Mood

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

 

 

 

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.

Tromp.png

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.

  

References:

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