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. http://diabetes.diabetesjournals.org/content/67/Supplement_1/770-P?fbclid=IwAR1W8LRbx1fSu02Tr3b19ANtu2qpkZRhnwySvCj8uUC4TpRhvzypNH6lERg

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. http://doi.org/10.1007/BF02899000

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. http://doi.org/10.3892/etm.2018.6986

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). http://doi.org/10.1002/14651858.CD004827.pub4

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. http://doi.org/10.1097/MIB.0000000000001221

Metchnikoff, E., & Metchnikoff, I. I. (1908). The Prolongation of Life: Optimistic Studies. Our post human future. Consequences of the biotechnology revolution. Retrieved from http://books.google.com/books?hl=en&lr=&id=U8bgKGvZJV0C&pgis=1

Trinkaus, E. (2011). Late Pleistocene adult mortality patterns and modern human establishment. Proceedings of the National Academy of Sciences. http://doi.org/10.1073/pnas.1018700108


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I wrote this book several years again and am in the process of creating a new, more complete text on the subject. Please feel free to download and share. All I ask is that you leave some comments on what you liked or disliked about it.

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Seasonal thyroid fluctuations, biology and mood

 As you may have read from previous blogs, the thyroid, its pituitary stimulator - thyroid stimulating hormone (TSH) and the other thyroid hormones are heavily influenced by environment, nutrition and stress. Additionally these hormones can present as normal when relied upon purely by biochemical analysis from the blood. The seasons, differing temperatures, light exposure and effects of hibernation hormones and neurotransmitters can also be a key factor in the expression of adequate energy, organisation and coherence of an individual’s biology. We get sick more so in winter when our function is suppressed and the immune system is called upon to mount a response.


S.W. Tromp Biometerology 1967.

“ The yearly influenza peak in the Netherlands, around February. Which may be related to the usually low humidity and wind-speed in this period, but which effect is probably accelerated by the decreased thermoregulation efficiency of the body as a result of the preceding cold months and the accompanying changes in the physico-chemical state of the blood such as y-globulin level.”

 Ambient temperature can have a significant effect on TSH production in as much as a colder environment increases TSH and warmer temperatures decrease TSH production and thyroid requirement. Observations have suggested a biphasic seasonal nature of TSH secretion, with increased TSH readings during winter time suggesting what could be a functionally hypothyroid or subclinical hypothyroidism which resolved during the summer months (Kim et al., 2013). As this stress increases throughout longer days of darkness, organisational hormones decrease, whilst stress hormones increase. If chronic enough, or in an unstable biology, stress can decrease the accuracy of TSH to predict a low thyroid state

 Light, both red and ultraviolet (UV) are well-known modulators of immune function, metabolism and mitochondrial production of energy or  adenosine triphosphate (ATP) (Wong-Riley et al., 2005) (Karu, 2010). These aspects of sunlight, exert their influence via enhancement of aerobic metabolism (at cytochrome c) and immunity enhancing via infra-red (NIR) and vitamin D synthesized by UV respectively.  The variation in light exposure as a consequence of daily sleep, darkness and seasonal variations present relationships that may explain the secretory patterns of TSH in healthy subjects. More than 100 years ago, thyroid function could be suggestively viewed via uptake of thyroid iodine levels in seasonal variations. (Fenger and Siedell 1913). Thyroid iodine levels rose during the summer in sheep, pigs and cows and decreased during the winter reflecting the variations in the need for TSH/TH production in healthy organisms. 

Seasons, Thyroid and Mood

 Depression is a known symptom of hypothyroidism and some studies have highlighted the need for a lower TSH value in the presence of depressive symptoms (Talaei, Rafee, Rafei, & Chehrei, 2017) (Hage & Azar, 2012). The former authors suggest a cut-off value of 2.5 mU/L for TSH as a point for treating hypothyroidism, which highlights the need for assessing symptoms as part of an effective strategy for diagnosing hypothyroidism. This compares to the attitude taken to expecting mothers where values should be decreased to compensate for hypothyroid states but in reality should be applied across the board.

 Relationships concerning seasonal variations of mood are well documented and decreased Beck mood scores are associated with the shorter days of winter (Harmatz et al., 2000). Seasonal affective disorder (SAD) may be a reflection of the increase in serotonin and melatonin and depression of thyroid hormone, which are increased by shorter days and in mammals are associated with hibernation. This aspect seems to be lost on those treating transient depressed states but light therapy does appear to be taken seriously these days. I would encourage anyone wanting more information on serotonin and mood to check out the extremely well written blog Against Utopia.

 As days become shorter and light exposure is decreased, influencing cellular function and metabolism negatively. The extended effects of melatonin from the shorter days can antagonise TSH secretion via its inhibitory action on TH, increasing prevalence throughout winter. Whilst fluctuations in TSH levels in response to seasonal changes are well-known to occur, these fluctuations are also under the influence of the nutritional and environmental factors that can suppress TSH values.

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Wake me up when it’s spring?

Violent suicides increase with the onset of spring from March to May. I was trying to think why this might occur? After speaking to a friend recently about depression, they said that holding onto the feelings of a blanketed, safe, dark environment by being it home (in a somewhat hibernation like state), and gorging on boxsets or podcasts was easy to do and a comfort. I wonder if the shorter phases of darkness and increased light remove that blanket of increased serotonin and melatonin and the light itself might become a stressor that takes away that comfort? Those most at risk might explain this seasonal increase in suicides?

Ray Peat (1997) has discussed various aspects of stressors such as darkness, oestrogen-cold sensitive enzymes and nutritional factors affecting endocrine systems, adding an interesting perspective on hormone production and relationships with temperature changes (Peat, R. and Soderwall, 1972) (Peat, 1997)(Peat, 1972).

In states of undetectable SCH mediated by the stress, a hypothermic state may stimulate the adrenal stress system to compensate for a low-metabolic and decreased temperature state.  Activated compensatory stress response pathways may explain poorly detected hypothyroid patients. Decreased metabolic rate, lowered temperature and pulse rate are well-known signs of hypothyroidism. β adrenergic mechanisms involving increased catecholamine production such as adrenaline and noradrenaline (NA) can increase Tb and RHR. In my previous blog on body temperature, I explained how low temperature can be indicative of low thyroid function when blood tests appear normal.



