Last partial update: August 2019 - Please read disclaimer before proceeding
Note: Before studying this chapter, people will need to have read the section on fat in the section on nutrition. (See Fat and nutrition section.)
The recent controvery regarding saturated fat intake and illness from cardiovascular disease (Written August 2019)For the last thirty years it has been accepted medical wisdom that a high saturated fat intake is a major cause of increased LDL cholesterol (bad cholesterol) and thus a significant cause of cardiovascular disease. This had important implications for Australians as traditionally they had a diet based on animal products rather than plant foods and animal products are the main source of dietary saturated fat. Recent examination of the evidence supporting this role for saturated fat has shown that this postion is difficult to support; thus the questioning in medical circles and in the media about the wisdom of continuing to support saturated fat reduction. HOWEVER, THIS IS NOT THE WHOLE STORY. The evidence from the extensive research that has looked at replacing some saturated fat with unsaturated fats (mainly from plants) does show a real benefit in reducing cardiovascular disease. Luckily, this is what many Australians have done over the past 30 years and it is what the National Heart Foundation has promoted and continues to promote. And the approach has provided great results. The heart attack incidence has decreased by around 70% over this period and, while factors such as reduced smoking and better treatment of blood pressuse and high cholesterol are important contributors to this reduction, change in diet has also conributed significantly. When the aged pension started in Australia it commenced at the age of 65 years. The average life expectancy of men at that time was 55 years!! It is now about 80. So what is current thought regarding fat intake. 1. Australians eat too much in general, including too much fat. Thus, where appropriate, they promote a reduction in total fat consumed and / or replacing some saturated fat with unsaturated fat. The best way of doing this is to adopt a Mediterranean-type diet. Luckily this tastes good and increases the intake of fruit and vegetables which in turn significantly reduces the risk of getting many types of cancer. 2. Trans-saturated fats are an important cause of cardiovascular disease and should be excluded from the diet as much as possible. (See section on trans-saturated fats.) Adopting this type of diet is examined more closely in the section below. |
Why do Australians need to be worried about their cholesterol?
High cholesterol is a major risk factor for cardiovascula disease and unfortunately about 50% of Australians over 25 years of age (6.4 million people) have a high blood total cholesterol level (over 5.5mmol/L) and in women over 70 years of age the rate is about 70%. These percentages have not changed significantly since 1980(!!), even though most people know cholesterol is a risk factor for heart disease. High blood cholesterol levels cause about 3% of all illness, mainly through increasing coronary artery disease (heart attacks and angina) and strokes.
Inadequate treatment: Importantly in Australia, about 30% to 40% of people who have a high overall cardiovascular disease risk (see section on assessing risk of cardiovascular disease) and would benefit from medication to reduce their blood cholesterol level are not receiving that medication; and about 60% are undertreated (i.e. do not reach target levels).
Elevated blood cholesterol levels can be reduced in most people, with a healthy diet usually reducing total blood cholesterol levels by at least 10% and medications, when needed, producing a further reduction of up to 25%. Such reductions can reduce death rates from heart attacks (and strokes) by about 25%!! Reducing an elevated total cholesterol by 1.0mmol/L (roughly a 17% drop) reduces heart disease by about 20%. At present over one million Australians take medication to lower cholesterol at a cost of over one billion dollars per year.
This chapter details the causes of raised blood lipids and explains how diet and medication can be used to reduce lipid levels.
The causes of adverse blood lipid (fat) levels
As stated in the section on dietary fat consumption, cholesterol is an insoluble fat and therefore needs to be transported in the blood inside larger compounds called lipoproteins. The two principal lipoproteins are low density lipoprotein (LDL) and high density lipoprotein (HDL). LDL (often called ‘bad cholesterol’) takes cholesterol from the liver to the tissues and in doing this increases cholesterol deposits in artery walls, thus making vascular disease worse. Conversely, HDL (often called ‘good cholesterol’) transports cholesterol from the body tissues back to the liver and in doing this removes some cholesterol from artery walls, thus reducing vascular disease. The total blood cholesterol level measures the cholesterolcontained in these two lipoproteins as well as that contained in other less important lipoproteins. As LDL is the largest component of the total blood cholesterol reading, a high LDL level is almost always associated with a high total cholesterol level.
