PMS

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

 

 

 

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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.

If you need any assistance with resolving energy, sleep, digestion, mood, libido, pain or other hormone issues then please check out the members area for more information or even the free resources section.

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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?

 

References:

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

 

Can a bad smell create pain, dysfunction and weakness?

We know about the feedback of pain and painful stimulus (nociception) and the creation of pain to warn us but what about the effects of noxious and more subtle smells on the nervous system? Over the last few years I have found that nothing ceases to amaze me when it comes to the human body. As it becomes possible to dissect systems and assess interactions of specific stimulus, observing the input/output relationship between stimulus and body. Pain stimulus is observed to be chemical, thermal or mechanical in nature. Please bear with the technicalities before I explain the simplified mechanisms or skip to the last part of the blog, if you get bored!

There are many factors that contribute to a patient’s perception and physical feeling of pain. Pain is the central nervous systems response to an event that has the capacity to injure the tissues of the body. Nociception or pain can be qualified from the following pathways.

The ‘First’ pain is usually a withdrawal mechanism (Nociceptive Withdrawal Reflex or NRA) mediated by the neurotransmitter glutamate and utilises the neospinalthalmic (new pain) tract in the anterolateral system or ALS. This typically lasts less than 0.1 of a second and the signal, suggested to be dampened in the substantia gelatinosa, an area found in the dorsal aspect of the spinal cord. Think about that sharp initial pain experienced causing you to move away from a stimulus, which has been detected by free nerve endings.                               Smelly pain

The ‘Second’ pain is also part of the ALS but is part of the paleospinalthalmic tract (old pain). It typically takes over from the initial first pain/neo. It is mediated by the compound substance P and can be associated with that long, lingering pain experienced from an injury.

In addition to pain, we have the capacity to assess many other features of mechanical distortion such as pressure, stretch and touch. The Dorsal Column Medial Lemniscus or DCML, allows the nervous system to provide adequate feedback to tasks and environmental stimulus.

Another part of the pain detection system is the trigeminal chemosensory system, which has nociceptive/pain and temperature pathways that feedback to cranial nerve five, called the Trigeminal nerve (CNV). When a noxious or toxic substance is processed by the neurons in the mucosal areas of the nose, mouth, eyes and lips it is relayed into the thalamus. The VPMN (or ventral posterior medial nucleus) relays signals to the sensory cortex and provides responses, such as watery eyes, sneezing and withdrawal

When we inspire air with small particles of pollutants, they pass from the lungs into the blood stream. Although the blood brain barrier is supposed to prevent any unwanted chemicals, crossing from the blood to the brain; the Circumventricular organs present an area that does not have the capacity to restrict compounds that can create dis-organisation of neurological signals entering and leaving the brain. The area postrema, also has a chemosensory role to initiate vomiting to deal with exposure to harmful compounds

So let’s have something a little easier on the eyes and brain to read now. For example:

Perhaps you are walking across the road in heavy traffic. Sucking up all the pollutants such as benzene, carbon monoxide and other waste products of burning fossil fuels into your lungs as you find your way from one side of the road to another.

For a few seconds your brain, exposed to the onslaught of pollution, has a hard time processing the compounds that have made their way into areas such as the pineal gland or chemoreceptors that can induce vomiting in response to a noxious stimulus.

You are in a rush and bump into someone, his or her shoulder hitting you firmly in the chest. It was slightly painful but you don’t really notice it, the pain pathway, along with pressure, stretch and touch receptors provided some form of feedback. The brain, perhaps still not capable of processing this feedback due to the short exposure of increased pollutants, is just trying to get on with the milieu of everything else that your body demands of it.

Meanwhile the pectoralis muscle, which is being used with each step that you take, has been exposed to increased pressure, a state of contraction or small window of pain that necessitated a withdrawal reflex. The intrafusal muscle fiber that monitor both stretch and contraction now have increased signal towards sustained contraction due to the chaos of external compounds that entered areas of the brain.

So now we might have some level of muscle dysfunction. We probably don’t even know about it. That level of muscle dysfunction now increases and decreases tension demands to receptors found in the ligaments and tendons. The joint mechanoreceptors have a different signal. The skin exteroreceptors perhaps have a different signal. There’s no pain to remind us of the event. In fact we have now gone to the gym and started doing a bunch of push-ups or gone shopping for food and simply carrying the bag home with that hand and shoulder. This doesn’t create pain, but simply sets the foundation for increased areas of dysfunction from distorted neurological signalling.

The concept of this neurological/chemical chaos is often referred to as ‘brain fog’. It seems to be in the literature for many reasons, blood sugar issues, gluten, estrogen (PMS and menopausal females are particularly susceptible) and other factors. It’s also possible that brain fog can be created from specific food stressors, once again eliciting the same response, proposed in the heavy traffic.

Some might say, how can the body be so fragile? Surely we are more robust than that? But it is possible to create these specific dysfunctions but they can be unravelled. Understanding specific stimulus can give us a solution to what dysfunction exits. We might never find out how it came about but a thorough history taking can help to influence where we assess and how to treat it. This is where a technique like P-DTR or Proprioceptive Deep Tendon Reflex, developed by Dr Jose Palomar is unique and effective at uncovering specific neurological dysfunction.

If emotions, visual, auditory, mechanical, chemical and pain factors perpetuate dysfunction, then using those stimulus can pose an effective form of assessment and treatment.