Hage, M. P., & Azar, S. T. (2012). The link between thyroid function and depression. Journal of Thyroid Research. http://doi.org/10.1155/2012/590648

Harmatz, M. G., Well, A. D., Overtree, C. E., Kawamura, K. Y., Rosal, M., & Ockene, I. S. (2000). Seasonal variation of depression and other moods: A longitudinal approach. Journal of Biological Rhythms. http://doi.org/10.1177/074873000129001350

Karu, T. I. (2010). Multiple roles of cytochrome c oxidase in mammalian cells under action of red and IR-A radiation. IUBMB Life. http://doi.org/10.1002/iub.359

Kim, T. H., Kim, K. W., Ahn, H. Y., Choi, H. S., Won, H., Choi, Y., … Park, Y. J. (2013). Effect of seasonal changes on the transition between subclinical hypothyroid and euthyroid status. Journal of Clinical Endocrinology and Metabolism. http://doi.org/10.1210/jc.2013-1607

Peat, R. and Soderwall, A. L. (1972). Estrogen stimulated pathway changes and cold -nactivated enzymes. Physiol Chem Phys, 4((3)), 295–300.

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

Peat, R. (1999). Thyroid Therapies, Confusion and Fraud. Retrieved from www.raypeat.com/articles/articles/thyroid.shtml

S.W., Tromp. (1967). Biometeorology, iia and b. Symp. Publ. Div. Pergamon Press (Oxford).

Talaei, A., Rafee, N., Rafei, F., & Chehrei, A. (2017). TSH cut off point based on depression in hypothyroid patients. BMC Psychiatry, 17(1). http://doi.org/10.1186/s12888-017-1478-9

The Armour Laboratories. (1945). The Thyroid Gland and Clinical Application of Medicinal Thyroid. Armour Laboratories.

Wong-Riley, M. T. T., Liang, H. L., Eells, J. T., Chance, B., Henry, M. M., Buchmann, E., … Whelan, H. T. (2005). Photobiomodulation directly benefits primary neurons functionally inactivated by toxins: Role of cytochrome c oxidase. Journal of Biological Chemistry. http://doi.org/10.1074/jbc.M409650200


Poly Cystic Ovary Syndrome (PCOS) - inheritance, environment and stress.

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Poly Cystic Ovary Syndrome - inheritance, environment and stress. Recently I took on a client who was diagnosed with polycystic ovary syndrome (PCOS), a slightly wayward insulin profile and the ‘best practice’ of oral contraceptives and Glucophage (metformin- blood sugar regulating drug) were suggested. My client had started bleeding daily and was informed that this was normal for three months but would help out with PCOS and weight gain. However this seemed at odds with my current knowledge and experience of biology and endocrinology. There are plenty of studies highlighting the diabetes inducing effects of estrogen and oral contraceptives.

Glycemia constitutes a fundamental homeostatic variable, and hence its alteration can lead to a number of pathophysiological conditions affecting the internal milieu of the human being. Since the early 1960s, the intake of oral contraceptives has been associated with an increased risk of developing disorders of glucose metabolism.(Cortés & Alfaro, 2014)

Is best practice the efforts of a global network of doctors or simply a corporate led strategy? Don’t get me wrong; the world is full of competent, passionate and well-meaning doctors who signed up to help others. But the concept of both best practice and clinical governance seem a utopian ideal when those that are responsible for drug development are companies whose primary function is to make as much money as possible, without appropriate direction.

Joseph Dumitt in his book Drugs for Life (2012) highlights that there hasn’t been a scientist at the head of a pharmaceutical company for many years and their direction being driven by economists and marketers. As there are many examples of absolutist statements regarding drugs and their positive effects on health that lack congruence over time, you’ll forgive me for sounding like a conspiracy theorist. How about hormone replacement therapy (HRT) for better health despite its negative outcomes related to cardiovascular events or cancer? Or statin therapy for decreasing unnecessary risk factors based upon skewed data and early terminated trails with no public access to trial data (Lorgeril & Rabaeus, 2016)?

Back to PCOS. I have written previously about the effects of metformin and its use in gestational diabetes, and the problems it poses trans-generationally. It’s possible to suggest that the failure to act with appropriate biological interventions perpetuates the cycle of acquired traits from parents that are passed to offspring, treated ineffectively and generations of reproductive (and other tissues) tissue conditions continue without being resolved.

The biologist Jean Baptiste Lamarck's fourth law stated:

“ Everything which has been acquired..or changed in the organisation of an individual during its lifetime is preserved in the reproductive process and is transmitted to the next generation by those who experienced the alterations. “

It's worth pointing out that this is not isolated to the female of the species as the factors below have been shown to be instrumental in reproductive issues (testicular dysgenesis, hypospadias etc) in males.

The environment has been shown to be instrumental in the development of reproductive tissue disorders, diabetes and cancer but more emphasis is placed on the individual and their food choices rather than acknowledgement of industrial responsibility. Positive associations between levels of polychlorinated bisphenyls (PCBs), pesticides, polycyclic aromatic hydrocarbons (PAHs) and dichlorodiphenyldichloroethylene (DDE) have been confirmed in multivariate data analysis (Yang et al., 2015). Relationships between increases of luteinising hormone (LH) PCO, hyperandrogenism, annovulation, insulin resistance and pollutants are significant and may add to issues of detection, due to the subtle long term perturbations that often affect endocrine function. Stress, other pollutants and medications contribute to further problems that burden not only reproductive tissue but also other organizational hormones such as thyroid hormone.

PCOS is defined medically by the following: One of the main problems of treating PCOS with contraception is the many studies that clearly show a relationship between estrogen and decreased insulin sensitivity (Godsland et al., 1992)(Cortés & Alfaro, 2014). Progestin’s, the synthetic version of progesterone, also pose many problems but this has not deterred the inclusion of estrogen and progestin contraceptives as another inappropriate form of treatment. The burden of estrogen induced by the sources suggested above comes at a cost and it’s well known that an excess of estrogen can suppress thyroid function (thyroid is necessary for detoxification of estrogen and another organisational hormone progesterone.

Both thyroid and progesterone are known to improve insulin sensitivity and can create beneficial changes to disorganised tissue induced by an excess of estrogen. Thyroid nodules and uterine fibroids appear to be intimately linked by an excess of estrogen (Kim et al., 2010) and suppression of thyroid tumours can be achieved by thyroid stimulating hormone (TSH) suppression by thyroxin supplementation (Grussendorf, Reiners, Paschke, & Wegscheider, 2011). An old rambling on thyroid nodules and fibroids.

Breaking the cycle requires interventions that address inheritance, environment and individual stressors. Strategies that involve adequate nutrition that build biology not reduce it, use of protective compounds like progesterone, thyroid and adequate carbohydrate can be of great benefit. Although this stands in contrast to the best practice of contraception, blood sugar medication and poorly thought out nutritional advice of restricting carbohydrates. As the environment appears to drive most of the increasing numbers of issues like PCOS, it becomes important to increase robustness, restrict exposure to what we can control and become more adaptable to what we can’t.

