My previous motivation to write blogs was to inform everyone of all the things I knew, how I could help them and why I was probably correct with a healthy smattering of dogma. These days my motivation has changed and I suppose it goes with the old adage - The more you know, the less certain you become of a subject. Sometimes my purpose to write is to take what I have learnt or discovered and set it down for others to contest it, or to go back years later to compare current to previous writings and if my thoughts have stood the test of time.
With auto immune disease (AI) protocols, I intend to discuss some of the problems associated with assuming that
a) that the immune system has lost sense of self and is attacking itself at will.
b) most of the foods suggested are optimal from an AI perspective
For an example let’s take one of the most common AI diseases related to thyroid function such as Hashimoto’s which is the most common cause of hypothyroidism.
‘Hashimoto/lymphocytic thyroiditis is an immunologic disorder in which lymphocytes become sensitised to thyroidal antigens and auto-antigen bodies are formed react with those antigens (Gardner et al., 2011).’
Many recommend and invoke a drastic change to diet. The suggestion of an auto immune paleo type diet, which actually has some merit segmentally but perhaps loses sight of the main issues that drive an auto immune reaction. I’ll address the positives and negatives in the next blog but a common theme that dairy is problematic, and should be removed might better serve an individual if they were aware that it’s their stressed system that drives the response. Much like the assumptions that fruit should be restricted due to sugar content, which matches the dogma that sugar causes diabetes and removes key nutrients that enable efficient metabolism.
So, on to what might be the most pertinent point of this post. A definition of an auto immune disease (AI) is the following:
Auto-immune disease may result from the interaction of the genetic load of the individual, modification of self-tissue antigens by environmental agents such as virus or drugs and abnormalities of the immunological system itself such as the loss of controlling or suppressor T cells with age. In the majority of people the outcome is tolerance, maintenance of normal tissue architecture and function. In the unfortunate few the outcome is auto-immune disease, that is, failure to recognize ‘self’. (Panayi, 1976)
This seems quite logical doesn’t it? The body must be attacking itself because it’s producing antibodies against its own tissues, a clear case of autoimmunity. Diagnosis of Hashimoto’s is usually based upon levels of the anti thyroid peroxidase (ATPO) and thyroglobulin antibodies (TgAb). The higher the levels the increased likelihood of autoimmunity. Increased and sustained antibodies must mean increased autoimmunity and the nefarious nature of attacking oneself.
However there are some that theorise a different view. Enter the Danger Theory proposed by Dr Polly Matzinger who suggests that the immune system is particularly good at recognising damaged and potentially dangerous tissue.
Invoking Occam’s razor and the simplest explanation seems the best choice, although the issues are just as complex. Using the example of the thyroid again as it’s the most common cancer diagnosed and susceptible to a number of insults namely pollution, stress, poor nutrition, preservatives like nitrates/nitrites and a significant factor is estrogen. Matzinger’s suggestions that heat shock proteins (HSP’s) could be at the heart of the AI response to a viral infection and increased temperatures. Estrogen’s actions would be slightly different but their action ultimately decreases body temperature by inhibition of thyroid function, inactivating enzymes, leading to unfolding of proteins.
Estrogen and disorganised tissue has long been implicated in cancer. L.C. Strong who bred mice for genetic evaluation found back in the 1930’s the implications of estrogen and mutations.
Leonell C. Strong
‘“ The second contribution of genetics was the production and control of biological states that differed in cancer susceptibility and cancer resistance. This contribution made possible the discovery that the female hormone estrogen, was involved in the origin of several kinds of cancer in mice.”
AI disease is 80% more likely in females and estrogen can be considered a primary driver. Increasingly the role of environmental pollutants and their estrogen like effects have been implicated in diabetes, heart disease, thyroid dysfunction and fertility and AI disease doesn’t escape its noose (Gawda, Majka, Nowak, & Marcinkiewicz, 2017).
In my recent Masters thesis I referenced that malondialdehyde (MDA) as suggested by others is a useful marker for determining the effects of stress on a system why?
‘Increased malondialdehyde (MDA) levels have been noted in overt and sub clinical hypothyroidism. As MDA levels reflect increased oxidation of lipids and may represent a suppression of CHO metabolism, this might be another useful marker for analysis when euthyroid serum values are recorded, yet hypothyroidism is suspected.
Airborne pollutants create changes to reactive oxygen and reactive nitrogen species (RONS), which when increased, are pro-inflammatory and increase MDA via increased fat oxidation . Maybe the primary drivers behind AI action is part of the global response that decreases thyroid hormone communication, production and assimilation? An inability to regulate both blood sugar and utilise carbohydrate through the glucose-fatty acid/Randle cycle is a specific loss of function induced by pollution and thyroid inhibition. Thyroid is organisational, estrogen is a stimulator of growth and suppresses the organisational and protective actions of progesterone increasing growth and disorganisation (Peat 1992).
The strongest predictor for the development of the AI disease Lupus (SLE) is female sex with a female to male ratio of 9:1 (McMurray & May, 2003). Seems to be a pretty constant ratio with development of hypothyroid disease doesn’t it?
The markers below give a common overview of altered hormone levels shown in patients with Lupus. Once again the commonality of increased estrogen/estradiol and its stimulation of the pituitary hormone prolactin is observed. Suppression of the anabolic hormones and thyroid appears to be a key driver of the AI state.
In a previous blog, I suggested factors that could influence thyroid hormones and their appearance when tested. It might be normal for thyroid antibodies to persist being elevated for some time due to many factors which include use of T4 in isolation, excessive pollution, poor food choices, medical estrogens, lack of selenium and more. Again, blood tests may or may not offer a real time evaluation of thyroid status, which would be the main driver of resolving an AI state. Temperature and pulse rate to track thyroid hormone use and thyroid function at large is extremely useful. Maintaining energy, thyroid hormone and light exposure seems to be the most prudent action when it comes to having better conversations with the environment and what might a long term solution to resolving AI disease.
In part 2 I’ll elaborate on the problems associated with a reduced diet that promotes a decrease in function over time.
Gardner, D. G., Shoback, D. M., Greenspan, F. S. (Francis S., Beers, Mark H., ed.Berkow, Robert, ed. Bogin, Robert M., ed. Fletcher, Andrew J., ed. Merck Rahman, M. I. M. H. B. ; R. B., Schaffer, Alexander J.Avery, Mary Ellen Finberg, Laurence Markowitz, M., Ferrero, Narciso A., dir.Debaisi, Gustavo Ferrero, Fernando C. Gil, Stella Maris Mazzucchelli, María Teresa Nizzo, Dante D. Ossorio, María Fabiana Veber, S. E., … Hoskins, J. D. (2011). Greenspan’s Basic and Clinical Endocrinology. McGraw Hill.
Gawda, A., Majka, G., Nowak, B., & Marcinkiewicz, J. (2017). Air pollution, oxidative stress, and exacerbation of autoimmune diseases. Central European Journal of Immunology. http://doi.org/10.5114/ceji.2017.70975
Matzinger, P. (2012). The evolution of the danger theory. Expert Review of Clinical Immunology. http://doi.org/10.1586/eci.12.21
McMurray, R. W., & May, W. (2003). Sex hormones and systemic lupus erythematosus: Review and meta-analysis. Arthritis and Rheumatism. http://doi.org/10.1002/art.11105
Panayi, G. S. (1976). Auto-immune disease. Rheumatology. http://doi.org/10.1093/rheumatology/15.1.1
Peat, R. (1997). From PMS to Menopause: Female Hormones in context.