estrogen

Improving brain health - amyloid, tau, and energy

Neurological and neurocognitive diseases have often been associated with the peptide amyloid beta (AB) and considered a main culprit in the onset of Alzheimer’s disease (AD) due to its elevations in the central nervous system (CNS) or brain. Initial ideas behind AB accumulation were derived from Dr Alois Alzheimer’s observations in 1906 that peptide deposits, entangled structures and plaques were present in a patient with severe neurological and neurocognitive function. Much of the research over the last three decades has focused on AB which has two pathways, non amyloidogenic forming 3 soluble fragments and the amyloidogenic pathway providing the AB associated with AD (Gosztyla, Brothers, & Robinson, 2018).

The Verve - The Drugs Don't Work

The drugs don’t work they just make you worse but I know I’ll see your face again.

Despite many promising drugs, interventions ( y secretase inhibitors) focusing on lowering AB have been found to worsen cognitive function and increase susceptibility to infection (Penninkilampi, Brothers, & Eslick, 2016). Estrogen has often been touted as a protective hormone against both cardiovascular disease and cancers despite large bodies of conflicting and unsupportive data (Derwahl & Nicula, 2014)(Felty & Roy, 2005) (Benjamin, Toles, Seltzer, & Deutsch, 1993). In the last ten years or so further confusion has been added to most people’s (including doctors) understanding of  estrogen and its so called protective mechanisms. In AD and dementia studies, estrogen was shown to decrease AB production, therefore it must be protective. The only downside to this observation is that it decreased AB, worsened cognition and increased susceptibility to infections (Gosztyla et al., 2018).

These observations tie in well to the current hypothesis that AB is found in most life forms, is protective, and increases as a form of anti-microbial action against certain agents such as viral and bacterial. Another interesting observation is the comparison between the actions of estrogen and progesterone in AD and dementia. Estrogen lowers AB but progesterone does not. Progesterone also decreases another key component of AD,  a structure in the CNS called tau. Tau is a neuronal microtubule associated protein and a structural factor within the brain, which major functions are the promotion of self assembly and tau stabilisation (Carroll et al., 2007). The commonality of AD and dementia like states is tau aggregation and can be elevated in AD and also  traumatic brain injury (TBI). Progesterone not only decreases damaged/entangled (hyperphosphorylated) tau it’s shown to be protective in TBI cases.

Increased estrogen is associated with increased excitability, seizures and neuronal degradation and this appears elevated in the premenstrual and estrous phases (Broestl et al., 2018). With increased aspects of pollution such as aluminium, mercury and cadmium and air and water borne pollutants that mimic estrogen, the potential of increased neurological damage is at an all-time high (Exley, 2013) (Annamalai & Namasivayam, 2015). Perhaps instrumental in the incidence and prevalence of neurological disease in the industrialised world?

Dietary fats, glucose and thyroid.

There’s far too much resistance in medicine to consider both neurological decline and diseases such as cancer as issues of metabolism. Mutations occur when biology degrades, when the mitochondrial aerobic function is compromised and there’s much that can be done to improve that area of function. The insistence that unsaturated fat is protective to neuronal structures appears problematic. In Parkinson’s disease for example degradation of polyunsaturated fats (both n3s and n6s) appears to increase lipid peroxidation, neuronal damage and that maintaining cholesterol levels appears to be protective (Alecu & Bennett, 2019). A common theme between all the neurological and oncological diseases is an abundance of PUFA and their oxidation, decreased glucose efficiency, decreased thyroid availability and mitochondrial damage(Schönfeld & Reiser, 2013)(Choi et al., 2017)

Some of the conflicts between the connection of low thyroid function and decreased neurological function are grounded in the persistence that biochemical evaluation of TSH and thyroid hormones  (FT4 and FT3) are reliable and indicators of tissue saturation both in the hypothalamus, pituitary, neuronal and other tissues. Given the vast aspects of organisation allowed by adequate thyroid hormone and its effects on metabolism, movement, digestion, temperature, pulse rate, sleep, blood sugar, cholesterol and blood pressure, these variations might be of more value than reliance on poorly defined blood tests.

Endotoxin, gut and blood brain barrier.

Hyperphosphorylated tau.jpg

Chronic digestive stress increases endotoxin, serotonin and histamine and can cross the blood brain barrier

 

Intestinal hyperpermeability or leaky gut syndrome has been very fashionable for the last ten years and holistic narratives of detoxing, raw green foods and probiotics seems to still be the Zeitgeist. Endotoxin or LPS (lipopolysaccharides) are well known to induce stress responses, stimulating the production of both serotonin and histamine and adrenal pathways. Histamine and serotonin can increase the permeability of the blood brain barrier to  endotoxin induced increases of damaged tau structures is another aspect of neurological degradation(Wang et al., 2018). It also increases AB but know we have an idea that increasing AB is protective and it’s progression to plaques might be problematic. Attempting to lower AB is a reductionism that should best be avoided.

The concepts of detoxing and fasting might temporarily decrease endotoxin but they also have the capacity to make you colder, metabolically less efficient, decrease liver efficiency and lower thyroid hormone responsiveness that does not automatically increase after re-feeding (Boelen, Wiersinga, & Fliers, 2008). Ensuring adequate energy availability, endotoxin reducing foods like orange juice, carrots (Peat, 1997) (Ghanim et al., 2010) (Babic, Nguyen‐the, Amiot, & Aubert, 1994), and promoting restoring oxidative metabolism with compounds like methylene blue and caffeine (Eskelinen & Kivipelto, 2010)(Berrocal, Caballero-Bermejo, Gutierrez-Merino, & Mata, 2019), moderate exercise, engaging in life affirming activities and light exposure might be the some of the most effective factors in the fight against neurological disease.


References:

Alecu, I., & Bennett, S. A. L. (2019). Dysregulated lipid metabolism and its role in α-synucleinopathy in Parkinson’s disease. Frontiers in Neuroscience. https://doi.org/10.3389/fnins.2019.00328

Annamalai, J., & Namasivayam, V. (2015). Endocrine disrupting chemicals in the atmosphere: Their effects on humans and wildlife. Environment International. https://doi.org/10.1016/j.envint.2014.12.006

Babic, I., Nguyen‐the, C., Amiot, M. J., & Aubert, S. (1994). Antimicrobial activity of shredded carrot extracts on food‐borne bacteria and yeast. Journal of Applied Bacteriology. https://doi.org/10.1111/j.1365-2672.1994.tb01608.x

Benjamin, F., Toles, A. W., Seltzer, V. L., & Deutsch, S. (1993). Excessive estradiol secretion in polycystic ovarian disease. American Journal of Obstetrics and Gynecology, 169(5), 1223–1226. https://doi.org/10.1016/0002-9378(93)90286-R

Berrocal, M., Caballero-Bermejo, M., Gutierrez-Merino, C., & Mata, A. M. (2019). Methylene Blue Blocks and Reverses the Inhibitory Effect of Tau on PMCA Function. International Journal of Molecular Sciences. https://doi.org/10.3390/ijms20143521

Boelen, A., Wiersinga, W. M., & Fliers, E. (2008). Fasting-Induced Changes in the Hypothalamus–Pituitary–Thyroid Axis. Thyroid, 18, 12–129. https://doi.org/10.1089/thy.2007.0253

Broestl, L., Worden, K., Moreno, A. J., Davis, E. J., Wang, D., Garay, B., … Dubal, D. B. (2018). Ovarian cycle stages modulate alzheimer-related cognitive and brain network alterations in female mice. ENeuro. https://doi.org/10.1523/ENEURO.0132-17.2018

