Consequences of the Menopause

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When oestrogen levels begin to fall around the peri and post menopause, the risk of heart disease and stroke begins to increase.

There are many factors why this may occur but the most likely ones are as follows:

• The artery wall constriction-  a fall in oestrogen can result in the wall of the artery constricting causing stiffening and partial closure of the artery. This results in reduced blood flow. Because of the narrow diameter of the blood vessel, the heart has to contract harder to drive blood through the arteries and this can cause damage and inflammation of the artery lining.
• Inflammation of the artery lining - persistent inflammation due to lack of oestrogen from a generalised inflammatory factors or higher blood pressure leads to damage of the artery wall and this predisposes to deposition of cholesterol plaque even if the cholesterol is normal. Eventually the plaque hardens and the lumen-diameter of the arteries reduces even further. If this is treated before the plaque has hardened then some of the damage can be reversed but if the arteries have already hardened it is almost impossible to reverse this.
• High cholesterol - lack of oestrogen results in an increased productions of low density lipoproteins (LDL) compared to high density lipoproteins (HDL cholesterol). Low density lipoprotein is smaller and stickier and predisposes to plaque formation (see above). 

Studies have shown that patients who are commenced on adequate oestrogen prior to the whole formation of plaque and arterial stiffening, their risk of cardiovascular disease, cerebrovascular disease and dementia is reduced in the long term.

Some studies have tried to reverse pre-existing damage and plaque formation by the addition of oestrogen because oestrogen - particularly oral oestrogen, has a dissolving effect on plaque. This can increase the risk of thrombosis or clot whereas taking oestrogen well in advance of arterial hardening and plaque formation is more beneficial for long term protection.

However, this does not mean oestrogen cannot be commenced many years after the menopause or in the existence of pre-existing plaque or arterial damage but caution must be applied and may wish to discuss this with your cardiologist and possibly take blood thinning medication alongside oestrogen for the high-risk time ie. the first 6-8 weeks. Following that, once the initial risk has reduced then long term benefit may well be achieved by preventing any further plaque formation.

In women, bone is very sensitive to oestrogen. Usually it is in a state of constant placement of old bone with new and oestrogen maintains this process preserving the strength of the bone. Loss of oestrogen results in increased breakdown of bone but inadequate replacement of new bone and a reduction of bone density can occur. If this is left too long, then even replacing oestrogen or using other medications to try and improve bone density will not work as there are already micro factors within the honeycomb of the bone.

The highest risk areas are:

• Radius (wrist)
• Hip - especially neck of femur and the spinal vertebral bodies

In patients who are at high risk of osteoporosis such as early menopause, sedentary lifestyle, previous use of steroids, family history of osteoporosis, it is worth considering a baseline bone density scan at the beginning of the menopause to ensure that deterioration does not occur before it is reversable.

Collagen in the female body is very sensitive to oestrogen and as oestrogen levels begin to decline, the collagen matrix begins to thin and becomes less elastic. This can present in many different ways and supplementing adequate oestrogen replacement can completely or partially reverse this change. This is why women who experience an early menopause or who are under replaced such as after a hysterectomy or with down regulation of the ovaries early (Mirena, contraceptive pill), without adequate addback oestrogen can exhibit signs of premature ageing. The concern is that if collagen ages externally this can indicate premature ageing internally (bone, artery wall, ligaments etc.) Collagen affects:

• Oestrogen and joints - all joints are supported by ligaments which become thin and less elastic when oestrogen levels fall. The cushion (synovial fluid) between the joint surfaces also reduces with loss of oestrogen. The total result therefore means that there is more likelihood of the articular surfaces of the joints closing in and rubbing during movement of the joints. Loss of oestrogen also increases inflammatory changes in the joints -which is why the risk of arthritis increases or worsens with loss of oestrogen.
• Skin - the skin contains several layers of collagen. The upper layer (epidermis) sheds and is replaced by the cells from the lower layers (dermis and sub dermis.) Loss of oestrogen results in the slowing of this process so that while shedding occurs, replenishment of the underlying cells does not occur. The result is that the thickness of the skin reduces, becoming much weaker, less elastic and less liable to recover. At the same time, these sebaceous glands producing oily protective serum reduces so that the skin becomes drier. Applying moisturiser externally may help slightly but the penetration into the lower dermis is usually not enough to maintain the elasticity of the skin if there is not enough oestrogen.
• Eyes - Loss of oestrogen results in the thinning of the collagen and connective tissue to the eye with dry eyes being much more common in the peri and post menopause with falling oestrogen levels. At the same time, as the blood vessels constrict and blood supply is reduced, there are increasing problems with circulation through the eyes such as glaucoma. Inflammation also worsens after the menopause which is why cataracts are more common in the post menopause and this can be seen more commonly in women who undergo premature menopause so is not simply linked to age only.

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