To find out more about coaching for these issues.


Burkhardt, R. W. (2013). Lamarck, evolution, and the inheritance of acquired characters. Genetics, 194(4), 793–805. http://doi.org/10.1534/genetics.113.151852

Cortés, M. E., & Alfaro, A. a. (2014). The effects of hormonal contraceptives on glycemic regulation. The Linacre Quarterly, 81(3), 209–218. http://doi.org/10.1179/2050854914Y.0000000023

Dumit, J. (2012). Drugs for Life. Duke University Press.

Godsland, I. F., Walton, C., Felton, C., Proudler, A., Patel, A., & Wynn, V. (1992). Insulin resistance, secretion, and metabolism in users of oral contraceptives. Journal of Clinical Endocrinology and Metabolism, 74(1), 64–70. http://doi.org/10.1210/jcem.74.1.1530790

Grussendorf, M., Reiners, C., Paschke, R., & Wegscheider, K. (2011). Reduction of thyroid nodule volume by levothyroxine and iodine alone and in combination: A randomized, placebo-controlled trial. Journal of Clinical Endocrinology and Metabolism, 96(9), 2786–2795. http://doi.org/10.1210/jc.2011-0356

Kim, M.-H., Park, Y. R., Lim, D.-J., Yoon, K.-H., Kang, M.-I., Cha, B.-Y., … Son, H.-Y. (2010). The relationship between thyroid nodules and uterine fibroids. Endocrine Journal, 57(7), 615–21. http://doi.org/10.1507/endocrj.K10E-024

Lorgeril, M. De, & Rabaeus, M. (2016). Beyond confusion and controversy, can we evaluate the real efficacy and safety of cholesterol-lowering with statins? Journal of Controversies in Biomedical Research, 1(1), 67. http://doi.org/10.15586/jcbmr.2015.11

Is testosterone replacement therapy necessary?

In a world where it is increasingly normal to be convinced that we fall into a risk classification, need a treatment and can convince our doctor accordingly, negating any experience that he or she might have. The marketeers and economists that run pharmaceutical companies are doing a great job of increasing profits. Before we keep looking for the next wonder treatment we should take stock of what food and exercise can do.

Testosterone can be increased by some very simple strategies such as:

  1. Having adequate liver and vitamin A in the diet to assist in the conversion of cholesterol to pregnenolone - the base hormone responsible for production of testosterone and other androgens.

  2. Ensuring that adequate energy and thyroid hormone are available to maintain communication of the hypothalamic- pituitary- (signalling centres for hormone production-brain to testicles) gonadal axis.

  3. Understanding stress, sleep and interactions between excesses of estrogen and their impact on testosterone production.

  4. Less understood but increasingly keeping mobile communication devices out of pockets and bags that are close to reproductive tissue, including females (ovaries, endometrium etc), appears to be a pragmatic approach in the future. Steroid producing tissues have increased production of problematic compounds that may be prone to damage.

Here's some of the technical aspects to the situation that are taken from a recent assignment as part of my masters degree..


Testosterone is a hormone found in both males and females but is the major reproductive hormone in men that also has a variety of other beneficial functions for maintaining physical and psychological aspects to health. Testosterone levels may decrease with disease and/or be part of an age related decline of output. The use of testosterone supplementation has increased substantially in recent years counter these states, primarily due to increased marketing as an agent of change for energy, strength, fat loss and sexual function. Whilst its use appears beneficial in some areas, caution has been recommended on the effects of T supplementation use and it’s effects on the cardiovascular system.


Testosterone (T) is the most important androgen found in males and produced primarily within the testes, when low it is defined as hypogonadism. Hypogonadism is classified as either primary, derived from the testes or secondary, which involves the hypothalamus, pituitary or derived from illness or disease. A low serum testosterone (<300ng/dL) is suggestive, but not definitive of hypogonadism and measurements of luteinising (LH) and follicle stimulating hormone (FSH) is used to establish a primary or secondary diagnosis (Crawford & Kennedy, 2016). A worry trend is that despite striking increases of testosterone prescription a substantial amount (approximately 29% in this review) of patients often fail to have their levels checked prior to undertaking testosterone replacement therapy (TRT). (Corona G, Rastrelli, Maseroli, Sforza, & Maggi, 2015). Additionally only 45 % had their testosterone levels checked during or post TRT intervention.

Low testosterone and cardiovascular risk

Previous studies have highlighted an increase in all cause mortality associated with low testosterone levels in men (Araujo et al., 2011). Conditions that increase risk of mortality related to low testosterone are increased abdominal obesity, inflammatory biomarkers, dyslipidaemia, diabetes mellitus and metabolic syndrome. However the diagnosis of an isolated low testosterone level should be qualified by ruling out other potential diagnosis such as long-term illness, nutritional deficiencies and other endocrine issues such as subclinical or overt hypothyroidism.

Testosterone supplementation and risks

A number of studies and meta analysis have demonstrated a number of beneficial effects of TRT which extend to increased sexual satisfaction, muscle mass, strength mood and metabolic function (Corona G et al., 2015) (Gagliano-Jucá & Basaria, 2017). However the suggested risk to increased CV adverse events have appeared vague in many studies and previous extrapolations/anecdotes between men having increased levels of testosterone (and therefore increased cardiac risk) and females having less testosterone and more oestrogen were not just problematic but incorrect. Many studies have correlated low testosterone to low biomarkers of health and increased cardiovascular disease (Pastuszak, Kohn, Estis, & Lipshultz, 2017) (Kloner, Carson, Dobs, Kopecky, & Mohler, 2016).

TRT reductionism and treating symptoms

A comprehensive review of the data compiled by Oskui et al (Mesbah Oskui, P., French, W.J., Herring, 2013) described the major CV implications of TRT which can be observed below. The authors draw attention to previously conducted studies, that did not show any relationships between low levels of testosterone and CV risk and suggest that both the subfraction of testosterone (Total T compared to Free T) and method of analysis for CVD were inappropriate and therefore unreliable for inclusion. 

