hypothyroidism

Sub Clinical Hypothyroidism

Strange, must-try exotic fruits!.jpg

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

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

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

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

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


Thyroid hormone is necessary for all aspects of organised biology.

Thyroid hormone is necessary for all aspects of organised biology.

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

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

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

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

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

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

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

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

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

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

 

References: 

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Better gut health with less bacteria?

Can you have better gut health with less bacteria? There’s an old saying in the integrative health world that ‘ Death begins in the colon.’ These were the words of the 1906 Nobel science award holder Elie Metchnikoff, a Russian scientist who did much to elaborate on the mechanisms of embryology, immunology and other aspects of health and disease. These days there’s much that has been written about the micro biome and the suggestion that diverse microbes within the bowel are an important factor in health. How we need to eat plenty of fibrous and fermented foods for better health. But how true is this and are more bacteria necessary for better digestion and longer life? “The retention of faecal matter for several days very often brings harmful consequences. Organisms which are in a feeble state from some cause are specially susceptible to damage of the kind referred to.” (Metchnikoff & Metchnikoff, 1908)

Ok so you aren’t likely to die anytime soon from being constipated for several days, you might feel like crap (excuse the pun). But what if the repetition of constipation is over years? We have seen that hypothyroidism and constipation is clearly linked and can induce small intestinal bacterial overgrowth (Lauritano et al., 2007). An inability to remove the waste products is a particular burden on a stressed system.

"Not only is there autointoxication from the microbial poisons absorbed in, cases of constipation but microbes themselves may pass through the walls of the intestines."

This description of endotoxin and other bacterial end products damaging and permeating the intestinal wall is a well-known modern concept of leaky gut or intestinal hyper permeability. Metchnikoff’s describes the putrefaction (think fermenting mass of stinky stuff) of foods within the bowel that lead to the damage described in a permeable gut lining that allows bacteria and endotoxin into the blood stream.

There’s a theory that I have, as it’s clear that not all people have constipation. Many present with irritable bowel syndrome (IBS) like states, loose and perhaps a product of irritation induce by high serotonin and histamine (which by keeping to a minimum can also improve sleep and mood). It’s plausible to suggest that some people have already gone through a constipated phase induced by either a low energy or thyroid state, which may give way to a high adrenaline state over time. The lack of movement in the bowel for some can set the scene for future IBS reactions due to the accumulative damage induced by constipation, putrefaction, bacterial end products and increased irritation. Some clients have noticed that they previously went through a constipated phase before they arrived at their suggested IBS.

So if the current theme of recommending probiotics, raw and fermented foods is in vogue. What does that mean for the digestive system. I remember a newsletter from Ray Peat suggesting that animals born in a sterile environment generally live longer and have a higher metabolic rate. This in itself is a hard, near impossible feat to achieve outside of a sterile laboratory but consider this - Most babies are grown within a womb that does not contain any bacteria, as soon as they come through the birth canal and into the world at large. The bacterial management of life comes into play and had it come any sooner, may have had disastrous consequences. Other observations of Metchnikoff related to the longevity of birds, which have a high metabolic rate and limited intestinal flora -

‘Even in birds of pray which feed upon putrid flesh, the number of microbes in the intestine is remarkably limited. I have investigated the case of ravens which I fed flesh which was putrid and swarming with microbes. The droppings contained very few bacteria, and it was remarkable that the intestines had not the slightest smell of putrefaction. Although the opened body of a herbivorous mammal, such as a rabbit, gives off a strong smell of putrefaction, the body of a raven with its digestive tube exposed has no unpleasant smell. The absence of putrefaction in the intestine is probably the reason of the great longevity of such birds as parrots, ravens, and their allies.’

Metchnikoff also states that despite the absence of bacteria, their organisation and metabolism may be the primary driver for long health. Therefore if we were to keep bacterial interference at bay might we be better at living longer lives by improving our gut health? Our metabolism and cellular health is the key to prevention of many disease states. Extra bacteria may just be another factor that our immune system has to contend with and may be at the heart of autoimmune issues. From a comparative biology standpoint many other herbivorous animals don’t live as long as omnivorous animals. Horses, cows, and sheep live very short lives in comparison to other mammals that eat a wide range of foods. The main exception being the elephant, which has an extremely large intestine like other vertebrates.

