The most common cause of death in the UK is heart
disease, which kills more than 40% of the population. It is caused
by a process known as atherosclerosis which damages the blood
vessels, and occurs with a gradual build up of plaque in the blood
vessel walls, commonly known as furring of the arteries.
Atherosclerotic plaques are the most prominent cause of all
heart disease cases. They gradually narrow blood vessels resulting
in a reduction of blood flow to tissues further downstream.
Problems occur if the blood supply becomes limited and so the
muscles or other tissues do not get enough oxygen to function
normally. In the heart, this initially results in pain, typical of
angina, but can progress to a heart attack. Alternatively, rather
than a gradual narrowing of the vessel, a portion of the plaque can
break off the vessel wall and get carried down the blood vessel. As
the vessels branch and get smaller, the piece of plaque eventually
gets stuck in a small blood vessel, blocking any further blood
flow. The tissue on the other side of the blockage is starved of
oxygen and damaged and in the heart or the brain, this results in a
heart attack or stroke. The acute treatment for a heart attack
focuses on unblocking the blood vessel and getting the supply of
oxygen re-established to the muscles, either using drugs or
surgery.
Over the last fifty years, research has focused on identifying
risks of developing atherosclerosis in the hope that this might
enable us to modify them and subsequently reduce an
individual’s chance of suffering a heart attack. We now
recognise more than twenty such risk factors. Of these some are not
modifiable.
Whilst you are stuck with your own personal history, there are
many recognised factors that you can modify to reduce your risk of
suffering a heart attack, including:
- Stopping smoking
- Avoiding obesity
- Taking regular physical exercise
- Eating a well balanced diet
- Reducing high cholesterol
- Reducing high blood pressure
- Managing stress and anger. But also reducing your homocysteine
levels.
Homocysteine’s causal association is relatively new.
However, this relationship is not only very significant, but you
can also actively do something about it.
In 1968 a doctor called McCully recognised that children with a
genetic defect that resulted in high homocysteine levels developed
heart disease like that of middle-aged patients. He proposed that
homocysteine may be an independent risk factor for heart disease.
Since then it has been increasingly recognised in association with
the development of atherosclerosis and heart attack. Elevated
homocysteine levels are now also associated with developing several
other diseases including stroke, liver cirrhosis, kidney failure,
hypothyroidism, Alzheimer’s and dementia, depression and eye
disease.
Homocysteine is a normal part of a healthy metabolism. Its
formation is a by-product of normal cell control, converted from
the amino acid, methionine, to regulate gene expression and protein
function. Once made, homocysteine is then either converted back to
methionine which requires folic acid (B9) and B12, or is converted,
through a couple of reactions requiring vitamin B6, to another
amino acid, cysteine. When homocysteine is bound as an amino acid,
it is inactive and therefore safe. As homocysteine levels rise,
free homocysteine gets released into the blood stream, then causing
damage to the blood cell walls and other tissues and altering blood
clotting.
The level of homocysteine in our blood is affected by our
genetics (one in ten of us has a mutation in the gene that controls
the conversion processes and results in a moderately elevated
levels), our diet (particularly the B vitamins) and our age (as we
age our ability to absorb nutrients declines), but homocysteine
levels are also increased by smoking, high alcohol and coffee
intake, eating large amounts of red meat (which contains a lot of
methionine), lack of exercise, obesity, stress and a number of
drugs.
The drugs that increase homocysteine are:
- Fenofibrate - to reduce cholesterol
- Niacin - to reduce high blood pressure
- Metformin - to control non-insulin-dependent diabetes
- Antiepileptics - to control epilepsy
- Levodopa - to manage Parkinson’s disease
- Methotrexate - to treat cancer, psoriasis, arthritis and
lupus.
It is now possible to have your blood level of homocysteine
assessed:
- 5-15umol/L - Normal (ideally <8umol/L)
- 16-30umol/L - Mildly elevated
- 31-100 umol/L - Moderately elevated
- >100umol/L - Severely elevated.
By the age of 42 the mean homocysteine level in the population
is 11umol/L in men and 9umol/L in women and even at these modest
levels there are clear associations with an increased risk of
disease. This is why your level should ideally be kept below
8umol/L.
To reduce the like-lihood of developing a high homocysteine
level, you can:
- Stop smoking
- Drink alcohol in moderation (less than three units a day)
- Drink coffee in moderation
- Eat red meat no more than five times a week or less if your
homocysteine level is elevated
- Avoid being overweight
- Exercise regularly. Obtain a good intake of vitamins B6, 9 and
12 from your diet:
- B6 (pyridoxine): avocados, bananas, carrots, lentils, brown
rice, tuna, salmon.
- B9 (folic acid): spinach, aparagus, root vegetables,
wholegrains, kidney sprouts, beans, oysters, salmon,
avocado.
- B12 (cyanocobalamin): beef, cheese, eggs, fish, milk.
A recent review of all the studies using folic acid to reduce
homocysteine levels has demonstrated that taking just 0.8mg of
folic acid a day lowered them by 3umol/L and reduced the risk of
suffering a heart attack by 15% and stroke by 25%. These are small
actions having a massive effect. In the UK there are about 61,000
heart attacks each year. Folic acid supplementation could have
reduced this number by 9,150. I would go further and suggest that
those with an elevated homocysteine level should also take
100-200mg/day of B6 and 1-2mg/day of B12.
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