energy

Fasting and calorific restriction- Increased longevity or just a slower death?

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Intermittent fasting and calorific restriction (CR) seem to be the Zeitgeist of today’s nutrition and wellness sphere and has comparisons with the raw green sludge breakfast smoothie and these approaches to health. CR is often being touted as health enhancing because of a premise that sounds something like this. You fast or eat less than X calories and that has the capacity to slow down metabolism, ensuring that you produce less oxidative stress, autophagy ensues, and this opens up your 8th chakra ready for your beyond meat whopper. It’s true that fasting and CR can probably enhance your health when you are prone to over eating, and beyond that nothing else. Yes you will lose weight (seen as that’s the only variable that many people care about these days), but that result is down to one key fact. You are in a calorie deficit. Can you rebound from that restriction is the question that most need to evaluate.

CR and fasting promotes improvements to health and extending lifespan but the main reasons that it promotes longevity is probably for several reasons that include.

1. The restriction of polyunsaturated fats or PUFA.

2. The restriction of methionine, cysteine and sometimes tryptophan.

3. Perhaps less consumption of pesticides and metals.

The question of do you need to fast, should be rephrased with do you even need to fast? What about addressing what can extend lifespan and still maintain an optimal level of metabolism?

PUFA and mitochondrial uncoupling

Let’s start with PUFA which are commonly known as vegetable, seed, fish, soy and other oils, including olive oil (which is the better of the lot and when used cold has some useful qualities). The other oils share similarities, as they are all unstable especially so when heated. The most unstable oils in general use and over recommended are the omega 3’s particularly DHA and EPA. I’ve recently seen so called holistic practitioners recommending in excess of 6 grams of DHA to improve anti-inflammatory responses and so-called membrane fluidity. One of the key problems with this approach is that increased DHA levels are known to occur in the obese and diabetics (Madison Sullivan et al., 2018) and this increase is associated with reduced mitochondrial enzymes (metabolic enhancers).

 

PUFAs like DHA are often touted as protective because they induce a process called mitochondrial uncoupling. This can occur when your’e cold, when you don’t produce enough thyroid hormone and other stressors. It can indeed be protective but DHA for example creates something called proton leak within the cells, and decreases the efficiency of the cell. Oxygen efficiency is lost and production of energy or adenosine triphosphate (ATP) is also wasteful. This sits well with many who promote theoretical mechanisms of longevity such as the rate of living theory (Speakman et al., 2004) (Vaanholt, Daan, Schubert, & Visser, 2009) and the membrane pacemaker theory (Hulbert, 2007; Hulbert, Kelly, & Abbott, 2014). A. J Hulbert is a well-respected thyroid researcher who completed a large body of work on the role of thyroid hormones and fatty acids and their role in ‘membrane fluidity’. Interestingly Hulbert proposes that mammals and birds with a high metabolic rate (much like Elie Metchnikoff’s theories that link low gut bacteria with metabolism in birds, mammals and longevity) and increased longevity often have this key feature in common. They generally have low saturation of PUFAs as determined by something called the peroxidation index (PI). Conversely animals with high PUFA and PI have decreased longevity, but the membrane pacemaker theory postulates it as high metabolic rate, inducing uncoupling and characterized by increased reaction oxygen species (ROS) and the production of superoxide and superoxide dismutase (SOD).

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“There’s an inverse relationship between the peroxidation index of skeletal muscle phospholipids and maximum lifespan of mammal and bird species of different sizes.” A.J.Hulbert

 

 This forms a major component of the rate of living theory or that increased metabolism generates ROS ergo slowing metabolism down, produces less ROS and that’s productive. Although it’s not and this is where many people get confused about efficient thyroid function, enhanced metabolism and potential oxidative stress. I was reminded by a Ray Peat Newsletter earlier on the year how SOD remains elevated throughout the lifespan of those with Down syndrome and that serotonin increases SOD, contributing to decreased longevity. With excess PUFA consumption and tissue saturation, SOD increases as does uncoupling, lipid peroxidation and high levels of malondialdehyde (MDA) are observed with excess lipid peroxidation (Chen & Li, 2016). SOD can be counteracted by glutathione (SOD/G ratio) but this diminishes over time. This enhances the reductive state and perpetuates the gain of electrons, which are a hallmark of damaged physiology and shift efficient energy production away from oxidative metabolism of glucose and metabolic inflexibility.

 

PUFA, like DHA does initiate mitochondrial uncoupling but it’s inefficient and increases SOD degrading aerobic metabolism, which comes at a cost to lifespan. Hulbert notes that a 24% decrease in PI, is associated with doubling of lifespan and that calorific restriction alters the acyl composition of the cell membrane. Why?  Because PUFA are removed from the cell membrane to be used as fuel. Again this can be problematic if you persistently use unsaturated fatty acids as fuel. Not to mention that refeeding fasted subjects and those on a ketogenic diet are well known to depress thyroid hormone responsiveness, thyroid hormone receptors and glucose tolerance(Boelen, Wiersinga, & Fliers, 2008)(Garbow et al., 2011)(Kose, Guzel, Demir, & Arslan, 2017). Yes there are indeed many short-term studies showing positive changes from CR and ketogenic dieting. If one can benefit from these modalities great but if not metabolically flexible, it isn’t always going to be as fruitful as you think. It’s often these interactions that muddy the water between carbohydrate restriction and beneficial results. Hint, it’s never usually the carbohydrate, and if you’ve been prone to over eating, then that calorie deficit is always going to show a temporary positive effect.

If you’re someone that has tried many different interventions for improved health or even body composition and failed to get the results that you need, then the body requires a level playing field of energy and nutrients to create balance. Further stress from skipping meals, long hours without eating and failure to meet metabolic demands are some of the reasons why many develop metabolic inflexibility. The more stressed your physiology, the more prone it is to activating stress pathways and suppressing thyroid hormone, decreasing insulin responses and creating inflammation. More often than not those with tis existing inflexibility may not benefit from increased fatty acid oxidation mediated by a lack of available glucose.

Thyroid, PUFA and membrane composition and fluidity

My understanding of the so-called membrane, membrane pump theory and even membrane fluidity is certainly not of an expert but If I’m wrong here, I’m certainly willing to throw my hands up on in the air and say – I told you I wasn’t an expert.  I am reasonably sure of the interactions of thyroid hormone, its generality, it’s actions, organizational qualities and much like the theories of low serotonin, low estrogen, high cholesterol treated by statins, and that glyphosphate is a safe and friendly compound, that people with vested interests promote otherwise. I’m not going to go into the complexities of Gilbert Ling’s work (Gilbert N. Ling, 1965 1997, 2014) I’d be lying if I said I truly understand it but my attempt to summarize such a vast body of work.

The membrane pump theory has been a widely accepted unproven theory that appears on paper, to be unable energetically to support and each pump requiring unaccountable levels of ATP. Ling’s work suggests that membrane interactions are largely supported by organised or structured water interfaces and that there is no cellular membrane to speak of. Thyroid hormone, proteins and cholesterol are other integral components of this interface.

It’s always contentious when someone ends up disproving a theory that’s widely accepted without being proven.

Does it make sense that during fasting, these essential PUFA’s are depleted from this so-called membrane and replaced with cholesterol? Can they really be that essential? Thyroid hormones have been shown to modify this “membrane permeability”, cooperatively influencing behavior of enzymes and can penetrate the phospholipid bilayers  (Issé, Yunes Quartino, Fidelio, & Farías, 2013). Triiodothyronine or T3 appears similar to cholesterol’s action, increasing fluidity in ordered gel phases and decreasing in liquid crystalline states of phospholipids. I’m guessing that alterations in structured water through positive/ negative charges, and interactions between organisational qualities of thyroid hormones and cholesterol could be the ideal interface. This may explain why in hypothyroidism the so-called membrane, becomes more disorganised, less gel like and more abundant in PUFA (PUFAs degrade cholesterol).

 Restriction of PUFA, methionine and other agents which reduce biology need to be compared with so called decreased rate of living theories to ascertain what really increases longevity. If we keep looking at theories that promote decreased function instead of maintaining and improving order. The end result may be decreased lifespan and a slow death of cellular function.

 

References:

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

Chen, Y., & Li, P. (2016). Fatty acid metabolism and cancer development. Science Bulletin, 61(19), 1473–1479. https://doi.org/10.1007/S11434-016-1129-4

Garbow, J. R., Doherty, J. M., Schugar, R. C., Travers, S., Weber, M. L., Wentz, A. E., … Crawford, P. A. (2011). Hepatic steatosis, inflammation, and ER stress in mice maintained long term on a very low-carbohydrate ketogenic diet. American Journal of Physiology - Gastrointestinal and Liver Physiology. https://doi.org/10.1152/ajpgi.00539.2010

Hulbert, A. J. (2007). Membrane fatty acids as pacemakers of animal metabolism. In Lipids. https://doi.org/10.1007/s11745-007-3058-0

Hulbert, A. J., Kelly, M. A., & Abbott, S. K. (2014). Polyunsaturated fats, membrane lipids and animal longevity. Journal of Comparative Physiology B: Biochemical, Systemic, and Environmental Physiology. https://doi.org/10.1007/s00360-013-0786-8

Issé, B. A., Yunes Quartino, P., Fidelio, G. D., & Farías, R. N. (2013). Thyroid hormones-membrane interaction: Reversible association of hormones with organized phospholipids with changes in fluidity and dipole potential. Chemistry and Physics of Lipids. https://doi.org/10.1016/j.chemphyslip.2013.08.007

Kose, E., Guzel, O., Demir, K., & Arslan, N. (2017). Changes of thyroid hormonal status in patients receiving ketogenic diet due to intractable epilepsy. Journal of Pediatric Endocrinology and Metabolism. https://doi.org/10.1515/jpem-2016-0281

Ling, Gilbert N. (1997). Debunking the Alleged Resurrection of the Sodium Pump Hypothesis. Physiological Chemistry and Physics and Medical NMR.

Ling, Gilbert N. (2014). Canwe see living structure in a cell? Physiological Chemistry and Physics and Medical NMR.

