The ability to keep your bones strong depends to a large extent on how your body makes use of calcium, magnesium and phosphorus, all of which are incorporated into bone. Of these, calcium is the most abundant mineral in bone. However, more and more evidence is accumulating to show that dietary calcium intake is only one of a number of factors that influence the proper use of calcium in the body.
Your intake of magnesium, vitamin D and protein, plus weight bearing exercise, play a significant role. Although our calcium intake has stayed relatively constant, the incidence of osteoporosis has rocketed. Consequently, one in three women, and one in 12 men, has a fracture by the age of 70, most commonly of the hip. In the UK, 50,000 people fracture a bone as a result of osteoporosis every year – that’s one every three minutes.
Four-fifths of fractures occur after the age of 50 and the risk becomes quite significant from 70 onwards. One in two women and one in five men will suffer a fracture after the age of fifty. It is estimated that the cost of treating all fractures resulting from osteoporosis in postmenopausal women is £2 billion.
BONE MASS TESTING
However, before a diagnosis of osteoporosis is made, often following a fracture, bone mass starts reducing. This can be measured and if your bone mass is low you’ll be diagnosed with osteopenia – not as bad as osteoporosis but potentially heading that way. If measured and your T score is -1 to -2.5 then osteopenia is diagnosed. This is based on a bone mass density scan, the most common type called a DEXA scan (Dual energy X-ray absorptiometry) which is a bit like having an x-ray. It’s 96-98 percent accurate in detecting osteoporosis at moderately advanced stages but does not capture all the risk factors for osteoporosis so also having a bone turnover test is really helpful.
Research has shown that in postmenopausal women osteoporosis levels of bone resorption markers, measured in urine, above the upper limit of the range are associated with an increased risk of hip, vertebral (spinal) and nonvertebral fractures, independent of bone mineral density. Markers of bone turnover can also be used to predict the rate of bone loss in post-menopausal women and also be used to assess the risk of fractures. Research suggests that markers of bone turnover appear even more strongly associated with fracture risk than bone mineral density.
The test I like is the NTx test which can be arranged for home testing, the urine sample then sent to the lab by Glenville Nutrition headed by Marilyn Glenville PhD. They can also arrange a DEXA scan for you and provide guidance regarding osteoporosis reversal using a nutritional approach.
About half of people over 50, if tested, have osteopenia. Many, but not all will go onto develop osteoporosis over time.
Yet osteoporosis is far from inevitable. In fact, in some communities, there is no apparent loss of bone density after the menopause. Even though we have a better diet, analyses of skeletal remains show less bone loss in the 18th century than the late 20th century. So what has changed? It seems to be a case of too much of some things and too little of others.
OSTEOPOROSIS RISK FACTORS
Before we look at the treatments on offer to restore bone mass what are the risk factors?
Women are more at risk than men of developing osteoporosis. The female hormones oestrogen and progesterone are protective to women’s bones, just as the male hormone testosterone is protective to men’s. But, from the age of 35, women regularly fail to ovulate, minimising their production of progesterone, the major hormone for bone strength. Women at most risk for developing osteoporosis are those that have had an early menopause (before the age of 45), either naturally, or surgically by removing the womb and one or both ovaries.
Major Well Known Risk Factors:
• Early menopause
• Previous fracture from slight injury
• Significant corticosteroid use
• Lost several inches in height
• Close relatives with brittle bones
• Over/under exercised
• Heavy intake of alcohol and drugs
• Many missed periods
• History of heavy cigarette smoking
Osteoporosis is mostly a ‘silent’ disorder and a fracture is often the first indication of a problem. Loss of height, back pain, tooth loss and a bent posture are indicators for osteoporosis, particularly after the age of 50.
DOES HORMONE REPLACEMENT THERAPY (HRT) WORK?
The interplay of hormones is fundamental for preventing osteoporosis. Oestrogen works by removing old damaged bone and when oestrogen levels decline at menopause bone loss is accelerated. Progesterone is the bone builder as it works on bone cells that rebuild new bone to replace the old bone. The stress hormone cortisol, when chronically elevated, can contribute to bone loss. The balance of parathormone and calcitonin help control calcium balance between the blood and bones. Thyroid hormones, testosterone and growth hormone also affect bone health.
Osteoporosis is a slow, progressive disease: bone loss starts in most women from the mid-thirties. It does not happen overnight with the last menstrual period. Children and young adults are generally building bones, between 30 and 40 the balance between bone growth and bone loss is about equal and after 50 bone growth decreases and bone loss increases. Developing, supporting and maintaining bone health is a lifelong commitment.
