Estrogen and aromatase – Keeping the wolves from the door.

Estrogen and aromatase,  (and the  role of prolactin and a lack of progesterone) in cancer are well documented and so are the stimulatory effects of the neuro-endocrine (nervous system/hormones) disruptors termed xenoestrogens, which mimic the action and excess of estrogen (Kim, Kurita, & Bulun, 2013) (Mungenast & Thalhammer, 2014). Estrogen and notably estradiol/E2 is often measured by a standard blood test, which remains as problematic as other blood tests such as TSH, which I have previously described.

“ At first, it was assumed that the amount of the hormone in the blood corresponded to the effectiveness of that hormone. Whatever was in the blood was being delivered to the “target tissues.” But as the idea of measuring “protein bound iodine” (PBI) to determine thyroid function came into disrepute (because it never had a scientific basis at all), new ideas of measuring “active hormones” came into the marketplace, and currently the doctrine is that the “bound” hormones are inactive, and the active hormones are “free.” Ray Peat

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

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

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

Myopic thinking.

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

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

Solutions.

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

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

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

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

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

  

References: 

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

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

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

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

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

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

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

 

Gestational diabetes and metformin-Is that the best that medical thinking has to offer?

Gestational diabetes or elevated blood sugar is often treated with metformin to improve blood sugar levels and considered the standard approach to treating gestational diabetes. The research suggests that it has little negative effects on the pregnant mother. However, does significant risks to both mother and baby if the incidence of premature birth count? Here are a few aspects to consider regarding the use of metformin to control blood sugar during pregnancy.

A study of patients receiving a dose of metformin, combination of Clomiphene citrate (CC) and metformin both faired better than CC alone for the induction of ovulation (Neveu, Granger, St-Michel, & Lavoie, 2007).  As the combined group showed no benefit compared to metformin alone, one might consider that metformin alone may be considered for the positive effects.

In another study metformin and diet interventions showed a significant outcome compared to non-metformin-diet interventions. The metformin diet showed a reduction of 14 adverse events in a group of 76 expectant mothers, compared to the non-treated group of 36 adverse events out of 76 pregnancies (Glueck et al., 2013).

Thatcher and Jackson (Thatcher & Jackson, 2006) compared pregnancies of 188 women. 61 experienced miscarriages and 11 of those had stopped taking metformin, suggesting other abnormalities beyond metformin’s actions. 81% of women with pregnancies before metformin, 67% had prior miscarriages. 37% of these also miscarried again. Whilst metformin appeared to show minimal effects to mother and foetus 22% were born prematurely.

Whilst metformin has shown favourable outcomes in PCOS states, questions around pertinent biological mechanisms should warrant further discussion. It’s well known that two key endocrine actions may be compromised during the failure to achieve full gestation. Estrogen induces hypoxia in the uterus (Peat, 1997) and failure to produce adequate progesterone to counter the effects of estrogen may be implicated in the commonly fragile time around weeks 9-10 of pregnancy and incidence of miscarriage.

A concern of metformin are its affect transplacentally. Metformin appears to influence testicular size in males and affects sertoli cells. In females it may also lead to decreased androgen synthesis. Birth weight percentile is also significantly lower in pregnancies treated with metformin (Bertoldo, Faure, Dupont, & Froment, 2014)I Metformin has generally appeared safe in expecting mothers but considerable concern should be made regarding its long term effects to offspring and development most notably to reproductive tissues.

Hypothyroidism is a key factor in maintenance of pregnancy and alongside progesterone, thyroid hormone deficiency can be implicated in poor cellular energetics, production of adenosine tri phosphate (ATP) and blood sugar regulation. There remains much debate about the issue of subclinical hypothyroidism, values and when to treat and perhaps metformin’s role despite showing some promises may be treating a symptom related to insulin sensitivity. Failure

So perhaps these questions might be more pertinent before prescribing an agent that shows potentially negative effects to the fetus?

