Estrogen and aromatase – Keeping the wolves from the door.

Estrogen and aromatase,  (and the  role of prolactin and a lack of progesterone) in cancer are well documented and so are the stimulatory effects of the neuro-endocrine (nervous system/hormones) disruptors termed xenoestrogens, which mimic the action and excess of estrogen (Kim, Kurita, & Bulun, 2013) (Mungenast & Thalhammer, 2014). Estrogen and notably estradiol/E2 is often measured by a standard blood test, which remains as problematic as other blood tests such as TSH, which I have previously described.

“ At first, it was assumed that the amount of the hormone in the blood corresponded to the effectiveness of that hormone. Whatever was in the blood was being delivered to the “target tissues.” But as the idea of measuring “protein bound iodine” (PBI) to determine thyroid function came into disrepute (because it never had a scientific basis at all), new ideas of measuring “active hormones” came into the marketplace, and currently the doctrine is that the “bound” hormones are inactive, and the active hormones are “free.” Ray Peat

In addition to the obvious production of estrogen in the reproductive tissues, it’s possible to increase estrogen conversion via aromatase, an enzyme which converts androgens such as testosterone to estrogen, is one of the other main factors. Adipose tissue is a prime location for increased aromatase activity.

Another problem with measuring hormones in the blood is that it rarely accounts for the intracellular accumulation of hormones. Estrogen in excess in the cell, promotes fluid retention, swelling and causes an increase in calcium. Measuring pituitary hormones and in particular prolactin (PRL) may give us a better indication of the relative excess of estrogen due to estrogens stimulatory effect on the anterior pituitary and PRL.

PRL excess is associated with issues such as breast cancer, prostate cancer, resistance to chemotherapy, infertility in both men and women, male reproductive health and galactorrhea (Sethi, Chanukya, & Nagesh, 2012) (Rousseau, Cossette, Grenier, & Martinoli, 2002). Treating PRL excess, particularly linked to the most common form of pituitary tumour (1:1000), the prolactinoma is often treated effectively by the dopamine agonists Bromocriptine or Cabergoline. However, it’s not beyond the realms of possibility that prevention and treatment of excess PRL production, be achieved with decreasing synthesis and exposure to estrogens both endogenous and from external sources.

Myopic thinking.

Modern medical thinking and analysis has led us to a reduced proposition when it comes to diseases like cancer. Cancer is essentially a metabolic disease, and the proposed respiratory defect, the idea of scientist Otto Warburg, is often replaced by the mechanistic thinking of the receptor theory of disease. Estrogen receptors are one of the main evaluations for assessing types of cancer but the very essence of the testing leads us to an increased myopic line of questioning, failing to ask the necessary questions that underlie a persons health status.

If a city is being evacuated, its railroad transportation system, will be quickly “saturated,” and the impatience of a million people waiting for a ride wont make much difference. But if they decide to leave on foot, by bicycle, boat or balloon, in all directions, they can leave as soon as they want to, any number of people can leave at approximately the same time. A non-specific system is ‘saturable,” a nonspecific system isn’t saturable. The idea of a cellular “receptor” is essentially that of a “specific” transport and/or response system. Specific transporters or receptors have been proposed for almost everything in biology – for very interesting ideological reasons– and the result has been that the nonspecific processes are ignored and supressed. Ray Peat

Solutions.

Sometimes there are minimal opportunities for people to change their environment. Perhaps creating more solutions to enable better conversations with the environment, is the most pragmatic solution available?

Maintaining the body’s production of energy by optimising thyroid production, suppression of TSH (thyroid stimulating hormone) and lowering of other stress hormones like ACTH, intake of carbohydrates, protein and adequate light can support the necessary energy needed for the liver and digestive system to enhance detoxification of estrogen and estrogen mimickers.  A sluggish, fatty or hypothyroid state of the liver, makes it difficult for estrogen to be excreted. In states of constipation, beta glucaronidase converts inactive estrogen to the active form.  Keeping both estrogen and aromatase low seems a step in the right direction.

