oestrogen

The Big Estrogen Hoax

Routine spraying with potent pesticides was deemed safe previously.

Routine spraying with potent pesticides was deemed safe previously.

One of the reasons I decided to pursue a master’s degree in endocrinology was to challenge my own bias and what I had learnt from reading the works of people like Ray Peat PhD and Dr Katherina Dalton. Prior to my thesis I had to undertake a post graduate diploma due to my lack of medical training. It became apparent early on that discussions were heavily centred around endocrine mechanisms that occur in isolation that have become almost indoctrinated throughout text books and the plethora of funded research to support these narratives. My own research investigated the dogmatic belief that thyroid blood tests are accurate when faced with ongoing stress, nutrition and pollution issues that can render such blood tests inaccurate and more often than not appear normal. I thought having better conversations with clinicians might be a positive outcome of this study but anytime I attempt to discuss its always the same deflection that blood tests are accurate. It’s clear they are not in many different scenarios

One of the biggest problems and what could indeed be deemed as the biggest hoax in medicine (although the perpetuation of the need to lower cholesterol levels with statins is on a par with that) is the dogmatic belief that a female becomes estrogen deficient during the menopause. After reading Ray Peat’s PhD thesis and book (Peat, 1997)(Peat, 1972) that stated the counter argument, I’ve tried to look at this argument extensively over the last few years. It seems complex on the outside but consider the following and think about if for a minute or two.

Why is pregnancy protective?

When a woman becomes pregnant, she can produce up to 100 x more progesterone than normal. Why? It’s well known that progesterone is a hormone of organisation. It’s been shown to be associated with differentiation (regulate tissue growth induced by estrogen) compared to estrogen’s action of tissue growth, therefore just like thyroid hormone it’s a potent factor in creating tissue oxygenation and enhances blood sugar regulation. It’s well known that many miscarriages occur in the first trimester due to hypoxia induced by increased estrogen levels. Excess estrogen is also associated with disorganised biology and cancer. We know progesterone is protective and organisational so why does the madness persist that ovarian decline is associated with a lack of estrogen?

Recently I’ve thought about the comparison between economics and environment and how analogous it is with an excess of estrogen. The world needs more progesterone, it’s exposure to estrogen like processes of growth, unrestricted profits and resource draining that is excessive and unrestrained. It needs less leadership, more organisation, more differentiation and more cooperation. So do cells when they are exposed to the same forces.

The biggest study to date assessing the effects of hormone replacement therapy or HRT was the women’s health initiative (Rossouw et al., 2002). The main findings of this study were that HRT increased breast cancer and cardiovascular risk by increasing thrombosis. Further problems were encountered when progestins were added to estrogen replacement therapy.

Now go back and read that last part again because this is where a vast problem exists in medicine and advice given to females. Not just going through menopause but equally any advice they are generally given related to hormone health, effects of contraception etc. Why? Because progestins are not progesterone, they are synthetic versions of progesterone that act very differently to natural progesterone and the real problem is the acceptance by medical practitioners that they are one in the same.

Why so much confusion?

Take the following paper Progesterone action in endometrial cancer, endometriosis, uterine fibroids, and breast cancer by Kim et al (Kim, Kurita, & Bulun, 2013). This is a well-respected group of progesterone researchers who do make the distinction that progesterone antagonizes estrogen driven growth in the endometrium and that insufficient progesterone increases endometrial cancer. Throughout the paper they often cite the negative effects of supplemental progesterone (particularly with breast cancer) combined with estrogens that increase the progesterone receptor (PR) and increase cancer growth. Yet all the studies cited have used progestins and not natural progesterone. This is a primary factor in the perpetuation of mass confusion between progestins and natural progesterone.

Not that the receptor is a great way to test a hormones actions and in particular the PR can be stimulated by estrogen, other hormones such as cortisol and like other receptors can be hijacked and regulated by a variety of pollutants that mimic estrogen. Ray Peat points out that receptors have been proposed for everything in biology to bring order to complexity and an attempt to limit biology to lock and key mechanisms. Receptors do exist but they don’t explain all the processes that occur.