Carroll, J. C., Rosario, E. R., Chang, L., Stanczyk, F. Z., Oddo, S., LaFerla, F. M., & Pike, C. J. (2007). Progesterone and estrogen regulate Alzheimer-like neuropathology in female 3xTg-AD mice. Journal of Neuroscience. https://doi.org/10.1523/JNEUROSCI.2718-07.2007

Choi, H. J., Byun, M. S., Yi, D., Sohn, B. K., Lee, J. H., Lee, J. Y., … Lee, D. Y. (2017). Associations of thyroid hormone serum levels with in-vivo Alzheimer’s disease pathologies. Alzheimer’s Research and Therapy. https://doi.org/10.1186/s13195-017-0291-5

 Derwahl, M., & Nicula, D. (2014). Estrogen and its role in thyroid cancer. Endocrine-Related Cancer. https://doi.org/10.1530/ERC-14-0053

Eskelinen, M. H., & Kivipelto, M. (2010). Caffeine as a protective factor in dementia and Alzheimer’s disease. In Journal of Alzheimer’s Disease (Vol. 20). https://doi.org/10.3233/JAD-2010-1404

Exley, C. (2013). Human exposure to aluminium. Environmental Sciences: Processes and Impacts. https://doi.org/10.1039/c3em00374d

Felty, Q., & Roy, D. (2005). Estrogen, mitochondria, and growth of cancer and non-cancer cells. Journal of Carcinogenesis. https://doi.org/10.1186/1477-3163-4-1

Ghanim, H., Sia, C. L., Upadhyay, M., Korzeniewski, K., Viswanathan, P., Abuaysheh, S., … Dandona, P. (2010). Orange juice neutralizes the proinflammatory effect of a high-fat, high-carbohydrate meal and prevents endotoxin increase and toll-like receptor expression. American Journal of Clinical Nutrition. https://doi.org/10.3945/ajcn.2009.28584

Gosztyla, M. L., Brothers, H. M., & Robinson, S. R. (2018). Alzheimer’s Amyloid-β is an Antimicrobial Peptide: A Review of the Evidence. Journal of Alzheimer’s Disease. https://doi.org/10.3233/JAD-171133

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

Penninkilampi, R., Brothers, H. M., & Eslick, G. D. (2016). Pharmacological Agents Targeting γ-Secretase Increase Risk of Cancer and Cognitive Decline in Alzheimer’s Disease Patients: A Systematic Review and Meta-Analysis. Journal of Alzheimer’s Disease. https://doi.org/10.3233/JAD-160275

Schönfeld, P., & Reiser, G. (2013). Why does Brain Metabolism not Favor Burning of Fatty Acids to Provide Energy? - Reflections on Disadvantages of the Use of Free Fatty Acids as Fuel for Brain. Journal of Cerebral Blood Flow & Metabolism. https://doi.org/10.1038/jcbfm.2013.128

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). https://doi.org/10.1371/journal.pone.0114455

Wang, L.-M., Wu, Q., Kirk, R. A., Horn, K. P., Ebada Salem, A. H., Hoffman, J. M., … Morton, K. A. (2018). Lipopolysaccharide endotoxemia induces amyloid-β and p-tau formation in the rat brain. American Journal of Nuclear Medicine and Molecular Imaging.

 

The Big Estrogen Hoax

Routine spraying with potent pesticides was deemed safe previously.

Routine spraying with potent pesticides was deemed safe previously.

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

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

Why is pregnancy protective?

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

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

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

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

Why so much confusion?

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

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

Progesterone is protective across many aspects of function

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

 

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

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

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

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

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

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

 References: 

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

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

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

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

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

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

 

 

 

Autoimmunity part 2: The autoimmune paleo diet - The Pro's and Cons

Where's the ice cream?!.jpg

 In this post I’m going to explore the mechanisms of the recommended autoimmune paleo diet (AIPD)  and suggest why it has very useful short term applications which are a mixed bag of interventions, reductionisms and shouldn’t be considered as a long term solution.

 In the last autoimmunity post you might remember how scientists like Polly Matzinger give an insight of auto immune disease that’s often not given enough credit. In summary of the danger theory, which is the body recognising self and the potentially damaged self. These damaged tissues be they thyroid or another tissue, is marked for removal from the system to prevent more damage occurring. The body is a pretty impressive organism that should be credited with being able to recognise its own tissues and respond with an effective response to restore best working order. So why should we discount this theory?  It’s essential to remember that a significant driver of autoimmunity is the increased prevalence of the disease in females (some 10 x more than males)  is driven by estrogen, estrogen like compounds and their ubiquity in the environment. Recently I’ve seen more people in the preceding months with vitiligo than I have seen in my entire lifetime but then I do live in a very polluted city.

 The recommendations for the autoimmune paleo diet protocol has some positives but the thought process behind such a diet has shortcomings and it’s important to tease out why it can be successful for some. I’ve always found the idea that a paleo lithic diet be entertained for health somewhat problematic. Archaeological specimens of older adults are generally lacking, suggesting mortality ranges commonly found between 20-40 year old samples (Trinkaus, 2011). That’s not to say that there weren’t older adults, ,but to base the efficacy of a diet strategy on a previous era without any data is problematic.

 There are several reasons why the AIPD might have some positive outcomes.

1.     It removes many offending compounds that are known to irritate the digestive tract. Sweeteners,  emulsifiers and thickeners are well documented to increase intestinal inflammation. Gums like guar, locust bean and Irish sea moss (carrageenan) can cause substantial damage over time and is also implicated in blood sugar regulation and diabetes. http://diabetes.diabetesjournals.org/content/67/Supplement_1/770-P?fbclid=IwAR1W8LRbx1fSu02Tr3b19ANtu2qpkZRhnwySvCj8uUC4TpRhvzypNH6lERg

2.     Alcohol is restricted. It should come as no surprise that alcohol has the capacity to affect multiple aspects of function. Most forms of alcohol contain phytoestrogens and just like long term soy consumption has the capacity to influence the body as a source of external estrogens . Additionally, many other additives like yeasts, colorants and preservative like sulphites appear equally problematic. Drinking alcohol in moderation isn’t necessarily problematic but the more susceptible that one is to estrogen issues, alcohol will often be problematic. I have seen many old ladies in their 90’s have been prone to a tipple of sherry or whiskey.

3.     Nuts, seeds and oils which are high in unstable unsaturated fatty acids are also restricted ,decreasing lipid/fat oxidation and improve mitochondrial function. The restriction of grains can also be useful for a similar reasoning and grains like millet, sorghum and barley are known to slow metabolism, but the action of seeds and grains can promote increased intestinal serotonin and histamine production, increasing the burden and damage to digestive function. Both poly and monounsaturated fats appear to promote compromised liver function, degrade metabolism and contribute to obesity.

4.     Nightshades, legumes, egg whites and gluten are well known for their role in irritability of the digestive system.

When all is said and done, there’s every reason why many people should feel better when removing these usual suspects. But there are problems with the AIPD and I have seen individuals who despite following this protocol still present with both digestive and energy issues, primarily because deficits in energy still arise and potential autoimmune reactions persist. Given some of the problems associated with determining cause and effect of specific interventions. It would be easy to speculate why someone who was prone to eating lots of fast food, high in unstable oils, high fructose corn syrups, preservatives, binding agents and suffering autoimmune, digestive, energy and other hormone disturbances might respond well to this in the short term?

