Pain makes man think. Thought makes man wise. Wisdom makes life endurable.

–John Patrick, Playwright

f the statistics are to be believed, it seems that a great many Americans have yet to find a suitable solution to the problem of chronic and recurring pain. According to the 1999 research report, Pain in America, an estimated 26 million Americans suffer from severe pain on a regular basis; and various other surveys have reported that between 9% and 24% of American adults are suffering with chronic pain (defined as pain which persists for six months or longer). Perhaps the saddest statistic of all is that almost a full third of pain sufferers feel that their affliction is an unavoidable part of getting older – they feel that there is simply no solution for their pain.

With so many of us in constant pain, it comes as no surprise that the use of over-the-counter and prescription pain medication is rampant. In fact, the top three drugs consumed in America (acetaminophen, ibuprofen, and aspirin) are all pain killers. And although many pain sufferers have taken to popping these drugs like candy, the side effects associated with both acute and long-term use of anti-inflammatory drugs simply cannot be ignored. Anti-inflammatory drug-use results in over 100,000 hospitalizations and between 10,000 and 20,000 deaths in the US each year, and it’s estimated that 15% of chronic pain sufferers who regularly use non-steroidal anti-inflammatory (NSAIDs) medications (aspirin, ibuprofen, indomethacin, naproxen, etc.) develop stomach or duodenal ulcers as a result. NSAIDs (besides aspirin) have also been associated with increased risk of heart attack and stroke, and the most common over-the-counter pain reliever, acetaminophen, is well-known to be a major cause of liver failure.

As educated pain sufferers become increasingly wary of the side effects associated with over-the-counter and prescription pain medications, the role of nutrition in pain management has begun to garner increased attention. In recent years, many nutritional supplements have made the foray into our pain-relieving pharmacopoeia; but, mimicking the “treat-the-symptoms-only” approach of modern medicine, some nutritional supplements marketed as “natural pain relievers” or “anti-inflammatory nutrients” may offer only short-term symptomatic benefit, while actually predisposing us to increased pain and tissue degeneration in the long-run.

By examining the underlying causes of pain, we’ll see that a proper nutritional solution involves not only reducing inflammation safely, but also supplying our body with a balance of protective nutrients – and the proper metabolic environment – for healing injured tissue. In this issue of the Integrated Supplements Newsletter, we’ll begin by taking a look at the true role dietary and supplemental fats play in driving the process of pain and inflammation. We’ll also discover dietary practices which will allow us to reduce pain, not only by blocking the pain signal in the short-term, but by fostering the actual growth and repair of injured tissue for good.

The Purpose of Pain

When we’re suffering from a sports injury, or a splitting migraine, or an arthritis flare-up, it can sometimes be difficult to remember that pain does serve a very important biological purpose – pain is nature’s way of warning us that something’s wrong, or that our body is being damaged or threatened in some way. Of course, it doesn’t help matters that the duo of pain and inflammation comprise one of the many “vicious cycles” in biology – the more inflammation we experience, the more damage is done to our tissues; the more damage is done to our tissues, the more inflammation we experience - and the harder it is for our body to complete the healing process which is necessary in order for the pain to ultimately subside. Under the influence of this downward spiral, it’s no wonder that so many people feel hopelessly cursed by the burden of unrelenting pain.

But, to start solving the puzzle of chronic or recurring pain, the question we should ask isn’t simply: “How can I make the pain go away?” but rather, “Why isn’t my body healing properly?” When we seek out the answer to this question, and not just symptomatic relief, we’ll see that the scientific literature is bursting with reasons for the pain sufferer to be optimistic about the prospect of natural, lasting pain relief through dietary and lifestyle changes.

A Brief Look at Pain and Inflammation

Joint pain, low-back pain, migrane headaches, or muscle soreness - it’s clear that pain can make its presence known almost anywhere in our body. But for as varied as these manifestations of pain may seem, it’s now thought that, on a very basic level, all occurrences of pain may share a common biochemical thread.