Treatment strategies have largely been focused on HRT, bisphosphonate drugs, e.g. Fosamax, and calcium and vitamin D supplementation. Although, as mentioned earlier, the Women’s Health Initiative trial showed a small decreased risk of hip fracture,  there is now a substantial body of evidence that HRT should not be recommended to women to prevent or treat osteoporosis, and that the risks outweigh the benefits. It seems that bone mass is only preserved in those who take HRT for seven years or more and, even when you take it for that long, bone mineral density rapidly declines once you stop taking it.
Following a European-wide review of the balance of risks and benefits of HRT, it is no longer recommended as first choice of therapy for prevention of osteoporosis, according to advice from the Medicines and Healthcare products Regulatory Agency (MHRA) in 2003.  HRT does, however, remain a treatment option for those who cannot use other osteoporosis prevention therapies or for whom other therapies have been shown to be ineffective, although the decision must be made with care.
Younger women who use short-term HRT will probably gain little or no protection against fracture beyond the age of 70, according to a study from 1993.  At 75, the women’s bone mineral density was found to be only just over 3 per cent higher than that of women that had never taken HRT. So, unless you are prepared to take HRT for life, it is unlikely to protect you against osteoporosis – and the longer you take it, the greater your risk of developing breast and womb cancer.
Eighteen European specialists reviewed the data on HRT and osteoporosis. No long term benefits were identified. Hip fracture risk was as great for women who stop HRT as those that had never used HRT. Protection from HRT is lost within five years of stopping. Many women cannot tolerate HRT and stop within a year of using it. Other women may trial many forms of HRT before finding one that suits them.
The conclusion of the European specialists was: ‘For healthy women without menopausal symptoms the benefit – risk analysis of HRT for the prevention of osteoporosis is not favourable’. Officially, doctors in the UK are now told that the risks outweigh the benefits, and not to prescribe it for osteoporosis prevention. But it is still commonly prescribed for this reason in other parts of the world.
HOW EFFECTIVE ARE BISPHOSPHONATES?
The official figure given for the effectiveness of bisphosphonates in lowering the risk of having a hip fracture is 32 per cent, but although this sounds positive it’s very misleading. A study undertaken in 2010 by researchers in Finland and published in the British Medical Journal concluded that if everyone in that country over the age of 50 had been put on a bisphosphonate – that would be 1.86 million people – just 343 hip fractures would have been avoided. Meanwhile, the drug would have failed to prevent 7,068 of them. That is a long, long way from preventing 32 per cent, so how can the results be so poor and confusing?
The reason is that there is a big difference between how well drugs perform in clinical trials – the 32 per cent – and their results in the real world. Clinical trials are very artificial. Subjects in trials are usually quite young, healthy and not taking any other drugs, and nurses will ensure that they take the drug for the trial. The patients who are given them on prescription, however, will very likely be older, frailer and starting to decline; usually they will have three or more other disorders and will be on several drugs for each of them. Furthermore, only about half the drugs prescribed are actually taken.
How effective did bisphosphonates turn out to be when they became available on prescription? As a result of this mismatch between the trials and the real world, the Finnish researchers calculated that if everyone who had at least a 3 per cent risk of developing a fracture over the next ten years were treated with bisphosphonates, for every 667 people who took the drugs only one would avoid a fracture.
Side effects include upset stomach and inflammation of the oesophagus, if you don’t remain sitting upright for 30–60 minutes daily after taking the drug. You might also develop cancer of the jaw bone (although this is rare), and what are called ‘atypical’ fractures of the thigh bone (femur) and a disturbed heart rhythm if you are female. So you need to weigh your chances from benefiting from the drug with that kind of rate of efficacy against the side effects.
What is more, if you are taking one of the proton pump inhibitor (PPI) drugs that suppress stomach acid – often given with bisphosphonates because heartburn can be a side effect – the benefit of the drug can drop to zero.  These stop you making stomach acid, which is required for the absorption of calcium, magnesium and vitamin B12. These drugs are known to increase the risk of fracture, doubling the risk in those over 50 if taken long term, according to a study in the Journal of the American Medical Association. If you are on these drugs, at the very least have your homocysteine level checked.
Many women with digestive problems cannot take Fosamax and it is associated with many side-effects, including esophageal irritation and ulceration, bone and muscle pain. Intravenous Fosamax is linked with a horrendous condition called osteonecrosis of the jaw that results in deterioration and death of the jawbone. Fosamax also increases risk of atrial fibrillation.
There is also little point taking this medication if your vitamin D level is low (see Vitamin D section overleaf). Not only does research show that 75 per cent of people on bisphosphonates don’t respond at all if they have the kind of low levels very common in the UK (below 50 nmol/l) but also getting double that amount would mean that you would be seven times more likely to have a favourable response to the drug.  It only costs your doctor a small amount – a fraction of the cost of a drug prescription– to have your vitamin D levels tested, but if your doctor doesn’t want to test you, you can do it yourself.