 

There’s another plus to the AIPD - it includes fruit but there’s a caveat that natural sugars which include fructose should be kept to a minimum. There’s also an emphasis on eating fruits that are high in intestinal irritating seeds like berries. Carbohydrate is essential for optimal energy production. It promotes adequate carbon dioxide production and allows more efficient energy production and oxygenation of tissues that you just don’t get with sustained fat oxidation. Even refined table sugar shouldn’t be frowned upon and would only be problematic if your diet contained large amounts of refined sugar and devoid of other key nutrients like fats, proteins, and lack of potassium or magnesium as an example.

 

So is the AIPD useful? Yes, but it’s extremely limited. So how about a strategy that allows function to improve systemically rather than in isolation? Studies are limited on the effectiveness of AIPD. Whilst not autoimmune as such, a study that utilised the AIPD in patients with IBD (irritable bowel disease) completed remission in 11/15patients or 73% (Konijeti et al., 2017). That’s great, but it shouldn’t be surprising, if you’re removing all the intestinal irritants and this reasoning should extend to some improvements in autoimmune patients, resolving digestive function should follow. Gut function improved but markers of inflammation such as CRP did not, and one participant withdrew due to irritation from raw food consumption.

 

Aspects of the autoimmune and or autointoxication theory of disease is derived from Elie Metchnikoff’s work on immunology, bacteria and gut function (Metchnikoff & Metchnikoff, 1908). Metchnikoff proposed that death and disease started in the colon. Whilst there’s little doubt  that optimising gut function has many beneficial effects, problems arise beyond the digestive tract that might occur in otherwise healthy diets. The bowel can be a hospitable place for problematic bacteria when hydrochloric acid is low, and motility is slow induced by a low energy/thyroid state. Metchnikoff proposed that beneficial strains of bacteria can be useful to prevent unwanted maladies related to bowel function. However he was keen to point out that animals blessed with longevity often shared features of high metabolic rates and low levels of gut bacteria. This may explain why supplemental probiotic studies are not consistent in results and may simply act as a competing factor against more problematic bacteria (Goldenberg et al., 2015). The AIPD preference for more fermented goodies might be useful, but more is definitely not better. As food is poorly digested and bacterial metabolites increase so does endotoxin, intestinal hyperpermeability (leaky gut) and changes to biochemistry and hormones.

 I won’t discuss dairy produce here as it’s rarely the issue, the stressed digestive system has a problem with dairy products. I have seen countless clients return to eating dairy products like cheese, ice cream and  milks.

Eating ice cream & walking in the sunshine is an easy way to lower aspects of autoimmunity.jpg

It’s rarely the dairy that’s at fault, it’s usually the stressed digestive system that’s the real issue.

The AIPD, well there’s plenty that can be improved upon to create longer lasting function without the need for reductionist notions like the greener, the more natural, the better. Especially the problems that have been known for many decades that cruciferous/brassica vegetables high in isothiocyanates and glucosinolates, are well known to increase levels of cyanide in tissues and are anti-metabolic in nature disrupting thyroid function.

Siri what is broccoli?.jpg

Broccoli was not a palaeolithic food

Brassica vegetables may have very little place in resolving autoimmune diseases.

The most effective form of preventing autoimmunity might be to keep metabolism at its best working order rather than slowing it down. The fascination of broccoli in the modern diet is not without paradox.  Broccoli certainly wasn’t consumed in the palaeolithic era, although other cruciferous vegetables may have been (Buck, 1956). It’s elevation to farmed commodity and food stuff appeared to take place in Hellenic culture and more rapidly promoted to support the invading Roman army.

Promoting a diet that has easily digested nutrients, energy and facilitates available thyroid hormone, addressing internal and external sources of estrogen, without increasing stress responses may be the most pragmatic approach of any diet to decrease autoimmune responses. Eating plenty of fruit, sugars and honey combined with good quality proteins, moderate saturated fat and low in unsaturated fats, seeds might be the best autoimmune diet.

Another problematic aspect of the AIPD is the emphasis on Omega 3 fatty acids such as DHA to lower inflammation and this isn’t limited to poorly constructed diets but a common error in autoimmune and inflammatory protocols (Constantin et al., 2018). Many studies and review such as this invoke the antioxidant effect properties of omega 3s due to their ability to lower markers such as triglycerides, cholesterol and crease metabolism. Surprisingly when you decrease metabolic rate, you decrease metabolic function, therefore inflammatory and oxidative markers are reduced. Sustained omega 3 and other unsaturated fatty acids accumulate in the brain and liver and decrease aerobic metabolism through sustained lipid peroxidation, especially so when carbohydrate metabolism is lost.


‘ Calorific restriction and well established diet supplementation with omega 3 regulates total cholesterol, LDL-C and triglycerides.’ (Constantin et al, 2018).

 In essence this has as much benefit as taking medication to lower cholesterol. Of course eating less calories produces less inflammation and if calories are restricted below a certain threshold, this lowers metabolism, giving the impression of less oxidation. If you’re going to support the notion that taking omega 3s lowers inflammation and as many espouse, lowers cardiovascular risk, the net effect will be degraded cholesterol that’s prone to oxidation and left with an excess of fatty acids also prone to lipid peroxidation. If we’re going to help more people with a so called autoimmune disease, perhaps we need to be thinking a little more holistically? If estrogen is a main driver of a perceived autoimmune state then improving its excretion through adequate energy, liver function and robust biology should be the answer. There’s no doubt that improving digestive function is helpful but the current zeitgeist, promoting plenty of undercooked vegetables in their most natural state, high in metabolic inhibitors is restrictive to decreasing aspects of autoimmunity.


References: 

Buck, P. A. (1956). Origin and taxonomy of broccoli. Economic Botany. http://doi.org/10.1007/BF02899000

Constantin, M., Nita, I., Olteanu, R., Constantin, T., Bucur, S., Matei, C., & Raducan, A. (2018). Significance and impact of dietary factors on systemic lupus erythematosus pathogenesis (Review). Experimental and Therapeutic Medicine. http://doi.org/10.3892/etm.2018.6986

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

Konijeti, G. G., Kim, N., Lewis, J. D., Groven, S., Chandrasekaran, A., Grandhe, S., … Torkamani, A. (2017). Efficacy of the Autoimmune Protocol Diet for Inflammatory Bowel Disease. Inflammatory Bowel Diseases. http://doi.org/10.1097/MIB.0000000000001221

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

Trinkaus, E. (2011). Late Pleistocene adult mortality patterns and modern human establishment. Proceedings of the National Academy of Sciences. http://doi.org/10.1073/pnas.1018700108

https://balancedbodymind.com/blog/2019/3/7/auto-immune-disease-is-it-really-in-your-genes-part-1




Free Happy Hormones Copy

happyhormones2-4.jpg

Feel free to share around.


Download Happy Hormones

I wrote this book several years again and am in the process of creating a new, more complete text on the subject. Please feel free to download and share. All I ask is that you leave some comments on what you liked or disliked about it.

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

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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

Poly Cystic Ovary Syndrome (PCOS) - inheritance, environment and stress.

Estrogen excess.png

Poly Cystic Ovary Syndrome - inheritance, environment and stress. Recently I took on a client who was diagnosed with polycystic ovary syndrome (PCOS), a slightly wayward insulin profile and the ‘best practice’ of oral contraceptives and Glucophage (metformin- blood sugar regulating drug) were suggested. My client had started bleeding daily and was informed that this was normal for three months but would help out with PCOS and weight gain. However this seemed at odds with my current knowledge and experience of biology and endocrinology. There are plenty of studies highlighting the diabetes inducing effects of estrogen and oral contraceptives.