From a cellular perspective, pain and inflammation involve a mind-boggling interplay of hundreds of chemical messengers – many of which have surely yet to be discovered. But although science has yet to explore every minute detail of the pain response, some of the major players have been identified, and their actions extensively studied. One such chemical is a particular fatty acid component of our cells called arachidonic acid (AA). For all intents and purposes, we can think of arachidonic acid as the fountainhead chemical of pain and inflammation.

Arachidonic acid is a component of phospholipids, the fatty acid-containing structures which comprise our cellular membranes; and when triggered by injury, infection, or other cellular stress, arachidonic acid is released from the cell, and is converted into a whole host of inflammatory chemicals collectively called eicosanoids. Eicosanoids produced from arachidonic acid include chemicals known as prostaglandins, prostacyclins, thromboxanes, and leukotrienes – and it’s largely these chemicals which are the molecular-level mediators of all types of pain and inflammation.

Two Types of Pain – One Common Thread

The type of pain most commonly associated with tissue injury, and with the common manifestations of inflammation, like redness and swelling, is called nociceptive pain (noci is a prefix from the latin for trauma or injury). It’s well-known that the arachidonic acid metabolites called prostaglandins (most notably a prostaglandin called PGE2), are largely responsible for causing and perpetuating nociceptive pain.

The other major category of pain is called neuropathic pain, or simply, nerve pain. Neuropathic pain is often described as being “electrical” in nature, the shooting pain of sciatica and the tingling sensation of diabetic neuropathies being common examples. And while nerve pain often exists in the absence of noticeable tissue damage, or inflammatory symptoms like redness or swelling, it’s known that arachidonic acid metabolites play a role in neuropathic pain as well.

Study Link - Altered spinal arachidonic acid turnover after peripheral nerve injury regulates regional glutamate concentration and neuropathic pain behaviors in rats.

Quote from the above study:

These data suggest that regulating spinal AA turnover may be a useful approach to improving the clinical management of neuropathic pain.

So, it’s very clear that our quest for the nutritional and lifestyle solution to pain and inflammation will surely center on modulating the effects of arachidonic acid.

But altering arachidonic acid metabolism is certainly not a new concept in the field of pain relief – in fact, it’s one of the oldest. Non-steroidal anti-inflammatory drugs (NSAIDs) like aspirin, ibuprofen, and naproxen exert their analgesic (pain-relieving) effects specifically by blocking some of the enzymes involved in the arachidonic acid cascade. But the long-term side effects associated with this class of drugs should serve as a clue that the manipulation of the inflammatory process (whether through diet, drugs, or supplements) should be approached very carefully, and always with long-term health in mind.

COX Inhibition

The NSAID class of drugs exert their pain-relieving (and anti-inflammatory, anti-fever) actions largely by inhibiting one or more of a family of enzymes known as cyclo-oxygenases, or COX, for short. COX enzymes catalyze the conversion of arachidonic acid into several inflammatory chemicals, but adding a wrinkle of complexity to the process, is the fact that cyclo-oxygenase enzymes exist as several variants, each with subtly different effects. The two most prevalent subtypes of COX enzymes are known as COX-1 and COX-2.

Different tissues and cells of the body contain varying amounts of the COX enzymes, and because each NSAID drug has different selectivity for which COX enzyme it blocks (and exactly how it blocks it, for that matter), the long-term effects of NSAID-usage has been notoriously difficult for scientists to predict.

For instance, aspirin, the oldest NSAID drug, is known as a “non-selective” COX inhibitor, meaning that it can block both COX-1 and COX-2 activity. COX-1 enzymes are expressed in blood platelets and aspirin’s ability to block the inflammatory cascade in these cells leads to reduced platelet “stickiness” and reduced blood clotting time. It’s thought that this “blood-thinning” effect is largely responsible for aspirin’s role in supporting proper blood flow and cardiovascular health. But on the flip side of the coin, it just so happens that the lining of the gastrointestinal tract also contains COX-1 enzymes, and the eicosanoids produced from COX-1 are needed for the maintenance of the intestinal mucosal barrier. This is the major reason why aspirin use may cause gastrointestinal bleeding and ulcers, and why the promotion of aspirin is always tempered by warnings about its gastrointestinal side-effects.