CALCIUM, MAGNESIUM AND BONE MASS DENSITY
Unless your calcium intake is very low indeed, calcium supplementation alone makes little difference. A review of all the evidence for calcium for calcium in the British Medical Journal concludes that increasing calcium intake from dietary sources or by taking calcium supplements produces small non-progressive increases in bone mass density, which are unlikely to lead to a clinically significant reduction in risk of fracture. 
Both magnesium intake and measure of serum magnesium predict fracture risk.  When post-menopausal women supplemented magnesium over a two-year period their fracture risk reduced and bone mass density increased.  According to data collected in the UK’s Biobank which tracks the health of over 150,000 people, higher dietary magnesium intakes correlate with slower muscle deterioration that supports the skeleton.  Also, measures of magnesium levels within cells predicts knee extension strength.  Stronger muscles means less osteoporosis and arthritis risk.
While calcium intake appears to effectively delay the tendency towards bone mass density decrease in postmenopausal women with a total intake of 1200 mg a day (diet plus supplements) your intake of magnesium, and vitamin D is just as important. With the average dietary intake of calcium being around 700mg (eg vegans) to 900mg (high dairy consumers) this suggests that supplementing 300mg or maybe 500mg in those, such as vegans or those not eating dairy products, whose intake might be lower might have a small advantage. However, estimates of calcium intake of our Paleolithic ancestors, and intakes of African communities, both with no evidence of substantial bone mass loss with age, are much lower, between 400mg and 600mg a day. Their diets, and living outdoors, would have meant more magnesium and vitamin D. Perhaps, with sufficient magnesium and vitamin D, even this extra calcium intake is not so necessary.
VITAMIN D DRIVES CALCIUM INTO BONE
More effective than calcium or vitamin D on its own, however, is the combination of calcium with vitamin D. The latest ‘meta analysis’ of the results of six good quality randomised controlled studies that used calcium with vitamin D supplementation versus placebo showed 6 RCTs that the combined supplementation with vitamin D (daily doses of 400-800 IU) and calcium (daily doses of 1000-1200 mg) was associated with a 6 per cent reduced risk of any fracture and a 16 per cent reduced risk of hip fracture.  Based on the included trials, it appears that the minimum effective dose of calcium is likely to be 1,000mg 1,200mg while vitamin D should not be below 800iu, which is twice the current winter ‘top up’ supplemental guideline for vitamin D alone. However, it is possible that the vitamin D dose given in most earlier trials was just too low.
The optimal daily dose of vitamin D is whatever gets your blood level above 75nmol/l (30ng/ml). You may need between 2,000iu and 5,000iu a day to achieve this. If your level is low, below 50nmol/l, having 100,000iu a week for four weeks, then 3,000iu a day (or the same dose times seven once a week, is more likely to get you there faster. Choose vitamin D3, which is more effective than D2. HOLFORDirect have a high strength vitamin D in the Essentials range.
It is best to take vitamin K2 especially if you are using these higher doses of vitamin D. This is because K2 helps keep calcium in bone and low calcium in the arteries.  My one concern with high dose vitamin D is it’s potential to increase calcium levels in the blood. High coronary artery calcium is a risk factor for heart disease.
A recent double-blind placebo-controlled trial showed that vitamin K, at a dose of 90mcg a day, but not 50mcg significantly reduced loss of bone density in post-menopausal women but not men.  I recommend a daily dose of at least this, or 100 to 200mcg, of vitamin K2, which is more effective than K1. Some supplements combine these. You may find vitamin K in your multivitamin. Vitamin K1 is found in brassica family of vegetables but then has to be converted to the more active K2 version, which is found in natto, a fermented soya product and in supplements of nattokinase.
Calcium balance in the body depends on many factors, not only vitamin D and K intake. A person with a relatively low intake of calcium, but none of the factors shown, may have better calcium status than someone apparently consuming enough calcium, but scoring high on the above factors.
FACTORS INFLUENCING BONE MASS DENSITY
• Lack of minerals – calcium, magnesium, boron
• Excess of Protein – resulting in high levels of acidity
• Lack of Vitamins – D, K, C and Bs
• Excess of refined carbohydrates – resulting in blood sugar problems
• Thyroid and parathyroid hormone deficiencies
• Lack of Oestrogen and progesterone after the menopause
• Lack of Exercise
• Lack of sunlight
• Excess of Alcohol and Stimulants – coffee, tea, cigarettes, chocolate
• Lack of stomach acid
Take a look at your own diet and lifestyle over the last 20 years. Which of these factors may have contributed to the state of your bones and joints? Since most of them are the direct consequence of diet and lifestyle, which do you think is more likely to help: leaving your diet and lifestyle as it is and taking drugs; or changing your diet and lifestyle for the better? One thing is certain. There’s a lot more to healthy bones than getting enough calcium.