Glycemia constitutes a fundamental homeostatic variable, and hence its alteration can lead to a number of pathophysiological conditions affecting the internal milieu of the human being. Since the early 1960s, the intake of oral contraceptives has been associated with an increased risk of developing disorders of glucose metabolism.(Cortés & Alfaro, 2014)

Is best practice the efforts of a global network of doctors or simply a corporate led strategy? Don’t get me wrong; the world is full of competent, passionate and well-meaning doctors who signed up to help others. But the concept of both best practice and clinical governance seem a utopian ideal when those that are responsible for drug development are companies whose primary function is to make as much money as possible, without appropriate direction.

Joseph Dumitt in his book Drugs for Life (2012) highlights that there hasn’t been a scientist at the head of a pharmaceutical company for many years and their direction being driven by economists and marketers. As there are many examples of absolutist statements regarding drugs and their positive effects on health that lack congruence over time, you’ll forgive me for sounding like a conspiracy theorist. How about hormone replacement therapy (HRT) for better health despite its negative outcomes related to cardiovascular events or cancer? Or statin therapy for decreasing unnecessary risk factors based upon skewed data and early terminated trails with no public access to trial data (Lorgeril & Rabaeus, 2016)?

Back to PCOS. I have written previously about the effects of metformin and its use in gestational diabetes, and the problems it poses trans-generationally. It’s possible to suggest that the failure to act with appropriate biological interventions perpetuates the cycle of acquired traits from parents that are passed to offspring, treated ineffectively and generations of reproductive (and other tissues) tissue conditions continue without being resolved.

The biologist Jean Baptiste Lamarck's fourth law stated:

“ Everything which has been acquired..or changed in the organisation of an individual during its lifetime is preserved in the reproductive process and is transmitted to the next generation by those who experienced the alterations. “

It's worth pointing out that this is not isolated to the female of the species as the factors below have been shown to be instrumental in reproductive issues (testicular dysgenesis, hypospadias etc) in males.

The environment has been shown to be instrumental in the development of reproductive tissue disorders, diabetes and cancer but more emphasis is placed on the individual and their food choices rather than acknowledgement of industrial responsibility. Positive associations between levels of polychlorinated bisphenyls (PCBs), pesticides, polycyclic aromatic hydrocarbons (PAHs) and dichlorodiphenyldichloroethylene (DDE) have been confirmed in multivariate data analysis (Yang et al., 2015). Relationships between increases of luteinising hormone (LH) PCO, hyperandrogenism, annovulation, insulin resistance and pollutants are significant and may add to issues of detection, due to the subtle long term perturbations that often affect endocrine function. Stress, other pollutants and medications contribute to further problems that burden not only reproductive tissue but also other organizational hormones such as thyroid hormone.

PCOS is defined medically by the following: One of the main problems of treating PCOS with contraception is the many studies that clearly show a relationship between estrogen and decreased insulin sensitivity (Godsland et al., 1992)(Cortés & Alfaro, 2014). Progestin’s, the synthetic version of progesterone, also pose many problems but this has not deterred the inclusion of estrogen and progestin contraceptives as another inappropriate form of treatment. The burden of estrogen induced by the sources suggested above comes at a cost and it’s well known that an excess of estrogen can suppress thyroid function (thyroid is necessary for detoxification of estrogen and another organisational hormone progesterone.

Both thyroid and progesterone are known to improve insulin sensitivity and can create beneficial changes to disorganised tissue induced by an excess of estrogen. Thyroid nodules and uterine fibroids appear to be intimately linked by an excess of estrogen (Kim et al., 2010) and suppression of thyroid tumours can be achieved by thyroid stimulating hormone (TSH) suppression by thyroxin supplementation (Grussendorf, Reiners, Paschke, & Wegscheider, 2011). An old rambling on thyroid nodules and fibroids.


Breaking the cycle requires interventions that address inheritance, environment and individual stressors. Strategies that involve adequate nutrition that build biology not reduce it, use of protective compounds like progesterone, thyroid and adequate carbohydrate can be of great benefit. Although this stands in contrast to the best practice of contraception, blood sugar medication and poorly thought out nutritional advice of restricting carbohydrates. As the environment appears to drive most of the increasing numbers of issues like PCOS, it becomes important to increase robustness, restrict exposure to what we can control and become more adaptable to what we can’t.

To find out more about coaching for these issues.

References:

Burkhardt, R. W. (2013). Lamarck, evolution, and the inheritance of acquired characters. Genetics, 194(4), 793–805. http://doi.org/10.1534/genetics.113.151852

Cortés, M. E., & Alfaro, A. a. (2014). The effects of hormonal contraceptives on glycemic regulation. The Linacre Quarterly, 81(3), 209–218. http://doi.org/10.1179/2050854914Y.0000000023

Dumit, J. (2012). Drugs for Life. Duke University Press.

Godsland, I. F., Walton, C., Felton, C., Proudler, A., Patel, A., & Wynn, V. (1992). Insulin resistance, secretion, and metabolism in users of oral contraceptives. Journal of Clinical Endocrinology and Metabolism, 74(1), 64–70. http://doi.org/10.1210/jcem.74.1.1530790

Grussendorf, M., Reiners, C., Paschke, R., & Wegscheider, K. (2011). Reduction of thyroid nodule volume by levothyroxine and iodine alone and in combination: A randomized, placebo-controlled trial. Journal of Clinical Endocrinology and Metabolism, 96(9), 2786–2795. http://doi.org/10.1210/jc.2011-0356

Kim, M.-H., Park, Y. R., Lim, D.-J., Yoon, K.-H., Kang, M.-I., Cha, B.-Y., … Son, H.-Y. (2010). The relationship between thyroid nodules and uterine fibroids. Endocrine Journal, 57(7), 615–21. http://doi.org/10.1507/endocrj.K10E-024

Lorgeril, M. De, & Rabaeus, M. (2016). Beyond confusion and controversy, can we evaluate the real efficacy and safety of cholesterol-lowering with statins? Journal of Controversies in Biomedical Research, 1(1), 67. http://doi.org/10.15586/jcbmr.2015.11

Is testosterone replacement therapy necessary?

In a world where it is increasingly normal to be convinced that we fall into a risk classification, need a treatment and can convince our doctor accordingly, negating any experience that he or she might have. The marketeers and economists that run pharmaceutical companies are doing a great job of increasing profits. Before we keep looking for the next wonder treatment we should take stock of what food and exercise can do.

Testosterone can be increased by some very simple strategies such as:

  1. Having adequate liver and vitamin A in the diet to assist in the conversion of cholesterol to pregnenolone - the base hormone responsible for production of testosterone and other androgens.

  2. Ensuring that adequate energy and thyroid hormone are available to maintain communication of the hypothalamic- pituitary- (signalling centres for hormone production-brain to testicles) gonadal axis.

  3. Understanding stress, sleep and interactions between excesses of estrogen and their impact on testosterone production.

  4. Less understood but increasingly keeping mobile communication devices out of pockets and bags that are close to reproductive tissue, including females (ovaries, endometrium etc), appears to be a pragmatic approach in the future. Steroid producing tissues have increased production of problematic compounds that may be prone to damage.

Here's some of the technical aspects to the situation that are taken from a recent assignment as part of my masters degree..

Introduction

Testosterone is a hormone found in both males and females but is the major reproductive hormone in men that also has a variety of other beneficial functions for maintaining physical and psychological aspects to health. Testosterone levels may decrease with disease and/or be part of an age related decline of output. The use of testosterone supplementation has increased substantially in recent years counter these states, primarily due to increased marketing as an agent of change for energy, strength, fat loss and sexual function. Whilst its use appears beneficial in some areas, caution has been recommended on the effects of T supplementation use and it’s effects on the cardiovascular system.