Probiotics and fermented foods provide a mixed bag of research(Goldenberg et al., 2015). In many studies bacterial infections and digestive issues have not been resolved by probiotics. They do seem to be particularly effective at reducing bacterial/food poisoning cases and decreasing the diarrhoea like state by a day or two. Primarily this acts as a competing organism in the battle of the bowel and maybe why faecal implants have been shown to beneficial in the short term for some.. Even beneficial strains of bacteria such as lactobacillus can be problematic in excess due to the high levels of lactic acid leading to d-lactate acidosis, decreasing our gut health and overall wellbeing.

After all increased bacteria equals increased immune system responses and constant battles, for some there’s only so much that a faltering metabolism and immune system that one can take. Providing easily digested nutrients that limit bacterial growth and metabolites, that doesn’t burden a compromised digestive system seems prudent. In hypothyroidism gastric secretions such as hydrochloric acid are often lowered, further compromising digestion. Easily digested nutrients equals easily available source of energy and macronutrients.

To read more on how to combat these issues, to improve your gut health, digestion, mood and energy, this article is extended in the members’ area or there's also some information in this blog from 2017.

References:

Goldenberg, J. Z., Lytvyn, L., Steurich, J., Parkin, P., Mahant, S., & Johnston, B. C. (2015). Cochrane Database of Systematic Reviews. The Cochrane database of systematic reviews (Vol. 12). http://doi.org/10.1002/14651858.CD004827.pub4

Lauritano, E. C., Bilotta, A. L., Gabrielli, M., Scarpellini, E., Lupascu, A., Laginestra, A., … Gasbarrini, A. (2007). Association between hypothyroidism and small intestinal bacterial overgrowth. The Journal of Clinical Endocrinology and Metabolism, 92(11), 4180–4184. http://doi.org/10.1210/jc.2007-0606

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

A biochemical approach to decreasing muscle pain with food and hormones.

pain and hormones

pain and hormones

A biochemical approach to decreasing muscle pain is often the last place most people look and that includes many pain specialists. Modulating pain and hormones through food and other variables can create some impressive results. Aches and pains are a common theme in every day living. Some people seek to push themselves harder with excessive training schedules, others spend more time in a seated position and other factors contribute to tissue not responding the way that it should. Pain and the concept of nociception is a system of feedback for the body that is protective in essence. You touch something you shouldn’t; first pain kicks in to remove you from the painful stimulus (lasts less than 0.1 seconds), after that and depending on severity of damage second pain kicks in.

First pain and second pain (both reside in the anterolateral system or ALS) utilise different chemical messengers and another factor for this form of feedback is that other nociceptive factors like touch, visual, auditory and other sensations of stress can be part of the problematic feedback if not resolved. All of these have the capacity to interrupt optimal motor control and functioning of joints and soft tissues and affect hormone profiles. Even a bad smell can create neurological chaos.

Another less well known aspect (in therapy based settings) of disruptive function in muscle tissue are the effects of hormones that may lead to decreased feed back and be responsible for pain. Hypothyroidism affects muscle tissue via energy and neurological deficiencies.

Hypothyroidism results in

Slower peripheral and central nerve conduction velocity Lower body temperature is a factor creating slowed velocity Decreased active cell transport in the cerebral cortex Decreased flux of sodium and calcium for contraction/relaxation Poor production of energy for contraction/relaxation Decreases depolarisation of action potential

cold body

cold body

In a nutshell a colder, slower body leads to a decreased   coordinated body that has a hard time contracting and relaxing muscle tissue. This can lead to increased incidence of injury and pain.

A slowed heart rate is a sign of hypothyroidism and the bradychardia (slowed heart rate) should serve the purpose of describing the decreased rate of function throughout all muscle tissue. Thyroid hormone can improve both rate of contraction and relaxation in both fast and slow twitch muscles but also exerts a cardio protective role on blood vessels and bowel function via smooth muscle tissue. The documented symptoms of hypertension and constipation along with the neuromuscular actions tend to resolve with adequate thyroid hormone (Gao, Zhang, Zhang, Yang, & Chen, 2013).