Progesterone is protective across many aspects of function

There are many studies on progesterone and its broad actions on fertility, blood sugar, sleep, mood and more. Katherina Dalton who produced over one hundred and fifty publications on the role of progesterone and showed that issues such as post-natal depression and morning sickness often resolved with additional progesterone  Dr Dalton even helped individuals in court whose aggressive actions were mediated by progesterone deficiency (Dalton, 1980). Many people often state that we’ve moved on from old medicine but in reality we have moved away from medicine that doesn’t make vast profits for companies. It wouldn’t be unscrupulous to suggest that the blurred lines have been purposeful to confuse both clinicians and the public alike. Don’t just take my word for it, there’s plenty of data to review . In a systematic review of thirteen studies of progesterone by Spark and Willis (Spark & Willis, 2012) they state:

 

‘ Even though the words progestogen and progesterone are not interchangeable they are often used interchangeably which results in confusion about therapeutic use of progesterone.’

‘ Even though the words progestogen and progesterone are not interchangeable they are often used interchangeably which results in confusion about therapeutic use of progesterone.’

Expanding that large randomised control studies in progesterone have not been undertaken and this might primarily be due to poor profit margins from a natural versus  synthetic compounds. It’s hard not to sound a like a conspiracy theorist but there really is no vast sums of money for large corporations when progesterone is used. Given that it also drastically reduces the need for blood pressure, blood sugar, infertility and menopausal medications it starts to make some sense.

Some old books on progesterone, post natal depression and PMS by Katherina Dalton are worth a read. I picked all mine up for a quid or two a few years back but you can still get them.

https://www.amazon.co.uk/Depression-after-Childbirth-Recognise-2001-05-31/dp/B01JXORBK0/ref=sr_1_1?keywords=katherina+dalton&qid=1560326142&s=gateway&sr=8-1

Ray Peats website has dozens of excellent articles too http://raypeat.com/

 References: 

Dalton, K. (1980). CYCLICAL CRIMINAL ACTS IN PREMENSTRUAL SYNDROME. The Lancet. https://doi.org/10.1016/S0140-6736(80)92286-2

Kim, J. J., Kurita, T., & Bulun, S. E. (2013). Progesterone action in endometrial cancer, endometriosis, uterine fibroids, and breast cancer. Endocrine Reviews. https://doi.org/10.1210/er.2012-1043

Peat, R. (1972). Age Related Oxidative Changes in the Hamster Uterus. University of Oregon.

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

Rossouw, J. E., Anderson, G. L., Prentice, R. L., LaCroix, A. Z., Kooperberg, C., Stefanick, M. L., … Writing Group for the Women’s Health Initiative Investigators. (2002). Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results From the Women’s Health Initiative randomized controlled trial. JAMA.

Spark, M. J., & Willis, J. (2012). Systematic review of progesterone use by midlife and menopausal women. Maturitas. https://doi.org/10.1016/j.maturitas.2012.03.015

 

 

 

Sub Clinical Hypothyroidism

Strange, must-try exotic fruits!.jpg

I’ve seen a number of assumptions from doctors suggesting that there’s no optimal diet for improving thyroid function. If that were the case there would be no optimal diet for heart disease, cancer or autoimmune disease but there are many proposed guidelines of certain foods that should be avoided.

 If you want to slow down the thyroid eating plenty of cruciferous vegetables, fish oils and exposure to oestrogens (environmental pollution, contraception and other medical drugs) seems to inhibit thyroid function dramatically and large amounts of anti-thyroid (goitregens) foods are certainly linked with thyroid cancer. Often an individual’s perceived healthy choices can suppress thyroid function and therefore be resolved with nutrition alone. A functionally suppressed thyroid state that’s treated with thyroid hormone may not yield the best results.

 Sub clinical hypothyroidism (SCH) is an issue that divides endocrinology but when you look at the process of thyroid dysfunction there are some clear indicators that should suggest that it’s treatment would be the most sensible (but not the most money making) action in the long run. Let’s start with defining what SCH is.

SCH is usually defined as an asymptomatic state in which free T4 is normal but TSH (thyroid stimulating hormone or TSH is the pituitary stimulator of thyroid hormone) is elevated. If serum TSH is >10mU/L there is consensus that the patient should be treated with thyroxine because of the likelihood that the patient will develop overt hypothyroidism with subnormal T4 and because this degree of SCH predisposes to cardiovascular disease. When the TSH is in the range of 4.5 to 10 mU/L, there is controversy about the efficacy of T4 therapy (Lavin, N, Ali, Omar., Beall, M.U., Bhutto, 2016).

