Whilst fibromyalgia syndrome is generally characterised by systemic unexplained pain, it can also be accompanied by various psychological symptoms that include depression, anxiety and fatigue. Research on different parameters in fibromyalgia indicates that there are a multitude of factors involved in the functional changes that lead to the syndrome. These include genetic factors, abnormalities in pain mediators such as substance P, neurotransmitters such as serotonin and changes in the complex system known as the hypothalamic pituitary adrenal axis (HPA) involved in regulating how we respond to stress. Dysregulation of the HPA-axis results in the production of products called cytokines, proteins produced during inflammation that can themselves trigger, or exacerbate existing, inflammation. The fibromyalgia patient is subjected to a complex interaction of chemicals, hormones and proteins, all of which can contribute to their many symptoms. Not surprisingly, there are no specific biomarkers that can lead to a diagnosis of fibromyalgia.
Another area gaining increasing interest is the role of oxidative stress in the initiation and progression of fibromyalgia and its related symptoms. Oxidative stress is a complex condition that is characterised by the release of highly unstable products called free radicals. Free radicals are considered unstable because they are missing an electron; this gives them the ability to disrupt normal cellular function. Oxidative stress is a constantly occurring process within the body, but our bodies have evolved to limit the levels of these ‘reactive oxidants’ and the damage they inflict. Specific enzymes such as superoxide dismutase and glutathione peroxidase act directly to inactivate these potentially harmful products. However the consumption of dietary antioxidants also provides an effective defence mechanism by donating an electron to the free radical, rendering it harmless and thus removing it from the circulation.
Issues arise when the body’s store of superoxide dismutase and glutathione peroxidase are depleted, or if the diet contains low levels of antioxidants. Furthermore, eating excessive amounts of specific fats can also add to this problem of increased oxidative stress. Fat consumed in the diet is required as a constituent of cell membranes (as phospholipids). Polyunsaturated fatty acids within phospholipids are highly susceptible to oxidative attack and the lipid by-products formed as a result of this reaction are either rendered un-reactive by the reaction with glutathione peroxidase, or can react with metal ions to form reactive products such as aldehydes. The most common of these aldehydes is malondialdehyde, a known mutagen which is also formed during the omega-6 fatty acid arachidonic acid (AA) metabolism for prostaglandin biosynthesis. Under physiological conditions malondialdehyde reacts with DNA to form products called adducts and it is these adducts that, if not repaired, have the ability to disrupt normal DNA replication that, in turn, can alter a myriad of cellular processes. Significant increases in the levels of malondialdehyde and its adduct by-product (8-hydroxydeoxyguanosine), as well as decreases in the levels of antioxidants and the key enzymes superoxide dismutase and glutathione peroxidase within fibromyalgia patients, compared to healthy control individuals, suggests the possible involvement of oxidative stress.1
As such, there are several diet-based approaches which may be of benefit to fibromyalgia patients. Firstly by increasing consumption of fruit and vegetables, it is possible to modify the intake of key vitamins that are known to act as powerful antioxidants. We are all probably aware of ’superfoods’ which have earned their illustrious title by way of their high antioxidant content. Such foods include açai berries, blueberries and pomegranates, but more simple foods, highly available and cost effective, such as citrus fruits, avocado, broccoli, onions, peppers, spinach, and sprouts (to name but a few!) are also ‘superfoods’ in their own right.
Increasing levels of superoxide dismutase and glutathione peroxidase within the body can significantly help defend against the damaging effects of oxidative stress. Asparagus contains more glutathione than any other common food item, but generally it is difficult to increase levels of superoxide dismutase and glutathione peroxidase by direct consumption. Glutathione is a small protein composed of three amino acids, cysteine, glutamic acid, and glycine; the amount of cysteine in the body can determine how much glutathione the body can make. Consuming foods with a high cysteine content can therefore help as an indirect way of ensuring glutathione levels are maintained. Cysteine is found in a variety of foods including pork, poultry, yoghurt, egg yolks, red peppers, garlic, onions and broccoli.
Finally, it is possible to protect the body from the harmful by-products derived from lipid peroxidation by modifying dietary fat intake and reducing AA levels which, in turn, may reduce the production of malondialdehyde, reducing the depletion of antioxidants and detoxification enzymes. AA, gamma-linolenic acid (GLA) and linoleic acid (LA) are three forms of omega-6 fatty acids, all with differing actions. LA is converted to GLA in the body. Technically, GLA is considered to be an anti-inflammatory omega-6; however, if levels of omega-3 in the diet are low, this releases adequate amounts of enzymes that are then available to further convert GLA into inflammatory AA.
Omega-6 fatty acid in the form of AA can be found mainly in non-organic meats (organs in particular), and other animal-based food items. Our high intake of grains and oils rich in LA, coupled with our low intake of omega-3 fatty acids, has led to an overall increase of AA within our cell membranes. Because the AA pathway constitutes one of the main mechanisms for the production of pain and inflammation, reducing levels can have a major effect on reducing long-term pain. Increasing levels of omega-3 and in particular eicosapentaenoic acid (EPA) results in competition with AA for incorporation into cell membranes whilst also inhibiting the final conversion of GLA to AA, allowing GLA to convert to a family of anti-inflammatory products.
Consuming EPA therefore reduces the AA content of cell membranes, indirectly reducing the conversion of inflammatory products from AA and directly increasing the production of omega-3 anti-inflammatory by-products and the production of omega-3 anti-inflammatory by-products.
Not surprisingly, many fibromyalgia patients benefit from a taking Vegepa, a unique source of EPA and GLA. Furthermore, ensuring the body’s reservoirs of antioxidants detox enzyme precursors are kept in check can have a significant impact on many of the symptoms associated with fibromyalgia syndrome.
- Iqbal R, Mughal MS, Arshad N, Arshad M. (2011) Pathophysiology and antioxidant status of patients with fibromyalgia. Rheumatol Int. 31:149-52.