While most of these factors have been discussed in depth earlier on in this book there are two that need re-emphasizing, namely vitamin C and magnesium, and two we haven’t discussed. The first is the danger of too much protein; and the second is the extent to which hormone deficiencies contribute to arthritis and osteoporosis, and whether hormone replacement therapy is really advisable.
VITAMIN C CUTS RISK OF OSTEOPOROSIS BY A THIRD
The higher your vitamin C intake the lower is your risk of osteoporosis. A meta-analysis of 13 studies shows that greater dietary vitamin C intake was significantly associated with a 33 per cent reduction in risk of developing osteoporosis, and correlates with higher bone mineral density.  A more recent review of studies involving almost 20,000 people also showed that those with higher frequency of vitamin C intake had a 36 per cent lower risk of developing osteoporosis and having hip fractures.  They also had better bone mineral density.
MAGNESIUM SUPPLEMENTATION HELPS PROTECT YOUR BONES
The evidence for magnesium preserving bone mass at all ages, in both men and women, is substantial.  There are not, however, enough studies specifically looking at osteoporosis and bone mass density. One controlled trial of post-menopausal women with osteoporosis showed that magnesium supplementation for two years significantly improved bone mineral density. 
PROTEIN AND OSTEOPOROSIS
Osteoporosis is endemic in the Western world, particularly among post-menopausal women. The reason, it is thought, is that the hormone oestrogen, which ceases to be produced at the menopause, assists the retention of calcium in bone. Consequently, numerous trials have tested the effects of giving oral oestrogen, or calcium, or both. Neither have succeeded in completely ‘curing’ the problem, although both have an effect.
This suggests another cause, obvious when you know that many women from different cultures throughout the world have no increased incidence of osteoporosis after the menopause. Indeed, many cultural groups have no osteoporosis at all. Bantu tribes in Africa, for example, have an average calcium intake of 400mg (well below the recommended intake for post-menopausal women) and virtually no osteoporosis. In contrast, Eskimos, who consume vast amounts of calcium, have an exceptionally high incidence of osteoporosis. Why the difference? What have countries with a high incidence of osteoporosis got in common? The answer may be too much dietary protein. 
While we all need something in the region of 40g of protein a day, eating above 80g a day over the long term will boost your risk of developing osteoporosis. This is because protein is acidic, and excess amounts need to be neutralised, which can deplete the bones of calcium.
The Nurse’s Health Study, conducted in the US and analysed by the Harvard School of Public Health, recently found that women who consumed 95g of protein a day, as compared with those who consumed less than 68g a day, had a 22 per cent greater risk of forearm fractures.  In another study, eating more than 80g of protein a day, which is equivalent to bacon and eggs for breakfast and a steak for dinner, was found to increase your risk of osteoporosis. 
This happens because protein is made of amino acids and protein-rich foods therefore generate more acid in the body. Because the body cannot tolerate substantial changes in the acid pH of blood, it neutralises or ‘buffers’ this effect through two main alkaline agents – sodium and calcium. When the body’s reserves of sodium are used up, calcium is taken from the bones – a finding that has been confirmed by ‘metabolic ward’ studies in which people are kept in a controlled environment, fed precise diets and measured for their calcium loss.
Such studies have found that a negative calcium balance is created when 95g of protein is consumed while a person eats 500mg of calcium. The calcium intake must be raised to 800mg before calcium balance is achieved – that is to say, when the calcium entering the body is the same as the amount leaving. And the more protein you eat, the more calcium you need. The difference between the Bantus and the Eskimos is their protein consumption. According to a report in the American Journal of Epidemiology, an 11-year study of 40,000 elderly Norwegians also found increased risk of hip fractures among those eating high amounts of non-dairy protein (meat/fish/eggs), as well as among those who had either a high coffee or low calcium intake. 
The fact that high-protein diets lead to calcium deficiency is nothing new. Dr Shalini Reddy from the University of Chicago conducted a six-week study on ten healthy adults eating a low-carb diet. Volunteers lost an average of 9lb over the course of the study – that’s 1½ lb a week. That’s the good news. The bad news was that the acid excretion in the urine, which is an indication of acid levels in the blood, rose by 90 percent in some volunteers. There was also a sharp rise in the amount of calcium excreted in the urine during the low-carbohydrate, high-protein diets, and even the ‘maintenance’ diets for these regimes, despite only a slight decrease in calcium intake. This means the people were losing calcium from the body. Also, urinary citrate, a compound that inhibits kidney stone formation, decreased, implying an increased risk of kidney stone formation. 