Ibuprofen, currently the most popular NSAID in North America, has been marketed heavily as an aspirin-alternative which is gentle on the GI tract, but because it too is a non-selective COX inhibitor, the fact is that ibuprofen can stimulate gastrointestinal bleeding and ulceration similarly to the aspirin it is often promoted to replace.

Study Link - Over the counter non-steroidal anti-inflammatory drugs and risk of gastrointestinal bleeding.

Quote from the above study:

Risk of GI bleeding was increased 2-3 fold among recent users of aspirin, ibuprofen and other nonsteroidal anti-inflammatory drugs (NSAIDs) at OTC doses, with risk increasing in a dose-related manner.

So, ibuprofen is probably no safer to the gastrointestinal tract than aspirin, and yet unlike aspirin, whose cardio-protective benefits are well-recognized, ibuprofen has actually been linked to an increased risk of heart attack.

Study Link - Risk of myocardial infarction in patients taking cyclo-oxygenase-2 inhibitors or conventional non-steroidal anti-inflammatory drugs: population based nested case-control analysis.

Quote from the above study:

These results suggest an increased risk of myocardial infarction associated with current use of rofecoxib, diclofenac, and ibuprofen despite adjustment for many potential confounders. . . enough concerns may exist to warrant a reconsideration of the cardiovascular safety of all NSAIDs.

As evidence of aspirin and ibuprofen’s toxicity began to mount, drug manufacturers funneled their resources into the development of more “selective” drugs which blocked only the COX-2 enzyme. The thinking was that these drugs would be able to block the pain response without causing harm to the GI tract like drugs which blocked both COX-1 and COX-2 activity. But as further testament to the overwhelming complexity of the inflammatory cascade, it seems that even increased knowledge of the underlying biochemistry wasn’t enough to prevent modern medicine from producing the most toxic NSAIDs yet. Several years after their FDA approval, and much to the dismay of the pharmaceutical giants, it became clear that the wildly profitable selective COX-2 inhibitors were wrought with their own set of serious shortcomings. In one of the most publicized drug recalls in this countries’ history, the COX-2 inhibitor Vioxx ® was voluntarily withdrawn from the US market by its manufacturer in 2004, amidst overwhelming evidence of the drug’s cardiovascular toxicity.

Article Link - The Lessons of Vioxx — Drug Safety and Sales.

Quote from the above article:

The pharmaceutical industry spends more than $5.5 billion to promote drugs to doctors each year — more than what all U.S. medical schools spend to educate medical students. . . By the time of [Vioxx's] withdrawal from the market in September 2004, after a placebo-controlled study confirmed its cardiovascular risk, more than 100 million prescriptions had been filled in the United States. Tens of millions of these prescriptions were written for persons who had a low or very low risk of gastrointestinal problems.

With so many unforeseen side effects accompanying their long-term usage, it seems that the NSAID drugs are simply not the best answer for chronic pain. Despite the rampant promotion of these drugs, and their regular use by millions, far too many unanswered questions still remain about their safety. If we really want to reduce pain and safely foster healing, we’ll have to regulate the inflammatory cascade via diet; and to do this requires that we reduce our bodies’ levels of the upstream inflammatory chemicals in the first place, including and especially, the parent chemicals of arachidonic acid.

Fats and Inflammation

Many people, who have been conditioned to think of dietary fat as merely an energy source for the body, are surprised to learn that the production of pain and inflammation is fundamentally driven by the quantity and relative ratios of different fats in our diet. The inflammatory cascade we’ve been discussing is controlled, in large part, by the polyunsaturated fatty acids (PUFAs) known generally as omega-6 and omega-3 fatty acids. In particular, the arachidonic acid we identified as the major precursor to inflammatory and pain-producing chemicals is produced in our body from a very common omega-6 fat in our modern diet called linoleic acid.

