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

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.


 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).


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


 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.


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


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

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.


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.


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





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

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.


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.



Coconut oil, its protective effects both cellular and shellular.

Image-1 (2)I have written many times on why saturated fats have many proven benefits over unsaturated fats and the risk they pose. This blog is a brief summary of how and why coconut oil can be used for both cellular and shellular (ok I made that word up and yes my drawing sucks!). http://balancedbodymind.wordpress.com/2012/04/15/why-are-polyunsaturated-oils-so-dangerous/

One of the many problems associated with vegetable, nut and seed oils is their double carbon bond, which is pictured below and explains why these oils become problematic when aged or of most importance, when they become heated during cooking. Their propensity to cause inflammation and significant health issues is well documented and for further reading, please read the work of Ray Peat PhD.

molecular structure

Coconut oil has many advantages over so called essential fatty acids.
1. It doesn’t have the issues associated with cooking at high temperatures and instability.
2. It is readily used by the mitochondria or energy producing cells without the need for carnitine, which is used to transport fatty acids into the cell.
3. It provides structural cellular protection.

Many bloggers and health advocates have touted the use of coconut oil as a form of sun block. That’s fine, if you are of darker skin, where you are already protected from the suns harmful ultraviolet rays but if lighter skinned, here’s the huge fail that you may have experienced. Coconut oil despite it’s protective nature will burn fair skinned people, to which some of my friends have found out the hard way. However coconut oil can still be protective even for fair skinned people when used correctly and here’s how.

You may have found that when using regularly sun block, you now often burn quicker with less sun exposure. There are two reasons why this may happen.

1. The sunblock that you use often contains vegetable oils as recepient of the zinc oxide and allows it to soak into your skin.
2. Your diet is high in vegetable and seed oils, nuts, green vegetables and foods high in PUFA’s. Ever notice brown pigmentation spots on the skin too?
The use of coconut oil should be applied post sun and also at night as a natural moisturiser of the skin. Applying coconut oil in conjunction with lowering the amount of PUFA’s consumed in your diet and to avoid using sunblock. You should gradually introduce your time of exposure in the sun. Staying in the sun for long periods of time will ultimately age the skin but using these guidlines will help you to tolerate the suns ray’s and gain the essential, hormone like Vitamin D and healing red rays.

When spending longer periods of time in the sun and for children. My friend Eric Lepine has devised this useful home made sunblock that doesn’t have the PUFA’s often found in commercial products. To make it he recommends the following.

½ ounce of organic beeswax 2 ounces of coconut oil 2 ounces of shea butter one capsule of Unique E (for extra antioxidizing properties; for women, I’ve even had them use Progest-E, for similar effect, plus the added bonus of the progesterone).

2 TBS of micronized zinc oxide (at that concentration, it will be about 20% of total volume, and should confer an SPF of about 30). The micronized version will have you avoid the zombie/pasty white look. You can opt for the non-micronized version if you prefer though.

Just melt the first three ingredient one at a time, progressively, waiting until the preceding one has completely melted before adding the next one. Once the first 3 ingredients are melted, squeeze the vitamin E capsule into the melted mixture, followed by the zinc oxide powder (if using micronized zinc oxide, use caution while mixing it in. While its safety is well-proven when it comes to topical use, the safety issues with micronized powders arise from the risks associated with breathing in the fine particles. The risk is likely mostly a matter of how often one is exposed to these fine particles but, extra precaution is always warranted). Mix well using a whisk. Transfer to a small pot with a large opening before the mixture solidifies (small mason jar or something similar). The mixture might need one last good mixing once it solidifies so, preferably, the container should have enough space to allow for this without making too much of a mess.

It’s time for sunlight to get the credit it deserves for promoting health and stops being demonised. It’s free, it’s much better than poorly produced vitamin D supplements and an essential part of life. So if you need to use a block for longer periods. Try the one above or at least spend time getting used to sun light without the vegetable oils.