Prior to initiating thyroid therapy it’s essential to rule out functionally hypothyroid states induced by diet, stress, excess exercise and other environmental factors. Many clients often present with lowered temperature, with cold hands, feet and nose, altered bowel, sleep and emotional function, which can often be resolved with appropriate energy and decreased intestinal irritants.

Chronic pain increases cortisol production which decreases thyroid hormone production (Samuels & McDaniel, 1997) as does fasting or calorie restriction which induces a decrease in available T3 (thyroid hormone) (Hulbert, 2000).

This gives us two approaches 1) to reduce pain with appropriate therapy and to ensure that adequate energy modulates the suppression of excess cortisol and increases available thyroid for tissue organisation and recovery.

Hormones also affect tendons; diabetics and poor insulin profiles appear to create disorganised tendon structure but this may be a factor related to decreased available thyroid hormone. Hypothyroidism decreases available T3 within tendons, which can decrease growth, structure, and collagen production and create hypoxia of tissue leading to calcification.

Estrogen, although necessary for growth of tissue can often be found in excess creating problematic growth. Estrogen is also well known to decrease thyroid hormone and can provide an explanation why more females then men tend to be hypothyroid. The decrease in both thyroid hormone and progesterone can increase muccopolysacharides, which increase pressure in tissues, creating puffy, oedema like states. The swelling can be linked to many pain states which include carpal tunnel, which can be resolved with progesterone and thyroid in the absence of physical therapy. Progesterone also appears to induce myelination of nerves (surrounds and allows nerve conduction) and decreases inflammation (Milani et al 2010).

Energy production remains  a most potent form of therapy for decreasing pain, optimising rehabilitation and restoring tissue function.

References:

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

  2. Hulbert, A. (2000). Thyroid hormones and their effects: a new perspective. Biological Reviews of the Cambridge Philosophical Society, 75(4), 519–631. http://doi.org/10.1017/S146479310000556X

  3. Milani, P., Mondelli, M., Ginanneschi, F., Mazzocchio, R., & Rossi, A. (2010). Progesterone - new therapy in mild carpal tunnel syndrome? Study design of a randomized clinical trial for local therapy. Journal of Brachial Plexus and Peripheral Nerve Injury, 5(1). http://doi.org/10.1186/1749-7221-5-11

  4. http://raypeat.com/articles/aging/aging-estrogen-progesterone.shtml

  5. Samuels, M. H., & McDaniel, P. A. (1997). Thyrotropin levels during hydrocortisone infusions that mimic fasting- induced cortisol elevations: A clinical research center study. Journal of Clinical Endocrinology and Metabolism, 82(11), 3700–3704. http://doi.org/10.1210/jcem.82.11.4376

Sunlight, health and cancer

The more you read, the more holes you find in many theories.

The more you read, the more holes you find in many theories.

Increasing sunlight exposure increases an individuals health and decreases cancer risk. In the last year or two I remember reading a quote from a professor of dermatology at a university in the U.S. who stated, “ There is no amount of sun that is good for the skin.” Clearly said professor skipped basic biology in secondary school or has had a lifetime of examining patients with excess PUFA (polyunsaturated fatty acids) in their diet, which is associated with increased incidence of skin cancer (there’s also a hopeful possibility that he was quoted out of context but I live in hope). Sun and skin cancer are clearly linked. Or are they? It doesn’t appear so clear cut. I first became interested in light around 2009 and its benefits to health after reading Female Hormones in Context by Ray Peat. His suggestions that sunlight can, “cure depression, improve immunity, stimulate our metabolism, while decreasing food cravings and increase our intelligence, ” (Peat, 1997) intrigued me to gain a deeper understanding.Whilst I was aware of the harms of an excess of UV light, which can damage skin but is essential for increasing vitamin D levels. The far-reaching benefits of the spectrum of red and orange lights were unbeknownst to me.

Seasonal affective disorder or SAD is well documented and the mechanisms may be due to a number of factors such as increases in serotonin and melatonin. People generally get sicker and more depressed in winter and light therapy appears to be a useful tool in overcoming some of the symptoms associated with mood, energy and immune system related issues. If light is so harmful, why is it we often need more in these times and why has sunlight become so vilified?

