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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The term hemochromatosis describes a condition of excess iron in the body, and primary hemochromatosis (also known as hereditary hemochromatosis) and secondary hemochromatosis stand as the two main forms. A buildup of iron can be quite toxic and frequently damages such organs as the heart, liver, and pancreas (as well as joint tissues) [1].
Secondary or acquired hemochromatosis commonly manifests as a result of frequent blood transfusions, very high dietary or supplemental iron intake, significant hemolysis or the rupturing of red blood cells (can be due to microbial infection, autoimmunity, genetic disorders, etc.), too much alcohol consumption, or some kind of liver disease (like chronic viral hepatitis) [2] [3]. Signs and symptoms of hemochromatosis may include: abdominal pain, hair loss, fatigue, joint pain, weight loss, bronzing or darkening of skin color, and low libido [4]. The diagnosis of hemochromatosis may involve one or more of the following blood tests: serum iron, serum ferritin (iron storage protein), transferrin saturation (transferrin is an iron transport protein), and total iron-binding capacity (an indirect transferrin measure) [5]. An MRI, liver biopsy, or genetic test may also be employed to confirm or assess clinical findings [6]. The human body doesn’t really have a mechanism for excreting extra iron, so iron accumulation is largely a matter of intestinal absorption and release from macrophages. Phlebotomy or blood draws weekly or periodically is the chief method of treatment for iron overload issues, though pharmaceutical iron chelators like deferoxamine, deferasirox, and deferiprone are also available [7]. Erythrocytapheresis or the removing of red blood cells from whole blood extracted from the patient is another option. Hereditary hemochromatosis is often characterized by a mutation in the HFE gene promoting undue intestinal iron absorption, but mutations in other genes associated with iron metabolism (like HJV, HAMP, TFR2, and SLC40A1) can lead to forms of iron overload very similar to classical hereditary hemochromatosis, and since iron overload can arise in the absence of a strong genetic contributor, hemochromatosis can be more accurately viewed as an umbrella under which multiple conditions with similar clinical features exist [8] [9] [10]. And it’s important to understand, as Dr. Ernest Beutler has explained, that the simple presence of the hereditary or HFE hemochromatosis genotype is insufficient for the development of clinical disease [11]. Dr. Beutler agreed with the 1955 contention of Finch and Finch that the “hemochromatosis mutation” is common, but the hemochromatosis disease is rare or at least uncommon [12]. Fun fact: Ernest earned his doctorate degree in medicine from the University of Chicago at the age of 21. It would also be more correct to classify hemochromatosis as a disorder of iron metabolism (usually involving dysregulation of the hepcidin-ferroportin axis), rather than just iron abundance [13]. The pathophysiology for hemochromatosis conditions is complex, so let’s just focus on some highlights pertinent to this article. Firstly, hepcidin, encoded by the HAMP gene, is a major regulator of systemic iron homeostasis. Hepcidin is an antimicrobial peptide predominantly made by hepatocytes (liver cells) whose production is stimulated by inflammation, iron loading, and cellular signals from endoplasmic reticulum stress (endoplasmic reticula are organelles present in almost all cells of the body) [14] [15]. A rise in hepcidin normally coincides with a fall in serum iron due to lower iron absorption from the gut and higher iron trapping by macrophages. Hepcidin expression is inhibited by anemia (low hemoglobin or red blood cells), hypoxia (low tissue oxygen), and increased erythropoietic activity (the making of red blood cells in red bone marrow) [16]. So hepcidin levels go up with inflammation or microbial infection, and go down with anemia or hypoxia. Therefore, improving oxygenation (with a supplement like Germanium-132 for example) could be used to treat high iron levels. Coming back to the fact that endoplasmic reticulum stress triggers hepcidin release, since endoplasmic reticula perform the heavy lifting of cellular-level detoxification, the deficiency of hepcidin commonly seen in hemochromatosis may reflect an exhaustion of hepcidin expression from overstimulation due to toxicity and dysbiosis (bacterial lipopolysaccharide can induce hepcidin production in macrophages for example) [17] [18]. Accordingly, understanding the presentation