In visualizing how our cells respond to stress when they’re loaded with arachidonic acid, a good analogy would be that it’s like throwing a match into a fireworks factory. Arachidonic acid is very reactive chemically, and it’s prone to “go off” and stimulate inflammation and cellular destruction at the slightest provocation. The subsequent inflammatory response triggers even more tissue destruction than the initial stressor itself, liberating more arachidonic acid, and of course, stimulating a vicious cycle of even more inflammation, and even more cellular damage before our cells can stabilize themselves.

Ideally, we want our inflammatory response to be “short and sweet” - just sufficient enough to deal with the problem (injury, virus, bacteria, etc.) at hand – no more, and no less. But by consuming a diet with an excess of omega-6 linoleic acid, what we’re doing, in essence, is giving our body a nearly unlimited supply of inflammatory precursors. It’s no wonder, then, that the “alarm reaction” and stress response of inflammation so easily spirals out of control, and manifests as chronic pain and inflammation. And of course, with the increasingly recognized role of inflammation in all degenerative diseases, there’s sufficient reason to believe that perhaps every aspect of our health could benefit from altering our diet to drastically reduce our cellular inflammatory response.

The fact that the fats we consume will have a direct bearing on our levels of pain and inflammation is becoming more well-known as the marketing of various fatty acid supplements has increased in recent years. But much of the marketing you’ll currently hear touting the “anti-inflammatory” nature of “good fats” tends to miss the big picture entirely. Much like long-term NSAID usage, most of the “anti-inflammatory” fatty acid supplements currently popular, like those from fish oils, flax oils, evening primrose oils, borage oils, and a whole host of more exotic sources of omega-3s and omega-6s, are probably destined to do more harm than good in the long-run at the doses at which they’re currently recommended. With so many people turning to such “natural” supplements for relief, we think it’s time to take a look at the true role of dietary fats in inflammation.

Arachidonic Acid in Food

It’s true that animals store arachidonic acid in their tissues just like we do, so animal-based foods like meats, eggs, and dairy products will indeed contain arachidonic acid. And there is a direct relationship between the fats we eat and the fatty acids stored in our cells, so logically, you would think that animal-based foods would contribute greatly to our bodies’ level of arachidonic acid and inflammation.

But surprisingly, animal foods actually represent a relatively small contribution to bodies’ arachidonic acid stores – so, despite what you may often read, moderate consumption of meat and eggs probably won’t add to our inflammatory burden all that much.

For example, the following study estimated that the actual arachidonic acid intake of the Australian (and typically Western) diet ranged from 96 milligrams to 130 milligrams per day for men and women respectively; whereas the consumption of the arachidonic acid precursor, linoleic acid, has often been estimated to be on the order of 10 to 20 grams per day for the average person.

Study Link - The Arachidonic Acid Content of the Australian Diet Is Lower than Previously Estimated.

A much greater concern than dietary arachadonic acid is that our body is able to synthesize arachidonic acid from the omega-6 fat called linoleic acid. Linoleic acid from common oils such as soybean, safflower, sunflower, peanut, canola, cottonseed, and corn provides a nearly unlimited supply of arachidonic acid precursors.

Studies in rats indicate that just 0.33% of the diet as linoleic acid is able to load cell membranes with arachidonic acid, and what human studies exist in this area show that linoleic acid at just 2.5% of the diet is sufficient to produce more than enough arachidonic acid.

But unlike the pre-formed arachidonic acid we eat in meats and eggs, the production of arachidonic acid from linoleic acid uses up enzymes which could otherwise be used to produce anti-inflammatory substances.

This is a major reason why modern man in industrialized countries, where vegetable oils have become a common part of the diet for the fist time in human history, is uniquely prone to suffer pain, inflammation, and degenerative disease - an increased consumption of omega-6 fats, and subsequently, an increased level of unopposed arachidonic acid in the tissues.