Cardiovascular analysis Studies Major findings Association between T and mortality 8 8/8 studies found relationship between low T and increased all cause and CV mortality. Type 2 DM 6 6/6 studies showed improved insulin sensitivity through HOMA-IR/HgA!c and improved blood glucose Cholesterol 3 2/3 studies found no change to LDL/HDL from TRT Markers of inflammation (primarily C reactive protein CRP) 8 4/8 studies found reduced CRP Intima media thickness 8 8/8 found an inverse relationship between low T and IMT

The above studies reviewed by the authors, established a link between low levels of testosterone and increases in mortality (all cause and CV), insulin sensitivity and increases in intima media thickness that are resolved by TRT. Yet markers for lipids and inflammation markers such as CRP are less convincing. Hypothyroidism is related to low testosterone and hypogonadic states mainly through hypothalamic-pituitary dysfunction. Treatment of hypothyroid and subclinical hypothyroid states also resolves low testosterone and hypogonadic states, decreases intima media thickness, improves insulin sensitivity and decreases lipid levels (Crawford & Kennedy, 2016), (Krassas, Poppe, & Glinoer, 2010),(Donnelly & White, 2000) (Gao, Zhang, Zhang, Yang, & Chen, 2013). Is TRT the correct therapy for many males, given a) the rapid increases in often undiagnosed and prescription and b) when hypogonadic states, that have similar (cardiac) manifestations and are improved beyond the effects of TRT, are resolved with thyroid hormone?

Another factor concerning reliability of the studies used in previous meta analysis is the size to determine true risk between CV adverse events and TRT (Onasanya et al., 2016). The authors suggesting that to achieve a two-sided p value of 0.05 and power of 80% some 17664 participants would need to study to clarify any relationship. Observational data conducted over 5 years suggested that control groups treated with testosterone in short term had a lower mortality (HR 0.88 95 % CI 0:84 - 0.93) than controls (Wallis et al., 2016). From the meta analysis and other studies discussed above both age (>65) and predisposition to existing disease states may indicate the likelihood of adverse CV events when treated with TRT.

Another draw back of meta-analysis is the inclusion of data and bias produced by pharmaceutical companies that may not be adequately reflected or assessed. Much like cardiovascular end point studies being scarce. Testosterone studies that are funded by financial interests are usually in place to validate the benefits of TRT and fail to evaluate CV adverse events as end points. The increased adequate sample size needed to validate the safety and efficacy of this treatment often increase cost and decrease profit margin over time. The many studies that have been conducted so far, show much smaller sample sizes and a wide range of TRT delivery and dosing.

In a recent case crossover analysis that is not included in any current meta analysis, Layton et al (Layton et al., 2018) found a unique association between testosterone injections and short term cardio (and cerebrovascular) events in older men. Increased associations with myocardial infarction and stroke, post testosterone injection showed odds ratio (OR) were increased for all outcomes, OR =1.45 (95%: CI 1.07, 1.98).


Testosterone replacement does appear to have many positive effects on a number of markers related to cardiovascular health which include sexual performance, increased muscle mass, metabolic health, physical performance and decreasing mortality in a younger population. However, despite the many benefits of TRT the use of this therapy may have significant risk in late onset hypogonadal states, in ages >65 years of age, those susceptible to conditions associated with erythrocytosis and an association with acute cardiac events exists. It remains essential to ensure that not only adequate analysis of hypogonadal states are present but to ascertain if low testosterone levels are merely a symptom of other endocrine disturbances, such as hypothyroidism which has striking similarities to low levels of testosterone.

Want some more free resources on hormones?


1.Araujo, A. B., Dixon, J. M., Suarez, E. a, Murad, M. H., Guey, L. T., & Wittert, G. a. (2011). Clinical review: Endogenous testosterone and mortality in men: a systematic review and meta-analysis. The Journal of Clinical Endocrinology and Metabolism, 96(10), 3007–19. http://doi.org/10.1210/jc.2011-1137

2.Basaria, S., Davda, M. N., Travison, T. G., Ulloor, J., Singh, R., & Bhasin, S. (2013). Risk Factors Associated with Cardiovascular Events During Testosterone Administration in Older Men with Mobility Limitation. The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences, 68(2), 153–60. http://doi.org/10.1093/gerona/gls138

  1. Corona G, G., Rastrelli, G., Maseroli, E., Sforza, A., & Maggi, M. (2015). Testosterone Replacement Therapy and Cardiovascular Risk: A Review. The World Journal of Men’s Health, 33(3), 130–42. http://doi.org/10.5534/wjmh.2015.33.3.130

  2. Crawford, M., & Kennedy, L. (2016). Testosterone replacement therapy: role of pituitary and thyroid in diagnosis and treatment. Translational Andrology and Urology, 5(6), 850–858. http://doi.org/10.21037/tau.2016.09.01

  3. Donnelly, P., & White, C. (2000). Testicular dysfunction in men with primary hypothyroidism; Reversal of hypogonadotrophic hypogonadism with replacement thyroxine. Clinical Endocrinology, 52(2), 197–201. http://doi.org/10.1046/j.1365-2265.2000.00918.x

  4. Gagliano-Jucá, T., & Basaria, S. (2017). Trials of testosterone replacement reporting cardiovascular adverse events. Asian Journal of Andrology, 19(May), 1–7. http://doi.org/10.4103/aja.aja

  5. Gao, N., Zhang, W., Zhang, Y., Yang, Q., & Chen, S. (2013). Carotid intima-media thickness in patients with subclinical hypothyroidism: A meta-analysis. Atherosclerosis, 227(1), 18–25. http://doi.org/10.1016/j.atherosclerosis.2012.10.070

  6. Kloner, R. A., Carson, C., Dobs, A., Kopecky, S., & Mohler, E. R. (2016). Testosterone and Cardiovascular Disease. Journal of the American College of Cardiology. http://doi.org/10.1016/j.jacc.2015.12.005

  7. Krassas, G. E., Poppe, K., & Glinoer, D. (2010). Thyroid Function and Human Reproductive Health. Endocrine Reviews, 31(5), 702–755. http://doi.org/10.1210/er.2009-0041

  8. Layton, J. B., Li, D., Meier, C. R., Sharpless, J. L., Stürmer, T., & Brookhart, M. A. (2018). Injection testosterone and adverse cardiovascular events: A case-crossover analysis. Clinical Endocrinology. http://doi.org/10.1111/cen.13574

  9. Mesbah Oskui, P., French, W.J., Herring, M. J. et al. (2013). Testosterone and the Cardiovascular System: A comprehensive Review of the Clinical Literature. Journal of the American Heart Association. http://doi.org/10.1161/JAHA.113.000272

  10. Onasanya, O., Iyer, G., Lucas, E., Lin, D., Singh, S., & Alexander, G. C. (2016). Association between exogenous testosterone and cardiovascular events: an overview of systematic reviews. The Lancet Diabetes and Endocrinology. http://doi.org/10.1016/S2213-8587(16)30215-7