Although many people with most forms of thyroid disease often present with diverse symptoms due to the systemic effects of thyroid hormone action but are often ignored through reductionist observation. The table below lists most of the major actions of thyroid function and deficits created by a hypothyroid state.


Thyroid hormone is necessary for all aspects of organised biology.

Thyroid hormone is necessary for all aspects of organised biology.

Here’s a short history of some of the contrasting opinions on treating SCH. Biondi cites the original controversies of Wartofsky and Dickey (2005) who favoured a narrower TSH range (Wartofsky & Dickey, 2005), which was in contrast to the opposition to a lower TSH suggested by Surks et al. (2005) (Biondi, 2013).

 The latter authors stated ‘that there was little evidence supporting the treatment of SCH, citing a single small study by Kong et al. treating 40 women with SCH (Kong et al., 2002).  The main findings demonstrated that thyroxine treatment had no impact on lipids, energy expenditure, weight gain or composition despite decreases in TSH levels in the treatment group (8.0 +- 1.5 mU/L change from baseline -4.6 +-2.3 mU/mL compared to 7.3 +- 1.6  -1.7 +-2.0 mU/L in the placebo). However this study, perhaps like many others (Laurberg et al., 2011) (Surks et al., 2005), failed to assess the nutritional status of this small group of patients. For example, if calorific excess were present, these markers may show little change, as weight loss requires a calorie deficit.  Conversely if a patient were chronically undernourished through a low nutrient intake, attempting to enhance metabolic rate and weight loss with TH replacement may be negated when adrenaline, glucagon and cortisol are produced to regulate blood sugar levels.

 Problems associated with some of the smaller seemingly positive older studies, is often the lack of control groups for comparison. A smaller RCT (treatment n-22 control n-19) comparing treatment of subjects with biochemically euthyroid TFTs  yet clinical hypothyroidism with thyroxine, found the intervention no more successful than placebo (Pollock et al., 2001). Whilst the effect of placebo cannot be discounted, the study only focused on cognitive function and wellbeing, factors that are a limited component of thyroid function.  A friend of mine also pointed out that the use of T4 alone and female cohort with an increased weight some 20kgs over the control group are also problematic issues in studies like this.

 More studies trickle through that builds upon previous suggestions that measuring TSH is a poor way to accurately assess thyroid function, primarily due to the facts that stress, environmental pollutants and nutrition can cause biochemistry and in particular thyroid blood tests to present as normal. The problem with ignoring SCH is the following scenario.

 You have isolated or a number of hypothyroid symptoms such as weight gain, high blood pressure, high cholesterol, hair loss, fatigue, low libido, altered menstrual cycle, anxiety or depression, poor sleep, constipation, brain fog, inflammation of the brain, altered heart contraction, dry skin etc.

 Good news Mrs X you have normal thyroid function as your blood tests came back within the normal ranges. The symptom/s you have must be in your head. Here you have high blood pressure take this anti-hypertensive medication.

The pituitary should be considered a source of evaluation that could be useful but should be treated with suspicion. There are many factors that alter thyroid feedback which include the disparity between the enzymes in the pituitary (deioidinase 2 supports the conversion of thyroid hormone in the pituitary and can appear normal)  and other tissues, thyroid receptor and mitochondrial damage. Recent meta analysis and other studies support the role of treating SCH to prevent cardiovascular disease, high cholesterol, hypertension (Ochs et al., 2008)(van Tienhoven-Wind & Dullaart, 2015)(Udovcic, Pena, Patham, Tabatabai, & Kansara, 2017) (Sun et al., 2017) and there’s a strong possibility that hypothyroidism in the central nervous system in areas like the prefrontal cortex are associated with dementia and Alzheimer’s (Pasqualetti, Pagano, Rengo, Ferrara, & Monzani, 2015)(Davis et al., 2008).

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Temperature, pulse and symptoms can be a useful indicator of function when bloods appear to support the notion of sub clinical hypothyroidism

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 It’s worth suggesting that endocrinologists should be well aware of all of the factors that can create the perception of normal blood tests, especially when individual’s present with clinical findings of hypothyroidism as suggested above. My previous posts on assessing thyroid function through body temperature and Ray Peat’s well written post should also be considered an integral part of assessment of thyroid evaluation. The concept of SCH is really only related to the blood test, because the other findings should give the game away.  Treating SCH shouldn’t be problematic when a thorough understanding of nutrition and environmental stimulus are known, and the only people at risk from taking a gradually increased dose of thryroxine would be individuals at risk of an immediate heart attack who generally would  present with a certain set of symptoms.

