Rheumatoid Arthritis Cause and CurePosted: November 7, 2012
TUESDAY, NOVEMBER 06, 2012
The Cause and Cure for
Current medical science suggests that rheumatoid arthritis (RA) is an autoimmune disease, theorizing that white blood cells mistakenly attack healthy joints, tissues and organs causing chronic inflammation and degeneration of the joints and organs.
In contrast or in the reverse, my thirty years of hematological research suggests that any inflammation and/or degeneration of tissues, joints and/or organs is the result of tissue, joint and/or organ acidosis from the retention of dietary, metabolic, respiratory, and environmental acids that have not been properly eliminated or excreted through the four channels of elimination (urination, perspiration, defecation and/or respiration).
It is acid retention that breaks down tissues, joints and/or organs that causes the activation of the white blood cells as a protective mechanism rather than in reverse.
The main purpose of white blood cells is to maintain cleanliness of the blood and tissues as the primary janitors of the body fluids in the support of the body’s alkaline design. In the thirty plus years of looking at live unstained blood I have never witnessed white blood cells attacking healthy tissues, joints or organs.
My pH Miracle “New Biology” theory suggests that all sickness and disease, including rheumatoid arthritis is caused by the over-acidification of the blood and then tissues due to an inverted way of living, eating and thinking. I call this retention of acid, “Latent Tissue Acidosis.” Simply put, inflammation can only exist when acid is present and when acid is present this causes inflammation that leads to tissue and/or organ degeneration. There is no other cause of inflammation then the retention of dietary, metabolic, respiratory and/or environmental acids.
On the other hand, living an alkaline lifestyle and diet can lead to health, energy, vitality and fitness and the prevention of all sickness and disease, including the prevention or the reversal of rheumatoid arthritis.
The immune system contains a complex organization of cells and antibodies designed normally to “collect and eliminate” cellular debris NOT “seek and destroy” some phantom invader of the body, from the outside world. Patients with rheumatoid arthritis create antibodies which are then released to target, bind and neutralize dietary, metabolic, respiratory and/or environmental acids preventing inflammation of the tissues, joints and/or organs. Because acid can affect multiple other organs of the body, rheumatoid arthritis is a systemic acid retention condition I call “System Latent Tissue Acidosis.”
Picture of a joint with acid caused rheumatoid arthritis
While rheumatoid arthritis is a chronic acidic symptomology, meaning it can last for years, patients may experience long periods without symptoms. However, rheumatoid arthritis will become a progressive acidic illness as acids buildup in the connective and fatty tissues that has the potential to cause joint destruction and functional disability if the patient continues his/her acidic lifestyle and diet.
A joint is where two bones meet to allow movement of body parts. Arthritis means joint inflammation caused by tissue acidosis. The joint inflammation or acids of rheumatoid arthritis causes swelling, pain, stiffness, and redness in the joints. The acid caused inflammation of rheumatoid disease can also occur in tissues around the joints, such as the tendons, ligaments, and muscles when dietary, metabolic, respiratory and/or environmental acids are retained and not properly eliminated due to congestion of the bowels, lungs, skin and/or urinary tract system.
In some people with rheumatoid arthritis, the retention of dietary, metabolic, respiratory and/or environmental acids leads to chronic inflammation and the destruction of the cartilage, bone, and ligaments, causing deformity of the joints. Acidic damage to the joints can occur early in the disease and can be progressive as acids buildup in the connective and fatty tissues. Moreover, studies have shown that the progressive acidic damage to the joints does not necessarily correlate with the degree of pain, stiffness, or swelling present in the joints.
Rheumatoid arthritis is a common acidic rheumatic disease, affecting approximately 1.3 million people in the United States, according to current census data. The disease is a symptom of acid retention that is three times more common in women as in men. I would suggest that women tend to ingest more of the acid (lactic acid) or rheumatoid disease causing foods such as chocolate, ice cream, yogurt, milk, cheese, and sugar, in all of its forms.
Men and women with rheumatoid arthritis have a high prevalence of preclinical atherosclerosis independent of traditional risk factors, suggesting that chronic acidic inflammation, and, possibly, dis-ease severity are atherogenic in this population (1).
Regarding this matter an editorial published at Circulation Journal in 1999 have discussed about the many similarities shared by rheumatoid and atherosclerosis (2).
Researchers have found that the atherosclerotic process begins very early in the course of rheumatoid arthritis with the study revealing a significant increase in intima-media thickness, an indicator of atherosclerosis, in just 18 months (3).