  11. Pastuszak, A. W., Kohn, T. P., Estis, J., & Lipshultz, L. I. (2017). Low Plasma Testosterone Is Associated With Elevated Cardiovascular Disease Biomarkers. The Journal of Sexual Medicine, 14(9), 1095–1103. http://doi.org/10.1016/j.jsxm.2017.06.015

  12. Roos, A., Bakker, S. J. L., Links, T. P., Gans, R. O. B., & Wolffenbuttel, B. H. R. (2007). Thyroid function is associated with components of the metabolic syndrome in euthyroid subjects. The Journal of Clinical Endocrinology and Metabolism, 92(2), 491–6. http://doi.org/10.1210/jc.2006-1718

  13. Udovcic, M., Pena, R. H., Patham, B., Tabatabai, L., & Kansara, A. (2017). Hypothyroidism and the Heart. Methodist DeBakey Cardiovascular Journal, 13(2), 55–59. http://doi.org/10.14797/mdcj-13-2-55

  14. Wallis, C. J. D., Lo, K., Lee, Y., Krakowsky, Y., Garbens, A., Satkunasivam, R., … Nam, R. K. (2016). Survival and cardiovascular events in men treated with testosterone replacement therapy: an intention-to-treat observational cohort study. The Lancet. Diabetes & Endocrinology, 4(6), 498–506. http://doi.org/10.1016/S2213-8587(16)00112-1

  15. Xu, L., Freeman, G., Cowling, B. J., & Schooling, C. M. (2013). Testosterone therapy and cardiovascular events among men: A systematic review and meta-analysis of placebo-controlled randomized trials. BMC Medicine, 11(1). http://doi.org/10.1186/1741-7015-11-108


Scar tissue - is it an issue?

Is scar tissue really an issue? Alongside myself, scars may be one of the most under appreciated and neglected structures, when it comes to assessing aspects of an individual's pain and movement limitations.   For many people, which include physicians, surgeons and often the owners of said scars, there’s an acceptance that the scar has healed and is not involved in any process of pain, strength or movement dysfunction. Dr’s and surgeons often assume that time enables optimal healing and patients simply forget about the previous trauma. Time may be a great healer but the healing is only partial - the nervous system always remembers. Writing this, reminds me of a client who had filled in all historical injury and trauma that he had experienced on my intake forms, which might have been a factor in his chronic back pain. It wasn’t until he took his top off and under questioning revealed that he had  donated his kidney to his brother some twenty years ago. It wasn't a big deal though as it was twenty years ago apparently.

This sequence of events has been summarised as homeostatic, inflammation, granulation and remodelling phases (1) which are undergoing symbiotic relationships with other structures and dependant on energetic, endocrine and other functions of the individual, which often depend on environmental stimulus. During the granulation and proliferation phase, sub-phases, which include collagen deposition, remodelling of blood vessels and tissues occur. It’s likely that during these phases the health and energetic response of the individual will dictate the capacity to regenerate and may also influence the layers of dysfunction that are present with scar tissue.

“ In childhood, wounds heal quickly and inflammation is resolved, in extreme age, or during extreme stress or starvation, wound healing is much slower and the nature of inflammation and would closure is different. “Ray Peat.

Unsaturated vegetable fats, serotonin and estrogen promote collagen synthesis and resulting fibrosis and keloid scars are associated with these states (3). Perhaps the capacity to organise energy and regenerate are instrumental in decreasing the associated dysfunctions that can be found in all scar tissue? Most Drs that I have spoken to just assume that after 12 weeks the scar has generally healed and that normally activity can be resumed. As a rule, there is no thought given to mechanical, pain sensitising or emotional constraints induced by the presence of the scar. It’s generally accepted that most scars have 80% tensile strength of the previous structure, but again might that too be a product of the quality of healing available to the individual?

“ The amount of disorganised fibrous material formed in injured tissue is variable and depends on state of the individual and tissue situation. “

In hypothyroidism, high levels of the pituitary hormone TSH (thyroid stimulating hormone) are known to stimulate fibrosis (1) Maintaining adequate thyroid hormone production promotes DNA transcription, optimal energy production, carbon dioxide production and probably decreases the proliferative effects of 'estrogenic' states that can be attributed to keloid scar formation.

The bigger the scar, the more likely the associated dysfunction? Perhaps the more disorganised tissue that exists, the increased likelihood of fuzziness between the central nervous system and output to structures associated with that scar. In scar tissue that has not been assessed or treated, it's relatively easy to induce weakness or stress to the surrounding tissues by a variety of stimulus which might include thinking and different types of pain,  touch or vectors of stretch that create neurological chaos or threat to to the individual.

Good therapy should allow for conversations between the clinician and patient that create stimulus that may (or may not) affect the output of surrounding structures associated with the scar. Poor feedback mediated by the scar might involve the following:

Emotional: Aspects of recall of the event that the individual finds upsetting.

Nociception/pain: First and second pain, visual or auditory, crude/fine touch, tickle/itch temperature, stress or recall od suffering responses to stimulus. (Involve pain feedback related to spinothalamic, spinotectal, spinohypothalamic and spinomesencephalic tracts)

Mechanical: Pressure, rebound, stretch, joint mechanoreceptors and other responses to tissue and structures. (Related to Golgi, Pacini, Ruffini and other dorsal column feedback pathways.)

Improving the optimal healing of scar tissue might involve aspects such as adequate carbohydrate, proteins, sunlight (or red light), carbon dioxide, thyroid, progesterone, vitamin A and E. Avoiding phytoestrogens and low carbohydrate diets would also be prudent.

Despite optimised nutrition and endocrine function, it’s likely that many scars leave some artefact that prevents the nervous system communicating with tissues. C - sections, episiotomies, appendectomies, laparoscopies and most surgeries, injuries or trauma leave a trace that needs to be resolved with the right therapy. Inhibition can be purposeful but restoration might need a little nudge from therapies like proprioceptive deep tendon reflex (P-DTR).


  1. Kim, D., Kim, W., Joo, S. K., Bae, J. M., Kim, J. H., & Ahmed, A. (2018). Subclinical Hypothyroidism and Low-Normal Thyroid Function Are Associated With Nonalcoholic Steatohepatitis and Fibrosis. Clinical Gastroenterology and Hepatology, 16(1), 123–131.e1. http://doi.org/10.1016/j.cgh.2017.08.014

  2. https://emedicine.medscape.com/article/1298129-overview?pa=1ZDxXAnEOeNV9BUnYezdYpt49YJzASbxEvvw80YIDjlelzZDQj3XLvbI0V2MbTq%2FX8MwC0EECwzp432Skuf9qw%3D%3D

  3. http://raypeat.com/articles/articles/regeneration-degeneration.shtml

Being holistic versus (holistic) critical thinking.