  1. What is the nutrition of the mother, is it enough and does it contain enough nutrients to enhance/maintain adequate progesterone/thyroid production?
  2. Is estrogen increasing at a rate that suppresses progesterone/thyroid levels and persistently decreases insulin sensitivity?
  3. Is there enough carbohydrate in the diet to ensure that carbohydrate is effectively utilised instead of persistent conversion of fats, increasing overall stress to both mother and fetus?
  4. Are the values of hypothyroidism and the identification of subclinical/functional hypothyroid factors appropriate?
  5. Is gestational diabetes a reflection of the above points?

The use of metformin, without questioning these mechanisms, remains at best a reduced treatment that fails to address a range of biological interactions and function.

References:

Bertoldo, M. J., Faure, M., Dupont, J., & Froment, P. (2014). Impact of metformin on reproductive tissues: an overview from gametogenesis to gestation. Annals of Translational Medicine2(6), 55. http://doi.org/10.3978/j.issn.2305-5839.2014.06.04

Glueck, C. J., Goldenberg, N., Pranikoff, J., Khan, Z., Padda, J., & Wang, P. (2013). Effects of metformin-diet intervention before and throughout pregnancy on obstetric and neonatal outcomes in patients with polycystic ovary syndrome. Current Medical Research and Opinion29(1), 55–62. http://doi.org/10.1185/03007995.2012.755121

Neveu, N., Granger, L., St-Michel, P., & Lavoie, H. B. (2007). Comparison of clomiphene citrate, metformin, or the combination of both for first-line ovulation induction and achievement of pregnancy in 154 women with polycystic ovary syndrome. Fertility and Sterility87(1), 113–120. http://doi.org/10.1016/j.fertnstert.2006.05.069

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

http://raypeat.com/articles/articles/glucose-sucrose-diabetes.shtml

Thatcher, S. S., & Jackson, E. M. (2006). Pregnancy outcome in infertile patients with polycystic ovary syndrome who were treated with metformin. Fertility and Sterility85(4), 1002–1009. http://doi.org/10.1016/j.fertnstert.2005.09.047

What is functional hypothyroidism?

You won’t find the term functional hypothyroidism in the medical literature, or at least not yet. Primarily due to clinical hypothyroidism being bound to a rigid assessment usually diagnosed by the blood test thyroid stimulating hormone or TSH.

TSH secretion is controlled by synthesis of thyroid releasing hormone or TRH in the supraortic and supraventricular nuclei of the hypothalamus. TRH is transported to the anterior pituitary by the hypothalamo- hypophysial portal system where it stimulates synthesis of TSH. T4, T3 and TRH control the secretion of TSH (Gardner et al., 2011).

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

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

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

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

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

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

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

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

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

 

References:

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

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

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

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

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

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

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

 

An energetic approach to restoring gut function: Part 1.

Let’s kick this blog off with a question as to whether or not an energetic approach to restoring  gut function is useful when compared to over analysis? Let me clarify, that I have had my fair share of success stories with a reduced and diagnostic approach to improving gut health. Just like I have also had my fair share of kickbacks from the laboratory for recommending their tests. At one point I was using nearly 200 stool tests per year and making a little cash on the side. Many of the tests worked in isolating some specific disturbance to their gut bacteria, presence of a parasite or elevation of putrefied fatty acids. A ‘cleansing’ diet was promoted and a few supplements for good measure created some short term change whilst the client was in my care.

But here’s why the long-term approach to that type of assessment and treatment may not be the best response. A standard functional medicine approach  after spending quite a lot of cash on an integrated stool test is using the 4 R approach.

Remove (offending parties)- spend money on supplements

Restore function- spend money on supplements

Re-inoculate – spend money on nice expensive probiotics

Repair gut lining- spend money on supplements

Regurgitate. Ok the 5th one is mine but no supplements needed.

By taking this approach, an important question is not asked of the individual. Why is this person experiencing an overgrowth of bacteria/SIBO, parasitic infection, endotoxin overgrowth, inflammation and degradation of the bowel lining? I like to think that it is not because of the easy kickbacks FM practitioners are getting for the lab tests and supplements they recommend? So what is the persons level of biological energy and immune system function that allows their digestive system to get in such a state. We know there are some usual suspects. Food, stress or alcohol perhaps?