of hemochromatosis as being reflective of a weak or overwhelmed liver coupled with adrenal stress, we can prioritize detoxification and adrenal support in the treatment program. Next, we know that the body can withhold iron from potential pathogens as a defense strategy for thwarting infection. This withholding is achieved by reducing the amount of iron bound to serum transferrin [19]. And the body can choose to absorb less iron from the gut during times of inflammation to deprive pathogens of iron. But with chronic inflammation and stress, I contend that the body’s iron withholding mechanism could become dysregulated or fatigued. Because iron overload can compromise the ability of phagocytes (like macrophages and neutrophils) to engulf and destroy pathogens, and because the virulence of many microorganisms can be enhanced by an abundance of iron, it’s hard to argue against microbial infection or dysbiosis being able to both promote the onset and fuel the maintenance of hemochromatosis [20]. So resolving microbial infections or dysbiosis may be very necessary in the treatment of chronic states of iron overload. Some of the microbial and viral genera containing species whose growth or virulence rises in response to iron availability include: Candida, Cryptococcus, Entamoeba, Plasmodium, Toxoplasma, Clostridium, Mycobacterium, Staphylococcus, Streptococcus, Escherichia, Klebsiella, Pseudomonas, Salmonella, Cytomegalovirus, Parvovirus, Hepatitis B virus, and Hepatitis C virus [21]. And I think it’s worth mentioning that Human cytomegalovirus protein US2 can downregulate the HFE gene’s expression (which fosters high serum iron), possibly encouraging the persistence or proliferation of viruses in general [22]. Also, remember that alcohol consumption is related to hemochromatosis. Yeast organisms like Candida albicans can ferment ingested sugar into ethanol, which can then be metabolized into acetaldehyde. Acetaldehyde is toxic and can hinder the function of white blood cells, as well as contribute to anemia by rigidifying the cell membranes of red blood cells [23]. So consider Candida overgrowth as a possible factor in the pathogenesis of iron overload. To quickly summarize, so far we’ve identified inflammation, dysbiosis, toxicity, and hypoxia as ingredients in the brewing of hemochromatosis. Now let’s look deeper into iron metabolism and homeostasis. Again, hepcidin plays a dominant role in iron trafficking, and an abnormally low presence of hepcidin yields a large uptake of iron from the gut and a large release of iron from storage sites, leading to tissue iron saturation [24]. Now, the liver stands at the central axis of iron metabolism, for it is the main site of ferritin (iron storage protein) and transferrin (iron transport protein) synthesis, and it is where HFE protein, transferrin receptor 2, and ferroportin are preferentially expressed. HFE protein modulates hepcidin and transferrin-mediated iron uptake, transferrin receptor 2 helps with the cellular uptake of transferrin-bound iron, and ferroportin exports iron or pushes it out of cells [25] [26] [27]. Iron is recycled by macrophages which break down senescent red blood cells and hand over the scavenged iron to transferrin for transport throughout the body and to red bone marrow so that it can be incorporated into hemoglobin. Summarizing again, there is a triad between the liver, the gut, and the immune system that is responsible for iron sensing, iron uptake, and iron release, and thus the systemic distribution and utilization of iron [28]. Ergo, in crafting a plan for the remedying of hemochromatosis, we should look to the liver, the gut, and the immune system and identify hindrances, weaknesses, and flaws in these components of the body. Moving on to some natural treatment options, let’s first pay heed to the following recommendations typically given to hemochromatosis patients [29]: - Obviously avoid iron supplementation. - Consume red meat in moderation. - Limit or abstain from alcohol consumption. - Limit supplemental vitamin C to 500 mg daily or take supplemental vitamin C away from meals. - Avoid raw shellfish. Now we can cover some recommendations and supplement options: - Intestinal iron absorption can be enhanced by vitamin C but diminished by calcium, zinc, and manganese, so many leafy greens are great for those with hemochromatosis [30] [31]. - Vitamin D seems to play a part in the hepcidin-ferroportin axis, and so getting some sun or supplementing with a reasonable dosage could be helpful [32]. - Alpha-lipoic acid is a potent antioxidant and anti-inflammatory, and because it can chelate and help remove excess iron, its