Systemic lupus erythematosus (SLE) is an autoimmune condition that usually presents as a constellation of signs and symptoms affecting multiple organs, including the skin, kidneys, heart, lungs, brain, and bone marrow [1]. SLE predominately affects women of childbearing age, and is more common in those of Hispanic, African American, Asian, and Native American ethnicity [2] [3].
Lupus is Latin for ‘wolf,’ and erythematosus means ‘characterized by erythema’ (redness of the skin), erythema being derived from the Greek word for red, erythros. The term lupus represents more of an umbrella and is often used somewhat loosely, but most frequently lupus is referring to SLE. SLE autoantibodies can be directed against components of the nucleus, cytoplasm, or surface of cells, though antinuclear antibodies are the most characteristic, and anti-double stranded DNA (anti-dsDNA) and anti-Smith (anti-Sm) antibodies are quite unique to SLE [4]. Necessary to mention is the condition of drug-induced lupus erythematosus (DIL), for over 100 pharmaceuticals and biologic agents have been associated with the onset or exacerbation of lupus-like autoimmunity [5]. Multiple mechanisms may be exploited by pharmaceuticals in their contributing to autoimmunity, such as direct cytotoxicity, nonspecific lymphocyte activation, central tolerance disruption in the thymus gland, and epitope spreading (antibodies are crafted against more and more antigens, basically expanded molecular mimicry) [6]. Aberrations in the function or activity of B cells, T cells, dendritic cells, Fc gamma receptors (found on IgG antibodies), proinflammatory cytokines, complement system proteins, and apoptosis can all play a role in the pathogenesis of systemic lupus erythematosus [7]. Overarchingly, SLE can be characterized by a global loss of self-tolerance that includes autoreactive T cell and B cell activation which leads to the making of autoantibodies and subsequent tissue injury. Noteworthy is the fact that Choi, Kim, and Craft have argued that innate immune system issues are necessary for the aberrant responses of the adaptive immune system seen in SLE [8]. We know that lupus macrophages seem to be hyper-responsive to stimuli from innate immune system effectors, and this hyper-responsiveness, coupled with immune complexes (a.k.a. antigen-antibody complexes), type I interferons, neutrophil NETs, and mitochondrial destabilization, may heighten activation of the NLRP3 inflammasome and drive disease progression [9]. Two major steps in the pathogenesis of SLE include the stressing of phagocytes (like macrophages and neutrophils) from a large induction of apoptosis and release of nuclear antigens by one or more triggers or agents (leading to flawed clearance of nuclear antigens), and the presentation of autoantigens to autoreactive T and B cells causing autoantibody production and the formation of immune complexes which heighten innate and adaptive immune activity (driving autoimmunity) [10]. Essentially, hyperactivation of antigen-presenting cells promotes a loss of self-tolerance and the inadequate clearing of immune complexes fuels autoantibody manufacturing. Immune attacking of self cells and tissue damage spreads from there. Said a little differently, abnormal apoptosis coupled with the insufficient clearing of cellular debris allows intracellular autoantigens to linger in the extracellular space, where they are highly proinflammatory and are recognized by autoreactive immune cells that respond with the crafting of autoantibodies [11]. Since an overabundance of apoptosis combined with an inadequacy in clearing apoptotic cells is an important factor in SLE’s conjuring, remedying mitochondrial ill-health could be critical to correcting this condition because mitochondria are heavily involved in activating apoptosis [12] [13]. Regenerating damaged or faulty mitochondria could help ameliorate apoptosis signaling and improve the efficiency of waste removal (if nothing else, allowing the immune system to take a breath) [14]. Furthermore, mitochondria have been seen to be dysfunctional in the T cells of lupus patients, and the hyperpolarization and ATP depletion of these mitochondria predispose their housing T cells to necrosis, which can then drive the activation of dendritic cells and the making of autoantibodies [15]. Lastly, quenching free radicals made by mitochondria has reduced the severity of disease and type I interferon signaling in a murine model of lupus, which supports the recommendation for mitochondrial support in