Medications: The table below mentions numerous commonly used medications that can adversely affect blood lipids. It is important that anyone who has an increased risk of cardiovascular disease (for any reason) has their medications reviewed to make sure they are not exaccerbating their risk level.
a. Causes of high LDL / high total cholesterol
In the vast majority of people with a high total blood cholesterol level, the high level is thought to be caused by a combination of dietary and unidentified genetic factors, a condition called polygenic hypercholesterolaemia. It is usually associated with an elevated LDL level and normal levels of HDL and triglycerides. At present it is estimated that over six million Australians have a cholesterol level of over 5.5mmol/L and about three million have a level of over 6.5mmol/L.
The most important factor contributing to raised total and LDL cholesterol is thought to be excess saturated fat in the diet. Part of the process of regulating LDL blood levels is the removal of excess LDL from the blood by the liver. While the whole story regarding how dietary fats affect cholesterol is not fully known, it is thought that the dietary intake of saturated fats increases blood LDL levels by reducing LDL uptake by the liver and that it does this by altering the LDL receptors on the membranes of liver cells. Unsaturated fats are thought to do the opposite. There has been much duscussion of recent times regarding whether reducing saturated fat intake actually improves patient outcomes with respect to cardiovascular disease as the evidence is far from conclusive. However, the National Heart Foundation still feels that the best diet with respect to reducing cardiovascular disease is a Mediterranean type diet that has more plant-sourced foods and is higher in unsaturated fats. Their advice is to try to adopt this type of diet.
Excess dietary cholesterol consumption also increases LDL, which it does by increasing the production in the liver of the LDL precursor, VLDL. While this is a much less important factor in raising LDL, people with a high cholesterol and/or a high overall risk of heart attacks should still make sure their cholesterol intake is not excessive.
Other causes of raised LDL and total cholesterol are shown in the table below.
b. Causes of low HDL
The major causes of low HDL are obesity and diabetes. (These are also the major causes of raised blood triglycerides and the two conditions often occur together.) Others causes are shown in the table below.
Factors causing of adverse changes in blood lipids (fats)
|
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Increased total / LDL cholesterol |
Decreased HDL cholesterol |
Increased triglyceides |
|
High intake of saturated fat relative to unsaturated fat |
Yes
|
|
|
| Any intake of trans saturated fats | Yes (important factor) |
||
High intake of cholesterol |
Yes (but not a major cause) |
|
|
Obesity / inactivity |
Yes (important factor) |
Yes |
Yes (important factor) |
Diabetes / insulin resistance |
Yes |
Yes
|
Yes (important factor) |
Excess alcohol |
Yes |
(Small amounts may increase HDL) |
Yes |
Smoking |
|
Yes |
|
Inherited disease / genetic factors |
Yes |
Yes |
Yes |
Medications |
|
|
|
Other diseases / conditions |
|
|
|
Factors causing of beneficial changes in blood lipids (fats)
|
|||
|
Decreased total / LDL cholesterol |
Increased HDL cholesterol |
Decreased triglyceides |
High relative intake of unsaturated fats compared to saturated fats |
Yes
|
|
|
High dietary intake of antioxidants (mostly from fruit and vegetables) |
Yes |
|
|
High intake of foods rich in soluble plant fibre (mostly legumes) |
Yes |
|
|
Consuming plant sterols |
Yes |
|
|
Exercise |
|
Yes |
|
Other factors |
|
|
|
c. Causes of high triglycerides
Abdominal obesity and diabetes are major causes of raised triglycerides, with both conditions on the increase in Australia. In people with diabetes, an increased triglyceride level is a very important contributor to their overall increased risk of vascular disease. Other causes are mentioned in the table above.
Triglycerides are made up of three fatty acids joined together. Dietary triglycerides that contain longer fatty acids with more double bonds in their structure actually act to reduce overall triglyceride levels by reducing triglyceride synthesis in the liver. Omega-3 fatty acids fit both these criteria very well and are often prescribed, in the form of fish oil capsules, to reduce high triglyceride blood levels. (While fish oil capsules do reduce triglycerides, there is little evidence that they reduce cardiovascular disease and thus for using them for this purpose. A better alternative is to include fish in your diet two to three times a week.)
d. Lipoprotein A
Lipoprotein A is structurally similar to LDL and an increased blood level also raises cardiovascular risk level, with levels greater than 0.3g/L increasing cardiovascular disease risk by 20% to 30%.Very high levels (> 3.0g/L) are associated with very high risk of cardiovascular disease. Lipoprotein A levels are genetically determined and unfortunately most drug treatment, including statins, is ineffective. (A few patients respond to some extent to treatment with nicotinic acid.) People with high lipoprotein A levels are best treated by lowering Total cholesterol and LDL with statins.