 Diagnosis

Testosterone (T) is the most important androgen found in males and produced primarily within the testes, when low it is defined as hypogonadism. Hypogonadism is classified as either primary, derived from the testes or secondary, which involves the hypothalamus, pituitary or derived from illness or disease. A low serum testosterone (<300ng/dL) is suggestive, but not definitive of hypogonadism and measurements of luteinising (LH) and follicle stimulating hormone (FSH) is used to establish a primary or secondary diagnosis (Crawford & Kennedy, 2016). A worry trend is that despite striking increases of testosterone prescription a substantial amount (approximately 29% in this review) of patients often fail to have their levels checked prior to undertaking testosterone replacement therapy (TRT). (Corona G, Rastrelli, Maseroli, Sforza, & Maggi, 2015). Additionally only 45 % had their testosterone levels checked during or post TRT intervention.

Low testosterone and cardiovascular risk

Previous studies have highlighted an increase in all cause mortality associated with low testosterone levels in men (Araujo et al., 2011). Conditions that increase risk of mortality related to low testosterone are increased abdominal obesity, inflammatory biomarkers, dyslipidaemia, diabetes mellitus and metabolic syndrome. However the diagnosis of an isolated low testosterone level should be qualified by ruling out other potential diagnosis such as long-term illness, nutritional deficiencies and other endocrine issues such as subclinical or overt hypothyroidism.

Testosterone supplementation and risks

A number of studies and meta analysis have demonstrated a number of beneficial effects of TRT which extend to increased sexual satisfaction, muscle mass, strength mood and metabolic function (Corona G et al., 2015) (Gagliano-Jucá & Basaria, 2017). However the suggested risk to increased CV adverse events have appeared vague in many studies and previous extrapolations/anecdotes between men having increased levels of testosterone (and therefore increased cardiac risk) and females having less testosterone and more oestrogen were not just problematic but incorrect. Many studies have correlated low testosterone to low biomarkers of health and increased cardiovascular disease (Pastuszak, Kohn, Estis, & Lipshultz, 2017) (Kloner, Carson, Dobs, Kopecky, & Mohler, 2016).

TRT reductionism and treating symptoms

A comprehensive review of the data compiled by Oskui et al (Mesbah Oskui, P., French, W.J., Herring, 2013) described the major CV implications of TRT which can be observed below. The authors draw attention to previously conducted studies, that did not show any relationships between low levels of testosterone and CV risk and suggest that both the subfraction of testosterone (Total T compared to Free T) and method of analysis for CVD were inappropriate and therefore unreliable for inclusion. 

Cardiovascular analysis Studies Major findings Association between T and mortality 8 8/8 studies found relationship between low T and increased all cause and CV mortality. Type 2 DM 6 6/6 studies showed improved insulin sensitivity through HOMA-IR/HgA!c and improved blood glucose Cholesterol 3 2/3 studies found no change to LDL/HDL from TRT Markers of inflammation (primarily C reactive protein CRP) 8 4/8 studies found reduced CRP Intima media thickness 8 8/8 found an inverse relationship between low T and IMT

The above studies reviewed by the authors, established a link between low levels of testosterone and increases in mortality (all cause and CV), insulin sensitivity and increases in intima media thickness that are resolved by TRT. Yet markers for lipids and inflammation markers such as CRP are less convincing. Hypothyroidism is related to low testosterone and hypogonadic states mainly through hypothalamic-pituitary dysfunction. Treatment of hypothyroid and subclinical hypothyroid states also resolves low testosterone and hypogonadic states, decreases intima media thickness, improves insulin sensitivity and decreases lipid levels (Crawford & Kennedy, 2016), (Krassas, Poppe, & Glinoer, 2010),(Donnelly & White, 2000) (Gao, Zhang, Zhang, Yang, & Chen, 2013). Is TRT the correct therapy for many males, given a) the rapid increases in often undiagnosed and prescription and b) when hypogonadic states, that have similar (cardiac) manifestations and are improved beyond the effects of TRT, are resolved with thyroid hormone?

Another factor concerning reliability of the studies used in previous meta analysis is the size to determine true risk between CV adverse events and TRT (Onasanya et al., 2016). The authors suggesting that to achieve a two-sided p value of 0.05 and power of 80% some 17664 participants would need to study to clarify any relationship. Observational data conducted over 5 years suggested that control groups treated with testosterone in short term had a lower mortality (HR 0.88 95 % CI 0:84 - 0.93) than controls (Wallis et al., 2016). From the meta analysis and other studies discussed above both age (>65) and predisposition to existing disease states may indicate the likelihood of adverse CV events when treated with TRT.

Another draw back of meta-analysis is the inclusion of data and bias produced by pharmaceutical companies that may not be adequately reflected or assessed. Much like cardiovascular end point studies being scarce. Testosterone studies that are funded by financial interests are usually in place to validate the benefits of TRT and fail to evaluate CV adverse events as end points. The increased adequate sample size needed to validate the safety and efficacy of this treatment often increase cost and decrease profit margin over time. The many studies that have been conducted so far, show much smaller sample sizes and a wide range of TRT delivery and dosing.

In a recent case crossover analysis that is not included in any current meta analysis, Layton et al (Layton et al., 2018) found a unique association between testosterone injections and short term cardio (and cerebrovascular) events in older men. Increased associations with myocardial infarction and stroke, post testosterone injection showed odds ratio (OR) were increased for all outcomes, OR =1.45 (95%: CI 1.07, 1.98).

Summary

Testosterone replacement does appear to have many positive effects on a number of markers related to cardiovascular health which include sexual performance, increased muscle mass, metabolic health, physical performance and decreasing mortality in a younger population. However, despite the many benefits of TRT the use of this therapy may have significant risk in late onset hypogonadal states, in ages >65 years of age, those susceptible to conditions associated with erythrocytosis and an association with acute cardiac events exists. It remains essential to ensure that not only adequate analysis of hypogonadal states are present but to ascertain if low testosterone levels are merely a symptom of other endocrine disturbances, such as hypothyroidism which has striking similarities to low levels of testosterone.

Want some more free resources on hormones?

References:

1.Araujo, A. B., Dixon, J. M., Suarez, E. a, Murad, M. H., Guey, L. T., & Wittert, G. a. (2011). Clinical review: Endogenous testosterone and mortality in men: a systematic review and meta-analysis. The Journal of Clinical Endocrinology and Metabolism, 96(10), 3007–19. http://doi.org/10.1210/jc.2011-1137

2.Basaria, S., Davda, M. N., Travison, T. G., Ulloor, J., Singh, R., & Bhasin, S. (2013). Risk Factors Associated with Cardiovascular Events During Testosterone Administration in Older Men with Mobility Limitation. The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences, 68(2), 153–60. http://doi.org/10.1093/gerona/gls138

  1. Corona G, G., Rastrelli, G., Maseroli, E., Sforza, A., & Maggi, M. (2015). Testosterone Replacement Therapy and Cardiovascular Risk: A Review. The World Journal of Men’s Health, 33(3), 130–42. http://doi.org/10.5534/wjmh.2015.33.3.130

  2. Crawford, M., & Kennedy, L. (2016). Testosterone replacement therapy: role of pituitary and thyroid in diagnosis and treatment. Translational Andrology and Urology, 5(6), 850–858. http://doi.org/10.21037/tau.2016.09.01

  3. Donnelly, P., & White, C. (2000). Testicular dysfunction in men with primary hypothyroidism; Reversal of hypogonadotrophic hypogonadism with replacement thyroxine. Clinical Endocrinology, 52(2), 197–201. http://doi.org/10.1046/j.1365-2265.2000.00918.x