The typical gastrointestinal complaints people came to me with, were bloating, excess gas, constipation or irritated loose stools combined with poor energy. It was Ilya Mechnikov who originally stated that death starts in the bowel or colon and there’s’ certainly many degenerative and inflammatory conditions that appear at the last stop to poopy central. But is the bowel the main driver of this dysfunction? Many of the symptoms that I recalled earlier are also key symptoms of an energetic and perhaps a thyroid dysfunction. So instead of reaching for our drastic 4 R protocol with an expensive poo test lets consider the following.

 The likes of Broda Barnes and Ray Peat have highlighted how a lack of energy, either from a low or inappropriate food intake or a dysfunctional hypothalamic-pituitary-adrenal-thyroid axis can be evaluated by assessing body temperature and the combination of pulse. Additional information on Thyroid and TSH evaluation can be found here.

Most people are aware that when they get stressed or exercise, blood is shunted away from the digestive system to the periphery and other working tissues. Even the concept of high Adreno-corticotrophic hormone (ACTH), cortico releasing hormone (CRH) and adrenal production of cortisol is becoming common place in work and gym environments alike. These hormones suppress thyroid hormone and the energy compound ATP that provide energy for tissues.

It’s also well known that low energy states create tight painful muscles that are difficult to relax and one might be able to apply that line of thought to the smooth muscle tissues that regulate bowel contractility. Therefore a low energy state that does not allow for adequate energy production will not allow adequate digestion and bowel function to occur. Cold hands and feet can be a symptom of not eating enough carbohydrate and protein.

If the cold hands and feet, low body temperature, fatigue, constipation don’t resolve from eating energy rich meals that contain plenty of fruit and contains little of the foods that promote the bowel irritants histamine and serotonin (nuts, seeds, vegetable oils, grains, gluten free products, beans and pulses). Then, often factors that influence the hormones such as thyroid, estrogen and progesterone may need a deeper consideration.

I drafted a little flow chart that will be helpful for some quick strategies on what might be happening but what I would like to focus on the low energy state that might have its source from a food or hormone factor or perhaps both. Instead of using a strategy like the 4 R approach, these simple questions can help guide you to understanding whether it is the foods that you eat or an energetic factor that could be causing your digestive system to suffer. It’s not a complete algorithm but it does offer some simple solutions that have helped plenty of people resolve digestion and energy issues.

Foot note: I haven’t needed a stool test with a client for over 4 years now following this chart.

 

In part 2 I will elaborate on foods and basic supplements that can be used to resolve most long standing digestive issues and understanding other hormone actions that create digestive discord.

References:

Lokaj, J., & John, C. (2008). [Ilya Ilich Metchnikov and Paul Ehrlich: 1908 Nobel Prize winners for their research on immunity]. Epidemiologie, Mikrobiologie, Imunologie : Casopis Spolecnosti pro Epidemiologii a Mikrobiologii Ceské Lékarské Spolecnosti J.E. Purkyne, 57(4), 119–24. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/19069024

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

Peat, R. (2006). Autonomic Systems. Retrieved from raypeat.com/articles/other/autonomic-systems.shtml

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

Health, Thyroid and TSH.

Increasingly health is defined by a bunch of arbitrary numbers. High cholesterol? That’s not normal take a pill. Low iron? Here take this iron supplement. In Ivan Illich’s book, Limits to Medicine- Medical Nemesis, Illich makes the reader fully aware of his disdain of medical check ups –

” The medicalisation of prevention thus becomes another major symptom of social iatrogenesis. It tends to transform personal responsibility for my future into my management by some agency.”

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

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

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

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

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

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

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

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

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

References:

Hoang, T. D., Olsen, C. H., Mai, V. Q., Clyde, P. W., & Shakir, M. K. M. (2013). Desiccated thyroid extract compared with levothyroxine in the treatment of hypothyroidism: A randomized, double-blind, crossover study. Journal of Clinical Endocrinology and Metabolism, 98(5), 1982–1990. http://doi.org/10.1210/jc.2012-4107

Illich, I. Limits to Medicine – Medical Nemesis. Marion Boyars. 1976.