Inherited lipid disordersThere are numerous inherited lipid disorders. The two most common are mentioned here. Familial Hypercholesterolaemia The disease can occur in two forms. In the heterozygous form, only one gene in the pair is affected and about one in 500 individuals are affected. Total cholesterol readings in this group are usually between 7mmol/L and 13.0mmol/L and individuals tend to develop heart attacks from the age of thirty onwards. In the much less common homozygous form, both genes are affected and total cholesterol readings are usually above 13.0mmol/L. Affected individuals start developing heart attacks even earlier (sometimes in childhood) and they also develop deposits of cholesterol under the skin (called xanthomas). HDL is generally normal or low. The condition is present from birth. People with a family history of this condition need cholesterol checks in childhood so that affected individuals can start treatment early on in the disease process. Familial Combined Hyperlipidaemia |
Benefits of improving harmful lipid abnormalities
Lowering a high LDL level / a high total cholesterol level – Very beneficial
There is very strong evidence that lowering LDL (and thus total cholesterol) has a major impact on reducing the risk of major cardiovascular events such as heart attacks and strokes. Each lowering of LDL cholesterol by 1.0mmol/L reduces this risk by 25%.
This benefit occurs irrespective of the total cholesterol and LDL cholesterol levels prior to starting treatment, even when starting levels are in the ‘normal range’. This is an important concept to grasp as it means that medication to lower cholesterol can be used in people with high (and often moderate) risk of cardiovascular disease even if the starting cholesterol levels are normal.
Thus, the decision to start treatment with cholesterol lowering medication more often than not depends on the overall risk of cardiovascular disease rather than the person's cholesterol level. The exception is in people who have very high cholesterol levels who need to start medication as well.
Raising a low HDL level – Not shown to be beneficial
A low HDL level is a significant risk factor for cardiovascular disease. For example, a person with an HDL of 0.5mmol/L has three times the risk of cardiovascular disease as a person with an HDL of 1.2mmol/L. However, in contrast to lowering LDL, studies have not shown a significant cardiovascular disease benefit from increasing HDL levels. Thus, the aim when treating people with low HDL levels is to decrease their LDL by 30 per cent or more rather than raising their HDL level. (Statin drugs commonly used to lower LDL usually do increase HDL levels also.)
Lowering high triglycerides
While triglycerides do not cause vascular disease, they are usually high in people who get vascular disease because people with high triglycerides also tend to have low HDL levels. A rise in triglycerides from the optimum level of 1.5mmol/L (or less) to 4.0mmol/L increases cardiovascular disease risk by about 25 per cent. (Triglyceride levels above 4.0mmol/L do not add to this increased risk.) There are numerous factors that can alter the levels of triglycerides. (See tables above.)
Investigating blood lipids
When to start: There is no question that the elevation of blood lipids is a major risk factor in the development of cardiovascular disease. For this reason, all adults should have their blood lipid levels assessed. This should commence at 45 years in people who are at low risk of cardiovascular disease or earlier in people an increased risk, especially if there is a strong family history of high blood cholesterol or triglycerides. Assessment is usually not needed before 20 years of age.
Measurement: The measurement of blood lipids is done by analysing a blood sample. The minimum information required for proper assessment is total cholesterol, HDL, triglycerides and LDL. (Usually, the first three are measured and the LDL is calculated from them as follows.)