  4. Gagliano-Jucá, T., & Basaria, S. (2017). Trials of testosterone replacement reporting cardiovascular adverse events. Asian Journal of Andrology, 19(May), 1–7. http://doi.org/10.4103/aja.aja

  5. 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

  6. Kloner, R. A., Carson, C., Dobs, A., Kopecky, S., & Mohler, E. R. (2016). Testosterone and Cardiovascular Disease. Journal of the American College of Cardiology. http://doi.org/10.1016/j.jacc.2015.12.005

  7. Krassas, G. E., Poppe, K., & Glinoer, D. (2010). Thyroid Function and Human Reproductive Health. Endocrine Reviews, 31(5), 702–755. http://doi.org/10.1210/er.2009-0041

  8. Layton, J. B., Li, D., Meier, C. R., Sharpless, J. L., Stürmer, T., & Brookhart, M. A. (2018). Injection testosterone and adverse cardiovascular events: A case-crossover analysis. Clinical Endocrinology. http://doi.org/10.1111/cen.13574

  9. Mesbah Oskui, P., French, W.J., Herring, M. J. et al. (2013). Testosterone and the Cardiovascular System: A comprehensive Review of the Clinical Literature. Journal of the American Heart Association. http://doi.org/10.1161/JAHA.113.000272

  10. Onasanya, O., Iyer, G., Lucas, E., Lin, D., Singh, S., & Alexander, G. C. (2016). Association between exogenous testosterone and cardiovascular events: an overview of systematic reviews. The Lancet Diabetes and Endocrinology. http://doi.org/10.1016/S2213-8587(16)30215-7

  11. Pastuszak, A. W., Kohn, T. P., Estis, J., & Lipshultz, L. I. (2017). Low Plasma Testosterone Is Associated With Elevated Cardiovascular Disease Biomarkers. The Journal of Sexual Medicine, 14(9), 1095–1103. http://doi.org/10.1016/j.jsxm.2017.06.015

  12. Roos, A., Bakker, S. J. L., Links, T. P., Gans, R. O. B., & Wolffenbuttel, B. H. R. (2007). Thyroid function is associated with components of the metabolic syndrome in euthyroid subjects. The Journal of Clinical Endocrinology and Metabolism, 92(2), 491–6. http://doi.org/10.1210/jc.2006-1718

  13. 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

  14. Wallis, C. J. D., Lo, K., Lee, Y., Krakowsky, Y., Garbens, A., Satkunasivam, R., … Nam, R. K. (2016). Survival and cardiovascular events in men treated with testosterone replacement therapy: an intention-to-treat observational cohort study. The Lancet. Diabetes & Endocrinology, 4(6), 498–506. http://doi.org/10.1016/S2213-8587(16)00112-1

  15. Xu, L., Freeman, G., Cowling, B. J., & Schooling, C. M. (2013). Testosterone therapy and cardiovascular events among men: A systematic review and meta-analysis of placebo-controlled randomized trials. BMC Medicine, 11(1). http://doi.org/10.1186/1741-7015-11-108

 

Scar tissue - is it an issue?

Is scar tissue really an issue? Alongside myself, scars may be one of the most under appreciated and neglected structures, when it comes to assessing aspects of an individual's pain and movement limitations.   For many people, which include physicians, surgeons and often the owners of said scars, there’s an acceptance that the scar has healed and is not involved in any process of pain, strength or movement dysfunction. Dr’s and surgeons often assume that time enables optimal healing and patients simply forget about the previous trauma. Time may be a great healer but the healing is only partial - the nervous system always remembers. Writing this, reminds me of a client who had filled in all historical injury and trauma that he had experienced on my intake forms, which might have been a factor in his chronic back pain. It wasn’t until he took his top off and under questioning revealed that he had  donated his kidney to his brother some twenty years ago. It wasn't a big deal though as it was twenty years ago apparently.

This sequence of events has been summarised as homeostatic, inflammation, granulation and remodelling phases (1) which are undergoing symbiotic relationships with other structures and dependant on energetic, endocrine and other functions of the individual, which often depend on environmental stimulus. During the granulation and proliferation phase, sub-phases, which include collagen deposition, remodelling of blood vessels and tissues occur. It’s likely that during these phases the health and energetic response of the individual will dictate the capacity to regenerate and may also influence the layers of dysfunction that are present with scar tissue.

“ In childhood, wounds heal quickly and inflammation is resolved, in extreme age, or during extreme stress or starvation, wound healing is much slower and the nature of inflammation and would closure is different. “Ray Peat.

Unsaturated vegetable fats, serotonin and estrogen promote collagen synthesis and resulting fibrosis and keloid scars are associated with these states (3). Perhaps the capacity to organise energy and regenerate are instrumental in decreasing the associated dysfunctions that can be found in all scar tissue? Most Drs that I have spoken to just assume that after 12 weeks the scar has generally healed and that normally activity can be resumed. As a rule, there is no thought given to mechanical, pain sensitising or emotional constraints induced by the presence of the scar. It’s generally accepted that most scars have 80% tensile strength of the previous structure, but again might that too be a product of the quality of healing available to the individual?

“ The amount of disorganised fibrous material formed in injured tissue is variable and depends on state of the individual and tissue situation. “

In hypothyroidism, high levels of the pituitary hormone TSH (thyroid stimulating hormone) are known to stimulate fibrosis (1) Maintaining adequate thyroid hormone production promotes DNA transcription, optimal energy production, carbon dioxide production and probably decreases the proliferative effects of 'estrogenic' states that can be attributed to keloid scar formation.

The bigger the scar, the more likely the associated dysfunction? Perhaps the more disorganised tissue that exists, the increased likelihood of fuzziness between the central nervous system and output to structures associated with that scar. In scar tissue that has not been assessed or treated, it's relatively easy to induce weakness or stress to the surrounding tissues by a variety of stimulus which might include thinking and different types of pain,  touch or vectors of stretch that create neurological chaos or threat to to the individual.

Good therapy should allow for conversations between the clinician and patient that create stimulus that may (or may not) affect the output of surrounding structures associated with the scar. Poor feedback mediated by the scar might involve the following:

Emotional: Aspects of recall of the event that the individual finds upsetting.

Nociception/pain: First and second pain, visual or auditory, crude/fine touch, tickle/itch temperature, stress or recall od suffering responses to stimulus. (Involve pain feedback related to spinothalamic, spinotectal, spinohypothalamic and spinomesencephalic tracts)

Mechanical: Pressure, rebound, stretch, joint mechanoreceptors and other responses to tissue and structures. (Related to Golgi, Pacini, Ruffini and other dorsal column feedback pathways.)

Improving the optimal healing of scar tissue might involve aspects such as adequate carbohydrate, proteins, sunlight (or red light), carbon dioxide, thyroid, progesterone, vitamin A and E. Avoiding phytoestrogens and low carbohydrate diets would also be prudent.

Despite optimised nutrition and endocrine function, it’s likely that many scars leave some artefact that prevents the nervous system communicating with tissues. C - sections, episiotomies, appendectomies, laparoscopies and most surgeries, injuries or trauma leave a trace that needs to be resolved with the right therapy. Inhibition can be purposeful but restoration might need a little nudge from therapies like proprioceptive deep tendon reflex (P-DTR).