So, the first step in reducing pain and inflammation involves reducing omega-6 linoleic acid in our diet as much as reasonably possible. Of course, we’ll never be able to avoid linoleic acid in our diet completely, as almost all plant foods contain at least trace amounts. Even modern meats contain linoleic acid because animals are often fed feed containing corn and soybeans (chicken fat, for example has been estimated to contain over 20% linoleic acid – even more than many vegetable oils).

Along these same lines, while they are certainly healthier than isolated oils – some fatty foods can easily add to our burden of pain and inflammation if consumed in excess. Peanuts, almonds, and avocados are examples of foods which are often marketed for their health benefits, but the linoleic acid they contain is sure to add to the bodies’ inflammatory burden if they are consumed regularly. Just a handful of almonds, for example, will give most people far more linoleic acid than they require for an entire day, so the regular use of such linoleic acid-containing foods should be judged in this context. Trying to limit our linoleic acid intake to the trace amounts found in a diet of fruits, fresh leafy vegetables, along with some eggs, dairy, and quality meats, will go a long way towards reducing our inflammatory burden.

Note: A quality protein supplement like our CFM® Whey Protein Isolate is a good choice for those needing high-quality proteins, while wishing to avoid or minimize the fat and cholesterol often found in other protein-rich foods. Because undenatured whey proteins possess properties not found in typical foods, CFM ® Whey Isolate may even play a unique role in combating chronic pain as we shall see in the next Integrated Supplements Newsletter.

Enter Omega-3s

It seems logical that reducing our intake of linoleic acid – the precursor to arachidonic acid – would be able to reduce the level of arachidonic acid in our cells. In theory this is true, and in laboratory experiments, animals which are fed diets with extremely low levels of linoleic acid do indeed produce far less arachidonic acid in their tissues. But it’s unlikely that most people will ever eat a diet low enough in linoleic acid so as to significantly reduce the level of arachidonic acid in their cells. You may ask why then, is reducing linoleic acid in our diet so important for reducing the actions of arachidonic acid in our body?

The reason has to do with omega-3 fatty acids. In a general sense, omega-3 fatty acids are often thought of as the opposite of, or as a “counter-balance” to the inflammatory omega-6 fatty acids. This is true in many ways, but just knowing that omega-3s “balance” omega-6s can often lead to the indiscriminate and excessive consumption of omega-3s if a person isn’t careful. For example, the simplified logic employed by those recommending omega-3 supplementation is usually something along the lines of:

1) Due to the over-consumption of modern oils from soy, corn, cottonseed, canola, sunflower, safflower, etc., our modern diet is relatively very high in the omega-6 fat, linoleic acid, a precursor to the inflammatory arachidonic acid (this fact is very much true).

2) Omega-3 fats compete with omega-6 fats for the enzyme (called delta-5 desaturase) which produces arachidonic acid. Therefore, omega-3 fats reduce arachidonic acid levels and tend to reduce inflammation (these facts are also true, but the conclusions often drawn from these facts leave much to be desired).

The typical conclusion drawn from the above facts is that we should “balance” our ratio of omega-6 to omega-3 by consuming more omega-3s in the form of things like fish or flax (or supplements from these sources).

But for the omega-3s to exert their true anti-inflammatory action without long-term side effects, it’s important that the level of omega-6 linoleic acid in our diet be very low. Omega-3 fatty acids exert most of their anti-inflammatory action simply by competing with omega-6 fatty acids for the enzymes which metabolize both classes of fats. The enzymes which convert omega-6 linoleic acid to arachidonic acid actually tend to show a preference for omega-3s, so if our omega-6 intake is low enough, the net result will naturally be an increase in the relatively “anti-inflammatory” metabolites of omega-3 fats. But the problem is that most of us have so much omega-6 fats in our diet, that it takes potentially dangerous amounts of omega-3s to “balance” them out.