Foods also have the capacity to enhance estrogen synthesis. Mushrooms have shown to be a potent inhibitor of aromatase enzymes and have the capacity to lower the systemic production of estrogen (Grube, Eng, Kao, Kwon, & Chen, 2001). However it’s important to note that mushrooms need substantial cooking to reduce the liver toxins present.

 
“The hydrazine-containing toxins that Toth and others wrote about are destroyed by heat. Since extracts made by boiling the mushrooms for three hours were very active, I think it’s good to boil them from one to three hours.

If you want to know more about prepping mushrooms and soups, then check out the link below for The Nutrition Coach, who reminded me why mushrooms for lowering estrogen and a great source of protein will be helpful when consumed regularly.

  

References: 

Grube, B. J., Eng, E. T., Kao, Y.-C., Kwon, A., & Chen, S. (2001). White Button Mushroom Phytochemicals Inhibit Aromatase Activity and Breast Cancer Cell Proliferation. J. Nutr., 131(12), 3288–3293. Retrieved from http://jn.nutrition.org/content/131/12/3288

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

Mungenast, F., & Thalhammer, T. (2014). Estrogen biosynthesis and action in ovarian cancer. Frontiers in Endocrinology, 5(NOV). http://doi.org/10.3389/fendo.2014.00192

Rousseau, J., Cossette, L., Grenier, S., & Martinoli, M. G. (2002). Modulation of prolactin expression by xenoestrogens. Gen Comp Endocrinol, 126(2), 175–182. http://doi.org/10.1006/gcen.2002.7789\rS0016648002977890 [pii]

Sethi, B. K., Chanukya, G. V, & Nagesh, V. S. (2012). Prolactin and cancer: Has the orphan finally found a home? Indian Journal of Endocrinology and Metabolism. http://doi.org/10.4103/2230-8210.104038

http://raypeat.com/articles/articles/pdf/Estrogen-Receptors-what-do-they-explain.pdf

http://www.thenutritioncoach.com.au/anti-ageing/how-i-prep-mushrooms-and-why-its-worth-the-bother/#more-2595

 

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 tri phosphate (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. Failure

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.

References:

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.

http://raypeat.com/articles/articles/glucose-sucrose-diabetes.shtml

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?

 

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

 

An energetic approach to restoring gut function: Part 1.

Let’s kick this blog off with a question as to whether or not an energetic approach to restoring  gut function is useful when compared to over analysis? Let me clarify, that I have had my fair share of success stories with a reduced and diagnostic approach to improving gut health. Just like I have also had my fair share of kickbacks from the laboratory for recommending their tests. At one point I was using nearly 200 stool tests per year and making a little cash on the side. Many of the tests worked in isolating some specific disturbance to their gut bacteria, presence of a parasite or elevation of putrefied fatty acids. A ‘cleansing’ diet was promoted and a few supplements for good measure created some short term change whilst the client was in my care.

But here’s why the long-term approach to that type of assessment and treatment may not be the best response. A standard functional medicine approach  after spending quite a lot of cash on an integrated stool test is using the 4 R approach.

Remove (offending parties)- spend money on supplements

Restore function- spend money on supplements

Re-inoculate – spend money on nice expensive probiotics

Repair gut lining- spend money on supplements

Regurgitate. Ok the 5th one is mine but no supplements needed.

By taking this approach, an important question is not asked of the individual. Why is this person experiencing an overgrowth of bacteria/SIBO, parasitic infection, endotoxin overgrowth, inflammation and degradation of the bowel lining? I like to think that it is not because of the easy kickbacks FM practitioners are getting for the lab tests and supplements they recommend? So what is the persons level of biological energy and immune system function that allows their digestive system to get in such a state. We know there are some usual suspects. Food, stress or alcohol perhaps?