References:

  1. Kim, D., Kim, W., Joo, S. K., Bae, J. M., Kim, J. H., & Ahmed, A. (2018). Subclinical Hypothyroidism and Low-Normal Thyroid Function Are Associated With Nonalcoholic Steatohepatitis and Fibrosis. Clinical Gastroenterology and Hepatology, 16(1), 123–131.e1. http://doi.org/10.1016/j.cgh.2017.08.014

  2. https://emedicine.medscape.com/article/1298129-overview?pa=1ZDxXAnEOeNV9BUnYezdYpt49YJzASbxEvvw80YIDjlelzZDQj3XLvbI0V2MbTq%2FX8MwC0EECwzp432Skuf9qw%3D%3D

  3. http://raypeat.com/articles/articles/regeneration-degeneration.shtml

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

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 triphosphate (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.

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

Osteoporosis- could your exercise, nutrition and medical advice be better?

Deer eating human ribs

Deer eating human ribs

Osteoporosis and bone health, like many other aspects of optimal biology is a product of an organisms inputs and reactions to environmental stimulus. Osteoporosis is a condition like others, where prevention is often easier than the cure but perhaps the cure has been overcomplicated? Osteoporosis is a multifactorial musculoskeletal disease that is usually associated with the ageing process, decreased bone mineral density (BMD) and its tendency to fracture easily.       It’s clear that a number of factors that can be maintained throughout life to reduce the incidence of Osteoporosis in both men and women. Before we review those and compare with current guidelines, here’s some background info on the subject.

Primary Osteoporosis is the age related decline in men at around 70 and suggested as being a postmenopausal state, induced through the decreased production of estrogen in females. This last point is accepted in medical literature as the main cause of osteoporosis in females but may be severely flawed (more on this point later).

Secondary osteoporosis can be related to the following factors

Hypogonadism - testosterone/estrogen deficiency

Endocrine disease - Cushing’s syndrome, acromegaly, thyrotoxicosis, Addison’s disease and hyperparathyroidism

Dietary or assimilation deficiencies of calcium, vitamin K, vitamin D and other nutrients

Inflammation-rheumatoid arthritis, systemic lupus and ankylosing spondylitis

Neoplasms- Myleoma, lymphoma and leukaemia

Reduced physical activity

Medical drugs - corticosteroids, antiretroviral, antipsychotic, chemotherapy, hormone therapy, nicotine and excessive alcohol

Family history/genetics

Diabetes

The financial burden from osteoporosis generally, will increase from 98 Million Euros to 121 billion with proportional increases of 27.5 million to approximately 34 million people between the years 2010 to 2025 (Hernlund et al., 2013). Despite these huge burdens there appears to be a lack of well-designed educational programs that are geared at prevention of osteoporosis through non-pharmacological means.

The supplementation of vitamin D and calcium are well documented in osteoporosis strategies but a strategy to avoid these states are diets containing adequate calcium, vitamin A, K, magnesium (and others) adequate sunlight and moderate exercise.

Ok, so there’s a problem, it’s big business and there’s a lot of great info on how to avoid it right? Well no and here are the major points why I believe its not.

Diagnosis

Dual energy X-ray absorptiometry (DEXA) is the recommended choice for osteoporosis diagnosis, serum calcium, phosphate, creatinine (with GFR) alkaline phosphatase, liver function, 25 OHD, total testosterone, estrogen CBC and 24 urinary calcium excretion are recommended for the interpretation of secondary causes of osteoporosis (Watts et al., 2012).

Hormones

Estrogen loss is touted as the most significant factor in decreasing BMD yet it’s action only retards resorption, or the removal of calcium from bone. Estrogen tends to inhibit the action of osteoclasts which ultimately reduce BMD. It’s the main reason the introduction of hormone replacement therapy (HRT) was considered as the primary treatment until its long-term use was found to induce clotting and cancer in women. So estrogen does not reverse Osteoporosis, it prevents further bone loss.

A variety of studies have suggested little influence of testosterone in males on BMD and that low estradiol levels combined with elevated sex hormone binding globulin appear to increase the loss of BMD (Cauley et al., 2010). A point worth noting from the correlation associated with higher estradiol levels and decreased BMD loss is that all participants in the study were recorded as having increased weight and BMD, which may influence skeletal modelling due to increased bone-loading parameters. Perhaps too much emphasis has been given to the suggestion that estrogen and its primary role of tissue proliferation amongst others, which should follow the course of age related decline?

Progesterone on the other hand has been shown to be a bone trophic or building factor that increases mineralisation of BMD, via osteoblasts (Prior, 1990). Stress increases cortisol and decreases progesterone binding at the receptor, with a preference for the glucocorticoid. Ray Peat (1997) points out that cortisol causes bone loss and its widely accepted that progesterone has an “antiglucocorticoid” action, it is reasonable to think that progesterone should protect against bone loss, and that it is a progesterone deficiency after menopause which is a major factor in the development of osteoporosis.

Thyrotoxicosis has been suggested as a mechanism of bone resorption but this appears inaccurate-  Ray Peat does a much better job at explaining this.

Medical treatment

Bisphosphonates are the first line medical treatment for treating osteoporosis and show modest changes to hip and vertebral BMD over 3 years. There use may come at a risk. Gastro intestinal side effects are well documented and in some the increase of osteonecrosis of the jaw has been observed. In some, the long-term use has been shown not only to increase the rate of fragility fracture but also to inhibit the healing process. It should be noted that adequate calcium and vitamin D in the diet are essential for bisphosphonate effectiveness

Nutrition

There tend to be two well-known stances to the fitness industries approach to nutrition. One, the transformation approach, where limiting of nutrients, particularly dairy and carbohydrates and intermittent fasting are the norm. Another, the holistic warrior whose consumption of chia seeds and all things green, raw and limiting of dairy and sugar again,  may be a factor into lowering BMD in later life. Calcium is an essential nutrient for bone health and dairy is indeed a great source of calcium. Here’s an old blog on the subject.

Despite the mis information, dairy is healthy, protective against the ageing and osteoporotic state.

Despite the mis information, dairy is healthy, protective against the ageing and osteoporotic state.

It’s clear that adequate vitamin D is a nutrient that is important in BMD maintenance. It regulates calcium levels, decreases the production of parathyroid hormone, which is a potent resorption factor of skeletal calcium when calcium or vitamin D are low. Here are the main points that relate to diet.

  • Vitamin D in isolation and particularly high doses increases fracture rates (Janssen, Samson, & Verhaar, 2002)

  • Unless vitamin D is accompanied by adequate calcium, BMD can decrease further.

  • Vitamin K2 can prevent the calcification of soft tissues and help improve blood calcium levels (Masterjohn, 2007)

  • High meat and diets high in pulses and beans can have a negative effect on calcium levels due to their high phosphate levels.

  • Unless you assess other key nutrients like magnesium and the factors discussed above

  • Low diary intake can be associated with poor bone health.

  • The low carbohydrate, raw green and seed eating diet suggested by holistic health practitioners may contribute to lower BMD.

Exercise

Regular exercise has been touted as a significant factor in maintaining muscle mass and increasing BMD. But is the type of exercise that people are doing, increasingly in their younger years, contributing to better or worse outcomes to BMD. For bone to form adequate carbon dioxide (CO2 ) is essential. Some exercise regimes are so challenging, they contribute to excess levels of metabolic acidosis (lactic acid) and passing of CO2 from the body (worth noting that sugar consumption can also help to increase CO2 production) . Perhaps for exercise to be effective it should be light to moderate, with adequate rest periods that don’t mean that the participant is lying in a pool their sweat and vomit.

Walking, strength training with adequate rest, yoga, Pilates and other modes of moderate exercise appear most suitable for modest improvements to bone health but the diet and hormone factors are key.