Ling, Gilbert Ning. (1965). THE PHYSICAL STATE OF WATER IN LIVING CELL AND MODEL SYSTEMS. Annals of the New York Academy of Sciences. https://doi.org/10.1111/j.1749-6632.1965.tb45406.x

Madison Sullivan, E., Pennington, E. R., Sparagna, G. C., Torres, M. J., Darrell Neufer, P., Harris, M., … Shaikh, S. R. (2018). Docosahexaenoic acid lowers cardiac mitochondrial enzyme activity by replacing linoleic acid in the phospholipidome. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.M117.812834

Speakman, J. R., Talbot, D. A., Selman, C., Snart, S., McLaren, J. S., Redman, P., … Brand, M. D. (2004). Uncoupled and surviving: Individual mice with high metabolism have greater mitochondrial uncoupling and live longer. Aging Cell. https://doi.org/10.1111/j.1474-9728.2004.00097.x

Vaanholt, L. M., Daan, S., Schubert, K. A., & Visser, G. H. (2009). Metabolism and Aging: Effects of Cold Exposure on Metabolic Rate, Body Composition, and Longevity in Mice. Physiological and Biochemical Zoology. https://doi.org/10.1086/589727

http://raypeat.com/articles/

http://www.gilbertling.org/

 

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.

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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.

 

Why fruit juice won’t give you cancer.

But it can protect you against it.

But it can protect you against it.

You may have noticed the carbohydrate fearing headline stating that - "One small glass of juice a day raises cancer risk, " yesterday. Do you know when you’ve been tangoed?

This is based upon the study by Chazelas et al (Chazelas et al 2019) and being used to justify the swathe of dogmatic headlines in the press.Apart from the study being based on food questionnaires (mean food log was 5.6 days over 5 years hardly conclusive) which are not reliable indicators of actual consumption, the authors suggest that the mechanisms that might drive the association are as follows.

1.    Excessive sugar consumption could contribute to obesity driven mechanisms. There's no doubt that excess carbohydrate, fat and protein contribute to obesity when an EXCESS of calories are consumed (and the other multifactorial issues associated with obesity.

2.    Sugar from juice contributes to increased glycaemic load and inflammation. This point doesn't add up because many fruit juices have a low glycaemic load, associated with anti- inflammatory responses (polyphenols, vitamin c, capacity to lower endotoxins, improve blood sugar regulation and cholesterol levels). Many grains have higher glycaemic loads and index than juices. So is this really a valid argument?

Of the 101, 000 or so participants the increased risk associated with sugary drinks was found in those who exercised less. In an important factor, if you combine over consumption and decreased activity. Another point that the authors suggest on sugary drinks is that additives to sweetened beverages like sodas could also contribute to risk. Indeed a valid point.

It starts with a hint of truth and a headline or meme tends to become written in folklore, the myth of the carbohydrate rich food churning out death in its path. These small, half or even quarter truths often disappear when you scratch beneath the surface. That’s why I actively encourage carbohydrate and specifically carbohydrate consumption in my programs. Even most people I have met rarely chug down large amounts of fruit juices in isolation and even if glycemic index\load were an issue, when you consume carbohydrate rich foods with proteins and fats, these concepts are somewhat irrelevant.

Orange juice (or any juices) is one of those foods that still seems to be getting a bad rap but many people who demean its nature often fail to look at the studies that have shown it to be protective. You might have heard...but the sugar levels or but it’s acidic. Just take a look at the tabloid’s permanent vilification of the simple juice drink, which is based on half-truths of small increased risk with limited data. To play devil’s advocate, there’s no doubting that some people with less money available have been seduced into purchasing more junk food. It’s cheap, it’s filling and it’s full of sugar, vegetable oils, preservatives, GMOs, fillers, emulsifiers, additives like flavouring, enhancers, gums and much more. Yet still, the sugar is the demon in this list. Not even the pollution that’s shown to increase cancer, heart diseases, diabetes and neurodegenerative diseases, it’s still sugar and even if you drink fruit juice, it’s the sugar that will kill you.

So, with that in mind let’s consider what a simple food like orange juice could do to hasten, I’m sorry I meant prevent neurological and metabolic decline. Let’s first add some context. It should be no surprise that if you just drink large amounts of juice on their own, without balancing their ability to enter the blood stream with fats and or proteins, it isn’t going to be as beneficial. This is also why throwing large amounts of sweetened fizzy drinks down one’s neck can be problematic. The Glycemic index becomes redundant when you add another food into the mix, therefore drinking fruit juices with fats and proteins helps to normalise blood sugar responses in isolation. So why orange juice? Here are just a couple of reasons

Orange juice decreases inflammation

Eating a variety of foods has the capacity to increase inflammatory and damaging agents like endotoxin. Endotoxin or lipopolysaccharides is well known to increase in high fat and carbohydrate meals, especially so when fibrous poorly digested foods are consumed. High fat diets also induce endotoxin, and this is well known to induce intestinal hyperpermeability or the more well-known leaky gut syndrome. Consumption of orange juice appears to significantly reduce the levels and effects of inflammation induced by endotoxin (Ghanim et al., 2010) . Unfortunately, many foods are often kept stable longer with additives like carrageenan and gums, which also promote increased endotoxin.

Orange juice attenuates metabolic dysfunction

 “ Despite media concern, daily orange juice consumption did not result in adverse metabolic effects, despite providing additional dietary sugars. Data from epidemiological and in vitro studies suggest that orange juice (OJ) may have a positive impact on lipid metabolism. “ (Simpson, Mendis, & Macdonald, 2016)

During times of stress, under eating or consuming foods low in carbohydrates the response is to liberate energy from stored fats in the form of triglycerides. As metabolism becomes compromised high levels of triglycerides are known to be present in blood sugar dysregulation. There’s much in the press to suggest that sugar from fruit juice consumption increases cardiac risk but there are many studies that suggest otherwise, with the observed effect being reduced triglycerides and cholesterol (Aptekmann & Cesar, 2013). The cardiac protective factors aren’t limited to orange juice alone, pomegranate and other juices also seem to offer similar results (Moazzen & Alizadeh, 2017)

Orange juice decreases carcinogen production

A very relevant and protective mechanism of orange juice (and others) and fruit peel consumption is the decreased risk of gastrointestinal cancers (Xu, Song, & Reed, 1993). Nitrates and nitrates are naturally occurring compounds found in a variety of foods. Nitrates are often used in preservatives and sodium nitrites are ubiquitous in preserved meats and have a significant relationship between cancers in many of the mucosal areas including the mouth, bowel and lungs.. Nitrates have been implicated in not just intestinal and stomach cancers but increasingly thyroid cancers (Hernández- Ramírez et al., 2009). This occurs through increases in N-nitroso compounds (NOC) which increase the capacity of cell mutation but there are extensive studies that show many classes of NOC inhibitors which include vitamin e and vitamin C that negate that risk.

Of course, for optimal effects, ensuring adequate protein and fats are consumed will always be beneficial. We’ve known that compromised blood sugar and insulin responses are rarely to do with consuming carbohydrates. Unless excessive eating and obesity are the association, there’s plenty more relevant relationships such as environmental pollutants and other stressors that show a clear effect on all aspects of metabolism and increased metabolic disease. Yet many people seem intent on shooting the messenger and vilifying protective carbohydrates such as fruit juice.

 

References: 

 1.    Aptekmann, N. P., & Cesar, T. B. (2013). Long-term orange juice consumption is associated with low LDL-cholesterol and apolipoprotein B in normal and moderately hypercholesterolemic subjects. Lipids in Health and Disease. https://doi.org/10.1186/1476-511X-12-119

2.   Chazelas Eloi, Srour Bernard, Desmetz Elisa, KesseGuyot Emmanuelle, Julia Chantal, Deschamps Valérie et al. Sugary drink consumption and risk of cancer: results from NutriNet-Santé prospective cohort BMJ2019; 366 :l2408

3.    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

4.    Hernández-Ramírez, R. U., Galván-Portillo, M. V., Ward, M. H., Agudo, A., González, C. A., Oñate-Ocaña, L. F., … López-Carrillo, L. (2009). Dietary intake of polyphenols, nitrate and nitrite and gastric cancer risk in Mexico City. International Journal of Cancer. https://doi.org/10.1002/ijc.24454

5.    Moazzen, H., & Alizadeh, M. (2017). Effects of Pomegranate Juice on Cardiovascular Risk Factors in Patients with Metabolic Syndrome: a Double-Blinded, Randomized Crossover Controlled Trial. Plant Foods for Human Nutrition. https://doi.org/10.1007/s11130-017-0605-6

6.    Simpson, E. J., Mendis, B., & Macdonald, I. A. (2016). Orange juice consumption and its effect on blood lipid profile and indices of the metabolic syndrome; A randomised, controlled trial in an at-risk population. Food and Function. https://doi.org/10.1039/c6fo00039h

7.    Xu, G. P., Song, P. J., & Reed, P. I. (1993). Effects of fruit juices, processed vegetable juice, orange peel and green tea on endogenous formation of N-nitrosoproline in subjects from a high-risk area for gastric cancer in Moping County, China. European Journal of Cancer Prevention. https://doi.org/10.1097/00008469-199307000-00007

 

 

Chronic stress, appetite suppression, control and metabolic inflexibility.

It was the famous stress scientist Hans Selye who suggested that stress can be a positive or negative force. But how do we know whether we are dealing with stress effectively? There’s a common theme among clients both male and female who have got used to feeling in control of their health by suppressing appetite, symptoms and a false sense of health by perhaps feeling in control. Is this control a false economy? A well-known symptom of stress is a loss of appetite and skipping breakfast, it feels better to perpetuate the production of stress hormones like adrenaline and cortisol to liberate energy from stored fats and stride through the day with their endorphin like qualities. A common theme of females suffering from poly cystic ovary syndrome (PCOS) is chronic irregular eating or over eating in the obese. High stress can be chronic and perceived as the norm. I’ve observed the former in my eldest daughter through under eating as a product of emotional stress

‘For those habituated to high levels of internal stress since early childhood, it is the absence of stress that creates unease, evoking boredom and a sense of meaningless. People may have become addicted to their own stress hormones, adrenaline and cortisol, Hans Selye observed. To such person’s stress feels desirable, while the absence of it feels like something to be avoided.’ Gabor Mate

It should come as no surprise why some studies suggest that short term fasting, and calorific restriction seem to be productive in reversing aspects of inflammation and auto immune disease. When the body is stressed even eating certain foods becomes stressful. Dairy, sugar, fruits, grains all get the blame. I feel better when I don’t eat these some say. I feel better when I don’t eat others say. Is it the food or is it you? Can you be so fragile that eating some fruit for example is enough to send your biology into a tail spin. Eating sugar in excess can be problematic but then so can eating fat or anything in excess.

