Garces et al, in the October 2010 issue of Obesity, reported that people who are obese had significantly elevated insulin levels and also had significantly elevated levels of PLA2, independently of whether or not diabetes was present.
Because insulin levels are strongly influenced by what you eat, and by exercise, diet can be used as a powerful lever to control pain. A low insulin diet, whether by calorie restriction, intermittent fasting (as I’ve advocated here and here) or just by restricting carbohydrates and proteins, has the little known benefit of enhancing the integrity of muscle cell membranes, thereby increasing resistance of muscle tissue to damage and inflammatory pain.
Calorie restriction improves the pain resistance of muscles in other ways as well. It directly spurs on the biosynthesis of mitochondria by activating endothelial nitric oxide synthase (eNOS), and it turns on a process known as autophagy, which repairs damaged mitochondria.
Essential fatty acids. It is a commonplace notion in health blogs that inflammation and pain are effectively reduced by increased consumption of omega-3 fatty acids–found in fish, grass-fed beef, flax and certain nuts– and decreased consumption of omega-6 fatty acids, found in eggs, meat and vegetable oils. This idea is everywhere, yet I think it is overblown. For one thing, the evidence from interventional studies is not convincing. For those interested, in those studies and the biology of essential fatty acids, I’d suggest reading Chris Masterjohn’s excellent article, Precious, yet perilous: Know your essential fatty acids. Masterjohn retraces the history and scientific basis for identifying the essential omega-3 and and omega-6 PUFAs, and makes several key observations that many overlook:
- The “essentiality” of the PUFAs is contingent. “Diets low in refined sugar and rancid vegetable oils, adequate in protein and total energy, and rich in vitamin B6, biotin, magnesium, and whole, fresh foods abundant in natural antioxidants are likely to reduce the essential fatty acid requirement to such a degree that it is impossible for a healthy, growing child under ordinary circumstances to develop a deficiency. The requirement in adults is likely to be even lower… levels of DHA are especially high in the brain and retina, where its concentration is tightly regulated. In the early development of these tissues, small amounts of omega-3 fatty acids are required to provide maximal DHA content; after this window is closed, however, the brain and retina are very resistant to the effects of deficiency, just as mature animals and adult humans are resistant to the effects of arachidonic acid deficiency under ordinary circumstances.”
- You aren’t precisely what you eat: “unbalanced” PUFAs in the diet don’t imply they are unbalanced in membranes or the bloodstream. “Animal experiments suggest that great excesses of linoleic acid are required to cause deficiencies in omega-3 fatty acids….When fed to weanling rats, the classic sucrose-casein essential fatty acid-deficient diet only depletes retinal DHA content by 15 percent. The addition of ten percent of calories as safflower oil, however, causes a much more dramatic 50 percent depletion. Feeding rats two percent of their calories as purified linoleic acid depletes the DHA content of the retina by 62 percent in the first generation and 92 percent in the second generation…Our bodies use the same enzymes to convert ALA to DHA as they use to convert linoleic acid to arachidonic acid. A great excess of one precursor can therefore outcompete the other for the enzymatic machinery. Large amounts of any PUFA, moreover, will cause the cell to make less of this enzymatic machinery by convincing the cell that it is no longer needed. This competition and cellular confusion can be avoided altogether by providing small amounts of preformed arachidonic acid and DHA in the diet.”
- The anti-inflammatory effects of omega-3 fatty acids are indirect. “Many authors consider EPA an “anti-inflammatory” essential fatty acid, but its “anti-inflammatory” activity is a result of its ability to interfere with arachidonic acid metabolism. The conversion of arachidonic acid to PGE2 in immune cells is an important initiator of inflammation, but it also turns on the genes necessary for the synthesis of compounds that resolve inflammation, some of which are derived from arachidonic acid and others of which are derived from DHA. Providing sufficient DHA to allow the synthesis of the full spectrum of inflammation-resolving compounds is a nutritional approach to inflammation. Providing high doses of EPA that interfere with arachidonic acid metabolism, however, is a pharmacological approach, and it is likely to have many adverse consequences.”
These are sobering observations! What it means is that we should not overdo the need for essential fatty acids by mega-dosing omega-3 fatty acid oils from fish or fish oil tablets, and avoiding meat and discarding egg yolks because of a fear of arachidonic acid. So long as we get a modicum of essential fatty acids, we should trust our metabolism to balance our essential fatty acids.