The typical gastrointestinal complaints people came to me with, were bloating, excess gas, constipation or irritated loose stools combined with poor energy. It was Ilya Mechnikov who originally stated that death starts in the bowel or colon and there’s’ certainly many degenerative and inflammatory conditions that appear at the last stop to poopy central. But is the bowel the main driver of this dysfunction? Many of the symptoms that I recalled earlier are also key symptoms of an energetic and perhaps a thyroid dysfunction. So instead of reaching for our drastic 4 R protocol with an expensive poo test lets consider the following.

 The likes of Broda Barnes and Ray Peat have highlighted how a lack of energy, either from a low or inappropriate food intake or a dysfunctional hypothalamic-pituitary-adrenal-thyroid axis can be evaluated by assessing body temperature and the combination of pulse. Additional information on Thyroid and TSH evaluation can be found here.

Most people are aware that when they get stressed or exercise, blood is shunted away from the digestive system to the periphery and other working tissues. Even the concept of high Adreno-corticotrophic hormone (ACTH), cortico releasing hormone (CRH) and adrenal production of cortisol is becoming common place in work and gym environments alike. These hormones suppress thyroid hormone and the energy compound ATP that provide energy for tissues.

It’s also well known that low energy states create tight painful muscles that are difficult to relax and one might be able to apply that line of thought to the smooth muscle tissues that regulate bowel contractility. Therefore a low energy state that does not allow for adequate energy production will not allow adequate digestion and bowel function to occur. Cold hands and feet can be a symptom of not eating enough carbohydrate and protein.

If the cold hands and feet, low body temperature, fatigue, constipation don’t resolve from eating energy rich meals that contain plenty of fruit and contains little of the foods that promote the bowel irritants histamine and serotonin (nuts, seeds, vegetable oils, grains, gluten free products, beans and pulses). Then, often factors that influence the hormones such as thyroid, estrogen and progesterone may need a deeper consideration.

I drafted a little flow chart that will be helpful for some quick strategies on what might be happening but what I would like to focus on the low energy state that might have its source from a food or hormone factor or perhaps both. Instead of using a strategy like the 4 R approach, these simple questions can help guide you to understanding whether it is the foods that you eat or an energetic factor that could be causing your digestive system to suffer. It’s not a complete algorithm but it does offer some simple solutions that have helped plenty of people resolve digestion and energy issues.

Foot note: I haven’t needed a stool test with a client for over 4 years now following this chart.

 

In part 2 I will elaborate on foods and basic supplements that can be used to resolve most long standing digestive issues and understanding other hormone actions that create digestive discord.

References:

Lokaj, J., & John, C. (2008). [Ilya Ilich Metchnikov and Paul Ehrlich: 1908 Nobel Prize winners for their research on immunity]. Epidemiologie, Mikrobiologie, Imunologie : Casopis Spolecnosti pro Epidemiologii a Mikrobiologii Ceské Lékarské Spolecnosti J.E. Purkyne, 57(4), 119–24. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/19069024

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

Peat, R. (2006). Autonomic Systems. Retrieved from raypeat.com/articles/other/autonomic-systems.shtml

Health, Thyroid and TSH.

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.     Thyroid pic

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.

References:

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

 

How to improve sleep-wake cycles.

Do you need to improve sleep? Why is it that sometimes, with the best intentions of going to bed early, we either find ourselves struggling to enter a sleep cycle, or wake up, deep in the hours of darkness? The prominent stress researcher Robert Sapolsky (Why Zebras don’t Get Ulcers) writes fondly of his near death experiences, of little sleep from the arrival of his newborn child.

It’s no surprise that security and intelligence operatives use a lack of sleep to disorientate prisoners. Just one nights lack of sleep from me and I will tell you anything! Despite the will to nod off, why is it that many people suffered from poor sleep, or struggle to enter sleep cycles?