Is being 'holistic' an advantage to holistic critical thinking? It’s relatively easy to get drawn into a naturalistic fallacy of consuming all foods in their most raw natural state. Perhaps you’re someone who went from a fast food diet, where you didn’t feel your best, to consuming more whole foods, fresh fruit and vegetables? It’s easy to see how a switch and positive changes can occur in the short term. The next step is to start preaching to the masses how sugar is bad, how your life will be saved with green smoothies, nuts, seeds and coffee butt cleanses. For the record this is a waste of coffee and not to far from what I was preaching a decade ago. So what does it mean to be holistic?There’s a large movement within the health fitness and wellness industry (and lay people) that are drawn to  'holistic' thinking, and their definition is often enforced by the fallacy that everything in its most natural state is better for human health. This appears to include foods like nut milks (yes you can milk a nut), kale smoothies, seed oils like flax and undercooked broccoli and other greens, despite their negative effects on human health when consumed in substantial amounts. It’s a religion, and much like religion and with this mind-set it isn’t going to make you any healthier. I’ll make reference here to the late, great Beastie Boy, MCA who despite being a vegan and a Buddhist died far too early from throat cancer.

It is true that eating plenty of foods in their most natural state f(or some foods) can be important for health. But the image on the right highlights the faulty narrative of being holistic without thinking about the consequences. Fruits, vegetables, dairy products, meats and the like require minimal processing but in the quest for longevity, taste and profit, adding preservatives and flavour enhancers causes our food sources to become problematic. The so called ‘holistic’ folk get lost in this narrative urging your diet to become abundant in the rawest, greenest and brownest foods, that are most indigestible and contain potent inhibitors of biological function.

To integrate a level of holism into nutrition and function requires a level of critical thinking. What do these foods contain? How do they affect physiology? It’s well known that the brassica vegetables like broccoli, cauliflower and sprouts contain potent compounds that decrease energy output. These goitregens inhibit thyroid output and isothiocyanates found in cruciferous vegetables affects TPO or thyroid peroxidase, both of which are exacerbated when iodine uptake or restriction is present. Research tends to support these problematic effects (Choi & Kim, 2014)(Truong, Baron-Dubourdieu, Rougier, & Guénel, 2010), but much attention is focused on the smaller compounds that seem to work well in test tubes, rather than its global effects. As the environment becomes more stressful for biology do we need more building or reducing factors within our control?

The environment can be a harsh place. There are plenty of pollutants that have a negative effect on fertility, metabolism and other key endocrine aspects of health, some of which are industrial, others purposively added to food (arguably another form of industry) (Rajpert-De Meyts, Skakkebaek, & Toppari, 2000)(Upson, Harmon, & Baird, 2016). We can argue that the environment has always been a harsh place and adaptation has taken place as a response to selective pressures at the heart of evolution. Yet currently we are heading towards a tipping point, as environmental stimulants appear to be at the heart of acquired biological damage that is inherited by offspring. Cancer, fertility and other metabolic diseases are more common than ever and yet the approach is to keep seeking the magic bullet to ameliorate the fate that awaits many of us.

If we were to ask:

What enhances biological function, makes us more robust and allows us to have a stronger conversation with a stressful environment?

Rather than succumb to its stressors.

The highway to health

The highway to health

A biological system in its best working order could be represented, as an infinite road stretching into the  distance, perhaps with the odd bump along the way or a slight deviation but an ability to get back on track is available. Compare that to the inhibitory T-junction where the body cannot function as the clear straight road, it deviates from its true organised direction. The journey is laboured and restrictive. The ability to flux and respond to stressors is key and adequate energy is an essential component of reorganisation.

Nutrition is an important factor for such conversations with the environment. Eating a diet that is dominated with foods that are difficult to digest, decrease energy availability and create more stress are not going to make chatting any easier. If we make the effort to understand what keeps a cell and its mitochondria functioning at its most efficient state, we can understand why aspects such as sugar, adequate protein, moderate exercise, light and other factors, can play a role in overcoming current stimulus that decrease function and increase disease states.

The following article is definitely worth a read for an understanding of the concepts that I have talked about. http://raypeat.com/articles/articles/vegetables.shtm


Choi, W. J., & Kim, J. (2014). Dietary factors and the risk of thyroid cancer: a review. Clinical Nutrition Research, 3(2), 75–88. http://doi.org/10.7762/cnr.2014.3.2.75

Rajpert-De Meyts, E., Skakkebaek, N. E., & Toppari, J. (2000). Testicular Cancer Pathogenesis, Diagnosis and Endocrine Aspects. Endotext. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/25905224

Truong, T., Baron-Dubourdieu, D., Rougier, Y., & Guénel, P. (2010). Role of dietary iodine and cruciferous vegetables in thyroid cancer: A countrywide case-control study in New Caledonia. Cancer Causes and Control, 21(8), 1183–1192. http://doi.org/10.1007/s10552-010-9545-2

Upson, K., Harmon, Q. E., & Baird, D. D. (2016). Soy-based infant formula feeding and ultrasound-detected uterine fibroids among young African-American women with no prior clinical diagnosis of fibroids. Environmental Health Perspectives, 124(6), 769–775. http://doi.org/10.1289/ehp.1510082

Gestational diabetes and metformin-Is that the best that medical thinking has to offer?

Gestational diabetes or elevated blood sugar is often treated with metformin to improve blood sugar levels and considered the standard approach to treating gestational diabetes. The research suggests that it has little negative effects on the pregnant mother. However, does significant risks to both mother and baby if the incidence of premature birth count? Here are a few aspects to consider regarding the use of metformin to control blood sugar during pregnancy. A study of patients receiving a dose of metformin, combination of Clomiphene citrate (CC) and metformin both faired better than CC alone for the induction of ovulation (Neveu, Granger, St-Michel, & Lavoie, 2007).  As the combined group showed no benefit compared to metformin alone, one might consider that metformin alone may be considered for the positive effects.

In another study metformin and diet interventions showed a significant outcome compared to non-metformin-diet interventions. The metformin diet showed a reduction of 14 adverse events in a group of 76 expectant mothers, compared to the non-treated group of 36 adverse events out of 76 pregnancies (Glueck et al., 2013).

Thatcher and Jackson (Thatcher & Jackson, 2006) compared pregnancies of 188 women. 61 experienced miscarriages and 11 of those had stopped taking metformin, suggesting other abnormalities beyond metformin’s actions. 81% of women with pregnancies before metformin, 67% had prior miscarriages. 37% of these also miscarried again. Whilst metformin appeared to show minimal effects to mother and foetus 22% were born prematurely.