Masterjohn’s analysis contradicts the meme that inflammation and pain result from an imbalance of omega-6 oils in the diet. As one example, in Lassek and Gaulin’s intriguing book “Why Women Need Fat“, the claim is made that
The single biggest change in the American diet over the past forty years has been an enormous increase in vegetable oils high in polyunsaturated fat. …The very high levels of omega-6 linoleic in our diet produce higher levels of arachidonic acid in our blood, and their is also more preformed arachidonic acid in our diets than in most other countries….Women’s weights are lowest when they have more omega-3 and less omega-6 in their diets…Omega-6 increases weight, omega-3 reduces it; omega-6 increases inflammation, omega-6 reduces it…Having more omega-6 in our bodies pushes omega-3 out of our bodies. (WWNF, pp. 23-33).
While it is true that consumption of linoleic acid rich vegetable oils has skyrocketed in the U.S. and Europe, if Masterjohn is right, the problem is not the general imbalance between omega-6, but specifically the metabolic effects of linoleic acid (from vegetable oils) and sugars, not the inherent balance between the essential fatty acids arachidonic acid and DHA. Eggs and meat are good — its the linoleic-rich vegetable oil that screws things up.
Diet and membrane integrity. For understanding pain, far more important than dietary intake of essential fatty acid, as it turns out, is the fate of essential fatty acids as retained in the cell membrane and their propensity for release from the membrane. In this regard, the findings of Jeff Volek and Stephen Phinney are especially pertinent. In their studies of hypocaloric carbohydrate restricted diets (10% carbohydrate, 65% fat, 25% protein calories), Under a carbohydrate restricted diet high in saturated fatty acids. Volek and Phinney found a reduction in multiple nflammatory markers despite a significant increased in plasma arachidonic acid (ARA). As they note,
Increasing ARA in membranes, however, does not inevitably lead to greater inflammation and may in fact have the opposite effect. The pro-inflammatory effects of ARA are due to metabolites produced subsequent to its release from membranes rather than the proportion of the intact fatty acid.
In their book, The Art and Science of Low Carbohydrate Living, Volek and Phinney discuss the interesting paradox
…when a person switches from a high carb diet to [a ketogenic diet], the body’s economy of essential fatty acids changes dramatically. This is seen as a rise in both arachidonate and DHA in serum phosopholipids, while at the same time, the levels of the intermediate products (the fatty acids half-way between precursor and end product…go way down. This is a bit vexing to say the least, because if the body was cranking out lots more end products through this pathway, one would expect the levels of the intermediates to go up in the process. (TAASLCL, p. 118)
Volek and Phinney argue that this occurs because the low carb / ketogenic diet suppresses ROS, resulting in better preservation of arachidonic acid in the membrane, despite lower levels of precursor.
In short, restricting carbohydrates and insulin reduces oxidative damage, preserves arachidonic acid, and inhibits its and release from cell membranes, with the subsequent inflammatory consequences. Which also means reduced potential for pain.
Piecing the above paragraphs together, we can draw the conclusion that reducing basal insulin levels, whether through restriction of carbohydrates or total calories, is likely to enhance the integrity of cell membranes and inhibit the release of pro-inflammatory omega-6 fatty acid arachidonic acid — regardless of the omega-3/omega-6 composition of the membranes, and regardless of the balance of those fatty acids in the diet. (In fact, there is some evidence that a diet high in EPA may actually increase the release of AA). If you chose to eat a high carbohydrate, high protein diet and raise your insulin levels, perhaps you should be careful of the omega-3/omega-6 balance. But insulin control is a much more powerful lever for controlling inflammation and pain.