Before I delve into some brief hormonal issues that can be manipulated to ensure a deeper sleep it’s worth noting that darkness itself is a stressful experience and we produce many restorative hormones during sleep to combat the metabolic stress of darkness. Therefore one essential component of adequate sleep is exposure to sunlight on a daily basis. This ensures uptake of vitamin D and exposure to the deeper penetrative orange and red lights, which help to restore metabolism and healing of cells. An old blog on light therapy.

Over the years I have found the following issues associated with poor sleep.

  • Low blood sugar levels
  • Increase in compounds of wakefulness
  • Exercise late at night
  • Excessive work stress/blue light exposure
  • Exposure to EMF-electromagnetic stress and Wi-Fi
  • Poor sleep and its vicious cycle
  • Emotional Stress

There are several models to be aware of when it comes to sleep theory and the phases of sleep are categorised as

NREM – Non rapid eye movement- pre REM sleep.

REM – Rapid eye movement- this is the deep restorative part of sleep
Active wake

Neurotransmitters and hormones associated with sleep:

Acetylcholine – AcH is the neurotransmitter associated with Rapid Eye Movement or REM sleep.

Serotonin – 5HT this neurotransmitter along with HA is associated with wakefulness.

Norepinephrine/Noreadrenaline – Ne – Hormone of wakefulness.

Gammaminobutyric Acid – GABA. GABA’s role in sleep is well documented but levels vary depending on location of the brain. It’s role is known in decreasing wakefulness and also decreasing deeper REM sleep and involved in producing wakefulness.
Histamine- HA involved in wakefulness.

Hypocretin Orexin- PCT /O Involved in wakefulness.

Adenosine- AD involved in entering NREM sleep.

Here is a rough depiction of key Neurotransmitters of REM and NREM sleep. Other neurotransmitters of wakefulness such as Histamine, Serotonin and noreadenaline (hormone) are not depicted but are elevated in waking state and should be lower during sleep cycles. It’s worth noting that the use of serotonin in mood related disorders such as depression is a key agent in insomnia like states.

sleep neurotransmitters

 

Common sleep disorders

Insomnia:  The inability to sleep restfully and I would categorise a good nights sleep from 6-9 hours depending on your own needs. The ability to enter deep sleep is dependant on many factors such as hormones, neurotransmitters, stress and available energy. It’s worth noting that the regenerative aspects of REM sleep and brain function have been shown to use as much glucose as when awake. Maintaining adequate available energy is key to getting sound-nights sleep.

Sleep apnoea: inability to enter REM sleep due to issues associated with optimal breathing. Obesity and sleep apnoea do seem to correlate and there is a suggestion of structural abnormalities in a small section of people.

The role of sleep in disease prevention

Sleep’s role in psychiatric disorders, depression, metabolic disease and addiction are well documented. A key feature of a lack of sleep, besides on-going fatigue and failure to regenerate is the elevation of adrenalin and cortisol. Elevated levels of cortisol are well known to decrease thyroid function, which can have a significant effect on levels of circulating thyroid hormone and energy production (key to regulation of sleep). The mechanism can tie in with its pervasive actions on management of blood sugar levels. Another noted effect from sleep loss is that we tend to overeat more when tired, which could impact weight gain (and if thyroid is part of the vicious cycle, weight loss becomes increasingly difficult).

Lack of quality sleep can therefore be responsible for an increasing amount of deleterious conditions, such as hypothyroidism, diabetes and obesity, other hormone dys-regulation and cardiovascular disease. Ascertaining whether the issue initially stems from a hormone imbalance can be key in resolving sleep wake issues.

Drugs

There are a variety of drugs on the market that help to improve onset of sleep, however if you seek to improve the biological mechanisms of sleep and perhaps look to the list suggested below, you may find that your sleep improves, without the need for medication.

Cognitive behavioural therapy

The role of CBT in reducing Insomnia has shown effective results even more so than prescriptive medications. Whilst the treatment is not determined whether it effectively targets the mechanics of insomnia its success suggests provides a more desirable approach than long term insomnia medication.

