Nowadays, we have new risk factors for inflammation, which spells more rheumatic arthritis (RA) such as psoriasis, lupus and ankylosing spondylitis.
Even as 10,000 years ago, RA risk starts with genetics. Some of us have an allele called HLA-B27 which is associated with arthritis. If you have HLA-B27, you have greater risk of autoimmune arthritis.
Well, because of a chain reaction that starts in joints. Estrogenics like bisphenol A (BPA) cause joint cells to produce IL-6, a pro inflammatory cytokine. In turn, IL-6 upregulates IL-17, which increases risk of collagen-induced arthritis.
Basically, anyone who readily produces IL-17 is in danger of autoimmune attack on joints. Having HLA-B27 upregulates IL-17, in a sense meaning you are an IL-17 factory waiting to happen.
Waiting to happen is the key, as benelles usually safeguard. But benelles can be overrun if everything goes wrong: accumulation of plastic contaminants in joints, a lack of exercise, excess body weight, and a lack of vitamin A, which down regulates collagen-induced arthritis.
Thus, autoimmune arthritis is strongly tied to sitting around and consuming lots of processed food and drink in plastic packaging. These are modern risk factors the ancients never faced.
Most of our common plastic bases like BPA cause estrogenic activity. Estrogenics accumulate in fibroblast-rich tissue. Incidentally, the collagen that makes up the hyaline cartilage of our joints is made up mostly of fibroblasts.
Essentially, rheumatoid arthritis sufferers are allergic to plastics that have accumulated in their joints. Indeed, plastics have accumulated in all of our joints, but those with HLA-B27 posses the allergy which causes joint tissue damage, and pain. For the allergic, the plastic in joints is interpreted as a bacterial, viral, or fungal infection…one which never ends. Over time, joint tissue becomes chronically ill, resulting in RA like ankolosing spondylitis.
The overweight and obese are at greater risk. Their excess fat tissue stores more estrogenic material; a storage tank of plastic antigen.
People with plenty of adipose tissue and even mild estrogen allergy are likely to chronically aggravate sundry tissue. We can’t just think of a potbelly as a fat store; today, it’s also a bank of plastic pollution. For those with the genetic allergy, the plastics are constant deposits which aggravate joint tissue, heart tissue, pancreatic tissue, vascular tissue, breast tissue, etc.
Even for those with the allergy, benelles have a natural mechanism of using organic vitamin A to prevent the allergy from becoming a chronic tissue issue. But those consuming the most processed food, rich in chemicals and plastics, are the least likely to be eating a fresh assortment of organic food that’s rich in vitamin A.
In the end, many factors align for joint disease to occur. The right allele. Consuming plastics. Not exercising. Getting heavy. Not eating fresh foods. Our benelles have to have a great deal go wrong before they get sick, and even then the power of benelles is so strong, most people remain healthy.
Sadly, our healthcare system ignores the interplay and safeguards. It goes looking for a drug to control HLA-B27, when that allele isn’t the true problem and probably provides a key genetic advantage that would be foolish to give up.
To solve this, the government could share the placebo effect. The placebo effect is the largest government subsidy in the world. Right now, it’s given strictly to pharma companies. A doctor can’t be paid the same—and insurance won’t cover—putting an RA patient on filtered water and fresh organic food, even when the evidence shows that is the safest and most effectual path. For the doctor to make his money, he must provide toxic drugs, which pluck benelles, and which work largely based on the placebo effect. If the government says only prescription drugs work, that is a subsidy of hundreds of billions of dollars to pharma companies. Instead, government policy should help create market demand for safe, long-term solutions like organic farming, selling organic foods, etc. This starts with how the placebo effect is distributed.
My contention is that evidence-based healthcare should be reimbursed at a similar rate. Evidence-based doctors should control the placebo effect at a local level; not by decree of a central government. We need to brush past lobbyists and provide a new path for those with ankylosing spondylitis to get well.
I have no idea if my family has HLA-B27 but I suspect I carry the gene because my father has suffered from joint pain and a stiff back for over a decade. But I’m unconcerned; usually these types of genes confer some special advantage when treated properly, which we do in my house. My wife, kids and I drink RO water, and from glass containers. We don’t eat from cans. We never use prescription drugs or vitamins. We exercise daily, and eat an assortment of organic food, including carrots and raspberries. As a result, our benelles give us health you can’t find in a big healthcare system.
Shows BPA accumulates the most in animal tissue that’s rich in fibroblasts:
Doerge DR, et al “Distribution of bisphenol A into tissues of adult, neonatal, and fetal Sprague-Dawley rats” Toxicol Appl Pharmacol. 2011 Sep 15;255(3):261-70. doi: 10.1016/j.taap.2011.07.009
Shows DES, a synthetic estrogen, causes cartilage damage in animals:
Rowas S, et al “Effect of in utero exposure to diethylstilbestrol on lumbar and femoral bone, articular cartilage, and the intervertebral disc in male and female adult mice progeny with and without swimming exercise” Arthritis Research & Therapy 2012, 14:R17 doi: 10.1186/ar3696
Shows estrogen causes animal joint cells to produce IL-6 (proinflammatory cytokines):
Yun Kl, et al “Effect of estrogen on the expression of cytokines of the temporomandibular joint cartilage cells of the mouse” J Oral Maxillofac Surg. 2008 May;66(5):882-7. doi: 10.1016/j.joms.2008.01.034.
Shows BPA causes human fat cells to produce IL-6:
Valentino R, et al “Bisphenol-A Impairs Insulin Action and Up-Regulates Inflammatory Pathways in Human Subcutaneous Adipocytes and 3T3-L1 Cells” PLoS ONE 2013 8(12): e82099. doi: 10.1371/journal.pone.0082099
Reviews dysregulated IL-6 production and signalling being associated with chronic inflammatory diseases:
Camporeale A, Poli V “IL-6, IL-17 and STAT3: a holy trinity in auto-immunity?” Front Biosci (Landmark Ed). 2012 Jun 1;17:2306-26.PubMed link
Shows IL-6 upregulates IL-17:
McGeachy MJ et al “TGF-beta and IL-6 drive the production of IL-17 and IL-10 by T cells and restrain T(H)-17 cell-mediated pathology” Nat Immunol. 2007 Dec;8(12):1390-7. Epub 2007 Nov 11.PubMed link
Indicates HLA-B27 upregulates IL-17 in a pathogenic manner:
Bowness P et al “Th17 cells expressing KIR3DL2+ and responsive to HLA-B27 homodimers are increased in ankylosing spondylitis” J Immunol. 2011 Feb 15;186(4):2672-80. doi: 10.4049/jimmunol.1002653. Epub 2011 Jan 19. doi: 10.4049/jimmunol.1002653
Shows vitamin A down regulates IL-17:
Mottaghi A et al “Vitamin A Supplementation Reduces IL-17 and RORc Gene Expression in Atherosclerotic Patients” Scandinavian Journal of Immunology 2014 80: 151–157. doi: 10.1111/sji.12190