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A foundation of good health is built upon biological flexibility, potential and far away from equilibrium states.

The inability to utilise carbohydrate is a snapshot of the inflexibility of an individuals’ metabolism and not the carbohydrate. Evolutionary biology has provided efficiency by aerobic metabolism of carbohydrate and fat. The loss of efficient use of carbohydrate/sugar is the hallmark of a loss of function or flexibility and the chronic use of fats as a fuel is problematic due to increased oxidation of these lipids which can damage the aerobic apparatus within the mitochondria. The Randle cycle or glucose fatty acid cycle should allow flexibility between using either fats or carbohydrate as a fuel (Randle, Garland, Hales, & Newsholme, 1963). It’s often the lack of flexibility, decreased oxidation of carbohydrate and perpetual use of fats that damage the energy producing cells. Saturated fats are the preferred fuel of aerobic (oxidative) metabolism but in aggressive metabolism of cancer cells, unsaturated fats are utilised perpetuating the damage, promoting inefficient glycolysis or anaerobic metabolism that creates the acidic state of the cell.

The dogma that persists in nutrition circles is not based on sound reasoning but limited ideas that look at short term studies related to carbohydrate restriction. When a system loses its capacity to regulate sugar, we blame sugar instead of looking at the variety of factors that are responsible for degraded biology, carbohydrate utilisation and insulin responses.

Whether excessive exercise or inadequate nutrition the end result may be similar and its effects are far reaching into metabolism, cardiovascular, sexual and reproductive physiology.

By improving life conditions (in many ways) the hormones of pleasure can have a bigger role in our physiology. I think the experience of pleasure (whatever capacity for pleasure there is) increases the ability to experience pleasure, but I don't offer this with much hope as a therapeutic approach, since I know of people who say that running to exhaustion makes them "feel good" - neither "feeling good" nor "having orgasms" has a clear meaning, at present. Ray Peat

I’m not suggesting that going long periods without eating are necessarily bad, nor if you enjoy running is that bad either. Context is key. If you enjoy running run. If you have the capacity to go long hours without eating, then do that too. However if you have a system that lacks flexibility these actions can be problematic.

Have you ever considered not engaging in intense exercise for a couple of weeks to see how your body really feels?

I think this is a useful test to discover where your biology is really at. It can help determine whether you have been propping up a dysfunctional biology with intense exercise that falsely elevates your body temperature through activation of the sympathetic stress pathway. Slowing down and just focusing on walking and a few stretches shouldn’t feel stressful. Equally an individual who switches to eating regularly every 3 hours or so with the same amount of calories they were previously eating shouldn’t feel stressful. We all have patterns, routines and to the extent that they are effective or not is dictated by the metabolic flexibility that one should have. I’ll also suggest that metabolic flexibility could be analogous to emotional flexibility and mood states. A sign of improvements to metabolic flexibility and flux is return of energy, ability to tolerate exercise, good sleep, libido and emotional responses among other aspects of function. How do you know if it’s working? This diagram suggests what drivers are necessary and how to overcome your unwanted symptoms with the right inputs.

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Some patience seeking the return of these aspects of function is needed. After all, if you have spent decades constrained by negative symptoms then it may take more than a few weeks or months to fully resolve these patterns. In addition to the foundational work on hormones and chemistry, some people might find a need to address belief systems or require counselling for trauma or emotional grief to help resolve emotional stressors.

 References

Mate, G. (2008). In the realm of hungry ghosts. Close encounters with addiction. Canadian Family Physician.

Randle, P. J., Garland, P. B., Hales, C. N., & Newsholme, E. A. (1963). The glucose fatty-acid cycle its role in insulin sensitivity and the metabolic disturbances of diabetes mellitus. The Lancet, 281(7285), 785–789. https://doi.org/10.1016/S0140-6736(63)91500-9

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

Selye, H. (1987). Stress without distress. In Society, stress, and disease, Vol. 5: Old age. (pp. 257–262). http://doi.org/10.1080/00228958.1983.10517713

 

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

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 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.

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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.

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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

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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

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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

Seasonal thyroid fluctuations, biology and mood

 As you may have read from previous blogs, the thyroid, its pituitary stimulator - thyroid stimulating hormone (TSH) and the other thyroid hormones are heavily influenced by environment, nutrition and stress. Additionally these hormones can present as normal when relied upon purely by biochemical analysis from the blood. The seasons, differing temperatures, light exposure and effects of hibernation hormones and neurotransmitters can also be a key factor in the expression of adequate energy, organisation and coherence of an individual’s biology. We get sick more so in winter when our function is suppressed and the immune system is called upon to mount a response.

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S.W. Tromp Biometerology 1967.

“ The yearly influenza peak in the Netherlands, around February. Which may be related to the usually low humidity and wind-speed in this period, but which effect is probably accelerated by the decreased thermoregulation efficiency of the body as a result of the preceding cold months and the accompanying changes in the physico-chemical state of the blood such as y-globulin level.”

 Ambient temperature can have a significant effect on TSH production in as much as a colder environment increases TSH and warmer temperatures decrease TSH production and thyroid requirement. Observations have suggested a biphasic seasonal nature of TSH secretion, with increased TSH readings during winter time suggesting what could be a functionally hypothyroid or subclinical hypothyroidism which resolved during the summer months (Kim et al., 2013). As this stress increases throughout longer days of darkness, organisational hormones decrease, whilst stress hormones increase. If chronic enough, or in an unstable biology, stress can decrease the accuracy of TSH to predict a low thyroid state

 Light, both red and ultraviolet (UV) are well-known modulators of immune function, metabolism and mitochondrial production of energy or  adenosine triphosphate (ATP) (Wong-Riley et al., 2005) (Karu, 2010). These aspects of sunlight, exert their influence via enhancement of aerobic metabolism (at cytochrome c) and immunity enhancing via infra-red (NIR) and vitamin D synthesized by UV respectively.  The variation in light exposure as a consequence of daily sleep, darkness and seasonal variations present relationships that may explain the secretory patterns of TSH in healthy subjects. More than 100 years ago, thyroid function could be suggestively viewed via uptake of thyroid iodine levels in seasonal variations. (Fenger and Siedell 1913). Thyroid iodine levels rose during the summer in sheep, pigs and cows and decreased during the winter reflecting the variations in the need for TSH/TH production in healthy organisms. 

Seasons, Thyroid and Mood

 Depression is a known symptom of hypothyroidism and some studies have highlighted the need for a lower TSH value in the presence of depressive symptoms (Talaei, Rafee, Rafei, & Chehrei, 2017) (Hage & Azar, 2012). The former authors suggest a cut-off value of 2.5 mU/L for TSH as a point for treating hypothyroidism, which highlights the need for assessing symptoms as part of an effective strategy for diagnosing hypothyroidism. This compares to the attitude taken to expecting mothers where values should be decreased to compensate for hypothyroid states but in reality should be applied across the board.

 Relationships concerning seasonal variations of mood are well documented and decreased Beck mood scores are associated with the shorter days of winter (Harmatz et al., 2000). Seasonal affective disorder (SAD) may be a reflection of the increase in serotonin and melatonin and depression of thyroid hormone, which are increased by shorter days and in mammals are associated with hibernation. This aspect seems to be lost on those treating transient depressed states but light therapy does appear to be taken seriously these days. I would encourage anyone wanting more information on serotonin and mood to check out the extremely well written blog Against Utopia.

 As days become shorter and light exposure is decreased, influencing cellular function and metabolism negatively. The extended effects of melatonin from the shorter days can antagonise TSH secretion via its inhibitory action on TH, increasing prevalence throughout winter. Whilst fluctuations in TSH levels in response to seasonal changes are well-known to occur, these fluctuations are also under the influence of the nutritional and environmental factors that can suppress TSH values.

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Wake me up when it’s spring?

Violent suicides increase with the onset of spring from March to May. I was trying to think why this might occur? After speaking to a friend recently about depression, they said that holding onto the feelings of a blanketed, safe, dark environment by being it home (in a somewhat hibernation like state), and gorging on boxsets or podcasts was easy to do and a comfort. I wonder if the shorter phases of darkness and increased light remove that blanket of increased serotonin and melatonin and the light itself might become a stressor that takes away that comfort? Those most at risk might explain this seasonal increase in suicides?

Ray Peat (1997) has discussed various aspects of stressors such as darkness, oestrogen-cold sensitive enzymes and nutritional factors affecting endocrine systems, adding an interesting perspective on hormone production and relationships with temperature changes (Peat, R. and Soderwall, 1972) (Peat, 1997)(Peat, 1972).

In states of undetectable SCH mediated by the stress, a hypothermic state may stimulate the adrenal stress system to compensate for a low-metabolic and decreased temperature state.  Activated compensatory stress response pathways may explain poorly detected hypothyroid patients. Decreased metabolic rate, lowered temperature and pulse rate are well-known signs of hypothyroidism. β adrenergic mechanisms involving increased catecholamine production such as adrenaline and noradrenaline (NA) can increase Tb and RHR. In my previous blog on body temperature, I explained how low temperature can be indicative of low thyroid function when blood tests appear normal.

  

References:

Hage, M. P., & Azar, S. T. (2012). The link between thyroid function and depression. Journal of Thyroid Research. http://doi.org/10.1155/2012/590648

Harmatz, M. G., Well, A. D., Overtree, C. E., Kawamura, K. Y., Rosal, M., & Ockene, I. S. (2000). Seasonal variation of depression and other moods: A longitudinal approach. Journal of Biological Rhythms. http://doi.org/10.1177/074873000129001350

Karu, T. I. (2010). Multiple roles of cytochrome c oxidase in mammalian cells under action of red and IR-A radiation. IUBMB Life. http://doi.org/10.1002/iub.359

Kim, T. H., Kim, K. W., Ahn, H. Y., Choi, H. S., Won, H., Choi, Y., … Park, Y. J. (2013). Effect of seasonal changes on the transition between subclinical hypothyroid and euthyroid status. Journal of Clinical Endocrinology and Metabolism. http://doi.org/10.1210/jc.2013-1607

Peat, R. and Soderwall, A. L. (1972). Estrogen stimulated pathway changes and cold -nactivated enzymes. Physiol Chem Phys, 4((3)), 295–300.

