auto immune paleo

Autoimmunity part 2: The autoimmune paleo diet - The Pro's and Cons

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 In this post I’m going to explore the mechanisms of the recommended autoimmune paleo diet (AIPD)  and suggest why it has very useful short term applications which are a mixed bag of interventions, reductionisms and shouldn’t be considered as a long term solution.

 In the last autoimmunity post you might remember how scientists like Polly Matzinger give an insight of auto immune disease that’s often not given enough credit. In summary of the danger theory, which is the body recognising self and the potentially damaged self. These damaged tissues be they thyroid or another tissue, is marked for removal from the system to prevent more damage occurring. The body is a pretty impressive organism that should be credited with being able to recognise its own tissues and respond with an effective response to restore best working order. So why should we discount this theory?  It’s essential to remember that a significant driver of autoimmunity is the increased prevalence of the disease in females (some 10 x more than males)  is driven by estrogen, estrogen like compounds and their ubiquity in the environment. Recently I’ve seen more people in the preceding months with vitiligo than I have seen in my entire lifetime but then I do live in a very polluted city.

 The recommendations for the autoimmune paleo diet protocol has some positives but the thought process behind such a diet has shortcomings and it’s important to tease out why it can be successful for some. I’ve always found the idea that a paleo lithic diet be entertained for health somewhat problematic. Archaeological specimens of older adults are generally lacking, suggesting mortality ranges commonly found between 20-40 year old samples (Trinkaus, 2011). That’s not to say that there weren’t older adults, ,but to base the efficacy of a diet strategy on a previous era without any data is problematic.

 There are several reasons why the AIPD might have some positive outcomes.

1.     It removes many offending compounds that are known to irritate the digestive tract. Sweeteners,  emulsifiers and thickeners are well documented to increase intestinal inflammation. Gums like guar, locust bean and Irish sea moss (carrageenan) can cause substantial damage over time and is also implicated in blood sugar regulation and diabetes.

2.     Alcohol is restricted. It should come as no surprise that alcohol has the capacity to affect multiple aspects of function. Most forms of alcohol contain phytoestrogens and just like long term soy consumption has the capacity to influence the body as a source of external estrogens . Additionally, many other additives like yeasts, colorants and preservative like sulphites appear equally problematic. Drinking alcohol in moderation isn’t necessarily problematic but the more susceptible that one is to estrogen issues, alcohol will often be problematic. I have seen many old ladies in their 90’s have been prone to a tipple of sherry or whiskey.

3.     Nuts, seeds and oils which are high in unstable unsaturated fatty acids are also restricted ,decreasing lipid/fat oxidation and improve mitochondrial function. The restriction of grains can also be useful for a similar reasoning and grains like millet, sorghum and barley are known to slow metabolism, but the action of seeds and grains can promote increased intestinal serotonin and histamine production, increasing the burden and damage to digestive function. Both poly and monounsaturated fats appear to promote compromised liver function, degrade metabolism and contribute to obesity.

4.     Nightshades, legumes, egg whites and gluten are well known for their role in irritability of the digestive system.

When all is said and done, there’s every reason why many people should feel better when removing these usual suspects. But there are problems with the AIPD and I have seen individuals who despite following this protocol still present with both digestive and energy issues, primarily because deficits in energy still arise and potential autoimmune reactions persist. Given some of the problems associated with determining cause and effect of specific interventions. It would be easy to speculate why someone who was prone to eating lots of fast food, high in unstable oils, high fructose corn syrups, preservatives, binding agents and suffering autoimmune, digestive, energy and other hormone disturbances might respond well to this in the short term?


There’s another plus to the AIPD - it includes fruit but there’s a caveat that natural sugars which include fructose should be kept to a minimum. There’s also an emphasis on eating fruits that are high in intestinal irritating seeds like berries. Carbohydrate is essential for optimal energy production. It promotes adequate carbon dioxide production and allows more efficient energy production and oxygenation of tissues that you just don’t get with sustained fat oxidation. Even refined table sugar shouldn’t be frowned upon and would only be problematic if your diet contained large amounts of refined sugar and devoid of other key nutrients like fats, proteins, and lack of potassium or magnesium as an example.


So is the AIPD useful? Yes, but it’s extremely limited. So how about a strategy that allows function to improve systemically rather than in isolation? Studies are limited on the effectiveness of AIPD. Whilst not autoimmune as such, a study that utilised the AIPD in patients with IBD (irritable bowel disease) completed remission in 11/15patients or 73% (Konijeti et al., 2017). That’s great, but it shouldn’t be surprising, if you’re removing all the intestinal irritants and this reasoning should extend to some improvements in autoimmune patients, resolving digestive function should follow. Gut function improved but markers of inflammation such as CRP did not, and one participant withdrew due to irritation from raw food consumption.


Aspects of the autoimmune and or autointoxication theory of disease is derived from Elie Metchnikoff’s work on immunology, bacteria and gut function (Metchnikoff & Metchnikoff, 1908). Metchnikoff proposed that death and disease started in the colon. Whilst there’s little doubt  that optimising gut function has many beneficial effects, problems arise beyond the digestive tract that might occur in otherwise healthy diets. The bowel can be a hospitable place for problematic bacteria when hydrochloric acid is low, and motility is slow induced by a low energy/thyroid state. Metchnikoff proposed that beneficial strains of bacteria can be useful to prevent unwanted maladies related to bowel function. However he was keen to point out that animals blessed with longevity often shared features of high metabolic rates and low levels of gut bacteria. This may explain why supplemental probiotic studies are not consistent in results and may simply act as a competing factor against more problematic bacteria (Goldenberg et al., 2015). The AIPD preference for more fermented goodies might be useful, but more is definitely not better. As food is poorly digested and bacterial metabolites increase so does endotoxin, intestinal hyperpermeability (leaky gut) and changes to biochemistry and hormones.