Sunlight appears to get a bad rap in an ever increasingly reductionist causal relationship, in as much as sunlight causes skin cancer. Therefore wear sunscreen and avoid it. However current literature suggestions are along the lines of; “Wearing sunscreen increases sun exposure and increases incidence of melanoma and skin cancer.” Like many other approaches this A to B inference neglects to mention other pertinent mechanisms that can be attributed to increased incidence of cancerous states.

Cancer is a well known metabolic disease that can occur when specific effects to cells, namely mitochondria and the electron transport chain (ETC - often termed respiratory defects which allows problematic features of metabolism to occur, increasing damaging compounds). Cancer can be a feature of poor differentiation. Damage to tissues can often require new tissue to be formed. If an architect informs the site manager how to build the structure from just the blueprints without appreciation of the surrounding land and features, you can’t always guarantee success of completion.

Promoting better conversations between structures     

Vitamin A - promotes cell differentiation (this is very important when damaged tissue is rebuilt), improves immune system function and optimal hormone function. A meta analysis in 2016 highlighted vitamin A’s protective functions and usefulness in protection against skin related disease such as melanoma through inhibiting malignant transformation and decreasing tumour size and improving survival rates (Zhang, Chu, & Liu, 2014). It’s important to note that retinol from liver sources is the effective compound in this action and not carotenoids. Other findings such as anaemia are synergistic with decreased vitamin A levels due to its critical role in the immune system and fighting infection (Semba & Bloem, 2002). Vitamin A has similar actions to organisational compounds such as progesterone and thyroid.

A question worth exploring - Does a vitamin A deficiency decrease differentiation and lead to a potential increase in cancerous type states when exposed to UV light?

Estrogen

Estrogen has been implicated in many cancerous states, primarily due to its role in tissue proliferation. When unchecked by levels of progesterone, it can be responsible for unwanted tissue growth and mutagenicity (Mungenast & Thalhammer, 2014) (Troisi et al., 2014). Levels can be increased due to external sources in the environment and through increased conversion of testosterone in adipose tissue to estrogen via aromatase in both men and women (Skakkebæk, 2003)(Cargouët, Bimbot, Levi, & Perdiz, 2006). The potential increases in cancerous states such as melanoma due to modulation of estrogen might be an easy target for excess levels of U.V. light to exert a negative influence in susceptible tissues. Therefore keeping estrogen low and utilising estrogen lowering strategies through food choices and avoidance of certain compounds can be useful. Estrogen also lowers thyroid function

Thyroid failure

Hypothyroidism is well known to create disorganised tissue and its effects extend to all areas of physiology which include metabolism, fertility, mood, cognition and is instrumental in heart disease. As the need for thyroid hormone increases or the gland fails TSH or thyroid stimulating hormone - the pituitary hormone used to stimulate thyroid hormone increases, or at least it should do as a normal response. TSH has been associated with many pathological states but has been increasingly linked with melanoma (Ellerhorst et al., 2006). It appears that nearly all TSH receptors (TSHR) are present within melanoma cells and play a role in proliferation. Whilst the pituitary response and TSH is known to rise to increase thyroid hormone in response to increased need or thyroid failure. This action is a back-up and comes at a cost of increasing pituitary stimulation. Another factor for protection of the skin is that thyroid blood tests may not be accurate when individual nutrition, environmental pollutants and other stressors are present. Increased TSH is one factor, low undetectable thyroid function, poorly defined by blood tests could be another factor in skin damage that may not be picked up by clinicians.

Fat status of tissues.

I often found that when my diet was high in unsaturated fats my skin burnt extremely quickly. It’s been noted that people who often use sunblock often burn much quicker when in the sun without sunscreen. Increased consumption of unsaturated fatty acids appear to be linked to an increase in melanoma (Bourne, Mackie, & Curtin, 1987). Anecdotally I found that with a large decrease in PUFA my skin tolerates much longer bouts of sunshine before burning (not bad for a semi ginger pasty bloke from Kent!) , even in the intense middle-eastern heat. High fat diets, whether un/saturated also decrease mitochondrial activity and lower oxidative metabolism (Titov et al., 2016). It’s well known that vegetable oil consumption is linked to cancer (Niknamian, S., Kalamian, 2016) and heated vegetable oils that enter the body are already oxidised causing additional inflammation.