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

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

S.W., Tromp. (1967). Biometeorology, iia and b. Symp. Publ. Div. Pergamon Press (Oxford).

Talaei, A., Rafee, N., Rafei, F., & Chehrei, A. (2017). TSH cut off point based on depression in hypothyroid patients. BMC Psychiatry, 17(1). http://doi.org/10.1186/s12888-017-1478-9

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

Wong-Riley, M. T. T., Liang, H. L., Eells, J. T., Chance, B., Henry, M. M., Buchmann, E., … Whelan, H. T. (2005). Photobiomodulation directly benefits primary neurons functionally inactivated by toxins: Role of cytochrome c oxidase. Journal of Biological Chemistry. http://doi.org/10.1074/jbc.M409650200

 

A Bioenergetic Approach to Restoring Gut Function: Part 2

Copy of Your bowel function might be an expression of your biology.jpg

Oops - A bioenergetic approach to restoring gut function part 1 was almost two years ago, my studies got the better of me, I’m sorry. Following on from the information of how to restore energy and digestion by simply removing foods that are difficult to digest, promote endotoxin, decrease energy and digestion. Replacing them with easily digested, protective nutrients can negate the need for expensive, reduced testing and a supplement list that causes you to rattle as you stroll down the street. Much like the decreased need for stool testing, I have rarely recommended a food allergy or sensitivity test for the same reason that I haven’t used a stool test for many years (or had the luxury of a nice cash kickback from the labs I used to use). Why? Because these tests show the body in a stressed, energy wasting state that is prone to inflammation and reacts with many foods like dairy. Is it the food? No. Could it be you? It’s possible.

Metchnikoff.png

It’s not the dairy it’s you

Elie Metchnikoff suggested over 100 years ago that as putrefaction within the bowel occurs, function and immunity is compromised

 

Many clients have rolled into the office clutching their food sensitivity tests in a file, with dozens of other tests. Red bars, yellow bars, all highlighting so called problem foods. During bouts of stress (pollution exposure, psychological, under eating etc, excessive exercise, poor sleep) the body is prone to decreasing available levels of organisational hormones such as thyroid and progesterone. Usually the adrenal glands have to pick up the slack and compensatory stress hormones such as cortisol, glucagon, adrenaline and activation of serotonin (not a hormone) which  suppress thyroid and progesterone are perpetuated. This often creates a high sodium (salt) and magnesium wasting state and poor digestive function that facilitates increased sensitivity via increased serotonin and histamine levels. This also increases demand for vitamin C for gut mucosa maintenance and adrenal responses.

If this state is perpetuated increases in endotoxin (the by-product of bacterial metabolism and degradation ) burden the digestive system, liver, and can damage the gastrointestinal lining. Endotoxin levels are also  increasing through airborne environmental pollutants such as polycyclic aromatic hydrocarbons  from fossil fuel use and industry (Annamalai & Namasivayam, 2015), so it’s worth considering that some people in a high pollution area, with poor digestive function are at increased risk of presenting with food sensitivities. They get tested, part with their cash and told to cut out 20 foods that they eat on a regular basis. Problem solved? Well no, it’s an intervention that will have some success but it’s some distance of what the person really needs.

 To simplify some of the well-known digestive issues with two ends of the spectrum.

Your bowel function might be an expression of your biology.jpg

Restore function

Restore appropriate movement

Constipation – failure to go to poop daily, hard to pass.

 

IBS irritable bowel like issues. Loose often more than 3 times per day.

 

There’s plenty of reasons to link constipation with a low energy, functionally hypothyroid, subclinical or overt hypothyroid state (Lauritano et al., 2007) and increased bacterial overgrowth like SIBO or small intestinal bacterial overgrowth. The digestive system is energy and thyroid hormone dependant and restoring energy by supplying easily digested high energy foods can be a simple intervention with effective results.

Often when you dig into a person’s history, you might find that those with IBS like states often describe a period of constipation. It’s not impossible to suggest that sustained constipation will lead to increased endotoxin, serotonin and histamine that damages the bowel lining. When this environment is perpetuated by stress, poorly digested foods and low energy, the digestive system is maintained in a high stress state, sensitive and ready to reject any remotely objectionable substance. Any food can become problematic when the digestive system is over-burdened or sustains damage to enzyme producing structures in the villi and microvilli.

 If you follow the chart suggested in restoring gut function part 1, you should find yourself in a much improved state. If you need further improvement then the following factors have always worked well:

 

Constipation:

 Magnesium in forms such as chloride and glycinate or very useful for decreasing perceived stress and lowering the incidence of sensitivities and 400mgs to 1g is useful to experiment with and complements dietary changes suggested.

To restore bowel movement magnesium sulphate or Epsom salts will mobilise the digestive tract and I have found that clients if needed try half to a full teaspoon to grease the wheels.

Vitamin C is a great way of decreasing constipation. A few years back I would recommend a dose of 1-2 grams  but equally I feel adequate intake of orange juice will do a great job. The added benefit of orange juice (polyphenols) has been shown to decrease inflammation and endotoxin which is often present in both high fat and carbohydrate meals (Ghanim et al., 2010).

 

Cascara Sagrada If you need a good clear out to restart function then cascara is an extremely effective solution.


‘ An effective laxative (besides preventing inflammation) causes not only coordinated contraction of the smooth muscles of the intestine, but also adjusts secretions and absorption, so that an appropriate amount of fluid stays in the intestine, and the cells of the intestine don’t become water-logged.’ Ray Peat.

 

Caffeine seems a logical choice and the research on caffeine as a potent factor in the fight against cancer and neuro degenerative diseases such as dementia and Alzheimer’s disease is very positive. Coffee stimulates bowel function and like the suggestions above is useful to decrease the reabsorbed metabolites and toxins that may be instrumental in systemic inflammation. The aerobic/respiratory system is enhance and protected by coffee consumption, providing protection to the mitochondria (Eskelinen & Kivipelto, 2010).

 

Irritable bowel

Carrots I have posted about the power of grated carrot to reduce the irritated state many times and have seen some clients with over 20 years of IBS resolve with this simple addition. Carrots act as a natural antibiotic, lowering endotoxin and other bacterial end products (Babic, Nguyen‐the, Amiot, & Aubert, 1994) and bamboo shoots have the same effect. As increased bacterial issues stimulate endotoxin production the daily use of a carrot salad can be one of the simplest yet most effective tools that you can have to improve bowel function.

Bone broth, gelatin and glycine are also great for helping to support gastrointestinal mucosa, improve the brush border enzyme function and decrease the proinflammatory effects of eating tryptophan and iron rich muscle meats that can also irritate the bowel when excessive.

Mushrooms  when boiled also have a similar effect as the carrot by decreasing aromatase enzymes and estrogen  acting as a natural antibiotic.

I would challenge anyone who either has paid money for a food sensitivity test or who is thinking about it ,to simply try the suggestions set out in these two posts. Over the last few years I haven’t seen anyone who has failed to improve digestive function. Although sometimes other mechanisms involving hormones may need to be explored.

References:

Annamalai, J., & Namasivayam, V. (2015). Endocrine disrupting chemicals in the atmosphere: Their effects on humans and wildlife. Environment International. http://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. http://doi.org/10.1111/j.1365-2672.1994.tb01608.x

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). http://doi.org/10.3233/JAD-2010-1404

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. http://doi.org/10.3945/ajcn.2009.28584

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

 Peat, R. http://raypeat.com/articles/articles/cascara-energy-cancer-fda-laxative-abuse.shtml

Body temperature and health

Most people are so confused as to what constitutes good health these days and when they turn up to my office in low metabolic states with digestion, sleep, energy, mood and other issues. One of the first things that they say is that they eat really healthily. If you throw into the melting pot the obsession with the keto diet, chronic calorific restriction (CR) or other modalities, those short term gains have turned into long term deficits. I’ve long opined that health in general terms can be defined by:

 

·      Good energy

·      Good Digestion 2-3 bowel movements per day

·      Restorative sleep

·      Balanced mood free of depression or anxiety

·      Desire for life, motivation, hobbies and interests

·      Healthy libido

·      Absence of pain

Humans are endotherms that regulate their temperature at 37 degrees centigrade.jpg

What does your body temperature suggest about your health?

Get cold…read on

I’ll also add to that list a warm body and the ability to generate efficient energy,  a phrase biologists might use is a state of negative entropy. Entropy is a state associated with decay and disorder and as entropy increases, equilibrium is achieved - where a state of no energy in and no energy out or death of a living system occurs. The basis for life and metabolism is governed by the enzymes. Enzymes function well in an appropriate temperature and in a medium that is neither too acidic nor too alkaline. Mammals and specifically humans are endotherms that regulate their temperature in  tight range at approximately 37 degrees Centigrade (C) or 98.6 Fahrenheit (Bicego, Barros, & Branco, 2007). The central compartment theory of temperature  suggests that the head and the core should maintain a relatively stable temperature, due to the rich vascular supply and that the periphery may vary some 2-4 C.  

In a recent study that I conducted I suggested that the peripheral and core temperatures should remain at a similar level of about 37 C . The suggestion that a decreased body temperature recorded in the head, might be the last place that you would see a reduction due to the large quantities of glucose that the brain uses to maintain function. It’s possible to suggest that the slowing of function in low energy and hypothyroid states might be observed initially in the trunk or core. The well documented symptoms of constipation, decreased heart rate, slowed contraction relaxation of the heart and arteries and reduced peripheral relaxation of tendons (Achilles tendon reflex) might appear in the trunk and peripherally due to the preferential oxidation of glucose initially. Due to the vast systemic implications of low thyroid function, many different paths of decreased function might occur, dependant on nutrition, environmental stimulus and other stressors. In my study I didn’t find this but what I did find is strong linear correlations between low body temperature in both the mouth and armpit, multiple low thyroid symptoms (mean 6.8 per subject) and yet normal blood values.