The most frightening misconception fostered by the current omega-3 supplementation fad, is that we can somehow “make up for” or “balance” our excessive omega-6 consumption simply by taking in more omega-3 fats. But, because both omega-3 and omega-6 fats contribute to the free-radical burden known as oxidative stress, simply adding omega-3 fats to a diet already high in omega-6s is sure to increase overall free radical damage, tissue destruction, and degenerative disease in the long-run. From this standpoint, omega-3 fats are even more apt to increase oxidative stress than omega-6 fats because their greater degree of unsaturation makes them more prone to damage by oxygen. This is why omega-3 supplements spoil so easily and why the over-consumption of omega-3s is equally as problematic as the over-consumption of omega-6s.

Even the following study, which has a decidedly pro-omega-3 stance, recognizes the problems inherent in adding omega-3 fats to the typical Western diet which is already high in omega-6s. The study acknowledges that relatively little is known about the optimal amounts and ratios of omega-6s to omega-3s - but interestingly, we learn that:

“. . .there is enough scientific evidence to also state an upper limit for [linoleic acid] of 6.67 g/d based on a 2,000 kcal diet or of 3.0% of energy .”

Study Link - Human requirement for N-3 polyunsaturated fatty acids.

In other words, scientists still don’t know exactly how much omega-6 linoleic acid is optimal, but they do find it necessary to warn us against consuming more than the “upper limit” of 6.67 grams of it per day. To give you a frame of reference, this daily upper limit of linoleic acid could be exceeded by eating a mere two ounces of almonds, or three tablespoons of natural peanut butter, for example. If omega-6 fats pose health risks in such amounts – far lesser amounts than most people consume each day - then to recommend anything but a drastic reduction in omega-6 intake misses the point entirely. Can omega-3 supplements really be expected to “balance” an intake of omega-6s which is so grossly in excess of our bodies’ actual needs? Doesn’t it make more sense to simply limit our omega-6 consumption rather than to indiscriminately add omega-3 supplements to our diet? Why do we so often hear that we need to increase our omega-3 intake, but seldom hear that the real problem with our diet is an overwhelming excess of omega-6s? The answers to these questions should make it clear that much of the nutritional guidance we receive in this country – from our public health experts, and nutritional supplement hucksters alike – amounts to little more than product-driven marketing. Agricultural oils, and fatty acid supplements have been promoted in this fashion for decades, and their subsequent over-consumption is largely responsible for an untold amount of needless pain, suffering, and premature aging. Following the money made by massive oil industries over the past century should give you a clue as to why even “healthy” diets in the Western world have become so pro-inflammatory and destructive.

The above study goes on to speculate as to what the optimal amount of omega-3 fats in our diet may be – and if our omega-6 requirement is small, then we can extrapolate this to mean that the daily dose of omega-3s we actually require borders on the infinitesimal. The study recommends a mere 1% of calories as omega-3s – 2 grams per day at the very most in a 2000 calorie diet. With how frequently omega-3s are currently touted, its easy to loose perspective on how little of them we really need. In reality, a fish-meal a week, or regular consumption of green leafy vegetables should be more than sufficient to meet our omega-3 requirements. Not only are omega-3 supplements unnecessary, but with the food industry beginning to frantically fortify almost all classes of foods - from eggs to bread and even beverages with omega-3s, there’s actually a distinct possibility that we may have to choose our foods wisely to prevent omega-3 over-consumption before too long.

Of course, when omega-3 fats are added to the diet in the form of supplements, the initial effect could indeed be a reduction of inflammation, as these fats do compete with the omega-6 linoleic acid for the enzymes needed to produce arachidonic acid. Such symptomatic relief in the short-term probably explains why omega-3 supplements have been so well-received by millions of Americans. But over time, the cumulative effect of having fragile and easily damaged omega-3 fats in the body is likely to be massive tissue destruction, greater susceptibility to infection, an increase in oxidative stress, and overall, an acceleration of the aging process. As an example, the following study, in examining the effects of fish oil consumption in rheumatoid arthritis sufferers, found that the group consuming fish oil experienced less pain and stiffness in the short-term (by the end of the 12-week study). But four to eight weeks later, it was found that the subjects consuming fish oil were “significantly worse than the control group for pain and overall condition.”