What can you do?

  • Understand the link between production of inflammatory neurotransmitters such as Histamine and Serotonin and seek to lower them. This may be through diet adjustment or exposure to problematic chemicals/hormones.
  • If you get to sleep but wake up, this may be due to poor available energy. Maybe from a low carb diet, low thyroid function and poor production of energy. You may find having something light like a glass of milk with honey, or fruit juice with gelatin may help out. Salt also helps to decrease adrenalin production
  • Wi-Fi, blue light exposure, electromagnetic stress all play their part in interfering with stress and how the cells function. Stopping their use several hours before sleep can help. Do turn off Wi-Fi in house and no phones or electric devices by your bed.
  • Avoid stimulus such as caffeine or exercise in the evening, if you have sleep issues. Caffeine decreases production of adenosine.
  • If under emotional stress, a slow walk before bed may be a useful idea combined with ensuring adequate blood sugar levels are met.

References:

Neurobiology of Sleep. Course notes. Duke University. 2015.

Peat, R. From PMS to Menopause. Female Hormones in Context. 1997

Sapolsky R. Why Zebras don’t get Ulcers. St Martins Griffin. 1998

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2941414/

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3443758/

http://www.ncbi.nlm.nih.gov/pubmed/27091535

 

Muscles, pain, hormones and other stuff.

As a therapist who works within the fields of pain, movement, energy and digestion I have seen my share of pain and muscle dysfunction in clients. As my exposure to these situations increase, I realise more than ever, that the muscles are very rarely the problem.

Specific muscle dysfunction usually boils down to spindle cell

Thyroid pic

Muscle pain and thyroid hormone

dysfunction and notably Nuclear Bag Fibres (NBF) and Nuclear chain Fibres (NCF). The primary roles of these structures are related to stretch and contraction of muscle function. There can be other factors involving neuro transmitters, involved in nocicpetion such as glutamate, utilised in the withdrawal reflex and often referred to as first pain, (also known as Neospinalthalamic tract located in the Anterolateral system or ALS) and lasting, less than a tenth of a second. Problems can arise when the following pain pathway, called second pain (or Paleospinalthalmic tract also part of the ALS) has problematic feedback with first pain, this is mediated by Bradykinin.

Further complexities arise with serotonin and other structures associated with pain such as the Amygdala and Peri Aqueductal Gray (PAG) that are beyond the scope of this short blog. However a common, over looked feature of pain, may arise with hypothyroidism .

Low thyroid function can be classified effectively with assessment of a basal temperature test and a reading of between 36.6 and 37 degrees. Most blood tests designed to measure thyroid hormones such as TSH, T3, T4 and others, often do not reflect accurate function of thyroid hormone. This is often due to feedback loops between cellular function and the Pituitary gland. Some of the regular hallmarks of hypothyroidism are poor energy, weight gain, poor sleep, hair thinning, digestive dysfunction (constipation and also alternating loose stools), cold hands and feet and pain. Here’s an old blog on thyroid and adrenalin issues.

Another assessment of thyroid function is the Achilles return reflex. When stimulating the myotactic reflex a hammer hits the Achilles tendon stimulating, the dorsi flexors or calf muscles. The response should be a quick return of the foot to it’s resting position but with low thyroid the foot returns slowly. Low thyroid output equals low ATP (Adenosine Tri Phosphate – the energy used by the mitochondria/cells). This low energy state does not allow for optimal contraction and relaxation. This is where we can see specific issues with NCF and NBF’s within the muscle spindle cell.

Muscle tendons and associated ligaments provide a feedback loop via the Golgi Tendon Organs or GTO’s. There’s potential for pre-existing GTO dysfunction to drive muscle dysfunction and vice versa. As far back as the 1960s symptoms associated with muscle disorder from low thyroid were.