Whilst metformin has shown favourable outcomes in PCOS states, questions around pertinent biological mechanisms should warrant further discussion. It’s well known that two key endocrine actions may be compromised during the failure to achieve full gestation. Estrogen induces hypoxia in the uterus (Peat, 1997) and failure to produce adequate progesterone to counter the effects of estrogen may be implicated in the commonly fragile time around weeks 9-10 of pregnancy and incidence of miscarriage.

A concern of metformin are its affect transplacentally. Metformin appears to influence testicular size in males and affects sertoli cells. In females it may also lead to decreased androgen synthesis. Birth weight percentile is also significantly lower in pregnancies treated with metformin (Bertoldo, Faure, Dupont, & Froment, 2014)I Metformin has generally appeared safe in expecting mothers but considerable concern should be made regarding its long term effects to offspring and development most notably to reproductive tissues.

Hypothyroidism is a key factor in maintenance of pregnancy and alongside progesterone, thyroid hormone deficiency can be implicated in poor cellular energetics, production of adenosine triphosphate (ATP) and blood sugar regulation. There remains much debate about the issue of subclinical hypothyroidism, values and when to treat and perhaps metformin’s role despite showing some promises may be treating a symptom related to insulin sensitivity.

So perhaps these questions might be more pertinent before prescribing an agent that shows potentially negative effects to the fetus?

  1. What is the nutrition of the mother, is it enough and does it contain enough nutrients to enhance/maintain adequate progesterone/thyroid production?
  2. Is estrogen increasing at a rate that suppresses progesterone/thyroid levels and persistently decreases insulin sensitivity?
  3. Is there enough carbohydrate in the diet to ensure that carbohydrate is effectively utilised instead of persistent conversion of fats, increasing overall stress to both mother and fetus?
  4. Are the values of hypothyroidism and the identification of subclinical/functional hypothyroid factors appropriate?
  5. Is gestational diabetes a reflection of the above points?

The use of metformin, without questioning these mechanisms, remains at best a reduced treatment that fails to address a range of biological interactions and function.


Bertoldo, M. J., Faure, M., Dupont, J., & Froment, P. (2014). Impact of metformin on reproductive tissues: an overview from gametogenesis to gestation. Annals of Translational Medicine2(6), 55. http://doi.org/10.3978/j.issn.2305-5839.2014.06.04

Glueck, C. J., Goldenberg, N., Pranikoff, J., Khan, Z., Padda, J., & Wang, P. (2013). Effects of metformin-diet intervention before and throughout pregnancy on obstetric and neonatal outcomes in patients with polycystic ovary syndrome. Current Medical Research and Opinion29(1), 55–62. http://doi.org/10.1185/03007995.2012.755121

Neveu, N., Granger, L., St-Michel, P., & Lavoie, H. B. (2007). Comparison of clomiphene citrate, metformin, or the combination of both for first-line ovulation induction and achievement of pregnancy in 154 women with polycystic ovary syndrome. Fertility and Sterility87(1), 113–120. http://doi.org/10.1016/j.fertnstert.2006.05.069

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


Thatcher, S. S., & Jackson, E. M. (2006). Pregnancy outcome in infertile patients with polycystic ovary syndrome who were treated with metformin. Fertility and Sterility85(4), 1002–1009. http://doi.org/10.1016/j.fertnstert.2005.09.047

What is functional hypothyroidism?

You won’t find the term functional hypothyroidism in the medical literature, or at least not yet. Primarily due to clinical hypothyroidism being bound to a rigid assessment usually diagnosed by the blood test thyroid stimulating hormone or TSH. TSH secretion is controlled by synthesis of thyroid releasing hormone or TRH in the supraortic and supraventricular nuclei of the hypothalamus. TRH is transported to the anterior pituitary by the hypothalamo- hypophysial portal system where it stimulates synthesis of TSH. T4, T3 and TRH control the secretion of TSH (Gardner et al., 2011).

TSH production can also be affected by TSH receptor damage, medical drugs, disease states, iodide, blood glucose levels and other circulating hormones TSH may also be affected by environmental pollutants and heavy metals (Llop et al., 2015).  Metabolic disease and increases in Body Mass Index appear to be correlated with an increase in TSH levels (Ruhla et al., 2010).

Often, you will see clear links and studies to key micronutrients such as zinc, selenium, iodine and other important co-factors. These deficiencies can exist demographically but usually in westernised societies, there deficiency can be linked to impaired absorption rates, perhaps linked to digestive dysfunction and other factors.

“Measuring the amount of thyroid in the blood isn’t a good way to evaluate adequacy of thyroid function, since the response of tissues to the hormone can be suppressed (for example, by unsaturated fats) (Peat, R.1999).

 Dietary factors such as unsaturated fatty acids in the diet may potentially be one of the most overlooked factors that supress thyroid function. Other factors such as caloric restriction, stressful environments, over exercising and other factors are some of the others. It’s well known that in certain areas of hormone dysregulation such as menstrual cycle irregularities, oligoamenorrohea (loss of cycle), anovulation (failure to ovulate) and lack of libido and fertility in both men and women,  can be attributed to poor energy intake and environmental factors (Nieuwenhuijsen et al., 2014) (Skakkebæk, 2003). Dietary factors have synergy with hormonal imbalances perpetuating high levels of estrogen.

The functional suppression of thyroid function by unsaturated fats, eating a so-called healthy diet (full of uncooked brassica vegetables, nuts and seeds) orthorexic states and other factors is largely ignored by physicians.

I can say with some certainty, after completing postgraduate studies at university with a number of Doctors, that diet and inhibitory factors of diet rarely get assessed when it comes to assessing energy and thyroid function.

A persistent functional hypothyroid state, induced by unsaturated fats may lead to the pre-diabetic and diabetic states induced by an inability to utilise carbohydrate and the preferential shift to use of fats instead of sugars as suggested in the Randle or glucose fatty acid cycle (Randle, Garland, Hales, & Newsholme, 1963). Increased cortisol, oxidation, decreased carbon dioxide and an increased stress on the oxidative system, could potentially lead to glycolysis and an increase in lactic acid, further increasing damage, stress and further suppression of thyroid function.

Measurement of thyroid blood tests remains inaccurate and problematic without the inclusion of a variety of symptoms and previously accurate assessment, such as basal metabolic rate, body temperature and pulse. The suppression of both thyroid and adequate energy states will always remain.