use is indicated in hemochromatosis (note that alpha-lipoic acid can also chelate copper) [33]. - Low vitamin E levels have been seen in hemochromatosis patients, and since such patients need to be careful with their intake of vitamin C, vitamin E makes a great alternative antioxidant [34]. - Because S-adenosylmethionine (SAMe) can be low in those with liver disease due to a hampered conversion of methionine to SAMe, SAMe supplementation could up the body’s methyl donor supply and help knock down inflammation [35]. S-adenosylmethionine has been used to improve liver function in an animal with hemochromatosis, but it’s hard to say how much benefit was derived from the SAMe as deferoxamine and phlebotomy were also employed [36]. - N-acetylcysteine is another excellent antioxidant (NAC is a glutathione precursor) and anti-inflammatory, and has demonstrated liver protection in a murine model of alcohol-induced liver damage [37]. More importantly, NAC can bind to redox-active metals like iron (and copper) and therefore may improve iron overload (though a relatively high dose may be needed) [38]. - Curcumin is a well-known antioxidant and iron chelator and has been found to be very beneficial for those with iron overload or liver damage [39]. Specifically, curcumin decreased serum iron, spleen iron content, and liver iron content in mice [40]. - Intestinal sanitation can be imperative in the correction of iron overload and conditions of liver stress. Germane to liver status, probiotics can improve gut barrier health, modulate innate and adaptive immune function, and reduce the concentration of harmful gut microbes (note that the liver receives about 70% of its blood supply from the gut via the hepatic portal vein) [41]. Probiotics have demonstrated particular usefulness in the treatment of liver diseases [42] [43]. - It wouldn’t hurt to filter your drinking water to reduce iron intake from this source [44]. - As a supplement, pectin may be able to bind iron and partially block its absorption [45]. - Similar to curcumin, EGCG (epigallocatechin gallate) from green tea is an antioxidant and iron chelator, and can inhibit iron absorption from the gut, as can grape seed extract [46]. - The polyphenols quercetin, chrysin, rutin, and myricetin are all capable of chelating iron, and both quercetin and myricetin have rivaled the drug deferoxamine in vitro [47] [48] [49]. In a mouse model, quercetin and baicalin (another polyphenol) were shown to decrease liver iron content as well as iron-induced lipid peroxidation and protein oxidation in the liver, in addition to increasing iron excretion via stool [50]. - Milk thistle is commonly recommended for hemochromatosis and liver issues in general, and its flavonolignan complex silymarin can serve as a strong antioxidant, anti-inflammatory, antifibrotic, and regenerant tonic for the liver [51]. Silymarin can chelate iron, reduce iron absorption, and drop serum ferritin [52] [53] [54]. - Inositol hexaphosphate (IP6) or phytic acid possesses a familiar capacity to bind iron in the gut, but it can also protect the liver against free radical damage and lower both serum iron and serum ferritin [55]. Inositol hexaphosphate can be taken with food to blunt iron absorption, but it would be more effective for hemochromatosis when taken in-between meals so that it can readily enter the bloodstream. In conclusion, we know what can promote the manifestation of hemochromatosis and we know what can be done to address and even resolve those factors. Hemochromatosis patients need not be stricken of hope by incorrect and outdated understandings of conventional medicine. Hopefully this article was of some avail to you. References:
Unarguably, there is nothing that has been more misunderstood, wrongly chastised, battled against, unfairly blamed, and unhealthfully exploited than human sexuality. Its misapplication, suppression, and demonization is the source of more violence, disease, corruption, and detriment than any pathogen, economic scarcity, feudal bickering, or governmental unrest. Why then, is our sexuality, something as biologically innate as our need for oxygen, so powerfully at the crux of worldwide inharmony? The short answer is because sexuality stands as our most intrinsic connection to God. The central theme of human experience has been for quite some time, the separation between man and the divine. The most obvious expression of our creatorship is reproduction, the birthing of new life. Under the veil of metaphysical ignorance, this creative power is often heralded as miraculous yet enigmatic, for to the religious adherent, isn’t creation the sole office of God?