Hormetins. I have one more recommendation for what to consume to prevent and moderate muscle and back pain: eat hormetins. Specifically, eat foods and spices that make your mitochondria turn on their endogenous antioxidant defenses. The term “hormetin”, coined by Suresh Rattan, refers to any substance or stressor that activates a stress response at a cellular level. Rattan and other researchers like Edward Calabrese, have identified and quantified the behavior of hundreds of hormetins in a broad range of organisms and organ systems, from microbes to plants and animals. Bioflavanoid phytochemicals — Plant-derived polyphenolic compoiunds — are the hormetins are of greatest interest in the present context. As I have written about in my article, “The case against antioxidants“, the polyphenolic phytochemicals interact with the Nrf2 pathway to upregulate Phase II antioxidant enzymes, such as superoxide dismutase, and glutathione reductase. Because these Phase II enzymes catalytically neutralize ROS, regenerating themselves thousands of times, they are far more effective than biochemical antioxidant vitamins such as vitamins C, E, Co-Q10 or beta-carotene, which are expended stoichiometrically (one-for-one) when neutralizing oxidant species. And because these antioxidant enzyme are produced within the mitochondria, they are targeted to precisely where they are needed to boost cell defenses closely related to the integrity of cell membranes in healthy muscles and connective tissue.
In my other post, I’ve listed a range of hormetin-rich foods, including broccoli, asparagus, brussell spouts, green and red peppers, and mushrooms, strawberries and blueberries, and spices or herbs, such as green tea, ginger, and resveratrol. I draw a distinction between hormetins and supplements. A nutritional supplement is a substance you take in an effort to correct some apparent deficiency, such as that of a vitamin, mineral, or amino acid. A hormetin is not something you lack, but is rather a substance intended to stimulate your body to defend, repair, or strengthen itself using its own resources. Supplements make things easier for your body’s metabolism. Hormetins are stressors that make your body work harder, and thereby gain capacity in the process.
My favorite hormetin for preventing pain is one with a long history but relatively little fanfare: curcumin, the active compound in turmeric. This is one I highly recommend, based both on the research and personal experience. Curcumin is particularly effective in preventing release of arachidonic from membranes by inhibiting phospholipase A2. It does not do this directly, but rather by inibiting its phosophorylation, which is required for activation of the enzyme. Studies have found it particularly effective to treat or prevent eccentric-exercise induced muscle pain, tendonitis, joint pain, post-operative pain, and other types of inflammatory pain. It is somewhat amusing to learn that curcumin also functions as an anti-venom, but this makes sense in light of my earlier observation that PLA-2 is a major constituent of snake and insect venom, and curcumin inhibits PLA-2!
For the past year or so, I have taken curcumin on a somewhat regular basis. I sometimes add it as turmeric to my food. I noticed that after taking it for about a month, my recovery from running and intense exercise is more rapid, and I have no trace of pain. I’ve found that an oral supplement called Protandim to be particularly effective. It’s The curcumin in Protandim is co-formulated with several other Nrf2 activating herbs, but I think it is the curcumin that does most of the work. As a disclaimer, I have no financial interest in Protandim. It’s actually somewhat expensive, but I’ve found it to be convenient, well tolerated and effective.
To summarize, here are the four steps I recommend to reduce and prevent back and muscle pain:
- Minimize the use of anti-inflammatory medicines such as NSAIDs and corticosteroids — they impair the healing and growth of naturally pain-resistant muscles. Take them if you cannot tolerate the pain, but wean yourself away as expeditiously as you can. I avoid them entirely.
- Exercise intensely, but intermittently and with adequate rest, targeting the exercise to the muscle most vulnerable to pain. Gradually ramp up intensity, using good judgment to avoid causing further injury.
- Reduce your basal insulin levels by intermittent fasting and moderate or intermittent consumption of carbohydrates and protein. Consume both saturated and unsaturated fats, and fiber-rich vegetables (since gut microbes convert these to short chain fats). Don’t stress out about omega-3 versus omega-6 fats, but avoid excessive amounts of polyunsaturated vegetable oils like corn oil or safflower oil.
- Include hormetins such polyphenol-rich vegetables, herbs and spices in your diet on a semi-regular basis, to stimulate endogenous antioxidants and maintain strong cell membranes. As a food spice, or a supplement, I especially recommend curcumin.
In the above recommendations, the essential point is to understand pain as an important signal that the muscle or connective tissue is damaged and needs to be fortified to make it more resistant to damage.
Trying to mask pain with anti-inflammatory medications may provide temporary relief, but is counterproductive in the long term. It doesn’t address the root cause and worse, it can interfere with effective healing and strengthening. The sustainable way to prevent pain is strengthening muscle tissue at the cellular level, through targeted exercise and nutrition.