According to Dr Reddy, ‘Consumption of a low-carbohydrate, high-protein diet for six weeks delivers a marked acid load to the kidney, increases the risk for stone formation, decreases estimated calcium balance, and may increase the risk for bone loss.’ These studies all suggest that such high-protein diets may increase the risk of bone loss over the long term. Of course, we are going to have to wait a while to find out, but I’d rather you weren’t the guinea pig.
Research is also beginning to show that if you eat a high-protein diet, no amount of calcium supplementation can correct the imbalance. In one study, published in the American Journal of Clinical Nutrition, subjects were given a moderately high protein diet (12g nitrogen) and a very high protein diet (36g nitrogen) plus 1400mg of calcium.  The overall loss of calcium was 37mg per day on the 12g nitrogen diet and 137mg per day on the 36g nitrogen diet. The authors concluded that, ‘high calcium diets are unlikely to prevent probable bone loss induced by high protein diets’. The negative effects of too much protein have been clearly demonstrated in patients with osteoporosis. Some medical scientists now believe that a life-long consumption of a high-protein, acid-forming diet may be a primary cause of osteoporosis. 
Of course, this begs the question as to whether eating a lot of dairy produce (high in both protein and calcium) would be protective or contribute to osteoporosis risk. A 12-year study which involved over 120,000 women throughout the US, found that women who drank two or more glasses of milk per day actually had a 45 per cent higher risk of hip fractures and a 5 per cent higher risk of forearm fractures than women who drank less.  The director of the study, Diane Feskanich, said, ‘I certainly would want women to have adequate calcium in their diets, but I would not rely on that as the prime prevention against osteoporosis.’ There is no clear pattern of evidence that drinking milk prevents osteoporosis.
OSTEOPOROSIS AND HOMOCYSTEINE
People with osteoporosis tend to have high homocysteine levels, lowered by B vitamins. Also a decrease in bone mineral density (BMD) resulting in osteoporosis is a common symptom of the rare genetic disease homocystinuria, which is associated with very high homocysteine levels. Research from Japan has found that women with the greatest postmenopausal bone mass loss are much more likely to have a defect in the gene (MTHFR) that produces an enzyme that gets rid of homocysteine, resulting in a higher than normal homocysteine score.  These women may be particularly at risk for osteoporosis unless they follow a diet and supplement plan to lower their homocysteine level.
A number of studies suggest that having a high level of homocysteine in your blood may weaken bone and increase the risk of fractures.  One of these was a very large study (involving 2268 men and 3070 women) by Dr. Clara Gjesdal and her colleagues at the University of Bergen in Norway – known as the Hordaland Homocysteine study – which showed that elevated homocysteine and low folate levels were associated with reduced BMD in women, but not in men.  When it was fracture risk that was being evaluated, one study showed that risk of fracture was higher in men – almost 4 times higher for men; almost 2 times higher for women,  whereas another showed double the risk of fracture for both men and women. 
Another study, from China, finds that the higher a person’s homocysteine level the greater is their risk of having osteoporosis.  This study finds no risk below 10µmol/l which is pretty much the same level above which there is a greater risk of developing dementia, with increased brain shrinkage. Most people over age 50 have higher homocysteine levels than this. A further study calculates a 4 per cent increased risk for every 1µmol/l increase. So, if your homocysteine level were over 20µmol/l that’s likely to have increased your risk by 40 per cent! That’s why it is vital to check your homocysteiine level and act accordingly.
Dr. Markus Hermann, from the University of Sydney, Australia and colleagues from Germany and Italy reviewed a total of 28 studies and concluded that high homocysteine levels (and possibly B-vitamin deficiencies) have a detrimental effect on bone quality because they stimulate the cells that clear out old bone (osteoclasts). Since there is no direct effect on the bone-BUILDING cells (osteoblasts), old bone ends up being cleared away faster than new bone is produced. 
It is not yet clear if it is the homocysteine itself which is causing the damage to bone and increased fracture risk or whether homocysteine levels are just reflecting low levels or deficiencies of either folate or B12 – nutrients that DO have a direct effect on bone.  Some studies suggest that low folate levels influence bone mineral density (BMD) and/or fracture risk,  while others implicate B12.  Patients with a type of anaemia, called pernicious anaemia (caused by lack of B12 in the blood), have decreased BMD at the lumbar (lower) spine, and in comparison with the general population they have almost double the risk of hip fracture. 
Dr. Rosalie Dhonukshe-Rutten, from Wageningen University in the Netherlands, has shown that low B12 is associated with low BMD in adolescents and that frail elderly women with a B12 deficiency were seven times more likely to have osteoporosis than women with normal B12 levels.