Herein lies the origin of sexuality’s condemnation, for how dare the lowly human dabble in the celestial? Deplorably, it is all-too-well known that to control humanity’s sexuality is to control humanity. Preaching that copulation is for reproduction only, and that any other embodiment of intimacy is despicable, immoral, and sinful is an excellent way to ensnare human consciousness and fill it with fear, inferiority, and shame. On the contrary, natural sexual expression is something that unifies the human’s consciousness with that of the divine, it merges the male and female poles, and it opens the heart chakra to a streaming of unconditional love. Unconditional love is what God is, so inviting in such love invites in God and reminds us of our inseverable connection to the universe. Loving and respectful intercourse is capable of transcending material illusions, significantly healing and rejuvenating the body, and cleansing the aura of accumulated negativity and trauma. But here’s the kicker, it is terribly incorrect to assume that loving and respectful intercourse can only be shared by legally married individuals. Religious and cultural programming abhors anything outside of traditional monogamy, but this aversiveness exists purely as a human crafting. Now, please don’t mishear me, I am not stating that strict monogamy is inherently bad or wrong in any way. Every person is free to engage in the kind of consensual relationship that they wish. But to universally and unwaveringly restrain and confine human sexuality to strictly exclusive relationships dishonors our sovereign, free-willed, and divine nature. Again, please don’t mishear me. It is a wonderful and beautiful thing for two individuals to freely and willingly choose to commit to a traditional, monogamous partnership, regardless of how long it lasts (as opposed to two individuals reluctantly making such a decision because they believe they have no other permissible option in the eyes of God, society, or their parents). However, as long as respect, honor, and love stand as the foundation, other types of relationships can be equally wonderful and beautiful – and the right to unjustly prevent anyone from exploring or experiencing the kind of marital or romantic relationship they wish to belongs to no one. And by no one I mean no governmental figure, no religious figure, no celebrity, no imbecile on Twitter, no extraterrestrial, and not even God. We are unfoldings of the one Creator and we are infinite and eternal beings of light. It’s time we pull our heads out, grow up, and start acting like it. For far too long human sexuality has been enslaved by false teachings, fabricated beliefs, moronic superstitions, and even absurd legislation. Divine entities (which we are) are, by definition, sovereign and free to create and add to All That Is in the manner they choose. This means that we humans are free to experience God, love, ecstasy, union, partnership, higher states of consciousness, the spectrum of emotion, and, overarchingly, our creatorship as we desire. To limit the human is to limit God. We are here to create, to sense with all our senses, and to experience being empyrean within a physical body. We are not the possession of anyone or anything, therefore, when we unfurl self-acceptance and self-love we provide ourselves the opportunity to freely engage in relationships which nurture, warm, comfort, heal, and uplift us, without having to draft lengthy contracts that outline what we expect from and are owed by the other person. We can simply offer and receive love for the sake of loving. And when love is shared in such a pure way, unification with the true God is felt and known, and that is what connecting with other people is ultimately about – seeing God in all things. Shifting gears, it is very foolish for one to settle for or resort to a frustrating and miserable relationship simply because they believe that pursuing what they want is improper, iniquitous, or shameful. Commonly desperate attempts are made to inject new passion, excitement, or novelty into a relationship which end up procuring tension or even resentment because they get in the way of one or both partners authentically accepting and loving themselves as they are. As passion and lust fade, questions over one’s attractiveness and wantability often manifest or bubble to the surface. More detrimentally, questions over one’s deservedness or worthiness may soon follow. The blind and fearful adherence to artificial and invalid yet ego-serving moralism illustrates why “Adultery has been documented in every ostensibly monogamous human society ever studied, and is a leading cause of divorce all over the world today” [1]. Without the intention of preaching or proselytizing, it is clear that dogmatic suppression of affection and natural sexual expression fosters an increase in psychological dissonance and interpersonal violence [2]. It is also clear that emotional intimacy is a need quite universal in humans, but to assume that emotional intimacy can only arise within monogamous relationships is a mistake. For instance, Bergstrand and Williams, after surveying over 1,000 so-called swingers, concluded that swingers “are less racist, less sexist, and less heterosexist than the general population,” and that swingers “rated their marriages as happier, their overall life satisfaction as greater, and their lives as more exciting” [3]. Swingers engage in what can be