Humans are endotherms that regulate their temperature at 37 degrees centigrade-2.jpg

Thyroid hormone affects all aspects of biology

 

There are many factors that can decrease body temperature such as CR, fasting, estrogen, stress, pollution, over exercise and more. CR has been suggested as a mechanism for maintaining longevity but studies lack any conclusive evidence (Carrillo & Flouris, 2011) and a theory that a cold body, decreases metabolism, oxidation and damage therefore preserving tissues. Another emergent theory and results show in rodent studies, that mammals with a high energy intake, high metabolism and organised biology can increase life span (John R. Speakman et al., 2004) (J. R. Speakman, 2005). Think about this for a minute:

Calorific restriction makes the body cold, decreases metabolic rate  (via inhibition of thyroid hormone) and disorganisation of tissues. Entropy State

Adequate energy, maintains body temperature and organises tissues to function at their best. Negative entropy state.

From an evolutionary perspective fasting due to lack of food was a necessity. Fasting these days could be a useful tool, if you were prone to constant overeating but if your system lacks the flexibility to do so problems can occur. That’s not to say that calorie restriction for weight loss isn’t helpful but sustained CR in a system that doesn’t respond well might be counterproductive. Pollution has increased at a phenomenal rate clearly affecting physiology and hormones (Gore et al., 2015). Does it make sense that a so called detox diet, low in calories, protein, carbohydrates can enhance the function of detoxification, when liver function is energy and thyroid dependant? Skipping breakfast alone in some is associated with increased cortisol, glucagon and metabolic inflexibility (Jakubowicz, Wainstein, Ahren, et al., 2015) (Jakubowicz, Wainstein, Ahrén, et al., 2015). These factors can also decrease the mitochondrial uncoupling proteins which are responsible for increased body temperature.

Ageing is also associated with decreased metabolic rate, colder bodies and accepted increases in thyroid hormone stimulating values (TSH) (Laurberg, Andersen, Pedersen, & Carlé, 2005) . If symptoms of failing biology are present with isolated thyroid symptoms such as increased cholesterol,  , high blood pressure and sugar, cardiovascular issues and even cancer the acceptance of TSH and other thyroid hormone analysis to accurately predict hypothyroidism should be considered. Body temperature and metabolic rate was reliably used in the last century to diagnose hypothyroidism with qualitative analysis of symptoms and symptoms resolved with thyroid hormone treatment (Barnes, 1942) (McGavack, Lange, & Schwimmer, 1945) (Peat, 1999). Whilst thyroid is useful for restoring function, food and other factors can be used to restore and maintain function (previous blog on maintaining the aerobic system)

Certain nuances exist in temperature regulation that are dependant on acute or chronic exposure to stressors and a slowing down of the system through  a functionally, subclinical or overt hypothyroid state. In short term fasting, TSH is initially raised then decreases, negating thyroid blood tests. In the same manner the time frame of any stressor can dictate whether short or long term compensations of  the sympathetic adrenergic system is supporting the system. In well established feedback mechanism it’s known that as TSH increases so does cortisol and as body temperature approaches hypothermic levels (around 35C) cortisol, adrenaline and noradrenaline can increase body temperature as a protective response.

In a world where excess environmental and social stressors are ever increasing - it might make sense to maintain an efficient, organised warm body rather than reducing its function and heat.

 

References:

 

Barnes, B. (1942). Basal temperature versus basal metabolism. Journal of the American Medical Association, 119(14), 1072–1074. http://doi.org/10.1001/jama.1942.02830310006003

Bicego, K. C., Barros, R. C. H., & Branco, L. G. S. (2007). Physiology of temperature regulation: Comparative aspects. Comparative Biochemistry and Physiology - A Molecular and Integrative Physiology. http://doi.org/10.1016/j.cbpa.2006.06.032

Carrillo, A. E., & Flouris, A. D. (2011). Caloric restriction and longevity: Effects of reduced body temperature. Ageing Research Reviews. http://doi.org/10.1016/j.arr.2010.10.001

Gore, A. C., Chappell, V. A., Fenton, S. E., Flaws, J. A., Nadal, A., Prins, G. S., … Zoeller, R. T. (2015). Executive Summary to EDC-2: The Endocrine Society’s second Scientific Statement on endocrine-disrupting chemicals. Endocrine Reviews. http://doi.org/10.1210/er.2015-1093

Jakubowicz, D., Wainstein, J., Ahrén, B., Bar-Dayan, Y., Landau, Z., Rabinovitz, H. R., & Froy, O. (2015). High-energy breakfast with low-energy dinner decreases overall daily hyperglycaemia in type 2 diabetic patients: a randomised clinical trial. Diabetologia, 58(5), 912–919. http://doi.org/10.1007/s00125-015-3524-9

Jakubowicz, D., Wainstein, J., Ahren, B., Landau, Z., Bar-Dayan, Y., & Froy, O. (2015). Fasting until noon triggers increased postprandial hyperglycemia and impaired insulin response after lunch and dinner in individuals with type 2 Diabetes: A randomized clinical trial. Diabetes Care, 38(10), 1820–1826. http://doi.org/10.2337/dc15-0761

Laurberg, P., Andersen, S., Pedersen, I. B., & Carlé, A. (2005). Hypothyroidism in the elderly: Pathophysiology, diagnosis and treatment. Drugs and Aging. http://doi.org/10.2165/00002512-200522010-00002

McGavack, T. H., Lange, K., & Schwimmer, D. (1945). Management of the myxedematous patient with symptoms of cardiovascular disease. American Heart Journal. http://doi.org/10.1016/0002-8703(45)90476-5

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

Speakman, J. R. (2005). Body size, energy metabolism and lifespan. Journal of Experimental Biology. http://doi.org/10.1242/jeb.01556

Speakman, J. R., Talbot, D. A., Selman, C., Snart, S., McLaren, J. S., Redman, P., … Brand, M. D. (2004). Uncoupled and surviving: Individual mice with high metabolism have greater mitochondrial uncoupling and live longer. Aging Cell. http://doi.org/10.1111/j.1474-9728.2004.00097.x

 

Better gut health with less bacteria?

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

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

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

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

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

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

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

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

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

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

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

References:

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

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

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

Sleep, stress, sugar. Eat sugar for better sleep.

Onset of sleep

Onset of sleep

Can you improve sleep and decrease stress by eating sugar for better sleep? If you put sleep, stress and sugar in the same sentence, most people think they have already put the three together with something like; too much sugar causes stress and affects your sleep. If you read on you should find yourself advantageously aware of sleep biology and why consuming sugary foods before sleep, and indeed if you wake up are the answer for a deeper nights sleep.

Ah a good nights sleep. You remember one of those don’t you? As a father to 3 children I have had my fair share of sleepless nights but a recent 11 hour sleep whilst my kids slept for 12 hours, recently reminded me of why everyone should strive for better sleep and the common approaches that people tend to fail to implement. A couple of years ago I studied a short course on the neurobiology of sleep with the University of Michigan and I found it useful as it correlated with aspects of serotonin function that Ray Peat (7,8) had talked previously talked about.

Generalisations of sleep biology phases are:

Sleep latency - Getting your sorry arse to sleep

NREM sleep - Keeping your sorry arse asleep

REM sleep - Deep arsed sleep

Wakefulness - Wake your sorry arse up

One of the primary driving factors of the onset of sleep or sleep latency is the production of adenosine. Caffeine is a well-known antagonist of adenosine and therefore many a wise word about not drinking caffeine after 3-4 pm as it has a half-life of 6 hours are well heeded (yes I know there are some of you that metabolise caffeine really well after that time with no impact on sleep, STOP SHOWING OFF).  Avoiding caffeine though out the day isn’t necessary and caffeine is a widely mis-understand compound that shows many beneficial effects, if you follow the rules for its consumption.

Often there is much focus on the role of melatonin and sleep induction and structures like the suprachiasmatic nucleus and waking. Melatonin does indeed promote sleep but so does adenosine and I think the supplementing of melatonin misses key biological functions that induce sleep more effectively and without the negative effects associated with its use.

Serotonin and melatonin confusion

Sleep wake compounds

Sleep wake compounds

Just like the holistic health practitioner that suggests that coffee causes adrenal fatigue (it doesn’t but that’s another blog by itself), some practitioners recommend the use of 5HTP - tryptophan supplements (tryptophan converts to serotonin) for better sleep but this is misguided for the following reasons. It’s true that melatonin is a hormone of sleep and that it is derived from serotonin and that serotonin has a small but limited role in inhibiting the cholinergic system responsible for keeping you in an alert, thinking state. In the diagram below and born out of many studies is that serotonin is a powerful compound of wakefulness that synergises with histamine and the histaminergic system to bring you out of the deeper REM sleep, and start the process of waking you the hell up. The diagram from Brown et al (Brown, Basheer, McKenna, Strecker, & McCarley, 2012) highlights the complexities of the sleep wake compounds but also useful for highlighting serotonin's role (5HT) in the excitatory waking state. It’s also a great overview of the many areas and compounds that aren’t addressed in this blog. One thing that should become clear is that the neural structures controlling sleep are many and so are the interactions between hormones and other compounds of wakefulness. My advice below is not complete but merely a reflection of some of the simple changes that you can do (and which I have done with many clients) to create better sleep and recovery. 

Here are a few pointers on serotonin and melatonin.

  • Many people are aware of the fact that at least 95% of the body's serotonin is produced in the intestines - namely the enterochromaffin cells.

  • People associate serotonin as a hormone of calmness. 1) It’s not a hormone 2) well known side effects of serotonin excess are insomnia and anger.

  • Serotonin induces spasticity of the colons smooth muscle tissues

  • Eating excess muscle meats increases serotonin (as does eating poorly digestible foods), inflammation and can contribute to increased wakefulness by synergising with histamine.

  • Melatonin may be implicated in seasonal affective disorder due to increased levels in darker winter days. Sunglass wearing may pose similar issues (Alpayci, Ozdemir, Erdem, Bozan, & Yazmalar, 2012)

  • Supplementation with melatonin during the day can induce disruptive changes to fertility and also suppress thyroid hormone (Creighton & Rudeen, 1989).