* Weakness

* Cramps pain and stiffness

* Hypertrophy

* Myotonoid features.

A well-documented feature of hypothyroidism is muscular hypertrophied calf muscles and despite their size may often test weak to stimulation.

Muscle pain, may indeed not be muscle related, it may be due to many factors, suggested above and these may even be related to hormones and neurotransmitters. Many people often deal with muscle aches and pains by constantly focusing on mobility work but these structures continually return to their pre mobility work status (although this could also be an underlying stability issue). In reality there can be many factors that create dysfunction such as crude touch, vibration, nociception, Golgi, Pacini-pressure related structures and many more. But even after seeing a skilled therapist, these still don’t appear to get better, then addressing the chemical aspects of pain and function might be the next sensible thing to do.

References:

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

Ramsay I. Thyroid disease and Muscle Dysfunction. William Heinemann Medical Books. 1974.

Purves, D. et al. Medical Neuroscience. 5th Edition. Sinauer Assocates Inc. 2001

Starr, M Hypothyroidism Type II. Mark Starr Trust 2013.

http://raypeat.com/articles/articles/hypothyroidism.shtml

Why you really shouldn’t be giving up sugar in the New Year.

It’s that time of year again, the silly season is upon us and plenty of people using inaccurate words such as detox are thrown around like Christmas wrapping paper.

For many, the New Year is associated with dietary restrictions, born out of a period of over consumption from the festivities. May of those decisions such as stopping sugar or in particular fruit, as part of the so-called ‘detox ‘ is probably one the poorer choices that people do during this period of fad dieting. So it’s time to put the record straight on how to detox, or more appropriately how to maintain detoxification processes efficiently.

Detoxification and its suggested three phases, like most of the processes in the body is energy/nutrient/hormone dependant. Therefore the ability to detoxify efficiently is regulated by the amount of energy available and influenced greatly by how well your hormones function. The thyroid gland for example, is key to maintaining energy and this means energy for the liver to function. Detoxification is just one of the many functions of the liver, which also include glucose production and storage and the maintenance of adequate cholesterol.

The CDR or cell danger response suggests an evolutionary response to insults that affect the human body (and in particular cellular function) from a variety of sources. These can include:

  • Viral
  • Bacteriological
  • Chemical
  • Parasites
  • Electromagnetic stress
  • Physical and psychological trauma.

The net effects of the CDR can be suggested as a protective mechanism that stiffens cell membranes, perhaps to protect other cells, a decrease in processing of many nutrients and other compounds such as metals, and a decrease in metabolism. Whether this down regulation of function is protective or a result of the damage inflicted remains to be answered. Increased oxidative stress to how the body’s cells function can decrease the ability to generate energy using oxygen. Cellular respiration (ability to use oxygen to provide energy) using oxygen and carbohydrate remains the most efficient system for generating energy. Increased stress decreases the ability to utilise carbohydrate as a fuel. Other compounding factors with the CDR are a change to the gut bacteria, which can increase the fermentation of carbohydrates. So called beneficial bacteria such as Lactobacilli can produce lactic acid that disrupts the cells of the digestive system and increase the amount of gut damaging endotoxin.

For many the over indulgence will increase factors such as endotoxin, making them feel low, irritable and poor energy and sleep. An increase to neuro- transmitters such as serotonin and histamine, will exacerbate these issues and decrease sleep quality. The New Years resolution brings about a restriction of calories and eating less, burdening the digestive system less. People often make the assumption (one of many) that cutting out sugar has caused this miracle change but it may simply be the decrease in food itself. Perhaps it’s the lack of calories and the increase in adrenaline, much like the runners high, which makes people feel great?

For some, the equation of increased movement with less calories that is often employed at this time of year will have a good effect. For many others, and in particular, those who have a cell damage response, that is being resolved, this equation seems to have little effect. The decrease in available energy, to a cell that struggles to maintain adequate energy output, will find the move more, eat less, scenario a challenge.