LDL = Total Cholesterol - HDL - (Triglycerides / 2.2) mmol/L
(ApolipoproteinB (apoB): This equation is accurate only if triglycerides are less than 4.0mmol/L. Where the triglyceride level is higher, the measurement of LDL apolipoprotein B (apoB) level gives a more accurate indication of the LDL level. ApolipoproteinB is the main protein in LDL and there is always one apoB in each LDL. (Actually there is always one apoB in several types of lipoproteins; LDL, VLDL, VLDL remnant and IDL. All four of these lipoproteins cause cardiovascular disease and thus apoB is actually a slightly better indicator of cardiovacular disease than LDL. In some countries, such as Canada, it is replacing LDL as a lipid risk factor indicator. An apoB level of 0.8g/L is equivalent to a LDL level of 2.0mmol/L.))
(ApolipoproteinA-1 (apoA-1): There is one of these molecules in each HDL and it can be used as a measurement of HDL.)
A ‘pin prick’ cholesterol test usually only gives total cholesterol and triglyceride levels, which is not sufficient information to adequately assess the risk of vascular disease. (From the previous discussion it should be obvious that LDL and HDL levels are at least as important as the level of total cholesterol in assessing risk of vascular disease.)
Target levels for blood lipids are shown in the table below. As can be seen, the levels vary according to person's overall risk of cardiovascular disease.
Before deciding to initiate long-term drug therapy, tests should be repeated to guard against random error; for example, tests being mixed up. Repeat tests also avoid initiating treatment unnecessarily in people who only have temporarily abnormal level or in those whose levels fluctuate widely. (If levels vary markedly, a third test may also be required.)
When a person is commenced on either diet therapy or therapy with statin drugs, he or she should be on treatment for at least three weeks before being retested as it takes this length of time for cholesterol levels to stabilize.
Factors interfering with lipid test results
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Target levels for blood cholesterol – They vary depending on overall cardiovascular risk
Cardiovascular disease is very common and everyone should be aware of their cholesterol level and try to adopt a lifestyle to minimise it. Everyone should aim for a total cholesterol of 5.0mmol/L or less.)
Current thinking is that any reducuction in total cholesterol towards a level of about 3.8mmol/L and an LDL cholesterol of 2.0mmol/L is beneficial in reducing heart disease. Few people achieve these levels naturally and luckily most people are at insufficient 'vascular disease risk' to warrant trying to attain such low levels.
It is felt that the best approach in determining an individual’s optimum ‘target’ cholesterol is to assess their overall risk of cardiovascular disease; the higher the overall risk, the lower the target cholesterol should be.
In the section on assessing risk of cardiovascular disease, it was mentioned that doctors can work out a person’s overall risk of cardiovascular disease by collectively assessing their indivial risk factors using a risk calculator. While it is recommended that all people with a rasied blood cholesterol should adopt lifestyle measures to reduce their blood cholesterol, whether they should be commenced on medication for this purpose depends on their starting cholesterol level and their overall risk of cardiovasculare disease.
It is important to understand that any lowering of cholesterol will improve cardiovascular disease risk and thus a person at high risk of cardiovascular disease will benefit from lowering their blood colesterol even if it is normal to start with. (The same is true with respect of taking blood pressure medication to lower cardiovascular disease risk.) Unfortunately this treatment approach is not supported is not supported by Government and thus medication to lowerr cholesterol is not subsidised in some people at significantly increased risk but with normal blood cholesterol levels.
The table below states the target LDL, HDL and triglyceride levels for individuals in different risk categories. (The LDL cholesterol level is the target level that is most commonly focused on as it is the best ‘cholesterol indicator’ of cardivadsular disease risk.) These levels can be attained through diet or medication or both.
Target LDL levels keep decreasing: Those who have been observing LDL target levels for some time will be aware that they seem to be reduced fairly regularly. This is because evidence regarding best outcome use is changing and it is becoming increasingly evident that lower LDL (and triglyceride) levels can provide significant additional reductions in cardiovascular disease risk. The problem of course is that these lower levels imply that many more people have a medical problem and need to start taking or increase their dose of cholesterol lowering medication; mostly statins. Also, they make it harder for people already attempting cholesterol lowering to achieve the desired goal. This is good for drug companies but is it good for the general public? Using a person's overall cardiovascular risk rather than their starting blood cholesterol to decide whether medication to lower cholesterol is a good way of overcoming this problem as it means people at low cardiovascular disease riisk who have a mildly high cholesterol level may well not need cholesterol-lowering medication. (Of course, anyone with a raised cholesterol should be encouraged to lower their level using lifestyle initiatives.)