Perhaps melanoma is substantially increased when an individual has increased estrogen exposure, excessive amounts of unsaturated fatty acids in the skin, vitamin A deficiency and low thyroid function but does that still implicate sunlight as the cause of skin cancer? The A to B scenario hopefully seems less convincing when you read between the lines .

Modulating estrogen and decreasing PUFA in the skin is a step in the right direction. Increasing skin tolerance for longer days in the sun will be beneficial for many people. Using a homemade sun screen with minimal PUFA in can be useful for those wanting to spend extra time in the sun without damaging the skin and of course depending on the latitude, avoiding peak sun times is prudent to avoid excess UV light.

More information on resolving these issues can be found in the member’s area.

References:

Bourne, D. J., Mackie, L. E., & Curtin, L. D. (1987). Melanoma and Dietary Lipids. Nutrition and Cancer, 9(4), 219–226. http://doi.org/10.1080/01635588709513930

Cargouët, M., Bimbot, M., Levi, Y., & Perdiz, D. (2006). Xenoestrogens modulate genotoxic (UVB)-induced cellular responses in estrogen receptors positive human breast cancer cells. Environmental Toxicology and Pharmacology, 22(1), 104–112. http://doi.org/10.1016/j.etap.2006.01.002

Ellerhorst, J. A., Sendi-Naderi, A., Johnson, M. K., Cooke, C. P., Dang, S. M., & Diwan, A. H. (2006). Human melanoma cells express functional receptors for thyroid-stimulating hormone. Endocrine-Related Cancer. https://doi.org/10.1677/erc.1.01239

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

Niknamian, S., Kalamian, M. (2016). Vegetable Oils Consumption as One of the Leading Cause of Cancer and Heart disease. International Science and Investigation Journal, 5(5).

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

Semba, R. D., & Bloem, M. W. (2002). The anemia of vitamin a deficiency: Epidemiology and pathogenesis. European Journal of Clinical Nutrition. http://doi.org/10.1038/sj/ejcn/1601320

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

Titov, D. V., Cracan, V., Goodman, R. P., Peng, J., Grabarek, Z., & Mootha, V. K. (2016). Complementation of mitochondrial electron transport chain by manipulation of the NAD+/NADH ratio. Science, 352(6282), 231–235. http://doi.org/10.1126/science.aad4017

Troisi, R., Ganmaa, D., Silva, I. D. S., Davaalkham, D., Rosenberg, P. S., Rich-Edwards, J., … Alemany, M. (2014). The role of hormones in the differences in the incidence of breast cancer between Mongolia and the United Kingdom. PLoS ONE, 9(12). http://doi.org/10.1371/journal.pone.0114455

Zhang, Y.-P., Chu, R.-X., & Liu, H. (2014). Vitamin A intake and risk of melanoma: a meta-analysis. PloS One, 9(7), e102527. http://doi.org/10.1371/journal.pone.0102527

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

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

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

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

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

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

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

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

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

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

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

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

 

Sunlight, Low Level Laser Therapy and Photobiomodulation

Sunlight, Low Level Laser Therapy and Photobiomodulation I first became interested in the healing qualities of light about 5 years ago after reading From PMS to Menopause: Female Hormones in Context by Ray Peat. The obvious connotations to improved health during summer compared to a so- called Seasonal Affective Disorder or SAD was well known. The mechanics were intriguing but not limited to the obvious features of Ultra Violet light and the production of Vitamin D.

UV has been known to be problematic and excess, increases ageing of the skin but the mechanisms and links to cancer are misunderstood. An incomplete overview of other potential mechanisms that might promote mutogenic or cancerous processes are often left out of the explanation. The business of sunblock marketing, like many other fear mongering industries, continue to warn us of too much sunlight, yet often we often lack the right amount. An old blog highlights some points relating to this. The qualities of the healing properties of light are often glossed over instead of promoting the optimal rays of the sun..

