Metabolica Rheumatica
You don’t just get arthritis because it’s written in your genetic code, so that it suddenly kicks in on your 60th birthday. And it isn’t just a random event that lands on you out of nowhere, you know, randomly. There are reasons.
Arthritis commonly occurs alongside heart disease and diabetes as well as cancer and depression, and this too is not for no understandable or explainable reason. You don’t need to be a medical specialist to work out the main connections, in fact it probably helps if you aren’t. You do have to spend lots of hours reading through physiology texts and studies, and preferably with an open mind.
But I’m going to give you a heads up. The rheumatic diseases have to do with exposure to too much of the things that make it harder for the body to function optimally, and not enough of the things that the body needs in order to protect against those things. I’m not making this up. There are biological principles that help to explain this.
I’ll probably sound like a broken record, but I’m afraid stress and inflammation and the polyunsaturated fats (PUFAs) and sugar and thyroid energy metabolism will all be getting a mention. The way I see it, there is no other way.
Which is not to say that you can just wave your magic wand, and miraculously reverse the impact of decades worth of aging and degeneration, but your situation isn’t likely to improve much until you have a genuine understanding of what can make things better, and what can make things worse.
Arthritis and rheumatism are terms often used interchangeably to describe a large number of conditions – most commonly osteoarthritis, rheumatoid arthritis and gout – associated with chronic pain and stiffness, affecting the joints and connective tissue.
In reality there are a number of symptoms or indicators that are ignored, or simply not considered to be relevant. The truth is, however, that there is only one biology, and so applying biological principles honestly, provides a clearer picture of the relationship between symptoms and the progression of a variety of related conditions.
The stress of life is an obvious common denominator, and how great that stress is, how long it goes on for, and how it is dealt with, are probably the most important considerations. This is true for disease in general.
But some things make stress less manageable, and more of a chronic and potentially debilitating problem. The way I understand it (and have experienced it), you need to look for the things in your life that promote the damaging effects of stress, via their interference with energy metabolism. If you can get rid of some of the big ones, in the long run your whole system will function better, and you will be less likely to suffer from a range of conditions.
Exposure to the breakdown products from lipid peroxidation of the highly unstable PUFAs, is central to the progression of the symptoms of arthritis, as well as being a powerful factor causing metabolic interference.
When stress is high, blood sugar supplies get used up at a fast rate, and low glycogen stores means more fat is released out of storage for fuel. These days unfortunately, free fatty acids are composed of a higher percentage of PUFA, which is highly unstable and inflammatory.
So chronic stress promotes exposure to PUFA, and exposure to PUFA is a fundamental driver of stress and inflammation. This can become a vicious circle, able to be fed by an unlimited number of possible circumstances.
The breakdown products of PUFA directly interfere with blood sugar regulation, and blood sugar dysregulation issues – such as hyperglycemia and insulin resistance – have been shown to be involved in the progression of arthritis.
Too much exposure to PUFA is an obvious common denominator when it comes to inflammatory conditions like diabetes and arthritis, and if PUFA is a bullet, the low sugar high stress state easily pulls the trigger.
Proper thyroid function protects against stress and inflammation, and PUFA is powerfully anti-thyroid. Hypothyroidism – which very often goes hand in hand with blood sugar dysregulation – has been shown to be closely tied to the onset and progression of the symptoms of arthritis.
Considering the fact that the modern diagnosis of hypothyroidism commonly ignores what once were well understood symptoms of an under active thyroid metabolism, there is probably a far closer relationship between rheumatic disease and thyroid issues, than is seen in studies.
There is also evidence showing that thyroid related issues are an important reason for the link between arthritis and cardiovascular disease.
Unfortunately most studies don’t look closely at the intertwining stress promoting inflammatory things, from a big picture perspective, when considering the connection between arthritis and diabetes and heart disease, as well as even depression and cancer. PUFA, thyroid metabolism and proper blood sugar regulation are important influences with each of these conditions.
A suppressed (blood sugar dysregulated) metabolism often leads to chronically increased levels of a number of inflammatory stress substances, such as bacterial endotoxin (LPS), serotonin, nitric oxide and estrogen.