Other scientists have found a rapid increase in myocardial infarction risk following diagnosis of rheumatoid arthritis amongst patients diagnosed between 1995 and 2006 (4)
Having researched the blood of rheumatoid arthritis patients for years, I have found other studies investigating cardiovascular autonomic dysfunction in rheumatic diseases that validates my own conclusions. Although there are few studies in this direction, I have noticed that the sympathetic nervous system activity may be elevated in rheumatic diseases compared with health patients (5, 6). According, my view the sympathetic predominance is the primary factor in the cascade of events leading to increased lactic acid retention from oxygen deprivation and dairy products leads to an acidic environment and latent tissue acidosis, generating atherogenesis (7, 8).
Also, I have discovered a study from the eighties showing high values of lactate in seropositiverheumatic disease and crystal-induced arthritis, with the author suggesting that synovial lactate measurement could be a reliable indicator for differentiating inflammatory arthritides (9).
In parallel, the amount of lactate/lactic acid released by the myocardium has been shown to be related to the severity of coronary artery disease (10, 11).
Going deeper in my research I was happily surprised with the following information from a paper published in 1924 (12), entitled “The alleged role of lactic acid in arthritis and rheumatoid conditions”, that says:
“In 1858 Richardson published the results of extensive experiments on dogs in which the injection of large quantities of lactic acid, intraperitoneally, was followed by severe joint involvement. The condition of the joints was similar to that seen in acute arthritis, and Richardson suggested that the arthritic syndrome was due to an accumulation of lactic acid in the body. This theory found further support in 1877, when Foster reported that the administration of lactic acid by mouth to two diabetic patients resulted in painful and swollen joints. The pain and swelling persisted as long as the lactic acid administration was continued and disappeared promptly after the lactic acid was discontinued. These early experiments were apparently never repeated or extended but they have exerted some influence in the formation of hypotheses regarding the disease”.
This paper from 1924 strengthens my conviction, placed in the article, “Old experiments with rabbits and dogs,” provides powerful evidence of my acid retention theory causing All sickness and disease, including rheumatoid arthritis and atherosclerosis, where it was shown that lactic acid-fed rabbits and dogs may develop atherosclerotic lesions. (13)
Arthritis, Rheumatoid arthritis and Alkalinity
Alkaline Mineral Supplementation Decreases Pain in Rheumatoid Arthritis Patients
This incredible study from Institute for Prevention and Nutrition (Germany) provides clear and unquestionable evidence that using an alkaline mineral supplement (30g daily) reduced pain and increased movement in patients with moderately active Rheumatoid Arthritis over a 12-week period. (14)
1. Roman M. J, et al. Preclinical carotid atherosclerosis in patients with rheumatoid arthritis. Ann Intern Med. 2006; 144: 249-256. Full free text at: http://www.annals.org/content/144/4/249.full.pdf+html
2. Vincenzo Pasceri and Edward Yeh. Editorial, “A tale of two diseases – Atherosclerosis and Rheumatoid Arthritis“, Circulation, 1999; 100:2124-2126. Full free text at: http://circ.ahajournals.org/cgi/content/full/circulationaha;100/21/2124
3. Sodergren et al. Atherosclerosis in early rheumatoid arthritis: very early endothelial activation and rapid progression of intima media thickness. Arthritis Research & Therapy 2010, 12:R158. Full free text at: http://arthritis-research.com/content/12/4/R158
4. Holmqvist M. E. et al. Rapid increase in myocardial infarction risk following diagnosis of rheumatoid arthritis amongst patients diagnosed between 1995 and 2006”, J Intern Med 2010; 268:578-585.
5. Aydemir , V. Yazisiz et al. Cardiac autonomic profile in rheumatoid arthritis and systemic lupus erythematosus. Lupus (2010) 19, 255—261.
6. Dekkers JC et al. Elevated sympathetic nervous system activity in patients with recently diagnosed rheumatoid arthritis with active disease. Clin Exp Rheumatol. 2004 Jan-Feb;22(1):63-70.
7. Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project, January 28, 2008.
8. Sympathetic predominance: a primary factor in the cascade of events leading to the atherogenic spiraling, Carlos Monteiro, Monday, February 22, 2010.
9. Gobelet C and Gerster J. C. Synovial fluid lactate levels in septic and non-septic arthritides. Annals of the Rheumatic diseases, 1984, 43, 742-745.
10. G. Jackson, Lynne Atkinson, M. Clark, B. Crook, P. Armstrong, and S. Oram, Diagnosis of coronary artery disease by estimation of coronary sinus lactate. British Heart Journal, 1978, 40, 979-983 Full free text at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC483520/
11 Gertz EW, Wisneski JA, Neese R, Bristow JD, Searle GL, Hanlon JT: Myocardial lactate metabolism: evidence of lactate release during net chemical extraction in man. Circulation 1981, 63: 1273-1279. Full free text at: http://circ.ahajournals.org/cgi/reprint/63/6/1273