lupus patients [16]. It has been well documented that type I interferons (largely antiviral helpers) are usually released excessively and persistently in lupus, which illustrates that SLE behaves like a poorly controlled, ongoing viral infection [17]. Important is the fact that environmental toxins can activate the immune system in much the same way as pathogens do, even in the absence of a pathogen (like a virus), so the continual mounting of anti-pathogen fronts by the immune system can be caused by continual toxin exposure or toxin harboring [18]. Plasmacytoid dendritic cells are the chief fabricators of type I interferons, but neutrophils can also make them in response to chromatin exposure [19]. As more chromatin is released from apoptotic cells, more antibodies and immune complexes form, perpetuating the disease state. Essentially, lupus involves a vicious cycle of inflammation, apoptosis, autoantibody manufacture, and more inflammation. Neutrophils can kill pathogens by engulfing them or by secreting antimicrobial peptides and chromatin in meshworks named ‘neutrophil extracellular traps’ (NETs). Lupus neutrophils evidently have a greater propensity to undergo a form of cell death termed NETosis, and both interferon alpha and immune complexes can be triggers for increased NETosis [20]. NETs can injure tissues directly, and since lupus patients don’t clear NETs normally, a buildup of NETs may encourage disease progression. Also, significant neutrophil activity would suggest ongoing inflammation, possibly due to microbial infection or toxin exposure, items that may need to be addressed in treating lupus. Roughly 35 genes have, at least to some degree, been linked to SLE [21]. Specifically, certain major histocompatibility complex (MHC) class II and class III alleles (variant gene forms) may increase one’s risk for developing lupus. And single nucleotide polymorphisms (SNPs) in non-HLA genes like IRF5, STAT4, PTPN22, and multiple Fc gamma receptor genes have been tied to SLE’s inception with varying strengths [22]. Jeffries and Sawalha have expressed that hypomethylation of a few different overexpressed genes in lupus T and B cells seems to play a significant part in SLE’s genesis [23]. Inhibiting DNA methylation can make T cells autoreactive and facilitate their stimulating of macrophage apoptosis, and as macrophages die off through apoptosis, they release antigenic chromatin in addition to lessening the immune system’s capacity to clean up cellular debris, enhancing autoantibody production [24]. Accordingly, supplemental methyl donor support may be indicated in the treatment of at least some lupus cases [25]. Serum concentrations of the anti-inflammatory cytokine interleukin-10 are typically higher in those with lupus, and because IL-10 is a critical immunoregulator in the gut, persistently high IL-10 levels would suggest ongoing inflammation in the GI tract [26]. Therefore, in treating lupus, correcting intestinal dysbiosis, removing offending foods, and healing intestinal hyperpermeability will almost certainly be necessary. A leaky gut is the hallmark precursor to the presentation of most states of autoimmunity [27]. Very important: one paper reported three cases of patients whose gluten sensitivity was misdiagnosed as systemic lupus erythematosus (one of these patients was erroneously treated for years with steroids and immunosuppressive drugs) [28]. After a few months of nothing but a gluten-free diet, each of the three patients experienced subsiding of their symptoms. At least some degree of adrenal fatigue or HPA axis dysfunction has been found in human lupus subjects, suggesting the likely indication for stress reduction and adrenal support [29]. High concentrations of the problematic estrogen metabolite, 16-alpha-hydroxyestrone, have been demonstrated in SLE patients of both genders, suggesting unhealthy estrogen metabolism [30]. DIM (diindolylmethane) and indole-3-carbinol can both be used to improve estrogen metabolism and the ratio of 2-hydroxyestrone and 16-alpha-hydroxyestrone [31] [32]. Moreover, hormone replacement therapy and hormonal contraceptives have been associated with a small increase in SLE risk [33] [34]. A high prevalence of Epstein-Barr virus infection has been seen in lupus patients, and this virus has been identified as a possible etiological factor [35]. Antibodies against Epstein-Barr virus can cross-react with lupus-associated autoantigens, and through B cell epitope spreading, may target additional autoantigens and ultimately