The light which penetrates deeply into our tissues (mainly orange and red light) is able to improve the efficiency of energy production, and to suppress the toxic free-radicals that are always being formed in cells. “

Consideration of the healing properties of certain wavelengths of light is a must for health, metabolic and rehabilitation promotion. The useOrange and red rays of light therapy for improving pain, healing and many other issues has been used for decades. In 1903 a Nobel science prize was awarded to Niels Finsen for ultraviolet-phototherapy.

Low Level Laser Therapy and Photobiomodulation

The use of light therapy for improving pain, healing and many other issues has been used for decades.

Here are just some of the issues that have seen great improvement using LLLT and Photobiomodulation.

  • Pain reduction
  • Improved hormone function
  • Swelling reduction
  • Increased healing
  • Neurological issues
  • Improved cellular function
  • Promote recovery from exercise
  • Rehabilitation of injuries
  • Decreased inflammation
  • Improved hair follicle stimulation

The use of infra red heat lamps have been used for decades and often been recommended in rehabilitation or in the beauty world as an anti-aging protocol. I have used heat lamps with myself and clients for several years but it is clear that many gains can be had without the use of heat and just focusing on the use of light alone.

There are many factors that can make the use of light more effective and these illumination parameters include:

  • Wavelength
  • Fluence
  • Power density
  • Pulse structure
  • Timing

For many, even finding these variables may prove a difficult task. In fact even using the word Photobiomodulation becomes problematic! I think the exposure of bright light during the day through incandescent or LED lights is important to offset the lack of natural daylight and healing properties of various waveforms, (unless of course you do work or spend much of your day outside) with the use of red light after sunset to decrease impact to circadian rhythm.

One of the most prevalent mechanisms that appears to offer an explanation as to LLLT’s effectiveness is by increasing cytochrome c oxidase which improves mitochondrial function, increasing cell efficiency and function and improving energy production.

The wavelength of 600-950nm or optical window is a general guideline and appears to be where most of the research and the effects of LLLT has been conducted on. The toxinless website listed below has some great recommendations for the use of light and ideal set ups, which are very cheap to set up at home.

The use of LLLT for improving hormones and in particular thyroid function has gained a greater following of late. It’s worth noting, that in some studies which can be found on Valtsu’s website (a great resource for thyroid) , the use of LLLT improved thyroid function without the need for thyroid medication. Additional studies corroborate the effectiveness in reducing the need for thyroid medication and addressing autoimmune thyroiditis.  Therefore I think the use of LLLT for improving energy, digestion, mood and sleep is validated.

References:

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

http://www.ncbi.nlm.nih.gov/pubmed/22747309

http://www.ncbi.nlm.nih.gov/pubmed/12804422

http://www.ncbi.nlm.nih.gov/pubmed/26048721

Online resources:

http://valtsus.blogspot.fi/2015/09/hypothyroidism-could-it-be-treated-with.html

http://www.toxinless.com/red-light

http://www.photobiology.info/Hamblin.html

 

 

 

 

Adrenal fatigue or reductionist thinking? Part 2: Restoration of metabolic processes

adrenal Restoration of metabolic process- lowering the adrenal load.

Sugar, fat and other mal-aligned  factors.

Saturated fat is bad for you, so they said but it clearly wasn’t. Now it’s sugars turn. Sugar causes diabetes, cancer and many other modern conditions, if you are to believe many of the memes on social media. Well no, it doesn’t. Cancer for example is usually created from a specific defect to the respiratory apparatus of the cell. In English that means part of the cell that utilises oxygen. Sugar or Sucrose whose primary constituents are both Fructose and Glucose are readily available carbohydrates and the brain/central nervous system require plenty. Have you ever noticed that brain fog creep in when on that low carb diet? The reason? Restricted carbohydrates  equals reduced cognitive process’s. Yes we can generate glucose via oxidation of fat, in the form of ketosis and you can also break down protein to generate glucose too, but these methods are less than efficient forms of energy generation and long-term utilisation of these systems is not ideal.