Pantalone, K. M., & Nasr, C. (2010). Approach to a low tsh level: Patience is a virtue. Cleveland Clinic Journal of Medicine. http://doi.org/10.3949/ccjm.77a.10056

 

How to improve sleep-wake cycles.

Do you need to improve sleep? Why is it that sometimes, with the best intentions of going to bed early, we either find ourselves struggling to enter a sleep cycle, or wake up, deep in the hours of darkness? The prominent stress researcher Robert Sapolsky (Why Zebras don’t Get Ulcers) writes fondly of his near death experiences, of little sleep from the arrival of his newborn child.

It’s no surprise that security and intelligence operatives use a lack of sleep to disorientate prisoners. Just one nights lack of sleep from me and I will tell you anything! Despite the will to nod off, why is it that many people suffered from poor sleep, or struggle to enter sleep cycles?

Before I delve into some brief hormonal issues that can be manipulated to ensure a deeper sleep it’s worth noting that darkness itself is a stressful experience and we produce many restorative hormones during sleep to combat the metabolic stress of darkness. Therefore one essential component of adequate sleep is exposure to sunlight on a daily basis. This ensures uptake of vitamin D and exposure to the deeper penetrative orange and red lights, which help to restore metabolism and healing of cells. An old blog on light therapy.

Over the years I have found the following issues associated with poor sleep.

  • Low blood sugar levels
  • Increase in compounds of wakefulness
  • Exercise late at night
  • Excessive work stress/blue light exposure
  • Exposure to EMF-electromagnetic stress and Wi-Fi
  • Poor sleep and its vicious cycle
  • Emotional Stress

There are several models to be aware of when it comes to sleep theory and the phases of sleep are categorised as

NREM – Non rapid eye movement- pre REM sleep.

REM – Rapid eye movement- this is the deep restorative part of sleep
Active wake

Neurotransmitters and hormones associated with sleep:

Acetylcholine – AcH is the neurotransmitter associated with Rapid Eye Movement or REM sleep.

Serotonin – 5HT this neurotransmitter along with HA is associated with wakefulness.

Norepinephrine/Noreadrenaline – Ne – Hormone of wakefulness.

Gammaminobutyric Acid – GABA. GABA’s role in sleep is well documented but levels vary depending on location of the brain. It’s role is known in decreasing wakefulness and also decreasing deeper REM sleep and involved in producing wakefulness.
Histamine- HA involved in wakefulness.

Hypocretin Orexin- PCT /O Involved in wakefulness.

Adenosine- AD involved in entering NREM sleep.

Here is a rough depiction of key Neurotransmitters of REM and NREM sleep. Other neurotransmitters of wakefulness such as Histamine, Serotonin and noreadenaline (hormone) are not depicted but are elevated in waking state and should be lower during sleep cycles. It’s worth noting that the use of serotonin in mood related disorders such as depression is a key agent in insomnia like states.

sleep neurotransmitters

 

Common sleep disorders

Insomnia:  The inability to sleep restfully and I would categorise a good nights sleep from 6-9 hours depending on your own needs. The ability to enter deep sleep is dependant on many factors such as hormones, neurotransmitters, stress and available energy. It’s worth noting that the regenerative aspects of REM sleep and brain function have been shown to use as much glucose as when awake. Maintaining adequate available energy is key to getting sound-nights sleep.

Sleep apnoea: inability to enter REM sleep due to issues associated with optimal breathing. Obesity and sleep apnoea do seem to correlate and there is a suggestion of structural abnormalities in a small section of people.