Older women, but not men, with low BMD had significantly lower vitamin B12 levels than older women with higher BMD.  This is because B12 has a direct effect on bone-building cells and also stimulates an enzyme involved in the process of forming new bone called alkaline phosphatise, or ALP for short. Another of her studies showed that high homocysteine and low B12 were significantly associated with less bone strength, increased bone turnover and a three times higher risk for fractures in men and women. However, the impact of low B12 was more severe in women than men, whereas high homocysteine was more associated with fractures in men. 
A big driver of B12 deficiency is long-term use of antacid medication and specifically proton pump inhibitors (or PPIs) whose names often end in –azole. The long-term use of PPIs is a known risk factor for development of osteoporosis and osteoporotic fractures.  The reason is that stomach acid secretions are needed to absorb vitamin B12 and these drugs block stomach acid production.
Not many studies have been done to see what effects supplementing homocysteine-lowering nutrients has on BMD and fracture risk. However, since stroke increases the risk of subsequent hip fracture by 2 to 4 times, one Japanese study followed 433 stroke patients, aged 65 and over, for 2 years to see if treatment with folate (5mg) and vitamin B12 (1500 mcg) would have any effect. The combined treatment of folate and B12 was found to be a safe and effective way of reducing the risk of hip fracture in these patients. 
A low level of oestrogen, which is very common in postmenopausal women, also appears to raise homocysteine and increase osteoporosis risk. Theoretically, increasing oestrogen could help lower homocysteine.  This has been shown in some preliminary studies,  but not in others. Until more is understood about how homocysteine and oestrogen are related, we are reluctant to recommend oestrogen HRT as a means to lower homocysteine for two reasons.
One is that it is less effective than the nutritional strategy to lower homocysteine; the other is that it carries an increased risk of breast and uterine cancer. ‘Natural’ progesterone HRT (not to be confused with synthetic progestins used in most HRT preparations) does not have these associated risks. But no one has yet investigated whether this lowers homocysteine.
Also, having a raised homocysteine is associated with cognitive dysfunction, including loss of balance. This too may contribute to your risk of falls.
IS OSTEOPOROSIS A HORMONE-DEFICIENCY DISEASE?
Hormone balance, under the control of the endocrine system, is key to bone health. The endocrine system is made up of a network of glands that secrete hormones which control many of the processes that happen inside our bodies. Hormones can be protein-like, such as insulin, or fat-like, such as cortisol. Fat-based hormones are called steroid hormones. Most hormones are themselves controlled by means of feedback. An example of this feedback mechanism is seen in the working of the pituitary gland.
Often called the ‘master gland’, the pituitary governs the functioning of the thyroid gland, the adrenal glands and the sex glands. The thyroid gland, in turn, controls our rate of metabolism and, together with the parathyroid glands, the balance and utilisation of calcium. The adrenal glands control our ability to deal with stress, and, together with the pancreas, the balance and utilisation of glucose (sugar). And the sex glands control the production of sex hormones, including oestrogen and progesterone (which affects calcium utilisation). The adrenal glands also produce small amounts of sex hormones.
If you continually overuse or overstress any bodily organ or system, it will eventually under function. If the entire endocrine system is overstressed this can lead to slow metabolism, calcium imbalance, blood sugar imbalance, inability to cope with stress, sex hormone imbalances, and (in women) premature menopause with exaggerated symptoms. After noticing that many of my arthritic patients had a history of prolonged stress, overuse of stimulants, over-consumption of refined carbohydrates, and deficiency of the many essential vitamins and minerals needed for the endocrine system to work, I wondered whether arthritis couldn’t be caused, at least in part, by hormone imbalances caused by overstressing the endocrine system as a whole.
Rather than treating the effect – in other words giving hormones like cortisone, thyroxine, calcitriol and oestrogen – I experimented with treating the possible cause by encouraging my patients to change their diet and lifestyle and support their endocrine system by taking supplements of vitamins and minerals. This approach has proven most effective, and, although as yet unproven in clinical trials, research is beginning to confirm that it makes sense. 
OESTROGEN HRT IS NOT THE ANSWER FOR OSTEOPOROSIS
The previous conventional treatment for osteoporosis was hormone replacement therapy (HRT), employing either oestrogen alone or a combination of oestrogen and synthetic progesterone (called progestagens in the UK and progestins in the US). There is little doubt that oestrogen therapy does increase bone density and reduce the incidence of fracture. However, oestrogen HRT does also increase the risk of high blood pressure, gall bladder disease, blood clots and, most importantly, breast, uterine or endometrial cancer with or without progestagens.
In fact, a 5-year study involving one million women aged between 50 and 64 showed that the risk is substantially greater for oestrogen-progestagen combinations than for other types of HRT.  Since stopping oestrogen therapy rapidly returns bone mass to its previous osteoporotic level,  oestrogen therapy (or other forms of HRT) is only really effective as a long-term treatment, which means a long-term risk. Consequently, few doctors continue to advise this.