Ketogenic diets often have great short-term effects for weight loss. In the long term a ketogenic remains a stressed energy state requiring the need for more cortisol, a decrease in carbon dioxide (decreasing the amount of available oxygen for use) and a less efficient form of energy production. Those who have a large amount of weight to lose, potentially expose the metabolic system to increased stress by oxidising fatty acids.

The stressed body requires carbohydrate. Low blood sugar states require a balance of carbohydrate (with fat and protein), to maintain optimal detoxification you need carbohydrate. Unfortunately with the fear mongering on social media you can often observe the following.

  1. Sugar feeds and causes cancer.
  2. Sugar is addictive

Here’s the thing. There is not any scientific proof to validate those statements. The primary fuel for any cell is glucose, even in cancer cells, if sugar is not available, it will generate energy from protein. Otto Warburg’s research has often been misinterpreted to suit inaccurate memes. Damage to the respiratory function of the cell is often the source of mutagenic aspects of cellular/mitochondrial (energy producing cells) that potentiates the growth of cancer.

The sugar is addictive study; well if you look closely at the study you will see that sugar activates the same reward centre of the brain such as sex, exercise and receiving gifts. The science of addiction is beyond the scope of my expertise, however if you have someone that cannot regulate energetic processes that well, they may seek out adequate energy, with sources of easily processed carbohydrates. It would appear that insulin sensitivity becomes an issue when there is an excess of energy.

Are you eating too much? Or is it simply that you cannot process the energy available? Well, if you eating less and moving more but weight, energy, sleep, libido or emotional balance aren’t improving. Then you know which one it is.

I am not suggesting here is that you should over eat sugar and carbohydrates. Much like, I wouldn’t NUTRITIONsuggest overeating broccoli, or drinking too much water.

Either way removing the protective capacity of carbohydrates to create balance is probably not the way to go.

Is your diet and exercise program working for you?

Health, fitness and well-being are words that are often used interchangeably but more often than not fail to reflect the differences inherent in each person. Exercise, stress and diet are three components of wellbeing that are often grossly misunderstood not only is yourby the general public but by fitness professionals themselves. Companies wanting to sell products that supposedly enhance our well-being have largely driven our concept of health and of what it takes to achieve maximal health. Let’s take diet for example; the current trend is that we should eat foods such as raw green vegetables, drink plenty of water and try to eat less calories than we expend, usually supplemented with a fancy antioxidant that does what no other supplement currently does on the market. Exercise guidelines encourage us to exercise at least every day and in particular cardiovascular exercise is touted as the exercise that will help you lose weight and prevent heart disease.

Why is this unhealthy?

This approach may work with a number of people initially, especially with those who have been liberal with eating and drinking and exposure to limited exercise. The long term effect is an increasing number people who have a cold nose, hands and feet, low body temperature (below 36 degrees when the norm should be 37), poor energy, sleep, libido, digestive function, as well as mood swings usually dominated by poor adrenal regulation; and, ultimately, thyroid regulation. In fact one of the many flaws with the current recommendations with exercise guidelines is that it is most likely poor thyroid function that will contribute to elevated cholesterol levels (which is a protective response) and potential cardiovascular events, not a lack of exercise.

 Too much of a good thing?

Excessive exercise and malnutrition can also play havoc with the adrenal glands. Fatigue can also be linked to hypocortisolemia. Under and over production of the stress/anti-inflammatory hormone cortisol is well documented. Ever felt that fatigue early in the morning and inability to get out of bed? ‘But I eat a healthy diet and exercise regularly’ you say? The adrenals are responsible for getting our butt moving and are synergistic with other key glands, such as the thyroid, and have an impact on digestion, healing, blood sugar regulation and many other functions. The common approach to too much or too little cortisol production is adaptogenic herbs, such as Ashwaganda, Rhodiola and many others. However balancing stress responses with appropriate nutrition and a well-designed exercise and rest program can alleviate these issues without rattling as your walk down the street with your daily dose of supplements.