The role of sleep in disease prevention

Sleep’s role in psychiatric disorders, depression, metabolic disease and addiction are well documented. A key feature of a lack of sleep, besides on-going fatigue and failure to regenerate is the elevation of adrenalin and cortisol. Elevated levels of cortisol are well known to decrease thyroid function, which can have a significant effect on levels of circulating thyroid hormone and energy production (key to regulation of sleep). The mechanism can tie in with its pervasive actions on management of blood sugar levels. Another noted effect from sleep loss is that we tend to overeat more when tired, which could impact weight gain (and if thyroid is part of the vicious cycle, weight loss becomes increasingly difficult).

Lack of quality sleep can therefore be responsible for an increasing amount of deleterious conditions, such as hypothyroidism, diabetes and obesity, other hormone dys-regulation and cardiovascular disease. Ascertaining whether the issue initially stems from a hormone imbalance can be key in resolving sleep wake issues.

Drugs

There are a variety of drugs on the market that help to improve onset of sleep, however if you seek to improve the biological mechanisms of sleep and perhaps look to the list suggested below, you may find that your sleep improves, without the need for medication.

Cognitive behavioural therapy

The role of CBT in reducing Insomnia has shown effective results even more so than prescriptive medications. Whilst the treatment is not determined whether it effectively targets the mechanics of insomnia its success suggests provides a more desirable approach than long term insomnia medication.

What can you do?

  • Understand the link between production of inflammatory neurotransmitters such as Histamine and Serotonin and seek to lower them. This may be through diet adjustment or exposure to problematic chemicals/hormones.
  • If you get to sleep but wake up, this may be due to poor available energy. Maybe from a low carb diet, low thyroid function and poor production of energy. You may find having something light like a glass of milk with honey, or fruit juice with gelatin may help out. Salt also helps to decrease adrenalin production
  • Wi-Fi, blue light exposure, electromagnetic stress all play their part in interfering with stress and how the cells function. Stopping their use several hours before sleep can help. Do turn off Wi-Fi in house and no phones or electric devices by your bed.
  • Avoid stimulus such as caffeine or exercise in the evening, if you have sleep issues. Caffeine decreases production of adenosine.
  • If under emotional stress, a slow walk before bed may be a useful idea combined with ensuring adequate blood sugar levels are met.

References:

Neurobiology of Sleep. Course notes. Duke University. 2015.

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

Sapolsky R. Why Zebras don’t get Ulcers. St Martins Griffin. 1998

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2941414/

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3443758/

http://www.ncbi.nlm.nih.gov/pubmed/27091535

 

Muscles, pain, hormones and other stuff.

As a therapist who works within the fields of pain, movement, energy and digestion I have seen my share of pain and muscle dysfunction in clients. As my exposure to these situations increase, I realise more than ever, that the muscles are very rarely the problem.

Specific muscle dysfunction usually boils down to spindle cell

Thyroid pic

Muscle pain and thyroid hormone

dysfunction and notably Nuclear Bag Fibres (NBF) and Nuclear chain Fibres (NCF). The primary roles of these structures are related to stretch and contraction of muscle function. There can be other factors involving neuro transmitters, involved in nocicpetion such as glutamate, utilised in the withdrawal reflex and often referred to as first pain, (also known as Neospinalthalamic tract located in the Anterolateral system or ALS) and lasting, less than a tenth of a second. Problems can arise when the following pain pathway, called second pain (or Paleospinalthalmic tract also part of the ALS) has problematic feedback with first pain, this is mediated by Bradykinin.

Further complexities arise with serotonin and other structures associated with pain such as the Amygdala and Peri Aqueductal Gray (PAG) that are beyond the scope of this short blog. However a common, over looked feature of pain, may arise with hypothyroidism .

Low thyroid function can be classified effectively with assessment of a basal temperature test and a reading of between 36.6 and 37 degrees. Most blood tests designed to measure thyroid hormones such as TSH, T3, T4 and others, often do not reflect accurate function of thyroid hormone. This is often due to feedback loops between cellular function and the Pituitary gland. Some of the regular hallmarks of hypothyroidism are poor energy, weight gain, poor sleep, hair thinning, digestive dysfunction (constipation and also alternating loose stools), cold hands and feet and pain. Here’s an old blog on thyroid and adrenalin issues.

