Menopause and osteoporosis

What is osteoporosis? What is its relationship to menopause? How can we combat it?

What is osteoporosis?

Bone is a type of connective tissue. There are lots of different types of connective tissue in the body. Connective tissue is basically cells dotted around in a matrix of other stuff. A bit like a fruit cake. In bone the matrix is made up of 25% water, 25% collagen and 50% crystallised mineral salts. There are four types of cells but the ones we are interested in are the osteoblasts and osteoclasts. Bones are living organs designed to respond to the forces put through them. The osteoblasts and osteoclasts help bones to do this by creating new bone and breaking down old bone, respectively. This work is ongoing. It is referred to as bone turnover. For bones to be strong there must be a healthy matrix with the right balance of water, collagen and mineral salts and the osteoblastic activity must match osteoclastic. Osteoporosis is a disorder in which bones become weak, fragile and liable to fracture. It occurs when collagen is either lost or impaired such that mineral deposition is compromised and/or when bone reabsorption exceeds bone production (Studd et al, 2009).

Why is osteoporosis related to menopause?

Oestrogen is integral to bone health, being a key factor in bone turnover and healthy collagen (Trémollieres, 2019; Studd et al, 2009). As women approach menopause oestrogen levels fall. Osteoclastic activity out ways osteoblastic so more bone is re-absorbed than is made. In addition, collagen fibres lose their elasticity reducing flexibility and resilience. Bone is left weak, thin and brittle. Our nice rich, moist fruit cake becomes a Malteser. Bones give way under little force. Micro/stress and/or macro fractures may occur. 

Collagen is also an essential component of the intervertebral disc. This is the spongy, cushion-like structure that sits between each spinal vertebra. When collagen loses its integrity, the discs flatten under the weight of the body and the vertebrae come closer together. This causes accelerated degenerative change in the little joints between the vertebra. Osteoarthritis follows with spinal stiffness and discomfort.

How can we combat this?

There are several solutions.

Exercise

This should be frequent, consistent and weight bearing. The strength of bones develops in response to the forces put through them. Visit the National Osteoporosis website for ideas. Personally, I run and lift weights in a routine that takes about an hour. I do this three times a week.

Nutrition

Nutritionally, some, such as Dr Nitu Bajekal, gynaecologist and lifestyle medical physician, advocate a complete plant-based diet. Others talk about the inclusion of calcium and natural oestrogen-rich foods such as sesame seeds, sardines, soya and natto. There are, of course, plenty of supplements on the market. For myself, I have opted for a largely plant-based diet with a healthy side order of the suggested inclusions. I also take supplements.

Visceral Osteopathy

Osteopathy works to support overall health. Visceral osteopathy is a branch that concentrates on the body organs. The liver is one of the main structures of detoxification. Although there is no control trial evidence, patients have reported that enhanced detoxification by manipulation of the liver has helped to reduce certain menopausal symptoms (Personal experience and patient feedback).

Medication

These include the bisphosphonates, denosumab and teriparatide and hormone replacement therapy, HRT.

The first three act to increase osteoblastic or decrease osteoclastic activity, the net result being an accrual of bone mass thought to enhance strength. However, some report that bones become brittle (Glenville, 2008; https://courses.washington.edu). This may be because, in their natural state, osteoblasts and osteoclasts work together in a balanced way. The former produce bone and the latter shape it to create the intricate but strong/resilient bony architecture. In additional, these medications are not thought to have an effect on collagen (Muscat et al, 2007). Collagen continues to degenerate weakening the very framework that the new bone is being deposited into. What implications might this have for bony architecture and so strength? Furthermore, as mentioned above, impaired collagen undermines intervertebral and so spinal health.

HRT, as the name suggests, replaces the hormones lost during the time of menopause. The hormone of interest, with respect to osteoporosis, is oestrogen. Studies have shown that oestrogen reduces osteoclastic reabsorption (Wehrli et al, 2001), slows bone turnover (Trémollieres, 2019), repairs microfractures (Khastgir at al, 2001b) and restores collagen in both quantity and quality (Khastgir at al2001a). In essence, oestrogen reinstates and preserves bone and this lowers the risk of fracture (Zhu et al, 2016; Jackson et al, 2006; Cauley et al, 2003). Being a friend of collagen, it also sustains the intervertebral disc and so maintains spinal health, guarding against loss of height and flexibility (Studd, 2006). 

My choice? HRT. In a nutshell, “---- HRT is the only therapy available with randomized controlled trial-proven efficacy of fracture reduction in postmenopausal women ----” (Trémollieres, 2019). For more information about HRT, its efficacy and safety, please read my blog “To HRT or not HRT: A personal story”.

So, this is osteoporosis, its relation to menopause and some suggested ways to combat it. Personally, I am a plant eating, supplement gobbling, sardine-etarian who runs, lifts weights, takes HRT and has her liver manipulated by an osteopath occasionally. This is my anti-osteoporotic cocktail drawn from research and personal experience. Will it work? Tell you in ten years.

For more information or to book please contact Julieann, the Osteopath Clapham via [email protected] or 07929595685. You can also book on line.

 References

Cauley JA, Robbins J, Chen Z, et al. (2003) Effects of oestrogen plus progestin on risk of fracture and bone mineral density: the Women’s Health Initiative randomized trial. JAMA 2003;290:1729–1738

Glenville, M. (2008) The Silent Epidemic. Octopus books, UK

https://courses.washington.edu/bonephys/opbis2.html Internet Accessed 6/6/2020

Jackson RD, Wactawski-Wende J, LaCroix AZ, et al. (2006) Effects of conjugated equine oestrogen on risk of fractures, and BMD in postmenopausal women with hysterectomy: results from the Women’s Health Initiative randomized trial. J Bone Miner Res 2006;21: 817–828

Khastgir G., Studd J., Holland N., et al. (2001a) Anabolic effect of oestrogen replacement on bone in postmenopausal women with osteoporosis: histomorphometric evidence in a longitudinal study. J Clin Endocrinol Metab 2001;86:289–95

Khastgir G., Studd J., Holland N., et al. (2001b) Anabolic effect of long-term oestrogen replacement on bone collagen in elderly postmenopausal women with osteoporosis. Osteoporosis Int 2001; 12:465–70

Muscat Baron Y, Brincat MP, Galea R, Calleja N. (2007) Low intervertebral disc height in postmenopausal women with osteoporotic vertebral fractures compared to hormone-treated and untreated postmenopausal women and premenopausal women without fractures. Climacteric 2007;10:314–19

Wehrli FW, Ladinsky GA, Jones C, et al. (2008) In vivo magnetic resonance detects rapid remodeling changes in the topology of the trabecular bone network after menopause and the protective effect of estradiol. J Bone Miner Res 2008;23:730–740