drive the manifestation of clinical lupus [36]. Specifically, we know that lupus patients typically exhibit a dysregulated immune response against Epstein-Barr, and since some EBV proteins are molecular mimics of human immune system components, they can end up promoting impaired apoptosis and detrimental signaling of B cells [37]. Then again, Epstein-Barr virus may simply exacerbate already existing lupus, and the same may be said for cytomegalovirus and parvovirus B19, other viruses also associated with lupus [38] [39]. Molecular mimicry between human endogenous retroviruses and ribonucleoprotein complexes may also play a part in SLE’s initiation (though exogenous retroviruses delivered to the body through vaccines are more likely culprits) [40]. Root canal procedures can contribute to overwhelming of the immune system and the induction of autoimmunity, and so amending oral health could be requisite in the healing of lupus [41] [42]. Mercury has been identified as a potential causal agent in SLE, but other metals like cadmium, lead, and aluminum can be just as detrimental to the body and the functioning of the immune system [43] [44]. Certainly you’d be hard-pressed to find an individual with an autoimmune condition who wouldn’t benefit from an appropriate heavy metal detoxification program. Cigarette smoking and the use of permanent hair dyes have been connected with SLE, though not strongly [45] [46]. Aspartame is a very widely used artificial sweetener that can engender the autoimmunity seen in SLE. Aspartame is metabolized to phenylalanine, aspartic acid, and methanol (also known as wood alcohol) in the body. Aspartame is excitotoxic and can lower hemoglobin and red blood cell count, in addition to being able to damage the liver [47] [48]. Aspartame can ultimately be metabolized to formaldehyde, and formaldehyde can injure DNA and negatively modify proteins, inviting tumor formation as well as autoimmunity [49] [50]. The hepatitis B vaccine has been seen to trigger the onset of lupus erythematosus, and multiple instances of this triggering have been reported in the medical literature [51] [52] [53] [54] [55]. The appearance of a spectrum of SLE-like conditions has also been reported after administration of the HPV vaccine [56]. Relatedly, numerous cases of lupus vulgaris occurring after administration of the BCG (bacillus Calmette-Guerin) vaccine have also been reported (the BCG vaccine is typically given for tuberculosis but can also be used in the treatment of superficial bladder cancer) [57] [58] [59] [60]. Now let’s go over some aides that we can employ in the natural treatment of lupus. Firstly, let me just say that the conventional prescription of immunosuppressive drugs for lupus patients is riddled with side effects and fails to address underlying issues [61]. Vitamin D deficiency has been correlated with B cell hyperactivity and higher interferon alpha (a type I interferon) activity in the serum of lupus patients, so lupus patients may benefit from sufficient sun exposure or vitamin D supplementation [62]. Evidence exists for the use of vitamin E, vitamin A, selenium, fish oil, and evening primrose oil to be potentially helpful in the treatment of SLE, largely because of antioxidant and anti-inflammatory effects [63]. In using flaxseed to treat lupus nephritis, improvements in kidney function, plasma lipids, blood viscosity, and complement component 3 levels were demonstrated [64]. Turmeric can safely be of use in lupus nephritis, and curcumin can safely modulate Th17/Treg balance in SLE (basically helping to reestablish tolerance of self antigens) [65] [66]. The Chinese herbal formula Zi Shen Qing has proved to be a safe and effective agent for decreasing SLE disease activity and specifically lowering anti-dsDNA antibody and immunoglobulin G concentrations [67]. N-acetylcysteine has safely bettered lupus disease activity by blocking mTOR in T cells (mTOR regulates the production of interferon alpha and the maintenance of immune tolerance to an extent) [68] [69]. Perna canaliculus or green-lipped mussel has prevented the development of autoimmune conditions like SLE and rheumatoid arthritis in laboratory animals via potently dropping proinflammatory cytokines, inhibiting COX-1 and COX-2 enzymes, and suppressing immunoglobulin G [70]. In a study involving eight subjects with SLE given only a gentian supplement, six experienced complete remission and the remaining two experienced improvement with no apparent side effects [71]. In another study, six SLE subjects