Although not so striking in effect, ensuring adequate intake of calcium, vitamin D and other nutrients, especially magnesium, does increase bone density. Vitamin D is converted into a hormone, calcitriol, that improves calcium utilisation and retention in the body. Supplementing the hormone itself may be even more effective than taking vitamin D, and, unlike oestrogen, it has no apparent significant side-effects. 
A high calcium intake prior to the menopause does seem to improve bone density.  However, once osteoporosis has set in, calcium supplementation is only marginally effective in increasing bone density, except in people who eat a calcium-deficient diet. The recommended intake of calcium for a post-menopausal woman is in the order of 1000–1500mg per day. More than this is most unlikely to be of any benefit.
PROGESTERONE PREVENTS BONE MASS LOSS
Bones have two kinds of cell: osteoblasts, which build new cells; and osteoclasts which get rid of old bone material, such as calcium. Oestrogen, which influences osteoclast cells, doesn’t actually help build new bone. It only stops the loss of old bone.  Progesterone, on the other hand, stimulates osteoblasts which actually build new bone. Taking natural progesterone increases bone density four times more than taking oestrogen.
In the time leading up to the menopause, the peri-menopause, most women start to have cycles in which ovulation doesn’t occur (known as anovulatory cycles). After the menopause ovulation never occurs. If no egg is released, no progesterone is produced (because progesterone is only made in the ovary sac once the egg is released). However, the body does continue to produce small amounts of oestrogen, primarily oestradiol (there are three oestrogenic hormones – oestradiol, oestriol and oestrone or, in the US, estradiol, estriol and estrone).
Scientists are now starting to think that it is the relative excess of oestrogen to progesterone – creating, in effect, a progesterone deficiency – that precipitates osteoporosis, rather than the deficiency in oestrogen. This would explain why bone loss commonly starts from the age of 35, long before the actual menopause. In the pre-menopausal years, anovulatory cycles (in which no progesterone is produced) become increasingly common.
Loss of bone mass density is known to occur in women who have such anovulatory cycles.  A meta-analysis shows that almost 1 per cent a year of bone mass density is lost in women with such disturbed ovulatory cycles.  It estimates that much of this can be reversed, with natural or bio-identical progesterone plus estradiol adding back 0.7% bone mass per year and thus may be a highly effective osteoporosis treatment.
One trial, by Dr John Lee from California, found that giving nature-identical progesterone, as a transdermal skin cream, was four times more effective than oestrogen HRT, with none of the associated risks. 
Professor Cooper, from Southampton University, following this study, reported that there was no indication the creams did any harm, and there were some indications they could be beneficial in terms of reducing severe menopausal symptoms, such as hot flushes and night sweats. 
PHYTOESTROGENS & ISOFLAVONES PREVENT BONE MASS LOSS
Several factors in natural foods may also help to prevent osteoporosis in both men and women by keeping hormones in balance. While too much protein (especially from red meat) causes calcium loss and encourages inflammation, switching to a lower protein intake, with a greater proportion of vegetarian protein foods, helps protect against both arthritis and osteoporosis. Vegetarian protein foods include beans and soya which may be protective. Most interesting is the role of a group of naturally occurring hormone-like substances called isoflavones (a type of phyto-oestrogen) found in soya.
These seem to enhance bone-building and prevent the breakdown of bone. A study of 52 studies shows a significant improvement in bone mass over a year.  Ipriflavone, a derivative of these naturally occurring isoflavones, has been extensively tested and has proven, in over a dozen trials, to increase bone density and decrease bone loss, when given with either calcium, oestrogen HRT or vitamin D, significantly more than when these are given alone.  Concentrations of isoflavones can be derived from soya or red clover.
A one year trial giving 78 postmenopausal osteopenic women either a placebo or a combination of a red clover extract high in isoflavones plus probiotics reported a significant decrease in the rate bone mass decline and improved oestrogen status. 
While much attention has been focused on vitamin D and calcium, good bone health also depends on a lot of other nutrients. The minerals magnesium, zinc, manganese, boron and strontium all have a role to play in helping to build bone or cartilage. Vitamin K, anti-oxidants and B vitamins are also important. Women with osteoporosis often have low serum levels of vitamin K. Supplementing vitamin K2 decreases their loss of calcium. Therefore an all-round optimum nutrition programme, consisting of a healthy, balanced diet plus supplements containing all these nutrients, provides the best chance of keeping bones healthy.
THE EXERCISE FACTOR
One of the primary stimulants for bone growth and density is exercise, which will have profound effects on keeping your bones strong and protecting you from osteoporosis. This is because the body, unlike most mechanical devices, is unique in the way it responds to the amount of use it receives. Where most machines components wear down with regular use, the body does the opposite by building and strengthening the areas that are being used.