It’s clear that osteoporosis is in the rise but it can be reversed. But instead of heading advice like cutting out dairy, eating lots of uncooked vegetables and training to complete exhaustion. There are more suitable mechanisms for improving bone health

References:

Cauley, J. A., Ewing, S. K., Taylor, B. C., Fink, H. A., Ensrud, K. E., Bauer, D. C., … Orwoll, E. S. (2010). Sex steroid hormones in older men: longitudinal associations with 4.5-year change in hip bone mineral density--the osteoporotic fractures in men study. The Journal of Clinical Endocrinology and Metabolism, 95(9), 4314–23. http://doi.org/10.1210/jc.2009-2635

Hernlund, E., Svedbom, a, Ivergård, M., Compston, J., Cooper, C., Stenmark, J., … Kanis, J. a. (2013). Osteoporosis in the European Union: medical management, epidemiology and economic burden. Archives of Osteoporosis, 8(1–2), 136. http://doi.org/10.1007/s11657-013-0136-1

Janssen, H. C. J. P., Samson, M. M., & Verhaar, H. J. J. (2002). Vitamin D deficiency, muscle function, and falls in elderly people. The American Journal of Clinical Nutrition, 75(4), 611–5. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/11916748

Masterjohn, C. (2007). Vitamin D toxicity redefined: Vitamin K and the molecular mechanism. Medical Hypotheses, 68(5), 1026–1034. http://doi.org/10.1016/j.mehy.2006.09.051

Peat, R. (1999). Thyroid Therapies, Confusion and Fraud. Retrieved from www.raypeat.com/articles/articles/thyroid.shtml

Prior, J. C. (1990). Progesterone as a bone-trophic hormone. Endocrine Reviews, 11(2), 386–398. http://doi.org/10.1210/edrv-11-2-386

Watts, N. B., Adler, R. A., Bilezikian, J. P., Drake, M. T., Eastell, R., Orwoll, E. S., & Finkelstein, J. S. (2012). Osteoporosis in men: an Endocrine Society clinical practice guideline. The Journal of Clinical Endocrinology and Metabolism, 97(6), 1802–1822. http://doi.org/10.1210/jc.2011-3045

Estrogen and Progesterone

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

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

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

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

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

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

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

CYCLEovul

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

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

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

·      Increased body fat

·      Salt/ fluid retention

·      Clotting

·      Depression

·      Headaches

·      Decreased libido

·      Impairment of blood sugar

·      Reduced oxygen

·      Risk of breast cancer

·      Osteoporosis

·      Decreased thyroid

·      Increases CV issues.

·      Anti tumour effects·      Supportive to fertility

·      Sedative effects

·      Improves blood sugar

·     Decreases  Ovarian cysts

·      and Menopausal flushing

·      Removal of facial hair

·      Decreased Menstrual cramping

·      Improved auto-immune

·      Hormonal balance

·      Anti -Stress

·     Decreased arthritis

·      Promotes sleep

·      Thickens hair on head

 

 

 

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

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

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

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

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

References:

Dalton, K The Menstrual Cycle.

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

Peat, R. Nutrition for Women.

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

Online references:

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

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

 

 

Calcium- Don't ditch the dairy.

Calcium - don’t ditch the dairy. Like every nutrient that we have consumed over the last millennia or ten, there are reasons why some foods appear more beneficial than others. Using poor tests like Igg4 sensitivity/allergy analysis many ‘experts’ have convinced us that one of our most potent foods is causing us more harm than good. I am on the bandwagon that as far as my food goes (meat and dairy) grass fed, free range and organic remain a better choice for all concerned. Hormesis can only take us so far when it comes to pesticide and pollutant exposure and the individuality of tolerance and adaptation remains a knife-edge for many.

Don't ditch the dairy

Without getting into the arguments of which type of cows produce what compounds. This topic is merely aimed at why people have issues with calcium uptake and is the problem really a dairy issue?

Many people who have had blood tests are often told to take extra calcium supplements in response to presenting with low serum calcium. However the issue of lowered calcium in the blood may have nothing to do with the amount of calcium that they are ingesting. Here are some potential mechanisms:

• Low levels of vitamin D: Vitamin D is a well-known nutrient/hormone like substance that allows for the adequate uptake of calcium into bones and teeth. amongst many other functions which include immune system function. (This synergistic relationship can be observed in reverse also) • High phosphorus/phosphate diet. In addition to the added phosphates to foods and crops. Current recommendations suggest increasing portions of grains, beans and peas, which not only contain phosphates but also contain phytates, which can block mineral uptake. Low magnesium is also an issue. • Increased estrogens and xenoestrogens that increase the stress response and cause calcium to leach from the bones into soft tissues. A decrease in available progesterone can decrease bone density. • Poor reabsorption factors such as low intake of vitamin K2 • An actual calcium deficiency from low calcium intake • Excessive exercise which can be due to inadequate calcium and poor carbon dioxide retention. • Inability to absorb calcium from the digestive tract, low stomach acid levels/hypochlorhydria and damage to villi/intestinal lining, which can be observed in celiac but increasingly with intestinal hyper-permeability, endotoxin and chemical induced damage. • Decreased blood albumin levels which bind calcium. Digestion and dehydration issues mainly. • Regulation of PTH or parathyroid hormone.

Osteoporosis is on the rise but its increasing prevalence is not due to low calcium intakes but due to many complex interactions, between stress, pollutants, low sunlight exposure, excessive exercise and nutrient levels. The common reductionist approach is to throw the same nutrient at the problem in larger amounts and hope that this so called ‘deficiency’ is corrected.

It's worth noting that elevated serotonin levels in the blood are responsible for bone less. An increase in serotonin  can be viewed with both a temporary spasticity of smooth muscles tissues and loose or watery stools. The role of serotonin is to increase evacuation of the bowel, mediated by an increase in its production from the entero chromaffin cells in the digestive tract, where some 95% of the bodies own supply is created. A diet high in nuts and seeds, which contain serotonin are likely to irritate the digestive tract. From an evolutionary survival perspective, this allows for seeds to be passed out from the bowel without being digested, ensuring plants survival. Increased aggression and irritability have been noted in elevated serotonin levels, which also correlates with a decrease in bone density. Ensuring adequate calcium in the diet during these times is therefore essential.

When phosphorus increases and there is a lack of vitamin D, PTH increases to balance out the need for increased calcium, which is taken from bones and teeth. In essence much of the calcification of arteries and soft tissues can be attributed to this situation. Some of the signs that can be observed with low calcium levels are:

• Muscle cramps • Nose bleeds • Soft fingernails • Frequent cold sores, rashes • High or low blood pressure • Irritability • Fevers with mild colds

Administering calcium supplements to those with calcium deficiency is much like talking over someone before they have a chance to speak. You only here there initial words but fail to here what they are truly saying.

Much of the marketing and sales of supplements these days are suggestive that our food does not give us the nutrients that we need and that we need to stay plugged in to the rattle of supplement bottles opening daily. When in fact if we just strive to improve digestion and cofactor optimisation this simply isn’t the case. In the case of dairy, when we flippantly talk about super foods, when you look at the nutrients provided from dairy, it is indeed a food with plenty to say for itself, particularly in the situations of growth, stability and anti-stress.

References:

1. Christodoulou, S. , Goula, T., Ververidis, A., and Drosos, G. Vitamin D and Bone Disease. Volume 2013 (2013), Article ID 396541, http://dx.doi.org/10.1155/2013/396541 2. Weatherby, D. Blood Chemistry Analysis. Bear Mountain Publishing. 2002.

Online:

http://raypeat.com/articles/articles/phosphate-activation-aging.shtml

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.