  • Peak concentrations of thyroid stimulating hormone (TSH) occur at night and might be suggestive of thyroid hormone suppression induced by melatonin and other hormones. The pituitary responds by increasing TSH to bolster thyroid hormone supply.

Of course there are other compounds which include acetylcholine, GABA, oxycretin, histamine and many other areas of the central nervous system that could be mentioned but I have tried to stick to the mechanisms that can be changed and promote change in a short space of time.

If you find it hard to drift off, these are my suggestions as to why this might happen:

  1. You are eating foods that promote intestinal inflammation and increase serotonin and histamine.

  2. You are exposed to excess stimulus such as blue light, Wi-Fi or other source.

  3. Your blood sugar levels are not balanced and promote the stress hormones that liberate glucose from stored fats and proteins - adrenaline-glucagon-cortisol.

If you wake up at night the following might be also be an issue

  1. You are eating foods that promote intestinal inflammation and increase serotonin and histamine.

  2. Your blood sugar levels are not balanced and promote the stress hormones that liberate glucose from stored fats and proteins - adrenaline-glucagon-cortisol.

Point 2 may be a significant factor for many people and available efficient glucose production may be one of the most under-rated factors in both the onset of sleep and maintenance of sleep. Waking up to urinate at night is a feature of the diabetic like state. Poor blood sugar regulation requires, that instead of relying on blood and liver glucose stores, the stress response be relied upon to liberate energy from stored fats. This is an inefficiency that requires a stressed state. You should not be waking at night to go for a pee.

Morning Cortisol profile

Morning Cortisol profile

You can see from the average nighttime cortisol profile that cortisol generally starts to rise around 2 am, steadily increasing prior to the onset of waking. If your ability to regulate blood sugar levels is compromised this can increase the burden to blood sugar regulation and increase waking further. The REM phase of sleep uses a similar amount of glucose as the waking state.

Here are some useful tips that I use with clients to promote better sleep and recovery.

  1. Take a look at the previous post on resolving digestion issues. This helps to take away some of the factors related to serotonin and histamine excess.

  2. If you are exercising hard, low carb, busy parent or whatever form of stress and therefore don’t manage your blood sugar levels, you don’t manage your sleep. If you struggle getting to sleep a sweet drink like milk and honey (yes the old wives tale works like a charm). A glass of fruit juice with gelatin is also good. Any pattern with something with sweet with a little protein/fat is useful.

  3. Add some salt - increased stress burdens the adrenal glands, usually though thyroid hormone suppression. Salt is wasted in this state and so is magnesium. Salt spares magnesium, so adding a little salt also helps magnesium regulation.

  4. If you wake during the night. This can be common when trying to resolve these issues as liver function and hormone regulation take a little time to adjust. Therefore having something sweet by the bed can help to help you re-enter sleep. Squeezy honey tube or pouch of juice with straw I find useful so that the juice goes straight down rather than covering my teeth.

  5. I have often found that progesterone and thyroid play a key role in sleep and many clients have benefitted from resolving the states of low progesterone/thyroid, which may not have resolved with food alone.

  6. Optimal blood sugar regulation often starts with eating breakfast to decrease adrenaline, glucagon and cortisol (Jakubowicz et al., 2015)(Levitsky & Pacanowski, 2013). Drinking a kale smoothie or coffee on an empty stomach is not the best way to break your fast and set up the day.

  7. Of course aspects of sleep hygiene related to no phones, WI-FI etc goes without thinking and go as far as turning your router off at night.So armed with some facts that you can decrease stress and improve sleep by eating sugar in the right amount, you can go and experiment for yourself.

References:

  1. Alpayci, M., Ozdemir, O., Erdem, S., Bozan, N., & Yazmalar, L. (2012). Sunglasses may play a role in depression. Journal of Mood Disorders, 2(2), 80. http://doi.org/10.5455/jmood.20120529055051

  2. Brown, R. E., Basheer, R., McKenna, J. T., Strecker, R. E., & McCarley, R. W. (2012). Control of Sleep and Wakefulness. Physiological Reviews, 92(3), 1087–1187. http://doi.org/10.1152/physrev.00032.2011

  3. Creighton, J. A., & Rudeen, P. K. (1989). Effects of Melatonin and Thyroxine Treatment on Reproductive Organs and Thyroid Hormone Levels in Male Hamsters. Journal of Pineal Research, 6(4), 317–323. http://doi.org/10.1111/j.1600-079X.1989.tb00427.x

  4. Jakubowicz, D., Wainstein, J., Ahrén, B., Bar-Dayan, Y., Landau, Z., Rabinovitz, H. R., & Froy, O. (2015). High-energy breakfast with low-energy dinner decreases overall daily hyperglycaemia in type 2 diabetic patients: a randomised clinical trial. Diabetologia, 58(5), 912–919. http://doi.org/10.1007/s00125-015-3524-9

  5. Levitsky, D. A., & Pacanowski, C. R. (2013). Effect of skipping breakfast on subsequent energy intake. Physiology and Behavior, 119, 9–16. http://doi.org/10.1016/j.physbeh.2013.05.006

Online:

7. http://raypeat.com/articles/articles/serotonin-depression-aggression.shtml

8. http://raypeat.com/articles/articles/serotonin-disease-aging-inflammation.shtml

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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

 

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

Being holistic versus (holistic) critical thinking.

sunrise-2.png

Is being 'holistic' an advantage to holistic critical thinking? It’s relatively easy to get drawn into a naturalistic fallacy of consuming all foods in their most raw natural state. Perhaps you’re someone who went from a fast food diet, where you didn’t feel your best, to consuming more whole foods, fresh fruit and vegetables? It’s easy to see how a switch and positive changes can occur in the short term. The next step is to start preaching to the masses how sugar is bad, how your life will be saved with green smoothies, nuts, seeds and coffee butt cleanses. For the record this is a waste of coffee and not to far from what I was preaching a decade ago. So what does it mean to be holistic?There’s a large movement within the health fitness and wellness industry (and lay people) that are drawn to  'holistic' thinking, and their definition is often enforced by the fallacy that everything in its most natural state is better for human health. This appears to include foods like nut milks (yes you can milk a nut), kale smoothies, seed oils like flax and undercooked broccoli and other greens, despite their negative effects on human health when consumed in substantial amounts. It’s a religion, and much like religion and with this mind-set it isn’t going to make you any healthier. I’ll make reference here to the late, great Beastie Boy, MCA who despite being a vegan and a Buddhist died far too early from throat cancer.

It is true that eating plenty of foods in their most natural state f(or some foods) can be important for health. But the image on the right highlights the faulty narrative of being holistic without thinking about the consequences. Fruits, vegetables, dairy products, meats and the like require minimal processing but in the quest for longevity, taste and profit, adding preservatives and flavour enhancers causes our food sources to become problematic. The so called ‘holistic’ folk get lost in this narrative urging your diet to become abundant in the rawest, greenest and brownest foods, that are most indigestible and contain potent inhibitors of biological function.

To integrate a level of holism into nutrition and function requires a level of critical thinking. What do these foods contain? How do they affect physiology? It’s well known that the brassica vegetables like broccoli, cauliflower and sprouts contain potent compounds that decrease energy output. These goitregens inhibit thyroid output and isothiocyanates found in cruciferous vegetables affects TPO or thyroid peroxidase, both of which are exacerbated when iodine uptake or restriction is present. Research tends to support these problematic effects (Choi & Kim, 2014)(Truong, Baron-Dubourdieu, Rougier, & Guénel, 2010), but much attention is focused on the smaller compounds that seem to work well in test tubes, rather than its global effects. As the environment becomes more stressful for biology do we need more building or reducing factors within our control?

The environment can be a harsh place. There are plenty of pollutants that have a negative effect on fertility, metabolism and other key endocrine aspects of health, some of which are industrial, others purposively added to food (arguably another form of industry) (Rajpert-De Meyts, Skakkebaek, & Toppari, 2000)(Upson, Harmon, & Baird, 2016). We can argue that the environment has always been a harsh place and adaptation has taken place as a response to selective pressures at the heart of evolution. Yet currently we are heading towards a tipping point, as environmental stimulants appear to be at the heart of acquired biological damage that is inherited by offspring. Cancer, fertility and other metabolic diseases are more common than ever and yet the approach is to keep seeking the magic bullet to ameliorate the fate that awaits many of us.

If we were to ask:

What enhances biological function, makes us more robust and allows us to have a stronger conversation with a stressful environment?

Rather than succumb to its stressors.

The highway to health

The highway to health

A biological system in its best working order could be represented, as an infinite road stretching into the  distance, perhaps with the odd bump along the way or a slight deviation but an ability to get back on track is available. Compare that to the inhibitory T-junction where the body cannot function as the clear straight road, it deviates from its true organised direction. The journey is laboured and restrictive. The ability to flux and respond to stressors is key and adequate energy is an essential component of reorganisation.

Nutrition is an important factor for such conversations with the environment. Eating a diet that is dominated with foods that are difficult to digest, decrease energy availability and create more stress are not going to make chatting any easier. If we make the effort to understand what keeps a cell and its mitochondria functioning at its most efficient state, we can understand why aspects such as sugar, adequate protein, moderate exercise, light and other factors, can play a role in overcoming current stimulus that decrease function and increase disease states.

The following article is definitely worth a read for an understanding of the concepts that I have talked about. http://raypeat.com/articles/articles/vegetables.shtm

References:

Choi, W. J., & Kim, J. (2014). Dietary factors and the risk of thyroid cancer: a review. Clinical Nutrition Research, 3(2), 75–88. http://doi.org/10.7762/cnr.2014.3.2.75

Rajpert-De Meyts, E., Skakkebaek, N. E., & Toppari, J. (2000). Testicular Cancer Pathogenesis, Diagnosis and Endocrine Aspects. Endotext. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/25905224

Truong, T., Baron-Dubourdieu, D., Rougier, Y., & Guénel, P. (2010). Role of dietary iodine and cruciferous vegetables in thyroid cancer: A countrywide case-control study in New Caledonia. Cancer Causes and Control, 21(8), 1183–1192. http://doi.org/10.1007/s10552-010-9545-2

Upson, K., Harmon, Q. E., & Baird, D. D. (2016). Soy-based infant formula feeding and ultrasound-detected uterine fibroids among young African-American women with no prior clinical diagnosis of fibroids. Environmental Health Perspectives, 124(6), 769–775. http://doi.org/10.1289/ehp.1510082

Methylene Blue - Let’s play the blues.