  1. Palomar, J. Proprioceptive Deep Tendon Reflex: Course Notes.
  2. Purves D et al Neuroscience 5th edition. Sinauer Associates 2012
  3. http://www.neurology.org/content/77/12/1198.short

Estrogen and Progesterone

For the general public there is often no real need to understand what hormones are or what they do, unless faced with specific problems related to them. As hormones are affected increasingly by our environment, which includes: Food, air, water, physical and psychological stress, it seems that a basic understanding of problematic hormones can be helpful for maintaining or improving health. Before I attempt to give a brief overview of a complex subject, here are a few terms to be aware of, mainly related to female function.

Follicular phase- first 14 days of cycle to ovulation and increased production of estrogen, primarily E1

LH- Luteal phase, last 14 days, corpus luteum, which increases progesterone

Progesterone- Hormone of gestation, bone formation, anti clotting concerned with cell differentiation.

E1-E2-E3 – Estrogen classifications of Estrone, Estradiol and Estriol. Estrogen promotes growth and becomes problematic in the face of increased cellular division and changes or mutations.

Xenoestrogens – synthetic estrogen like compounds found in plastics, contraceptives, fuel and industrial waste. These have the capacity to increase estrogen levels in men, compounding issues related to testosterone function.

Progestin- synthetic progesterone. Lacking in the benefits of natural progesterone and increases unwanted symptoms.

CYCLEovul

Estrogen’s primary role is one of growth. It is used to stimulate growth of tissue, especially so in the endometrium. During the follicular phase estradiol increases and just before ovulation starts to decrease. Progesterone’s protective effects are enhanced via increased production of the corpus luteum.

Problems with excess estrogen have increased due to changes in diet, increased exposure to environmental pollutants and other factors that are not offset by increased production of progesterone. Below are just some of the actions of both estrogen and progesterone.

Effects of Estrogen Effects of Progesterone
·      Breast stimulation·      Endometrial proliferation

·      Increased body fat

·      Salt/ fluid retention

·      Clotting

·      Depression

·      Headaches

·      Decreased libido

·      Impairment of blood sugar

·      Reduced oxygen

·      Risk of breast cancer

·      Osteoporosis

·      Decreased thyroid

·      Increases CV issues.

·      Anti tumour effects·      Supportive to fertility

·      Sedative effects

·      Improves blood sugar

·     Decreases  Ovarian cysts

·      and Menopausal flushing

·      Removal of facial hair

·      Decreased Menstrual cramping

·      Improved auto-immune

·      Hormonal balance

·      Anti -Stress

·     Decreased arthritis

·      Promotes sleep

·      Thickens hair on head

 

 

 

Balancing blood sugar levels, particularly an issue during pre-menses, can be achieved with Progesterone. Hypoglycaemia is often present (especially so when engaged in exercise, low carbohydrate or calorie consumption) and particularly when oxidative damage occurs to cellular function, oxygen use is decreased and therefore a reliance on glycolysis, a sugar using energy system, which creates an abundance of lactic acid, occurs. Elevated levels of lactic acid are problematic, not only to cellular function but are also inefficient means of energy production. It’s transportation and conversion back to glycogen requires much more energy than it produces. Progesterone protects against estrogen’s anti-oxygen effects.

Progesterone is non-toxic even at elevated levels, however anaesthesia and euphoria has been recorded, along with changes to the menstrual cycle which can be noted as mainly positive. Symptoms related to PMS have often disappeared and its use is recommended only between ovulation and menstruation. Estrogen/progesterone balance can be achieved by supplementation, however diet can help to facilitate the change and serve to maintain the gains achieved with progesterone supplementation. In many cases decreased thyroid allows for excess estrogen in the body, via mechanisms of decreased energy to detoxify, which include liver and digestion mechanisms. The reverse can also be true due to increased estrogen decreasing thyroid function

Excess stress can be the cause of decreased progesterone and increased estrogen's, increased cortisol and decreased thyroid. The use of adequate protein within the diet and carbohydrates will ensure that thyroid is provided efficiently. Daily sunshine helps to promote optimal progesterone conversion, in addition to supplementation and those who live in areas with less sunlight should also consider progesterone supplementation.

During pregnancy, progesterone production can be one hundred times more than the amount seen during the premenstrual phase. A lack of progesterone during pregnancy has been associated with toxaemia. Symptoms include high blood pressure, excessive weight gain, oedema (fluid retention) and protein loss in the urine. If excess progesterone is available, the mother will simply use it, therefore an excess of progesterone would be preferred to a deficit and the likelihood of toxaemia induced by too little progesterone. Progestins seem to make many unwanted symptoms much worse

It is clear that decreasing exposure to environmental pollutants is helpful to lowering xenoestrogenic load. Foods that contain natural phytoestrogens can also affect estrogen/progesterone balance and where symptoms exist decreasing foods such as uncooked brassica vegetables, soy, nuts and seeds would be helpful in attempting to restore balance.

References:

Dalton, K The Menstrual Cycle.

Lee, J. Natural Progesterone, Multiple roles of a Remarkable Hormone. BLL Publishing

Peat, R. Nutrition for Women.

Tonilo, P.G. Endogenous estrogens and breast cancer risk: the case for prospective cohort studies. Environ Health Perspect. 1997 Apr;105 Suppl 3:587-92.

Online references:

http://raypeat.com/articles/articles/progesterone-summaries.shtml

http://raypeat.com/articles/articles/estrogen-age-stress.shtml