Another assessment of thyroid function is the Achilles return reflex. When stimulating the myotactic reflex a hammer hits the Achilles tendon stimulating, the dorsi flexors or calf muscles. The response should be a quick return of the foot to it’s resting position but with low thyroid the foot returns slowly. Low thyroid output equals low ATP (Adenosine Tri Phosphate – the energy used by the mitochondria/cells). This low energy state does not allow for optimal contraction and relaxation. This is where we can see specific issues with NCF and NBF’s within the muscle spindle cell.

Muscle tendons and associated ligaments provide a feedback loop via the Golgi Tendon Organs or GTO’s. There’s potential for pre-existing GTO dysfunction to drive muscle dysfunction and vice versa. As far back as the 1960s symptoms associated with muscle disorder from low thyroid were.

* Weakness

* Cramps pain and stiffness

* Hypertrophy

* Myotonoid features.

A well-documented feature of hypothyroidism is muscular hypertrophied calf muscles and despite their size may often test weak to stimulation.

Muscle pain, may indeed not be muscle related, it may be due to many factors, suggested above and these may even be related to hormones and neurotransmitters. Many people often deal with muscle aches and pains by constantly focusing on mobility work but these structures continually return to their pre mobility work status (although this could also be an underlying stability issue). In reality there can be many factors that create dysfunction such as crude touch, vibration, nociception, Golgi, Pacini-pressure related structures and many more. But even after seeing a skilled therapist, these still don’t appear to get better, then addressing the chemical aspects of pain and function might be the next sensible thing to do.

References:

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

Ramsay I. Thyroid disease and Muscle Dysfunction. William Heinemann Medical Books. 1974.

Purves, D. et al. Medical Neuroscience. 5th Edition. Sinauer Assocates Inc. 2001

Starr, M Hypothyroidism Type II. Mark Starr Trust 2013.

http://raypeat.com/articles/articles/hypothyroidism.shtml

Sunlight, Low Level Laser Therapy and Photobiomodulation

Sunlight, Low Level Laser Therapy and Photobiomodulation

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

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

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

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

Low Level Laser Therapy and Photobiomodulation

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

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

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

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

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

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

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

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

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

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

References:

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

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

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

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

Online resources:

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

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

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

 

 

 

 

Are probiotics essential for optimal gut health?

Probiotics are often being recommended to deal with a variety of digestive health complaints today. I have been intrigued for many years of the role of the digestive system; it’s functions and ultimately how bacteria can contribute to improved or decreased health. Recently, the last two newsletters from Ray Peat PhD have quoted studies, where animals that were born into sterile environments had improved metabolic rates. He also alluded to the increased lifespan of animals with higher metabolic rate in his book, Generative Energy.

Probiotics have been touted for many years to assist with optimal gut function but like many products these days have swiftly been elevated to cult status, with their miraculous, cure all capacity suggested by those that sell them. But what does the science say? A summary of The Cochrane database provides plenty of research that shows that probiotics do have a positive impact in the short term, decreasing acute diarrheal like symptoms; however it’s impact on issues such as IBS remain inconclusive and controversial.

The gut flora and microbial mass is suggested to weigh up to 7kgs, second only in weight to the skin as the largest mass found in the human body. There exist over four hundred different species of bacteria with a predominance of anaerobic bacteria found mostly in the lower bowel. The problem with anaerobic bacteria is that the by-product of these species is the production of lactic acid and other metabolites that are damaging to cellular function.