If Broda Barnes, an MD in the last century found that his patients didn’t succumb to heart disease when taking thyroid hormone. Shouldn’t we be looking for the more global implications of health improvements? Rather than treat high cholesterol, blood pressure, blood sugar, menstrual irregularities, metabolic syndrome (and many others) which all have a substantial relationship with thyroid function, with many studies that show substantial improvements when treated with thyroxine. Call me a cynic but perhaps a more detailed understanding of nutrition, environmental pollutants and their effects on thyroid physiology is probably more challenging to integrate into practice than completing genetic analysis with the proposed mutation driving a specific dysfunction.

 

References: 

BARNES, B. O. (1973). On the Genesis of Atherosclerosis. Journal of the American Geriatrics Society. http://doi.org/10.1111/j.1532-5415.1973.tb01239.x

Biondi, B. (2013). The normal TSH reference range: What has changed in the last decade? Journal of Clinical Endocrinology and Metabolism. http://doi.org/10.1210/jc.2013-2760

Davis, J. D., Podolanczuk, A., Donahue, J. E., Stopa, E., Hennessey, J. V, Luo, L. G., … Stern, R. A. (2008). Thyroid hormone levels in the prefrontal cortex of post-mortem brains of Alzheimer’s disease patients. Curr Aging Sci.

Kong, W. M., Sheikh, M. H., Lumb, P. J., Freedman, D. B., Crook, M., Doré, C. J., & Finer, N. (2002). A 6-month randomized trial of thyroxine treatment in women with mild subclinical hypothyroidism. American Journal of Medicine. http://doi.org/10.1016/S0002-9343(02)01022-7

Laurberg, P., Andersen, S., Carlé, A., Karmisholt, J., Knudsen, N., & Pedersen, I. B. (2011). The TSH upper reference limit: where are we at? Nature Reviews Endocrinology, 7(4), 232–239. http://doi.org/10.1038/nrendo.2011.13

Lavin, N, Ali, Omar., Beall, M.U., Bhutto, A. et al. (2016). Manual of Endocrinology and Metabolism (4th Editio). Lippincott Williams and Wilkins.

Ochs, N., Auer, R., Bauer, D. C., Nanchen, D., Gussekloo, J., Cornuz, J., & Rodondi, N. (2008). Meta-analysis: subclinical thyroid dysfunction and the risk for coronary heart disease and mortality. Annals of Internal Medicine, 148(11), 832–845.

Pasqualetti, G., Pagano, G., Rengo, G., Ferrara, N., & Monzani, F. (2015). Subclinical Hypothyroidism and Cognitive Impairment: Systematic Review and Meta-Analysis. The Journal of Clinical Endocrinology & Metabolism, 100(11), 4240–4248. http://doi.org/10.1210/jc.2015-2046

Pollock, M. A., Sturrock, A., Marshall, K., Davidson, K. M., Kelly, C. J., McMahon, A. D., & McLaren, E. H. (2001). Thyroxine treatment in patients with symptoms of hypothyroidism but thyroid function tests within the reference range: randomised double blind placebo controlled crossover trial. BMJ (Clinical Research Ed.). http://doi.org/10.1371/journal.pone.0098254

Sun, J., Yao, L., Fang, Y., Yang, R., Chen, Y., Yang, K., & Limin, T. (2017). The relationship between subclinical thyroid dysfunction and the risk of cardiovascular outcomes: a systematic review and meta-analysis of prospective cohort studies. International Journal of Endocrinology, 2017(2017). http://doi.org/10.1007/s00774-017-0828-5

Surks, M. I., Goswami, G., & Daniels, G. H. (2005). The thyrotropin reference range should remain unchanged. Journal of Clinical Endocrinology and Metabolism, 90(9), 5489–5496. http://doi.org/10.1210/jc.2005-0170

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

van Tienhoven-Wind, L. J. N., & Dullaart, R. P. F. (2015). Low-normal thyroid function and the pathogenesis of common cardio-metabolic disorders. European Journal of Clinical Investigation. http://doi.org/10.1111/eci.12423

Wartofsky, L., & Dickey, R. A. (2005). The evidence for a narrower thyrotropin reference range is compelling. Journal of Clinical Endocrinology and Metabolism. http://doi.org/10.1210/jc.2005-0455

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).

References:

  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