The question about what is normal and should doctors treat 'normal conditions' is a difficult one. For example, cholesterol levels vary significantly from country to country with dietary differences playing a significant role. Should the Australian average cholesterol be considered the normal, or the Japanese perhaps, or even the Scottish. All are very different and the population groups have different rates of heart attacks that are to some extent related to these differences in cholesterol levels. Probably the best solution is for doctors to ensure their patientsare aware of the advantages in lowering cholesterol and then patients need to make their own decision regarding what ultimate LDL level they wish to achieve and how they attempt to do this. (It is worth noting that many Australians choose to take the easy option of reducing cholesterol by taking medication in preference to seriously attempting weight reduction and increasing exercise.)
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Improving / optimising blood lipid levels.
Reducing total cholesterol, LDL cholesterol and triglycerides and raising HDL cholesterol can be accomplished in three main ways.
- Reducing lipid levels by diet modification. This involves:
- altering the balance of different types of fats present in the diet
- increasing soluble fibre in the diet
- consuming natural substances that improve blood lipids e.g. plant-sterols (in margarines) and fish oils.
- Maintaining a healthy weight and partaking in regular physical activity
- Using medication. The principle group of drugs used is the statins.
1. Reducing lipid levels by modifying diet
Modifying fat intake
Initially, everyone should try to achieve their optimum lipid levels through dietary change. The principal aim should be to consume the different types of fat in the correct quantities. The total amount of fat consumed is less critical, although most Australians consume too much fat and this makes keeping to a healthy weight difficult. It is best to keep to a total fat intake to that which provides about 30% of daily energy needs, although up to 35% is acceptable for people who are not overweight. The most important dietary fat modification recommendations are as follows and if people adhere to this advice they can lower their total cholesterol by 10% to 20%, depending on their existing dietary fat intake.
(Please remember that fat is an important part of everyone's diet and people should never aim to reduce their fat intake to less than that which provides about 20% of their daily energy needs.)
Reduce saturated fats as a proportion of total fat intake: As mentioned above, the role of saturated fats in causing cardiovascular disease is less certain than previously thought. The National Heart Foundationstill feels that many Australians consume a diet that is too high in animal products and thus saturated fats. Their advice is that a Mediterranean style diet, which contains more plant-based foods and thus more unsaturated fats, is the most beneficial in reducing cardiovascular disease.
Saturated fatty acids should idealy not contribute more than 10% of total energy intake (i.e. less than 30% of total fat intake). For most people this equates to a daily intake of saturated fat of 15 to 25 grams; as shown in the table below. (As a guide, 10 grams of saturated fat is contained in half a litre of full cream milk or in two ‘full fat’ cheese slices.)
(The section on Nutrition and fats includes a table showing the main food groups containing saturated fatty acids.)
Please remember that all types of fats are required by the body and the above advice does not mean that people should avoid all saturated fat. It just means that for most Australians, consuming the optimum balance of the different types of fat requires a reduction in saturated fat intake.
Increase monounsaturated fats and omega-3 fats: Generally, all unsaturated fats help reduce vascular disease and they should make up at least 70 per cent of total fat intake. However, most Australians consume enough polyunsaturated fats already (mainly through margarines and cooking oils) and an inadequate amount of Omega-3s and, to a lesser extent, monounsaturated fatty acids. Monounsaturated fats should make up about 35 per cent of unsaturated fat intake and people with a low HDL can benefit from an even higher relative intake. The sources of dietary unsaturated fatty acids are shown in a table in the section on Nutrition and fats.
Reduce cholesterol intake: Reducing dietary cholesterol is of secondary importance in improving blood lipids. Most foods high in cholesterol are also sources of saturated fat and thus people will hopefully already be avoiding them. These include lambs brains, offal, tripe, liver and pate. Egg yolks and sea foods such as prawns, while also being high in cholesterol, have numerous nutritional benefits and thus can still be safely consumed in moderation. Roughly 25 per cent of body cholesterol comes from the diet, the rest being made in the body in the the liver and muscles. Most people can reduce their body cholesterol production to compensate for a larger than usual intake. However, about 30 per cent of people can not and for these people, lowering cholesterol intake is more important. Determining who these people are is difficult and it is therefore best for all people with a high LDL to keep to a lowish cholesterol intake.