were given pycnogenol (a pine bark extract) and each of the six saw a reduction in free radical production, apoptosis, and erythrocyte sedimentation rate (a measure of inflammation) [72]. Cordyceps sinensis (or Ophiocordyceps sinensis) has aided kidney function and decreased anti-dsDNA antibodies in SLE rats [73]. In a murine model of SLE, the administration of royal jelly (a honey bee product) resulted in a lessening of interleukin-10, anti-dsDNA antibodies, splenic autoreactive B cells, and anti-ssDNA (anti-single stranded DNA) antibodies [74]. Gotu kola (a.k.a. Asiatic pennywort) could be of some help for lupus patients as it can help to calm the immune system, enhance circulation, regenerate collagen, and soothe inflammation [75]. I think it’s worth mentioning that burdock root can be used to effectively treat lupus skin rashes and has quite a long history of such employment [76]. Anecdotal reports of varying success have come from the use of aloe vera juice and apple cider vinegar for SLE, the major benefit probably stemming from these agents’ antifungal action in the GI tract [77] [78]. Active lupus disease can certainly predispose one to fungal infection, but fungal infections or overgrowths can also contribute to the appearance of lupus (Candida infection has been identified as the most common fungal infection in SLE patients) [79] [80]. Interestingly, a case study from a 1913 issue of the British Medical Journal reported correction of a lupus skin lesion using nascent iodine, though the treated patient also had tuberculosis, and so the improvement seen might have simply been due to iodine’s antibacterial effect [81]. Next let’s look at two hugely significant options available to us in the treatment of lupus: stem cell therapy and systemic enzymes. In one study, umbilical cord-derived mesenchymal stem cells (UC-MSCs) were administered to 16 subjects with SLE which resulted in significant improvements in serum antinuclear antibody and complement component 3 levels, bettered renal function, augmentation of peripheral Treg cells, and overarchingly, clinical remission in each of the 16 subjects [82]. In another study involving 15 subjects with SLE, mesenchymal stem cell transplantation yielded amelioration of disease activity in all subjects, with drops in serum titers of anti-dsDNA and other antinuclear antibodies, stabilization of renal function, and boosts in regulatory T cell numbers [83]. In a case study involving a 19-year-old woman who developed diffuse alveolar hemorrhage (a life-threatening event of bleeding from the lungs) about two months after her diagnosis of SLE, a single infusion of UC-MSCs was given and allowed the woman to make a dramatic recovery and be discharged from the hospital a few weeks later [84]. Similar results were also seen in a mice model of SLE using umbilical cord-derived mesenchymal stem cells [85]. Systemic enzyme therapy can have a widespread anti-inflammatory effect in the body, and has safely and effectively been used in the treatment of autoimmune conditions because of its ability to modulate pathogenic autoantibodies, inhibit the creation of immune complexes, and normalize T cell and cytokine activity [86] [87]. Systemic enzyme therapy is a highly overlooked yet invaluable modality for the natural treatment of autoimmunity. So, taking a step back, we can identify four standard, broad steps to be taken in the healing of lupus. First, restore normalcy to the gut microbiota and repair the overly permeable gut wall. Second, appropriately and sequentially detoxify the body to reduce the toxic burden, help extinguish inflammation, and calm the immune system. Third, utilize proteolytic enzymes to break up immune complexes, clean up cellular debris, and purify the blood. Fourth, administer stem cells to regenerate tissues that have been damaged by autoimmune attacking or use nutrition and herbs to do the same thing. In conclusion, some individuals have virtually cured lupus through diet alone, so to say that SLE is incurable is incorrect and precipitous (especially when conventional medicine claims that they don’t know what causes SLE). How can someone say that a condition is incurable when they don’t know what causes it? Obviously the cure lies in the cause. And correcting the cause is what natural medicine is all about. References:
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AuthorDenton Coleman is an Exercise Physiologist and Medical Researcher. Archives
October 2023
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