Study Link – Effects of manipulation of dietary fatty acids on clinical manifestations of rheumatoid arthritis.

Quote from the above study:

At follow up 4-8 weeks later, the [fish oil] group were significantly worse than the control group for pain and overall condition.

The pro-inflammatory metabolites of arachidonic acid are so incredibly toxic to all systems of the body, that merely blocking their production as omega-3s do can seem to produce nearly miraculous improvements in all aspects of health – including symptomatic improvement in pain and inflammation. But most people have so much omega-6 in their diet (and in their body) that the dose of omega-3 needed to “balance” it is also destructive and toxic in the longer-term. The above study, rather than being reason for us to run out and buy fish oil supplements, really gives us reason to reduce our linoleic acid consumption to the lowest levels possible. When we do this, the trace amounts of omega-3 fatty acids in our diet will naturally antagonize arachidonic acid production while allowing us to reap benefits even while our omega-3 intake remains at very low levels.

The following studies illustrate this fact very nicely.

Study Link – Fish oil reduces cholesterol and arachidonic acid content more efficiently in rats fed diets containing low linoleic acid to saturated fatty acid ratios.

Study Link &ndash Dietary saturated fat level alters the competition between alpha-linolenic and linoleic acid.

Both of these studies show that the lower the level of omega-6 linoleic acid in the diet, the more effective omega-3 fatty acids are at lowering arachidonic acid – even if the linoleic acid is replaced by saturated fat.

The Big Picture of EFAs

Selling essential fatty acid supplements has been a very profitable endeavor for hundreds of companies in recent years, but we can receive a balanced ratio of all of the fatty acids we require simply by eating a carefully-chosen diet of natural foods. This fact is often lost amidst the whirlwind of supplement promotion simply because there’s no money to be made by telling you which foods to avoid. It’s important to always remember that the human body’s requirement for essential fatty acids (both omega-6 and omega-3) is really very low. We probably couldn’t become “deficient” in omega-6s even if we tried, and, as we’ve seen, most of us consume far more omega-6s than we really need. Once we lower our omega-6 burden, our true requirement for omega-3s becomes easily obtainable through fresh, whole foods. The net result will be a reduction in pain and inflammation, and an improvement in overall health.

If you must include oils in your diet, extra virgin olive oil is a reasonable food choice, as the fatty acids it contains are relatively stable fats called monounsaturates (only around 9% of olive oil is polyunsaturated oil). Still, olive oil should not be used in high-heat cooking because even the relatively small amount of polyunsaturated fats it contains are easily damaged by heat. Save olive oil for salad dressings and even then, use it sparingly. Coconut oil, with its high amounts of very stable fats is suitable for medium-heat cooking and baking. Despite the bad rap coconut oil has gotten in previous decades (which some say was instigated by the sellers of the polyunsaturated seed oils), coconut oil can be part of a safe long-term solution to the effects of excessive omega-6 and omega-3 consumption.

Over time, as we alter our diet to exclude significant sources of linoleic acid, we’ll likely find we start to experience relief from pain and inflammation as our nagging injuries actually begin to heal. We won’t have to worry about long-term side effects with a whole-food diet like we will if we rely on NSAIDs or fatty acid supplements, and in fact, we’ll actually be protecting all aspects of our health in the process.

But while we can make great strides in reducing inflammation by altering the fats we eat, remember that this is only the first step – once our level of “background” inflammation is under control, we’ll next want to devise strategies to stimulate and support the bodies’ innate healing power. Such strategies will be the focus of the next installment of the Integrated Supplements Newsletter. All told, we’ll finally be able to reap the rewards of proper nutrition and a healthy lifestyle – building a strong, resilient, and pain-free body at any age – even well after many of our peers have begun to fall victim to the degenerative effects of aging.

About Us: At Integrated Supplements, our goal is to bring you the wellness information and products you need to live your life to the fullest. We are dedicated to producing the highest quality, all natural nutritional supplements; and to educating the world on the health promoting power of proper nutrition. You can find out more by visiting: www.IntegratedSupplements.com