Methylene blue - an overview: There’s been many times when I have recommended compounds/agents to create change in clients. Even the basic strategies of increasing sugar, not wearing sunscreen or the use of aspirin for improving energy and decreasing oxidative stress has moved the odd eyebrow to be raised. Objections often dissipate when presented with the line of reasoning and research that supports my recommendations. Effective clients will often do their own research and come back armed with significant questions for a better understanding of what is trying to be achieved. Research previously conducted by the Nobel scientist Albert Szent Györgi showed that previously damaged cells that produce energy inefficiently can be restored with methylene blue.

MB.jpg

Restoring respiration with colour.

So with the tradition of raising more eyebrows let’s suggest the use of a blue dye that can be added to aquariums for improving marine life health. That’s right you put it in fish tanks. Why indeed would you not think of consuming glassfuls of the stuff?

Methylene blue (MB) is a dye that has shown promising results in the following areas:

  • Tissue hypoxia

  • Hyper dynamic circulation of the liver post cirrhosis

  • Improved low blood pressure states

  • Hepato-pulmonary syndrome

  • Anti malarial agent

  • Improves mitochondrial function

  • Detects parasites such as h-Pylori

  • With additional treatment of red light has anti-parasitic effects.

  • Anti-microbial-kills MRSA

  • Hepatitis C and other conditions also effectively treated in tandem with red light application.

  • Anti-Alzheimer’s agent- attenuates amyloid plaques (which are often protective and responsive to bacterial/endotoxin/pollutant damage so presumably threat is decreased) and improves mitochondrial function.

  • Improves Parkinson disease states

  • Improves thyroid hormone availability

MB is able to decrease both nitric oxide and guanylate cyclase, both exert their influence on smooth cells and tissue, explaining its role in reversing severely low blood pressure states ( Medically termed - catecholamine refractory vasoplegia)

If we look closely at a couple of the major mechanisms, we can see that from a metabolic standpoint MB has some interesting benefits. It decreases hypoxia or increases oxygen saturation within the body, whilst also improving mitochondrial energy production.

Metabolic enhancer:

The respiratory/ electron transfer (ETC) chain, that is essentially the mechanism providing optimal use of oxygen, carbohydrate, fat, when this functions well, carbon dioxide is produced, which allows for optimal dissociation of oxygen from haemoglobin. When the respiratory chain is damaged, cells often have to switch to inefficient anaerobic sources of energy production, wasting sugar and increasing lactic acid, which continue to decrease aspects of cellular function.

I managed to find several papers on the restorative and protective effects of MB to improve T3 levels within the blood and lower TSH. MB also seems to arrest estrogen stimulated pituitary growth and tumour development (Schreiber, Nedvídková, & Jahodová, 1993) (Haluzik, Nedvidkova, & Schreiber, 1995) (Nedvídková, Pacák, Haluzík, & Nedvídek, 2000).

Methemoglobinemia is a state where haemoglobin is unable to carry oxygen. MB reacts within the red blood cell and converts ferric ions, which have been oxidised, to its former oxygen carrying state. Additionally it helps to repair the ETC that is often damaged due to pollutant, poison or inefficient metabolic induced changes as seen in states of Alzheimer’s (Oz, Lorke, & Petroianu, 2009).

Anti parasitic

Another novel aspect of MB is the treatment of parasitic infection. MB absorbs and reacts with the spectrum of red light acting as an antimicrobial/parasitic agent.

1.jpg

“ Protozoa require the invasion of a suitable host to complete all or part of their life cycle.”

So what constitutes an appropriate host? I offer the following definition.

An individual or organism that is unable to assimilate and produce energy effectively, organise optimal cellular function and provide an immune response capable of expelling or eradicating an opportunistic parasitic/bacterial infection.

I quote Ray Peat with the following:

“ Occasionally you have very vigorous parasites that have intentions. If they encounter you in a state when your blood sugar is low, for example, the parasites might find an opportunity and start disorganising your system. So the competing systems’ lower system getting a foothold in a higher system, counts as randomness. The assumption of randomness is usually that everything is always random. What has been ordered is achieved at a high cost, the arrow of time for these people is that you have to expend energy to create order, and get things piled up in a certain way can only do that by expending energy somewhere else. "

MB and the use low level laser therapy (or LLLT which uses red or near infra red light) have a commonality with their ability to reduce the inhibitory actions of nitric oxide. This leads to enhanced cytochrome c oxidase action at complex IV of the ETC ( in English this means the enzyme that promotes better function of the cells that use oxygen efficiently), promoting increased cellular respiration and energy production (ATP). These dual actions appear to be an effective anti-parasitic treatment.

If your still running around taking a rucksack full of supplements, restricting energy and immune enhancing foods to kill parasites and candida, this may be a far more effective therapy to consider. It should be no surprise that that considering these actions, the use of MB is being investigated as a serious therapy in the fight against cancer. The biology of cancer can be attributed to metabolic defects/damage within the mitochondria leading to mutations.

Of course like any compound whether it be oxygen, water, broccoli or vodka certain doses are problematic. However these are generally high. For example doses used to treat malaria are suggested as 36-72mg/kg over 3 days (Meissner et al., 2006) and safe therapeutic doses are suggested as <2mg/kg (Ginimuge & Jyothi, 2010). New born babies seem susceptible to MB side effects such as skin discoloration, respiratory distress and other unwanted symptoms. However, the mechanisms of why this might happen, requires a blog alone. It also appears problematic to those taking SSRI’s and can increase serotonin uptake to toxic levels.

A neurological restorer?

There are plenty of studies (in rodents) supporting the restorative effects of MB to the central nervous system. Improvements to cognition, smell, movement and other factors related to senescence and neuro degeneration seem to be improved or at least slowed (Smith et al., 2017) (Atamna et al., 2008) (Biju et al., 2018). Often when pollutants and endotoxin are able to cross the blood brain barrier an increase in protective beta amyloids (AB) can be observed often as an antimicrobial response and to prevent damage but also affects the tau structures in the brain. Damaged/entangled tau appear to be improved and decrease necessary AB with use of MB. The resistance of pro-metabolic therapies in areas of disease such as dementia, Parkinson’s and even cancer should be questioned when compounds like MB seem to have such restorative effects to the oxidative system, neurological function and beyond.

What I have learnt from taking MB.

I found that if I took doses of more than 5mg total within a day or two of each other, my urine turned blue. A self -limiting factor that probably suggests that I was taking too much. I also had the odd crazy dream. I generally found that a total intake of 2.5 mgs or around 5 drops 2-3 days per week seemed to serve me well. I titrated up and found the optimal dose, something which I strongly recommend doing for all but much higher doses have been found to medically safe (whatever that means these days). It should also be noted that medical IV dosing, which probably has more beneficial effects on blood borne parasites will differ from oral administration.

I found that my pulse oximeter readings improved from a general SpO2 93-97 to regular 98. Which is interesting as one side effect previously suggested is the ability of MB to underestimate pulse ox readings. It’s prudent to imply that any therapeutic dose may only create change as the system allows. Therefore basics strategies such as effective blood sugar regulation, through regular eating and other strategies should be applied.

Ps it’s also great at reversing cyanide and nitrate poisoning in fish. Might it be useful in humans consuming too much bacon?

References:

Atamna, H., Nguyen, A., Schultz, C., Boyle, K., Newberry, J., Kato, H., & Ames, B. N. (2008). Methylene blue delays cellular senescence and enhances key mitochondrial biochemical pathways. FASEB Journal. https://doi.org/10.1096/fj.07-9610com

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

Biju, K. C., Evans, R. C., Shrestha, K., Carlisle, D. C. B., Gelfond, J., & Clark, R. A. (2018). Methylene Blue Ameliorates Olfactory Dysfunction and Motor Deficits in a Chronic MPTP/Probenecid Mouse Model of Parkinson’s Disease. Neuroscience. https://doi.org/10.1016/j.neuroscience.2018.04.008

Ginimuge, P. R., & Jyothi, S. D. (2010). Methylene blue: revisited. Journal of Anaesthesiology, Clinical Pharmacology, 26(4), 517–20.

Haluzik, M., Nedvidkova, J., & Schreiber, V. (1995). Methylene blue--an endocrine modulator. Sb Lek.

Meissner, P. E., Mandi, G., Coulibaly, B., Witte, S., Tapsoba, T., Mansmann, U., … Müller, O. (2006). Methylene blue for malaria in Africa: Results from a dose-finding study in combination with chloroquine. Malaria Journal, 5. http://doi.org/10.1186/1475-2875-5-84

Oz, M., Lorke, D. E., & Petroianu, G. A. (2009). Methylene blue and Alzheimer’s disease. Biochemical Pharmacology, 78(8), 927–932. http://doi.org/10.1016/j.bcp.2009.04.034

Nedvídková, J., Pacák, K., Haluzík, M., & Nedvídek, J. (2000). The regulation of adenohypophyseal prolactin secretion: Effect of triiodothyronine and methylene blue on estrogenized rat adenohypophysis. Physiological Research.

Schreiber, V., Nedvídková, J., & Jahodová, J. (1993). Anterior pituitary weight, cAMP, cGMP and prolactin levels after combined treatment with estradiol and methylene blue. Physiological Research / Academia Scientiarum Bohemoslovaca.

Smith, E. S., Clark, M. E., Hardy, G. A., Kraan, D. J., Biondo, E., Gonzalez-Lima, F., … Lee, H. J. (2017). Daily consumption of methylene blue reduces attentional deficits and dopamine reduction in a 6-OHDA model of Parkinson’s disease. Neuroscience. https://doi.org/10.1016/j.neuroscience.2017.07.001

Ray Peat quote originally taken from a YouTube interview with Andrew Murray. (cant recall which one)

https://www.google.com/patents/WO2007038201A1?cl=en 6. http://valtsus.blogspot.ae/ contains over 2500 LLLT studies and is by far the best resource available on the actions of LLLT.