These substances interfere with oxidative metabolism and encourage greater release of polyunsaturated free fatty acids into circulation. PUFA breakdown products make all of these stress substances more of an issue for metabolism, creating a potentially inflammatory time bomb and a far higher likelihood that arthritis can take hold.
It’s all well and good for these studies to exist. The information they provide is enlightening and powerful. The problem is that how the different stress and inflammation indicators relate to each other, is not often talked about, and health practitioners are being trained to see things in a manner you could justify calling biologically confusing at best.
Insufficient availability of sugar leads to the release of PUFA out of storage. PUFA is inflammatory and interferes with digestive function, allowing bacteria to become overgrown. This increases exposure to endotoxin. Endotoxin causes inflammation, interferes with energy metabolism, and promotes serotonin and nitric oxide. Serotonin and nitric oxide suppress metabolism further, encouraging rising estrogen. All of these issues feed into each other, creating ongoing stress and inflammatory issues, and there are many variations on the theme.
However if for starters, you are being told that PUFA is a health food, that sugar is a dangerous and addictive substance, and that serotonin is the ‘happiness neurotransmitter’, you are going to struggle to figure out what causes the symptoms of arthritis. And you definitely will be thrown off the scent when it comes to solving the mystery of the connection between arthritis and other illnesses.
The fact that there are close ties between the development of arthritis, cancer, diabetes, depression, heart disease and other metabolic issues is obviously very important. But this won’t make sense, until the relationship between chronic inflammation, PUFA, sugar restriction, thyroid dysfunction, digestive distress, endotoxin, nitric oxide, estrogen, serotonin, even low cholesterol and vitamin D, is clearer.
Low cholesterol, exacerbated by PUFA consumption and sugar restriction, has been shown to promote arthritis, cancer, depression, suicidality and violent behaviour, and numerous other inflammatory issues, and the biological significance and protective role of cholesterol has been misrepresented for decades.
It’s obvious that there isn’t a relationship between arthritis and metabolic illness for no reason. You could call arthritis type 4 diabetes and not be too far off. But how things are for one person, will vary from the next largely because of diet and lifestyle, as well as hereditary/environmental factors.
The thing is, you don’t need to figure out what causes arthritis. That’s the wrong question. What you want to do is ask what kind of metabolic state is central to arthritic/rheumatic disease. You can then go on to look at how that plays out in relation to other diseases that tend to co-occur, whilst at the same time working out strategies for prevention and reversal.
Antibiotics (like minocycline), aspirin, methylene blue, caffeine, glycine, red light, vitamin K and some other vitamins, progesterone, pregnenolone, niacinamide, thyroid hormone and a number of other things have been shown to be helpful not just with arthritis, but in most cases, with all of the related metabolic diseases. Not by coincidence.
A diet avoiding PUFA and limiting difficult to digest grains and seeds and under cooked vegetable matter, with sufficient protein from milk and cheese and gelatin and plenty of sugar from sweet ripe fruit, fruit juice, white sugar and honey, is one good way to help promote metabolism and reduce inflammatory issues in general.
Lots of calcium and limited phosphorous is intended to be a by-product of this kind of diet, as a high calcium to phosphorous ratio is, metabolically speaking, another important factor protecting against stress and inflammation.
What amazes me most as I write an article like this one, is not that I was able to find the information and write about it, but that the whole world isn’t standing on the rooftops of buildings shouting about what can be found inside the 100 or so studies attached below, published online for everyone, including doctors, to see. Unfortunately sometimes the truth sounds crazier than crazy sounds.
Until the relationship between the substances of stress, chronic inflammation, blood sugar dysregulation and health propaganda becomes common knowledge, arthritis will most likely continue to be a problem without a solution.
See More Here
Cancer Morbidity in Rheumatoid Arthritis: Role of Estrogen Metabolites
Subclinical Hypothyroidism is Associated with Insulin Resistance in Rheumatoid Arthritis
Prevalence of Undiagnosed Diabetes in Rheumatoid Arthritis: an OGTT Study.