Sugar produces energy and when processed with oxygen is much more efficient than glycolysis or energy production without oxygen (anaerobic). In those who have damaged metabolism, there is a reliance on the production of energy in this manner, lactic acid is often produced even at rest. Therefore trying to exercise at intense levels poses a problem for those with both adrenal and metabolic issues.

Give the body what it needs?  Got cravings? You know those ones where you are dying for some food, starchy carbohydrates, a sugary drink? There are no demons at work here, just a simple case of biology, carbohydrates are a primary fuel source for the body. Want to avoid coming crashing down? Avoid having 3 big meals a day and maintain blood sugar levels by eating frequently. Some do better than others but allowing 4-6 meals a day and noting how you feel is a step in the right direction. Maintaining a body temperature of 37 degrees and a pulse rate of 70-85 beats per minute is ideal. This has been well documented in the work of thyroid researcher Broda Barnes and the work of Ray Peat PhD.

Eating readily available carbohydrates such as ripe digestible fruits, protein and saturated fats (in the right amounts) such as coconut oil help to maintain blood sugar levels throughout the day without the resultant elevations in cortisol, which affect adrenal regulation issues.

Stressful situations often warrant the use of supplements such as Vitamins A, B6, C, magnesium and potassium. In particular sugary foods, which should include fruit, maple syrup and honey are ideal choices to diminish the stress response (even table sugar could play a therapeutic role in lowering stress).

Salt is also a powerful anti-stress compound. During stress sodium is often passed more rapidly from the body. Sodium spares magnesium. If you drink too much water the level of sodium excretion increases, which further decreases available magnesium. The research on lowering salt intake is inconclusive but what is known, is that when a low sodium state exists, aldosterone, a hormone that is used to regulate both salt and blood pressure elevates in response. It would come as no surprise that in a low adrenal state, feeling dizzy when moving from seated to standing exits due to poor blood pressure regulation. Craving salt is a mechanism to improve such a situation.

The current mind set regarding exercise and wellbeing is

Increased exercise + Low carb and raw foods = Health

And in the short term, markers suggest that this could be favourable. So how do you tell if this working for you long term? The monitoring of both pulse and body temperature give a great insight into optimal biological function. Here are some of the symptoms, which combine both compromised cortisol and thyroid function.

  • Cold hands, feet and nose
  • Energy crashes
  • Poor wound healing
  • Poor sleep
  • Fatigue
  • Constipation or alternation between constipation and diarrheoa
  • Weight gain
  • Bloating
  • Skin issues
  • Low libido

In reality:

Intense exercise + low carb/raw food diets= compromised metabolism.

Historically in many, changing both the way you eat and completing more exercise may have worked previously, but as you push the markers of exercising more and eating less or certainly eating foods that do not support your activities. You may see many of those symptoms above start to creep into your daily life. There’s no doubt that eating well and exercising are productive pursuits for optimal body function. However for many the lines are blurred as to what actually is a healthy diet.  Consumption of large amounts of grains, margarine and low fat foods were being touted as healthy a decade or two earlier, now look at the research condemning that approach. The following information seems to be heading a similar route.

For the health conscious exerciser today a diet high in raw green vegetables, green juices, seeds nuts, fish oils, low carb, low starch seems to be the zeitgeist but is it that healthy? From a biological perspective the answer would be no. Eating these foods over a long period of time not only increases the stress response but may actually damage how our body’s cells actually function. Increasing available energy from easily digestible foods helps to assimilate energy for production. In contrast foods such as many raw green vegetables, nuts, seeds and vegetable oils, not only irritate the bowel, sit and accumulate bacteria damaging the intestinal lining, but also provide less than optimal nutrition, which will lower metabolic rate.

Moving is important, no doubt, but exercising to within an inch of total fatigue can be detrimental, especially so when dealing with issues related to both adrenal and metabolic based issues. Finding the right type of exercise and even stepping back and focusing on exercise that doesn’t produce high levels of lactic acid, causes hyperventilation and the loss of carbon dioxide should be considered in the short term. The goal of improving metabolic function, restoring deep sleep and raising energy should always predominate over the loss of body fat reduction. It’s a tricky issue to get your head around for some, but when you start to feel great again. You’ll understand why.