 I won’t discuss dairy produce here as it’s rarely the issue, the stressed digestive system has a problem with dairy products. I have seen countless clients return to eating dairy products like cheese, ice cream and  milks.

Eating ice cream & walking in the sunshine is an easy way to lower aspects of autoimmunity.jpg

It’s rarely the dairy that’s at fault, it’s usually the stressed digestive system that’s the real issue.

The AIPD, well there’s plenty that can be improved upon to create longer lasting function without the need for reductionist notions like the greener, the more natural, the better. Especially the problems that have been known for many decades that cruciferous/brassica vegetables high in isothiocyanates and glucosinolates, are well known to increase levels of cyanide in tissues and are anti-metabolic in nature disrupting thyroid function.

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Broccoli was not a palaeolithic food

Brassica vegetables may have very little place in resolving autoimmune diseases.

The most effective form of preventing autoimmunity might be to keep metabolism at its best working order rather than slowing it down. The fascination of broccoli in the modern diet is not without paradox.  Broccoli certainly wasn’t consumed in the palaeolithic era, although other cruciferous vegetables may have been (Buck, 1956). It’s elevation to farmed commodity and food stuff appeared to take place in Hellenic culture and more rapidly promoted to support the invading Roman army.

Promoting a diet that has easily digested nutrients, energy and facilitates available thyroid hormone, addressing internal and external sources of estrogen, without increasing stress responses may be the most pragmatic approach of any diet to decrease autoimmune responses. Eating plenty of fruit, sugars and honey combined with good quality proteins, moderate saturated fat and low in unsaturated fats, seeds might be the best autoimmune diet.

Another problematic aspect of the AIPD is the emphasis on Omega 3 fatty acids such as DHA to lower inflammation and this isn’t limited to poorly constructed diets but a common error in autoimmune and inflammatory protocols (Constantin et al., 2018). Many studies and review such as this invoke the antioxidant effect properties of omega 3s due to their ability to lower markers such as triglycerides, cholesterol and crease metabolism. Surprisingly when you decrease metabolic rate, you decrease metabolic function, therefore inflammatory and oxidative markers are reduced. Sustained omega 3 and other unsaturated fatty acids accumulate in the brain and liver and decrease aerobic metabolism through sustained lipid peroxidation, especially so when carbohydrate metabolism is lost.

‘ Calorific restriction and well established diet supplementation with omega 3 regulates total cholesterol, LDL-C and triglycerides.’ (Constantin et al, 2018).

 In essence this has as much benefit as taking medication to lower cholesterol. Of course eating less calories produces less inflammation and if calories are restricted below a certain threshold, this lowers metabolism, giving the impression of less oxidation. If you’re going to support the notion that taking omega 3s lowers inflammation and as many espouse, lowers cardiovascular risk, the net effect will be degraded cholesterol that’s prone to oxidation and left with an excess of fatty acids also prone to lipid peroxidation. If we’re going to help more people with a so called autoimmune disease, perhaps we need to be thinking a little more holistically? If estrogen is a main driver of a perceived autoimmune state then improving its excretion through adequate energy, liver function and robust biology should be the answer. There’s no doubt that improving digestive function is helpful but the current zeitgeist, promoting plenty of undercooked vegetables in their most natural state, high in metabolic inhibitors is restrictive to decreasing aspects of autoimmunity.


Buck, P. A. (1956). Origin and taxonomy of broccoli. Economic Botany.

Constantin, M., Nita, I., Olteanu, R., Constantin, T., Bucur, S., Matei, C., & Raducan, A. (2018). Significance and impact of dietary factors on systemic lupus erythematosus pathogenesis (Review). Experimental and Therapeutic Medicine.

Goldenberg, J. Z., Lytvyn, L., Steurich, J., Parkin, P., Mahant, S., & Johnston, B. C. (2015). Cochrane Database of Systematic Reviews. The Cochrane database of systematic reviews (Vol. 12).

Konijeti, G. G., Kim, N., Lewis, J. D., Groven, S., Chandrasekaran, A., Grandhe, S., … Torkamani, A. (2017). Efficacy of the Autoimmune Protocol Diet for Inflammatory Bowel Disease. Inflammatory Bowel Diseases.

Metchnikoff, E., & Metchnikoff, I. I. (1908). The Prolongation of Life: Optimistic Studies. Our post human future. Consequences of the biotechnology revolution. Retrieved from

Trinkaus, E. (2011). Late Pleistocene adult mortality patterns and modern human establishment. Proceedings of the National Academy of Sciences.


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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.

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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.

Sex Hormone changes in auto immune disease (McMurray & May, 2003)

Sex Hormone changes in auto immune disease (McMurray & May, 2003)

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.


  1. 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.

  2. Gawda, A., Majka, G., Nowak, B., & Marcinkiewicz, J. (2017). Air pollution, oxidative stress, and exacerbation of autoimmune diseases. Central European Journal of Immunology.

  3. Matzinger, P. (2012). The evolution of the danger theory. Expert Review of Clinical Immunology.

  4. McMurray, R. W., & May, W. (2003). Sex hormones and systemic lupus erythematosus: Review and meta-analysis. Arthritis and Rheumatism.

  5. Panayi, G. S. (1976). Auto-immune disease. Rheumatology.

  6. Peat, R. (1997). From PMS to Menopause: Female Hormones in context.