defined as emotionally monogamous yet sexually non-monogamous relationships. Accordingly, swinging should be made distinct from polyamory, where genuine love (which may or may not involve sexual intercourse) and emotional intimacy are shared with more than one partner concurrently. I’d like to mention that in the above study, the authors stated that their results suggested the surveyed subjects were no more likely to come from abusive or dysfunctional backgrounds than members of the general population, and that the sampled swingers seemed to be as committed to marriage, family life, and emotional monogamy in relationships as those in a comparative sample. Thus, it would not be fair or accurate to label swingers as social deviants or debauchers. In another interesting survey of a few thousand young adults who, in their adolescence, were presented with an opportunity to pledge to remain sexually abstinent until marriage, it was found that those who pledged to remain sexually abstinent were more likely to engage in anal or oral sex in place of vaginal sex, and were less likely to use a condom at first sex (before marriage) than those who did not pledge to remain sexually abstinent [4]. More relevant to our talk is the fact that 88% of the subjects who pledged to remain abstinent reported having engaged in intercourse before marriage. Certainly, the results of the above study cannot be extrapolated to everyone on the planet, but they do suggest that legally married individuals are unlikely the only humans who could possibly be interested in copulation. Taking a step back, prior to the rise of agriculture, early human civilizations thrived in close-knit bands, tribes, and villages. Within many of these hunter-gatherer communities, resources were freely shared, children were raised by the adult collective, and egalitarianism was the norm [5]. Importantly, gender equality thwarted possessiveness in primitive societies, and allowed for a more casual sharing of intimacy – turning communities into large families (not implying incest). Instead of the theme, “my spouse and I against the world,” “my large family and I living in harmony with nature” prevailed. Of course, this is in contrast to the picture painted by the atheistic, evolutionary biology classes we attended in college. Granted, this is not to say that pair bonding was completely absent in early man, as it wasn’t. But the standard narrative of human sexuality is erroneous and degrading, for it posits that male-female interaction is largely based on an exchange of sex for goods and services. We are not apes, men are not from Mars and women are not from Venus, and we are not biologically designed to confuse, manipulate, or psychologically torment one another. We are spiritual souls of which the human body constitutes only a fraction. Doesn’t it make more sense for us all to just get along? Instead of trapping ourselves within dualistic prisons of good and bad, or right and wrong, what if we freed ourselves from the silly perimeters of the ego and smoothly slid back into our true, heart-centered state in which we let unconditional (unconditional meaning without condition folks) love flow from, to, and through us? What if we put down our weapons and our fists, shut our mouths, closed our eyes, and opened our hearts to the greater reality that exists beyond the dividing, dehumanizing, debasing, and fear-inducing matrix that is itself, manmade? What would the human then perceive? What would the human then consist of? The human would perceive and consist of its essence – love and light. Imagine such a recasting. We are living in an unprecedented time, and right now we are serving as both descendants and forerunners. Vincit omnia veritas proclaim the illumined. The arms of Aquarius are open wide now, let us set our course for home. In conclusion, nirvana or moksha is not sought, it is realized. The human being is already complete, already whole – therefore enlightenment is allowed rather than achieved. The universe is not a work in progress, it is ever expanding perfection. We are eternal entities, so there is no true death, only a perpetual adding to all that we are. This life then, and all of our existence, is a flower that unendingly blossoms. The light waves which constitute the third dimension are always in motion, always in flux. As such, there is always an ongoing dynamism, a continual changing with the inbreath and outbreath of the cosmos. As Alan Watts has spoken to, if we imagine we are being carried along by a stream of water, then we feel as though we are one with the stream – we flow as the stream flows. But if we effort against the stream, we separate ourselves from it, and in doing so, we lose the power of the stream. If the stream represents our creative essence, then we create most effortlessly when we are in a state of oneness, in a place of love. Yet when we separate ourselves from God and the universe through fear, hate, and inharmony, we erect enormous resistance to the flow of our creative essence and we allow the mind to restrict the expression of our divinity. Let yourself be carried by the stream of your divinity, your God-hood, and there will be no place where you cannot be taken. Amun-Ra, Amen. References:
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AuthorDenton Coleman is an Exercise Physiologist and Medical Researcher. Archives
October 2023
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