Stressing the bones with weight-bearing exercise tells the body to ‘toughen up’, which is why astronauts in zero gravity conditions rapidly lose bone density. There is little difference between them and a person who sits at work all day, drives home and sits watching television all evening. We all need some weight-bearing activity every day, such as a 30-minute walk. On top of that, more strenuous activities at least once a week – hill walking, running, cycling, exercise classes – are necessary to keep your bones strong.
It’s also important to strengthen your quadriceps muscles in the thighs because, if you start to fall you’ll instinctively put your leg out in front of you. A simple exercise such as sitting with your back pressed against a wall, with your legs parallel and a right angle between your thighs and lower legs, for 30 seconds helps to strengthen these muscles, as do squats.
Knowing this we can start to make small changes in our lifestyle that will help to prevent the onset of osteoporosis. By making the skeleton perform load-bearing movements on a regular basis, it will respond by increasing the density of the bones being used thus making them stronger and less prone to breaks.
In conclusion, the best advice for anyone, whether suffering from arthritis or osteoporosis, is to avoid excess protein, sugar, fizzy drinks, alcohol and stimulants and to ensure optimal intakes of vitamins and minerals including magnesium, vitamin D, boron, zinc, vitamin C and other bone-friendly nutrients. These are often provided together in one supplement.
The best single food source is seeds – one heaped tablespoon of ground sesame, sunflower, flax or pumpkin seeds will give you significant amounts of calcium, magnesium and zinc, plus essential fats. Dairy produce is a good source of calcium, but a poor source of magnesium. Bear in mind that our ancestors didn’t milk buffaloes; they got their calcium and other minerals from seeds, nuts and vegetables.
If hormone replacement therapy is still needed, consider natural progesterone as opposed to oestrogen HRT. The combined supplementation of vitamins and minerals, plus hormones, has not only proven more effective in restoring bone density, but is also more effective in retaining it once hormone replacement therapy is stopped. 
Whether or not the complete approach recommended in this book – including diet, low stimulant intake, exercise and supplements – can replace hormone replacement therapy has yet to be put to the test.
The best way to prevent or reverse osteoporosis is to combine all these prevention strategies:
• Don’t consume more than 40g of protein a day. This is not usually a problem for vegetarians, who should aim to have two servings daily of a protein vegetable food, such as lentils, beans or tofu. For a meat-eater this means meat certainly no more than once a day and, ideally, no more than three times a week.
• Eat fish rather than meat. Fish is preferable, because it provides more anti-inflammatory essential fats and fewer oestrogenic hormones.
• Eat plenty of nuts, seeds and yellow and green vegetables. A heaped tablespoon of ground sesame, sunflower, flax or pumpkin seeds will give you significant amounts of calcium, magnesium and zinc, plus essential fats.
• Rely on seeds and nuts for minerals, not dairy products. Dairy products, especially cheese, are high in protein and oestrogenic hormones and low in magnesium.
• Eat plenty of wholefoods and follow low GL principles.
• Eat a varied diet that includes some soya milk, tofu or other soya products. Alternatively supplement isoflavones from soya or red clover.
• Avoid coffee. High coffee intake is associated with low bone density. It also raises homocysteine.
• Also avoid sugared fizzy drinks.
• Supplement a bone mineral complex or ensure your supplement regime includes at least 300mg of calcium, 300mg of magnesium, 1,000iu of vitamin D, 2mg of boron, 10mg of zinc, plus 2,000mg of vitamin C, 100 to 200mcg of vitamin K2 and B vitamins. Female Balance contains magnesium, B vitamins and zinc.
• Supplement vitamin D like my High Strength Vit D3. Ideally, test your vitamin D level and take whatever you need to get up to at least 75nmol/l. Many people need at least 50mcg (2,000iu) a day for the first three months. If your level is below 50nmol/l take 100,000iu a week for four weeks.
• Test your homocysteine and, if high, take a high strength homocysteine formula providing at least 500mcg of B12, plus folic acid, B6 and other homocysteine lowering nutrients.
• Exercise every other day. The best kind of exercise is weight-bearing, preferably using both lower and upper body muscles. Rowing, for example, is excellent. Even walking for 15 minutes each day makes a difference.
• Consider using natural progesterone cream. If pre-menopausal, check your hormone levels and, if oestrogen-dominant, use natural progesterone. If post-menopausal, use it anyway. Your doctor can prescribe it.
If you are at all concerned about osteoporosis there are many helpful tips in this article and as it is progesterone that is needed to help build new bone you will find the article below by Dame Dr Shirley Bond will also provide useful information. For a complete list of the 62 references cited in this article please email email@example.com
Osteoporosis – A Doctor’s View