Recommended daily fat intake (approximate) |
||||
|
Energy intake in kJ (Calories) |
Total fat intake with 30% of total energy intake from fat (in grams) |
Saturated Fat (30% of total fat intake) in grams |
Mono-unsaturated fat (About 35% of total fat intake) in grams |
Women |
||||
Moderately active |
8400 (2000) |
66 |
20 |
23 |
Sedentary |
6300 (1500) |
50 |
15 |
18 |
Men |
||||
Moderately active |
10500 (2500) |
83 |
25 |
29 |
Sedentary |
8400 (2000) |
66 |
20 |
23 |
Optimum fat intake is best achieved by adopting the following measures.
- Protein foods
- Eat more fish, two or three serves per week.
- Eat red meat that is lean and trimmed of all fat. Two to three servings a week is optimal. Servings should be about the size of a pack of playing cards or weigh about 80g.
- Cooking oils:
- Use a variety of unsaturated oil for cooking. Extra virgin olive oil is a good choice as it contains numerous antioxidants and other nutrients and contains mostly monounsaturated fat.
- Minimise the consumption of fried foods at home.
- Spreads
- Use monounsaturated spreads, such as canola and olive oil products or no spreads at all (or try mashed avocado). Sterol containing margarines give additional benefit with respect to lowering LDL cholesterol and are an option that people should consider. (See section below on plant sterols.)
- Minimise the consumption of butter or dairy blends products.
- Dairy products (See boxed section below.)
- Choose low-fat or reduced-fat milk and yoghurt
- Reduce the consumption of ice cream and cheese to a maximum of twice per week. These are not healthy food as they have added sugar.
- Minimise the consumption off butter and cream.
- Takeaway foods / confectionary / cakes & pastries
- Minimise the consumption of fried take away foods and foods fried at home.
- Limit takeaway foods such as pies, pizza, hamburgers, pastries and creamy pasta dishes to once per week.
- Eat minimal amounts of biscuits, cakes, pastries, chocolate products, potato crisps etc; preferably to no more than once per week.
- Try to make cakes etc at home from healthy products such as unsaturated oils, fruit and vegetables and minimise sugar content (e.g. carrot cakes and healthy muffins.) It is difficult to know what bought cakes and biscuits contain (e.g. extra sugar and salt, butter etc)
- Consume five to seven servings of a good variety of fruit and vegetables each day.
- Eat wholegrain bread.
- Eat a small handful of nuts regularly (a few times a week).
- Consume more legumes, such as peanuts, beans and lentils; preferably twice a week.
Heart Foundation advice regarding dairy products for those without an elevated risk of cardiovascular disease (2019)Milk, yoghurt, and cheese are healthy snack options in preference to discretionary foods and can contribute to healthy meals when eaten with vegetables, wholegrains or fruit. Milk, yoghurt and cheese can feature in a healthy eating pattern; as long as the primary sources of fat are foods such as fish, olives, seeds, nuts and oils made from them. Based on current evidence, there is not enough evidence to recommend full fat over reduced fat products or reduced fat over full fat products for the general population. Heart Foundation advice regarding dairy products for people with elevated cholesterol and those with existing coronary heart disease Reduced fat products are recommended. The evidence for milk, cheese and yoghurt does not necessarily apply for cream, butter, ice-cream and dairy based desserts; these products are not part of a heart healthy eating pattern. |
The advantages of unsaturated fats
For most Australians, vascular disease risk level is improved when any type of unsaturated fat is substituted for saturated fats. However, they achieve this in different ways. Replacing saturated fats with monounsaturated fats decreases total cholesterol and LDL cholesterol and increases HDL cholesterol. Replacing saturated fats with omega-6 polyunsaturated fats decreases total cholestereol and LDL cholesterol.
The benefits of increasing omega-3 polyunsaturated fats include lowering blood triglyceride level, helping prevent blood clotting, and reducing the likelihood of harmful irregular heart rhythms occurring. They also help reduce high blood pressure and make arteries more elastic. Omega-3s have an anti-inflammatory action that may help in preventing diseases such as arthritis and there is some evidence that they protect against prostate cancer. Finally, omega-3s are thought to improve brain function and may have a role in helping prevent diseases such as depression. Such benefits are yet to be proven.