Food for thought

Nutrition and eating to support your own body function was inherently about consuming enough calories to keep us alive throughout history. Our body is geared towards consuming calories and exercise based upon energy being available. Today’s culture is about working more and eating less but it just isn’t working for everyone. If the so-called Paleo approach was right, do you think we would have been scurrying around for a head of broccoli and calorie-poor foods, or looking for food that would have given us more bang for the buck like a wild boar and liberal use of fruits and calorie dense foods? The human genome hasn’t changed that much, so the way we function as organisms will not change radically for some time either.

The big question

So what is the right approach? Well there really is no ideal approach; it’s what works for you. Exercise and nutrition are stressors and have the potential to be positive or negative but how does it affect you? Ask yourself these questions and you should have the answer to either continuing or cessation with your current methodologies.

  1. Do I feel fatigued?
  2.  Do I sleep well?
  3. Good bowel movement once or twice per day?
  4. What’s my libido like?
  5. Is my skin clear
  6. Do I keep getting injured?
  7. Have I lost weight with my plan if that’s what is needed?

You probably already know the answers to these questions; any program that supports energetic processes doesn’t create injury and improves repair processes, such as sleep, is always what we want and you are bound to be doing that right? Unfortunately we mistake the buzz and excitement, release of stress hormones and pumped up music of the group exercise classes, destructive boot camps, cross fit and other over exercise methodologies as healthy. When clients come to me in a state of injury and fatigue they often say to me ‘but I don’t feel like I am doing anything unless I am wringing with sweat and red in the face.’  The fact that their movement is compromised, posture and energy are poor, and re-training the thought process on what is health and balance is the first part of the rehabilitation program. The problem is that we still don’t know what optimal health is; we just work along patterns that appear to be healthy.

Burn baby burn

One of the common misconceptions of health is that you need low levels of body fat and a six-pack to be healthy. This couldn’t be further from the truth. Many people who engage in excessive exercise regimes often take vast amounts of antioxidants in an attempt to combat the wear and tear of these programs.  An observation to be made in the future is will these people live longer than people who engage in a more balanced lifestyle? Many people who lived into their hundreds did not engage in excessive exercise routines and some of these never even drank water on its own, simply drinking tea and juices. The advice that comes from many professionals becomes flawed as we try to apply modern blanket nutrition approaches to the masses. Don’t get me wrong, certain foods can bring about changes to certain conditions and we certainly need water on some level, but for many the modern healthy diet isn’t doing everyone the good it should.

 The environmental factor

One other thing not discussed by many leading health and fitness bodies is the concept of environmental issues on the body. Your environment has the capacity to make or break any fitness or nutrition program. Toxins are ubiquitous and there is not one environment in the world that hasn’t been touched by PCBs, dioxins and PETs amongst hundreds of thousands of other chemicals. Food, water and the air we breathe may have a more significant impact on our ability to stay healthy. Your nutrition and exercise plan may become a sideshow to the inflammatory genes that are expressed when exposed to these estrogenic issues to both male and females.  Obesity and diabetes are now being linked to these issues.

Is more exercise and fewer calories a good idea to those that have less capacity to deal with these toxins than others? Probably not.

A balancing act

That’s not to say that you can’t assist your body towards balance, they key point here is to be aware that your environment may be responsible for many areas that you haven’t achieved with exercise and food. Manage your environment by decreasing infamous chemicals, found in perfumes, GM foods and even wireless technology can lead to great success with less exercise and less calorie restriction.

Ultimately life is about balance and finding your balance may not be the same as another person. Breathing correctly, flexibility, stability and strength may be what your body needs the most. Spending countless hours doing repetitive cardiovascular exercises, restricting calories or pushing your body to get down to low levels of body fat is not how your body perceives balance. Finding your own ideal diet may take time but in the end, time is on your side.