Excitatory amino acid profiles of synovial fluid from patients with arthritis.
Vitamin K and rheumatoid arthritis.
The onset of lipid peroxidation in rheumatoid arthritis: consequences and monitoring.
The use of vitamins in the treatment of chronic arthritis.
Aspirin Use in Rheumatoid Arthritis Patients with Increased Risk of Cardiovascular Disease
Depression in Rheumatoid Arthritis and its relation to disease activity
Abnormal Glucose Metabolism in Rheumatoid Arthritis
Blood serotonin and joint pain in seropositive versus seronegative rheumatoid arthritis.
A reevaluation of aspirin therapy in rheumatoid arthritis.
The role of endogenous serotonin in adjuvant-induced arthritis in the rat.
Benefits and risks of minocycline in rheumatoid arthritis.
Assessment of serum nitrite level in patients with rheumatoid arthritis
Malondialdehyde as a sensitive marker of inflammation in patients with rheumatoid arthritis.
Critical Role of Glucose Metabolism in Rheumatoid Arthritis Fibroblast-like Synoviocytes
Malondialdehyde-acetaldehyde adducts (MAA) and anti-MAA antibody in rheumatoid arthritis
Pain and synovial fluid concentration of serotonin in arthritic temporomandibular joints.
Lipid peroxidation in Rheumatoid arthritis; consequences and monitoring.
Use of minocycline in rheumatoid arthritis: a district general hospital experience Free
Pathogenic role of platelets in rheumatoid arthritis and systemic autoimmune diseases
Intraarticular progesterone: effects of a local treatment for rheumatoid arthritis.
Incidence of malignancy in adult patients with rheumatoid arthritis: a meta-analysis
Diabetes mellitus risk factors in rheumatoid arthritis: a systematic review and meta-analysis.
METHYLENE BLUE IN RHEUMATOID ARTHRITIS.
L-Glycine: a novel antiinflammatory, immunomodulatory, and cytoprotective agent.
IL-29 Enhances LPS/TLR4-Mediated Inflammation in Rheumatoid Arthritis
The Risk of Diabetes Among Patients with Rheumatoid Arthritis, Psoriatic Arthritis, and Psoriasis
PREGNENOLONE in the treatment of rheumatoid arthritis.
Reactivation of antigen-induced arthritis in mice by oral administration of lipopolysaccharide.
Energy metabolism and rheumatic diseases: from cell to organism
[Osteoporosis in Rheumatoid Arthritis: role of the vitamin D/parathyroid hormone system].
Total Cholesterol and LDL levels decrease before rheumatoid arthritis
Risk of diabetes in patients with rheumatoid arthritis: a 12-year retrospective cohort study.
Plasma lipid peroxidation and antioxidant levels in patients with rheumatoid arthritis.
Hypercalcemia in rheumatoid arthritis: relationship with disease activity and bone metabolism.
The effect of niacinamide on osteoarthritis: a pilot study.
Diabetes mellitus and arthritis: is it a risk factor or comorbidity?
The risk of cancer in patients with rheumatoid arthritis: a nationwide cohort study in Taiwan.
Lipid peroxidation and antioxidant status in patients with rheumatoid arthritis
Bacterial lipopolysaccharide acts as an adjuvant to induce autoimmune arthritisin mice
Treatment of Arthritis by Nicotinic Acid and Nicotinamide
Prevalence of hypothyroidism in rheumatoid arthritis and its correlation with disease activity.
Hypothyroidism in patients with rheumatoid arthritis and its relation to disease activity
The effect of hyperparathyroidism on the course of rheumatoid arthritis.
Lipid peroxidation and antioxidant status in blood of rheumatoid arthritis patients
Risk of cancer among rheumatoid arthritis patients in California
Caffeine downregulates inflammatory pathways involved in autoimmunity
Bone and joint manifestations of hypothyroidism.
Thyroid dysfunction in rheumatoid arthritis: a controlled prospective survey.
Oral administration of lipopolysaccharide exacerbates collagen-induced arthritis in mice.
High prevalence of thyroid autoimmunity and hypothyroidism in patients with psoriatic arthritis.
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