As the common approach for diagnosing hypothyroidism is having TSH above 4 or 5 mmUL and the preferred treatment is to supplement with synthetic levothyroxine. How much change can you realistically achieve if you fail to address the supressed metabolism induced by diet, an individuals susceptibility to stress and their own environment?



Gardner, D. G., Shoback, D. M., Greenspan, F. S. et al .(2011). Greenspan’s Basic and Clinical Endocrinology. McGraw Hill.

Llop, S., Lopez-Espinosa, M. J., Murcia, M., Alvarez-Pedrerol, M., Vioque, J., Aguinagalde, X., … Ballester, F. (2015). Synergism between exposure to mercury and use of iodine supplements on thyroid hormones in pregnant women. Environmental Research, 138, 298–305. http://doi.org/10.1016/j.envres.2015.02.026

Nieuwenhuijsen, M. J., Basagana, X., Dadvand, P., Martinez, D., Cirach, M., Beelen, R., & Jacquemin, B. (2014). Air pollution and human fertility rates. Environment International, 70, 9–14. http://doi.org/10.1016/j.envint.2014.05.005; 10.1016/j.envint.2014.05.005

Peat, R. (1999). Thyroid Therapies, Confusion and Fraud. Retrieved from www.raypeat.com/articles/articles/thyroid.shtml

Randle, P. J., Garland, P. B., Hales, C. N., & Newsholme, E. A. (1963). The glucose fatty-acid cycle its role in insulin sensitivity and the metabolic disturbances of diabetes mellitus. The Lancet, 281(7285), 785–789. http://doi.org/10.1016/S0140-6736(63)91500-9

Ruhla, S., Weickert, M. O., Arafat, A. M., Osterhoff, M., Isken, F., Spranger, J., … Möhlig, M. (2010). A high normal TSH is associated with the metabolic syndrome. Clinical Endocrinology, 72(5), 696–701. http://doi.org/10.1111/j.1365-2265.2009.03698.x

Skakkebæk, N. E. (2003). Testicular dysgenesis syndrome. In Hormone Research (Vol. 60, p. 49). http://doi.org/10.1159/000074499


Health, Thyroid and TSH. Assessing and treating the thyroid.

What is the impact of thyroid hormone on health?Increasingly health is defined by a bunch of arbitrary numbers. High cholesterol? That’s not normal take a pill. Low iron? Here take this iron supplement. In Ivan Illich’s book, Limits to Medicine- Medical Nemesis, Illich makes the reader fully aware of his disdain of medical check ups - " The medicalisation of prevention thus becomes another major symptom of social iatrogenesis. It tends to transform personal responsibility for my future into my management by some agency."

Instead of heavily reliant systems on numbers and markers. Should we not look to improve qualitative and quantitative pairings to get a better picture of health and improve outcomes? The last ten weeks of my life have been wrapped up in a post graduate diploma in endocrinology. Getting a better picture of how clinicians tackle complex areas has been a rewarding but at the same time frustrating area of study.

Sometimes the questioning has been a down the lines of - This patient has this endocrine feature, what are the medication used, which medications interfere, what surgical options can be pursued and what is the follow up? What is frustrating for me is there is little effort to understand why? Why? Why Donald why? Diet, stress and environmental aspects of hormonal health are often forgotten about, because the goal of getting that client back into the window of numerical health takes priority. But what if we took a better look at the why? Might it not yield better long-term outcomes for the patient?

I have a special interest in thyroid function, motivated by the writings of Ray Peat, Broda Barnes, Mark Starr and others. There’s a significant amount of work discrediting the role of combined T4/T3 therapy and in particular natural desiccated thyroid (NDT). In many endocrine textbooks the elevation of the active form of thyroid hormone, T3 was elevated significantly post NDT treatment.

A confounding factor in this assumption was based upon a previously incorrect conversion which can still be found in endocrine textbooks stating that 1mg of NDT was equivalent to 1ug of LT-4. There is recent evidence available showing a patient preference for NDT, which showed improved outcomes to weight loss, energy, happiness, sleep and memory (Hoang, Olsen, Mai, Clyde, & Shakir, 2013).

A reliance on TSH, T3 and T4 levels alone may be ineffective at analysing the effectiveness of combination therapy in comparison to synthetic monotherapy treatment of hypothyroidism. Additionally this study highlights the inaccuracy of the assumed conversion of 1mg: 1ug. Using more accurate 3rd generation TSH assays yields a suggested ratio of 1.47 mg’s to 1ug. This may explain the lack of effectiveness in previously conducted trials and the conclusion that increased transient T3 levels were decided as unacceptable. NDT in many cases may offer a better solution than synthetic thyroid hormone after all

Potential mechanisms of improvement may also lie in the actions of T1 and T2 and assumptions based solely on TSH, T3 and T4 may not explain the benefits recorded in this and other studies.      

Another pitfall of number reliance is well known in the reference of thyroid stimulating hormone (TSH). TSH is considered the gold standard for hypothyroid diagnosis but its limitations have become increasingly prevalent due to its production via the stimulating centers from TRH (thyroid releasing hormone) from the hypothalamus and then TSH from the pituitary, if a problem exists at the periphery the likelihood of getting an accurate assessment is diminished. A normal TSH reading is defined as 0.4-4.5 mU/L but generally many Doctors do not consider someone hypothyroid unless they present with a TSH over 4 mU/L.

Increasingly some Doctors are becoming aware of the reduction of hypothyroid symptoms when TSH is kept below 1mU/L and some evidence suggests that even at 0.5 mU/L (lowered but suppressed) is ideal to ensure that hypothyroid symptoms are decreased (Pantalone & Nasr, 2010).

Me? I am going to go back and contradict myself and say that numbers are useful. The basal temperature test with a cheap thermometer, as championed by Broda Barnes still suggests a good window of function of the thyroid test. 36.5 to 37 degrees is considered normal and reflects a well functioning metabolism. Couple that with a pulse rate test and you can also get a good indication of cortisol. So I am not against the numbers. I just think we need to ask better questions before we accept them as absolutes.


Hoang, T. D., Olsen, C. H., Mai, V. Q., Clyde, P. W., & Shakir, M. K. M. (2013). Desiccated thyroid extract compared with levothyroxine in the treatment of hypothyroidism: A randomized, double-blind, crossover study. Journal of Clinical Endocrinology and Metabolism, 98(5), 1982–1990. http://doi.org/10.1210/jc.2012-4107

Illich, I. Limits to Medicine - Medical Nemesis. Marion Boyars. 1976.

Pantalone, K. M., & Nasr, C. (2010). Approach to a low tsh level: Patience is a virtue. Cleveland Clinic Journal of Medicine. http://doi.org/10.3949/ccjm.77a.10056