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

 

What is functional hypothyroidism?

You won’t find the term functional hypothyroidism in the medical literature, or at least not yet. Primarily due to clinical hypothyroidism being bound to a rigid assessment usually diagnosed by the blood test thyroid stimulating hormone or TSH. TSH secretion is controlled by synthesis of thyroid releasing hormone or TRH in the supraortic and supraventricular nuclei of the hypothalamus. TRH is transported to the anterior pituitary by the hypothalamo- hypophysial portal system where it stimulates synthesis of TSH. T4, T3 and TRH control the secretion of TSH (Gardner et al., 2011).

TSH production can also be affected by TSH receptor damage, medical drugs, disease states, iodide, blood glucose levels and other circulating hormones TSH may also be affected by environmental pollutants and heavy metals (Llop et al., 2015).  Metabolic disease and increases in Body Mass Index appear to be correlated with an increase in TSH levels (Ruhla et al., 2010).

Often, you will see clear links and studies to key micronutrients such as zinc, selenium, iodine and other important co-factors. These deficiencies can exist demographically but usually in westernised societies, there deficiency can be linked to impaired absorption rates, perhaps linked to digestive dysfunction and other factors.

“Measuring the amount of thyroid in the blood isn’t a good way to evaluate adequacy of thyroid function, since the response of tissues to the hormone can be suppressed (for example, by unsaturated fats) (Peat, R.1999).

 Dietary factors such as unsaturated fatty acids in the diet may potentially be one of the most overlooked factors that supress thyroid function. Other factors such as caloric restriction, stressful environments, over exercising and other factors are some of the others. It’s well known that in certain areas of hormone dysregulation such as menstrual cycle irregularities, oligoamenorrohea (loss of cycle), anovulation (failure to ovulate) and lack of libido and fertility in both men and women,  can be attributed to poor energy intake and environmental factors (Nieuwenhuijsen et al., 2014) (Skakkebæk, 2003). Dietary factors have synergy with hormonal imbalances perpetuating high levels of estrogen.

The functional suppression of thyroid function by unsaturated fats, eating a so-called healthy diet (full of uncooked brassica vegetables, nuts and seeds) orthorexic states and other factors is largely ignored by physicians.

I can say with some certainty, after completing postgraduate studies at university with a number of Doctors, that diet and inhibitory factors of diet rarely get assessed when it comes to assessing energy and thyroid function.

A persistent functional hypothyroid state, induced by unsaturated fats may lead to the pre-diabetic and diabetic states induced by an inability to utilise carbohydrate and the preferential shift to use of fats instead of sugars as suggested in the Randle or glucose fatty acid cycle (Randle, Garland, Hales, & Newsholme, 1963). Increased cortisol, oxidation, decreased carbon dioxide and an increased stress on the oxidative system, could potentially lead to glycolysis and an increase in lactic acid, further increasing damage, stress and further suppression of thyroid function.

Measurement of thyroid blood tests remains inaccurate and problematic without the inclusion of a variety of symptoms and previously accurate assessment, such as basal metabolic rate, body temperature and pulse. The suppression of both thyroid and adequate energy states will always remain.

As the common approach for diagnosing hypothyroidism is having TSH above 4 or 5 mmUL and the preferred treatment is to supplement with synthetic levothyroxine. How much change can you realistically achieve if you fail to address the supressed metabolism induced by diet, an individuals susceptibility to stress and their own environment?

 

References:

Gardner, D. G., Shoback, D. M., Greenspan, F. S. et al .(2011). Greenspan’s Basic and Clinical Endocrinology. McGraw Hill.

Llop, S., Lopez-Espinosa, M. J., Murcia, M., Alvarez-Pedrerol, M., Vioque, J., Aguinagalde, X., … Ballester, F. (2015). Synergism between exposure to mercury and use of iodine supplements on thyroid hormones in pregnant women. Environmental Research, 138, 298–305. http://doi.org/10.1016/j.envres.2015.02.026

Nieuwenhuijsen, M. J., Basagana, X., Dadvand, P., Martinez, D., Cirach, M., Beelen, R., & Jacquemin, B. (2014). Air pollution and human fertility rates. Environment International, 70, 9–14. http://doi.org/10.1016/j.envint.2014.05.005; 10.1016/j.envint.2014.05.005

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

Randle, P. J., Garland, P. B., Hales, C. N., & Newsholme, E. A. (1963). The glucose fatty-acid cycle its role in insulin sensitivity and the metabolic disturbances of diabetes mellitus. The Lancet, 281(7285), 785–789. http://doi.org/10.1016/S0140-6736(63)91500-9

Ruhla, S., Weickert, M. O., Arafat, A. M., Osterhoff, M., Isken, F., Spranger, J., … Möhlig, M. (2010). A high normal TSH is associated with the metabolic syndrome. Clinical Endocrinology, 72(5), 696–701. http://doi.org/10.1111/j.1365-2265.2009.03698.x

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

 

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

It’s that time of year again, the silly season is upon us and plenty of people using inaccurate words such as detox are thrown around like Christmas wrapping paper. For many, the New Year is associated with dietary restrictions, born out of a period of over consumption from the festivities. May of those decisions such as stopping sugar or in particular fruit, as part of the so-called ‘detox ‘ is probably one the poorer choices that people do during this period of fad dieting. So it’s time to put the record straight on how to detox, or more appropriately how to maintain detoxification processes efficiently.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Adrenal Fatigue or Reductionist Thinking?

adrenal  

Here is the first part of my article, which published in the May 2014, Womens Health and Fitness Magazine.

Adrenal fatigue or reductionist thinking?

Often, being given a distinct diagnoses that can relate to modern living can   make sense to us, a modern condition that makes sense of the hectic lifestyle and the symptoms that we have been experiencing. Over the last decade there has been much literature on a so  called 'Adrenal fatigue', whose symptoms are wide reaching from fatigue, digestive dysfunction, weight and sleep issues.

Walther Canon and Hans Seyle, probably the most prominent  scientists to study and interpret the mechanics behind, adrenaline, cortisol and the stress response, showed that when  rats were exposed to high levels of stress, they developed issues such as ulcers, intestinal bleeding and then finally death. The common suggested auto immune diseases that are becoming more prevalent, such as intestinal hyper-permeability or leaky gut can therefore be interpreted as symptoms of chronic stressors.

The premise of adrenal fatigue works something along these lines.

  • You are exposed to stress
  • You produce stress hormones (Alarm phase)
  • Your body returns to normal
  • You become stressed again on a regular basis
  • You enter the adaptation phase
  • You constantly maintain the stress response through permanent exposure
  • The adrenal glands become exhausted
  • Suggestion that you have adrenal fatigue or exhaustion phase

There are many problems with this interpretation and deduction of adrenal fatigue, and how many practitioners treat this reductionist diagnosis.  If your adrenals were truly fatigued, you may not actually be with us anymore and ultimately be dead. Cortisol which is produced by the adrenal glands, is the primary hormone that directs immune function, inflammation and is involved in virtually all aspects of body function. Certainly the terms hypocortisolemia, too little cortisol and hyper, too much cortisol make sense, and that is what a typical adrenal stress test tells us. Are we producing too much or not enough cortisol , on that particular day, based around a suggested norm?

Cortisol does go up and down, and probably outside of suggested arbitrary norms especially if you experience or engage in the following:

  • Excessive physiological or structural stress, intense exercise without adequate rest.
  • Psychological stress
  • Diet or fail to eat enough calories, eating too much may also contribute over time
  • Eat a so called healthy diet based upon current guidelines
  • Fail to get adequate sleep.
  • Chronic exposure to environmental pollutants

The longer one stays in a state of chronic stress the more compromised all aspects of body function become. This can ultimately result in hormone, immune and metabolic systems dysfunction.

The positives from treating the aspects of adrenal fatigue are a compliance of those suffering from the suggested condition, to address aspects of why they have got to this current state of affairs. Overworking, too much or too little exercise, not enough sleep and psychological stress recognition can be aspects that can be changed with great effect.

To create effective change, should we not consider other aspects of function that would treat the root cause, rather than plaster over the symptom? Lets take a look at the cross over between symptoms of both adrenal and thyroid dysfunction, which have roots in energy and digestion. You may start to notice that there are many symptoms that you may experience a mixture of both and to highlight adrenal fatigue alone is problematic. The thyroid gland supports energetic process’s and when this becomes compromised we call on the adrenal glands to act in a supporting role. Addressing energy, metabolism and digestion, should be the target of any lifestyle or therapeutic interventions.

Adrenal symptoms Thyroid symptoms
Fatigue

Difficulty sleeping

Low blood pressure

Clenching teeth

Dizzyness

Arthritic issues

Crave salt

Sweats a lot

Allergies

Weakness

Afternoon crash

Need to wear sunglasses

Anxiety

Weight gain or loss

Difficult to lose or gain weight

Nervousness/anxiety

Constipation

Hair loss

Poor energy/fatigue

Feel cold hands and feet

Mentally sluggish

Morning headaches

Seasonal sadness

Poor sleep

 

 

 

 

However treating adrenal fatigue in isolation with adaptogenic herbs, restriction of sugar and other stimulants as is often the case, may be unwarranted and most importantly ineffective in resolving these issues. Treating any system in isolation is reductionist and often gives you at best, reductionist results. The complex interaction of the Hypothalamus-Pituitary-Adrenal-Thyroid-Gonadal axis is a system that helps our body manage many global aspects of our body's function and therefore addressing adrenal balance leaves a gaping hole in your treatment strategy. Consider that the adrenals and in particular cortisol production can be a slave to the your environment, nutrition, exercise and other lifestyle choices. Take stock, address what may be affecting your stress hormone production, If these factors can be changed do so. Stress is a double-edged sword. We need a certain amount of stress to improve our physiological function. Constant exposure to stress decreases our biological state.

Raising biological wholeness such as energy levels, cognition and increasing balance throughout the hormonal system can give much better results than focusing on the adrenals. Remember that the adrenals and ultimately cortisol production elevate in response to, what you eat, or fail to eat, the environment, psychological and physiological stress. All of these aspects are changeable.  In the next article I suggest some strategies that can be used to improve energy and lower adrenal stress.