progesterone

The Big Estrogen Hoax

Routine spraying with potent pesticides was deemed safe previously.

Routine spraying with potent pesticides was deemed safe previously.

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

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

Why is pregnancy protective?

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

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

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

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

Why so much confusion?

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

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

Progesterone is protective across many aspects of function

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

 

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

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

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

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

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

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

 References: 

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

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

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

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

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

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

 

 

 

Free Happy Hormones Copy

happyhormones2-4.jpg

Feel free to share around.


Download Happy Hormones

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

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

New logo Luara.jpg


                      

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); however 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.


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

Scar tissue - is it an issue?

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

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

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

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

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

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

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

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

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

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

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

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

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

References:

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

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

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

Sunlight, health and cancer

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

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

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

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

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

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

Promoting better conversations between structures     

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

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

Estrogen

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

Thyroid failure

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

Fat status of tissues.

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

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

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

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

References:

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

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

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

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

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

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

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

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

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

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

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

Estrogen and aromatase - Keeping the wolves from the door.

Estrogen and aromatase,  (and the  role of prolactin and a lack of progesterone) in cancer are well documented and so are the stimulatory effects of the neuro-endocrine (nervous system/hormones) disruptors termed xenoestrogens, which mimic the action and excess of estrogen (Kim, Kurita, & Bulun, 2013) (Mungenast & Thalhammer, 2014). Estrogen and notably estradiol/E2 is often measured by a standard blood test, which remains as problematic as other blood tests such as TSH, which I have previously described. “ At first, it was assumed that the amount of the hormone in the blood corresponded to the effectiveness of that hormone. Whatever was in the blood was being delivered to the “target tissues.” But as the idea of measuring “protein bound iodine” (PBI) to determine thyroid function came into disrepute (because it never had a scientific basis at all), new ideas of measuring “active hormones” came into the marketplace, and currently the doctrine is that the “bound” hormones are inactive, and the active hormones are “free.” Ray Peat

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

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

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

Myopic thinking.

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

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

Solutions.

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

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

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

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

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

  

References: 

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

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

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

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

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

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

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

 

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

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

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

Secondary osteoporosis can be related to the following factors

Hypogonadism - testosterone/estrogen deficiency
Endocrine disease - Cushing’s syndrome, acromegaly, thyrotoxicosis, Addison’s disease and hyperparathyroidism
Dietary or assimilation deficiencies of calcium, vitamin K, vitamin D and other nutrients
Inflammation-rheumatoid arthritis, systemic lupus and ankylosing spondylitis
Neoplasms- Myleoma, lymphoma and leukaemia
Reduced physical activity
Medical drugs - corticosteroids, antiretroviral, antipsychotic, chemotherapy, hormone therapy, nicotine and excessive alcohol
Family history/genetics
Diabetes

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

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

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

Diagnosis

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

Hormones

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

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

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

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

Medical treatment

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

 Nutrition

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

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

  • Vitamin D in isolation and particularly high doses increases fracture rates (Janssen, Samson, & Verhaar, 2002)
  • Unless vitamin D is accompanied by adequate calcium, BMD can decrease further.
  • Vitamin K2 can prevent the calcification of soft tissues and help improve blood calcium levels (Masterjohn, 2007)
  • High meat and diets high in pulses and beans can have a negative effect on calcium levels due to their high phosphate levels.
  • Unless you assess other key nutrients like magnesium and the factors discussed above
  • Low diary intake can be associated with poor bone health.
  • The low carbohydrate, raw green and seed eating diet suggested by holistic health practitioners may contribute to lower BMD.

Exercise

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

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

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

References:

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

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

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

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

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

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

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

Estrogen and Progesterone

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

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

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

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

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

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

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

CYCLEovul

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

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

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

·      Increased body fat

·      Salt/ fluid retention

·      Clotting

·      Depression

·      Headaches

·      Decreased libido

·      Impairment of blood sugar

·      Reduced oxygen

·      Risk of breast cancer

·      Osteoporosis

·      Decreased thyroid

·      Increases CV issues.

·      Anti tumour effects·      Supportive to fertility

·      Sedative effects

·      Improves blood sugar

·     Decreases  Ovarian cysts

·      and Menopausal flushing

·      Removal of facial hair

·      Decreased Menstrual cramping

·      Improved auto-immune

·      Hormonal balance

·      Anti -Stress

·     Decreased arthritis

·      Promotes sleep

·      Thickens hair on head

 

 

 

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

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

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

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

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

References:

Dalton, K The Menstrual Cycle.

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

Peat, R. Nutrition for Women.

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

Online references:

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

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

 

 

Calcium- Don't ditch the dairy.

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

Don't ditch the dairy

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

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

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

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

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

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

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

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

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

References:

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

Online:

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