Bones are alive and active. Starting before birth, they undergo constant turnover, such that our total bone mass is replaced every three years.
This ongoing process of bone dissolving (resorption), and bone formation (new bone growth), continues throughout life.
Osteoporosis is a progressive disease, (‘osteo’ means bone; ‘porosis’ means porous), where bone resorption exceeds new bone formation.
In other words, more bone is dissolved than that being replaced. Calcium is being eroded from the bone stores, faster than it can be replaced, and as a result, the bone calcium level, measured as bone mineral density, reduces.
The bony meshwork inside the bones (trabeculae) become thinner, and even the usually stronger supporting, outer (cortical) bone reduces in strength, and can eventually collapse.
When the outer bone collapses in the spinal column, the vertebral ‘block’ distorts, much like a collapsing concertina, and as a result, the spine becomes shorter and hunched over.
Maintaining bone strength in ageing vertebrae, hips and arms, will prevent fractures and significantly reduce the morbidity associated with such injuries.
Although there are many causes of osteoporosis, including thyroid and para thyroid disease, liver and kidney disease, disuse, nutritional deficiency or drug induced, the hormonal changes associated with ageing and menopause are the most common cause.
Two groups of bone cells are mainly responsible for bone turnover.
They are the osteoclasts (the bone dissolvers), and the osteoblasts (the bone builders).
Both work in harmony, reshaping and strengthening bone; dissolving old bone here and rebuilding new bone there.
Traditionally, medicine has been commercially geared to limit the dissolving rate at which the osteoclasts work. Most patented pharmaceutical osteoporosis drugs, such as oestrogen derivatives and diphosphonates are anti-resorption agents.
They slow the dissolving performance of the osteoclasts and have little or no new bone growing activity. They induce an osteoclast ‘go-slow’, so that in five years they will have dissolved less bone than they would have if they had been working at normal speed.
The benefit of such products is a meagre 1.15% reduction in the bone resorption annually, usually touted in medical journals as 11.5%* net gain in bone mineral density (* in ten years). Deceptive isn’t it?
Any emphasis on new bone growth tends to be conveniently ignored.
Although oestrogen plays a part in slowing bone loss, it is the new bone forming, osteoblast stimulating, hormone levels of testosterone, progesterone and growth hormone like molecules, that truly dominate bone turnover, with up to 15% new bone growth per year.
Our testosterone levels peak at 25 years, and naturally fall by 1-2% annually; progesterone levels suddenly plummet when a woman stops releasing eggs from her ovaries (becomes anovulatory), which occurs up to 10 years before menopause (when her periods cease).
Now most people, and most doctors, don't realise that spinal bone mass also peaks at 25, after which it declines at about 1% a year until 50.
In other words, bone mass declines at exactly the same rate that our testosterone levels decline. Women convert the progesterone released upon ovulation into testosterone in their ovaries (men made three times more in their testes).
This negative balance toward progressive osteoporosis is totally independent of low oestrogen levels, as the woman's oestrogen levels remain normal between 25 and 50, which allow her to have regular periods.
Osteoporosis associated with ageing and menopause can be successfully overcome by:-
- the maintenance of more youthful progesterone and testosterone levels in women and men
- to encourage new bone growth,
the maintenance of normal dietary calcium intake
- the use of pharmaceutical antiresorptive drugs where necessary
- the encouragement of weight bearing exercise, safe sunlight exposure
- and smoking cessation
- and by reducing the excesses of alcohol and caffeine consumption.
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