Endocrinology

How to keep your energy chain maintained. Protective compounds.

How to keep your (electron transport) chain-2.png

How to keep your energy chain ( electron transport or ETC) running might not be something you think about, but if you are concerned about being healthier, this is an often overlooked area of maintaining health. It came as a huge disappointment to find out that the historical use of a false tooth compartment to hide cyanide tablets (for soldiers and spies) to commit suicide was pure fantasy. Although cyanide hidden in glasses appears to be more likely, the role of cyanide to induce rapid death is indisputable. We are at a time where industrial pollutants are at an all time high and cyanide being one of those pollutants, might not induce a theatrical foaming of the lips and contorted last throws of life (as seen in many an old war movie); it may induce a slower, less dramatic affect on cell function and efficient biology over time.

Cyanide is certainly ubiquitous in the industrialised environment but unknowingly for many, trying to achieve a ‘healthier’ balanced diet, cyanides are present in many foods favoured by the health conscious.

There are more than 2500 plants associated with cyanide content, these include almonds, millet, lima beans, soy, spinach, bamboo shoots, and cassava roots (which are a major source of food in tropical countries), cyanides occur naturally as part of sugars or other natural compounds. Cassava consumption (especially so in poorer countries) is associated with the neurological, irreversible disease called Konzo (Nzwalo & Cliff, 2011). Some other major sources of cyanide are:

Seeds/kernels of apples, apricots, plums, peach and nectarine, millet, almonds, flax seed, , spinach, sorghum gluten free flour like cassava often used to replace normal flours. Simply type in cassava poisoning into a search engine and you'll see some cases where dozens of people from the same meal have died from a so called bad cassava. Most likely it was the poor preparation and failure to remove the cyanide from the cassava that lead to these numerous deaths. In one case in the Philippines in 2005, 27 children died in such a manner.

Other cyanide sources include vehicle exhaust, releases from chemical industries, burning of municipal waste, and use of cyanide-containing pesticides (Jaszczak et al 2017) and the more obvious smoking.

Excess cyanide (ions) is able to disrupt the efficient production of energy that is produced through the electron transport chain/mitochondria (energy producing cells) where water, carbon dioxide and energy are end products. The loss of this function often creates a decreased ability to utilise carbohydrate effectively and the result can be an excess of lactate, which diminishes cell function further and creates hypoxia. Lactic acid seems to be getting some praise of late but it is the hallmark of inefficient energy production, as observed in the so called Warburg state seen in cancer (5). As cyanide levels increase cellular death occurs through increased lactic acidosis. This is the death throw that you see our actors who have crunched down on that mythical hydrogen cyanide capsule. It's also observed as a cause of death to the unlucky Private Santiago in A Few Good Men, where he has a rag with cleaning fluid, stuffed into his mouth creating a not to dissimilar occurrence.

[embed]http://gph.is/1hyjRwN[/embed]

You want the truth? You can't handle the truth but it might be that a combination of dietary cyanide and pollutants might not be as healthy as you think.

If there’s a ubiquitous source of cyanide and other pollutants in the environment does it make sense to have plenty of cyanide containing foods? Let’s not take this out of context. Here and there - having foods that have some levels of cyanide in should pose no problem to a healthy individual but what if your diet contains a regular supply and also contains plenty of vegetables that contain goitregens or foods that slow down thyroid function (and also contain cyanide) it may be problematic. Many people seem to promote a diet high in raw green vegetables, nuts, seeds, often low in adequate protein and often deficient in adequate energy/carbohydrate. In this instance the so-called healthy diet, in a highly polluted area becomes a burden not a provider of energy to promote optimal thyroid health, energy and liver enhancer (energy, detox, hormones etc.).

Chris Masterjohn’s report - Thyroid toxins, highlights the out of context suggestions of nutritional science evaluation of compounds in a test tube compared to a real world scenario.

The line that divides nutrients from toxins is often thin and equivocal. Since any given chemical may react in any number of ways in a test tube depending on the other chemicals with which it is combined, it is often possible to prove such a chemical to be both a nutrient and a toxin.

If a diet is to be considered healthy, it should meet the body’s energetic demands without reducing its function. A healthy energy chain ensures that carbohydrate is metabolised efficiently without an excess of lactic acid production.

The abundance of glucosinolates found in broccoli, cauliflower (and other brassica vegetables) and other cyanide like food sources combined with other environmental pollutants may pose substantial problems over time. Heavy metals like mercury, which are also increasing environmentally can decrease selenium and iodine uptake creating another algorithm for decreased function.

 cell enhancers

cell enhancers

Caffeine can be considered a useful compound for preventing excess uptake of metals and may go someway to explain the anti-oxidant and other positive effects observed in neurological degeneration diseases such as Alzheimer’s and dementia (Liu et al., 2016). Other compounds like methylene blue can be seen in the next diagram that promote a better energy chain.

" As I have shown in my earlier days , one can knock out the whole respiratory chain by cyanide and then restore oxygen uptake by adding methylene blue  which takes the whole electron transport chain over between dehydrogenases and  O2 ."   Albert Szent Györgi

You can also reduce the risk of excess cyanides in foods through heating, boiling and other forms of processing but given that the zeitgeist is as raw, wholesome and as gluten free as one can be, it’s unlikely that this occurs in the upwardly mobile food neurotic.

References:

  1. Jaszczak, E., Polkowska, Ż., Narkowicz, S., & Namieśnik, J. (2017). Cyanides in the environment—analysis—problems and challenges. Environmental Science and Pollution Research, 24(19), 15929–15948. http://doi.org/10.1007/s11356-017-9081-7

  2. Liu, Q.-P., Wu, Y.-F., Cheng, H.-Y., Xia, T., Ding, H., Wang, H., … Xu, Y. (2016). Habitual coffee consumption and risk of cognitive decline/dementia: A systematic review and meta-analysis of prospective cohort studies. Nutrition, 32(6), 628–636. http://doi.org/10.1016/j.nut.2015.11.015

  3. Nzwalo, H., & Cliff, J. (2011). Konzo: From poverty, cassava, and cyanogen intake to toxico-nutritional neurological disease. PLoS Neglected Tropical Diseases. http://doi.org/10.1371/journal.pntd.0001051

  4. Masterjohn, C. Thyroid Toxins Report. 2007

  5. http://raypeat.com/articles/articles/cancer-disorder-energy.shtml

  6. Szent Györgi, A. Introduction to a Submolecular Biology. Academic Press. 1960.

http://www.keithlittlewoodcoaching.com

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

 pain and hormones

pain and hormones

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

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

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

Hypothyroidism results in

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

 cold body

cold body

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

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

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

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

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

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

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

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

References:

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

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

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

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

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

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

Estrogen excess.png

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

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

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

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

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

The biologist Jean Baptiste Lamarck's fourth law stated:

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

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

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

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

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


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

To find out more about coaching for these issues.

References:

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

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

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

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

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

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

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

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?

Is Testosterone replacement therapy (TRT) necessary or symptom chasing? [embed]https://www.youtube.com/watch?v=KC0-xL0JVrI&feature=youtu.be[/embed]

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.

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 and vitamin A deficiency but does that still implicate sunlight as the cause of skin cancer? The A to B scenario hopefully seems less convincing.

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

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.

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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

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