Bacteria are often classified as pathogenic or disease causing or ‘friendly’ whose role can assist in production of Vitamin K2, biotin and B vitamins amongst other compounds. Bacteria can also increase the production of nitric oxide and endotoxin ( a compound well known to disrupt the mucosal barrier and enzymatic process of the bowel) is known to increase it further. An intriguing question would be whether an increase of certain bacteria predominate when we have a lower intake of certain foods

It is clear that metabolites from all bacteria do pose a challenge to cellular function and certainly when there is an overgrowth or dysbiosis they produce increased compounds that can create health issues dependant on the host’s immune and metabolic status. Probiotics like other supplements are often recommended long term but even the so-called friendly bacteria have the capacity to cause metabolic disturbances. Some species of lactobacilli in excess, cause a condition called D-Lactate acidosis, which disrupts metabolism and has significant impact on mood, digestion and energy. I can recall a three-year-old client who presented with anger and constipation ( 1 bowel movement per week) whose mother thought she was doing the right thing by feeding plenty of fermented foods and yoghurts with natural bacteria. Within a week of removing these foods the issues had stopped.

Chis Masterjohn PhD suggests, ‘Not every fermented food is good for every person, and some people don’t tolerate fermented foods well at all. I think this is largely mediated by the biogenic amine content.’

A common diagnosis clients have been told is one of fructose or carbohydrate malabsorption. When carbohydrate in the diet is high in the absence of a healthy bowel this may be an issue. However if Lactobacillus levels have not been checked, we cannot rule out the possibility of fermentation of carbohydrate due to the action of increased Lactobacilli.

E.E. Metchnikoff’s view that disease starts in the colon is a widely accepted statement. Reducing the amount of bacterial agents in the bowel and increasing protective factors such as decreased adrenalin and improved thyroid function can complete elevating the biological status of a person. A stressed digestive system that does fails to produce adequate stomach acid (Achlorhydria or hypochlorhydria) often increases the amount of bacteria in the lumen of the bowel. Partially undigested food accumulates and elevates lipopolysaccharides from increased endotoxin, damaging the bowel. An increase in adrenaline and decreased thyroid hormone can contribute to decreased stomach acid production via stress pathways. Helicobacter pylori, bacteria that buries into the stomach wall may also contribute to this issue.

High protein diets have the capacity to increase bacterial action in the bowel and a metabolite of tryptophan degradation is indole. This increases ammonia and is problematic to the function of the bowel. This is often the reason for practitioners often suggesting an alkalinising type of diet. Alkaline environments pose just as much a problem as acidic environments. To decrease the bacterial actions of tryptophan, increasing the amount of gelatin like substances may be more beneficial than trying to restrict protein. The amino acids glycine, arginine and proline, found in gelatin do not have the carcinogenic properties associated with tryptophan, which is high when consuming muscle meats alone. Metchnikoff’s theory of putrefactive dysbiosis  would fit better here but fermentive dysbiosis of grains and carbohydrates is prevalent in the poor performing bowel also.

Whilst antibiotics have gotten a bad rep over the last twenty years there can still be much use for them especially when there are stubborn gastrointestinal infections. Antibiotics seems to also work well in reducing the impact of endotoxemia

Testing the bowel can be completed with a CDSA (comprehensive stool analysis) or to accurately assess metabolite an organic acid urine analysis. These tests often cost £250-400 and present a considerable expense to clients. I personally think these tests should be completed after you have tried to optimise the bowel with optimal foods that digest well and support hormonal function. A caveat to that would be, when a client presents with parasitic infections or autoimmune type systems that may need further investigation

To summarise, I think probiotics can be useful in the short term to people with acute problems, primarily due to restricting proliferation of problematic bacteria but in many cases long term use is unwarranted and may even contribute to health issues.

References:

 

  1. Lord, R.S and Bralley, J.A. Laboratory Evaluations for Integrative and Functional Medicine. Metametrix Institute. 2nd 2008.
  2. Peat, R. Generative Energy. Restoring the Wholeness of Life. 1994.
  3. Chris Masterjohns Blog http://blog.cholesterol-and-health.com/2015/08/weighing-in-on-fermented-cod-liver-oil.html
  4. .http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD003048.pub3/abstract;jsessionid=5315A28A4390280DD5D4257508AD7AC0.f04t02
  5. http://onlinelibrary.wiley.com/enhanced/doi/10.1002/14651858.CD005573.pub2
  6. Ray Peat Newsletters: Directing Epigenetic Adaptation/Imprinting and Aging