Cholesterol reduction using plant sterols and stanols (phytosterols)
Plant sterols and stanols are natural compounds similar in structure to cholesterol. When added to foods in appropriate amounts, they can help reduce the absorprtion of cholesterol from the bowel (by competing for cholesterol absorption sites) and this in turn reduces blood cholesterol. An intake of about two to three grams per day is optimal and is provided by about 25 g of sterol enriched margarine. This equates to about two teaspoons full or enough to cover about four slices of bread. This amount should not be exceeded as larger intakes provide no additional benefit and may interfere with the absoption of other nutrients such as fat soluble vitamins. The benefit gained from plant sterols varies depending on the degree to which the person absorbs sterols, a factor that is genetically determined. The reduction in LDL level that can be achieved thus varies from none at all to as much as 20 per cent. (A more detailed discussion appears in the section Nutrition and fats.)
Cholesterol reduction using soluble fibre
There is good evidence that a diet high in soluble fibre will lower LDL, with reductions in LDL of about five per cent being achievable. Foods rich in soluble fibre reduce plasma cholesterol levels by binding to cholesterol in the gut. This prevents the cholesterol from being absorbed into the body from the small intestine. (It is excreted in the feces attached to the soluble fibre.) A high intake of fibre, especially cereal fibre, has been shown to reduce the risk of coronary heart disease for the reason stated above.
Foods containing soluble fibre include oat bran, barley bran, rice bran (less than oat and barley bran), lentils, dried beans, fruit and vegetables. Psyllium husk (2 tablespoons full per day) is a good source.
Insoluble fibre, such as wheat bran, does not bind cholesterol and thus does not help reduce cholesterol levels. However, it is the better fibre for the bowel. A diet containing 30g of fibre a day is optimal, preferably a mixture of soluble and insoluble. This can be gained from a daily intake of the following:
- A bowl of bran cereal
- 3 slices of multigrain bread
- Two pieces of fruit
- 2 servings of vegetables
- A serving of beans
For more information, see section on Nutrition and fibre.
Dietary Carbohydrates (i.e. sugars and starches)
Recent evidence suggests that the type of carbohydrate eaten may also play a part in vascular disease, especially in people who are overweight. High intakes of carbohydrates that are digested quickly and therefore raise blood sugar quickly are associated with a significant increase in the risk of cardiovascular disease. This is due to several factors including raising blood triglyceride levels and LDL cholesterol levels and increasing insulin resistance. (The effect on triglycerides is more prominent in people who already have a high blood triglyceride level.) Highly refined carbohydrates such as biscuits, cakes and confectionery are examples of such foods.
The glycaemic index (GI) rates foods according to how quickly they raise blood sugar after consumption. Foods with a high GI raise blood sugars more quickly. People should try to include a large portion of at least one starchy food with a low GI in each meal and include as many other low GI foods as possible. They also should try to reduce their intake of refined carbohydrates such as confectionery (chocolates etc), cakes, biscuits, pastries and sugary drinks. (The National Heart Foundation suggests trying to limit eating cakes, biscuits and pastries to once a week.) A more detailed discussion on the GI occurs in the section on Nutrition and carbohydrates, which includes a table stating the GIs for various foods.
Fish oils
Fish oils are good at reducing high blood triglyceride levels, with reductions of up to 50 per cent being achievable. Fish oils can also raise HDL mildly, a beneficial effect. The only problem is that they can raise LDL slightly and this may require treatment if it occurs.
However, as mentioned previousy, there is litte evidence that this reduction in triglycerides results in a reduction in cardiovascular disease and thus they are generally not used in people with raised blood triglyceride levels. The exception is in people with very high levels of triglycerides where other treatment is inadequate.
For most people, fish in the diet is a better alternative to fish oil capsules and there are population-based studies that support consuming two to three fish meals per week to lower cardiovascular disease.
Mediterranean dietThe Mediterreanean diet has been shown to reduce the incidence of cardiovascular disease (heart attacks and strokes) and death rates overall. There is also evidence that it reduces the incidence of numerous types of cancer, Parkinson's disease and Alzheimer's disease. The key components of the Mediterreaean diet are as follows:
The Meditteranean diet food pyramid. |
2. Improving blood lipid levels through exercise and weight reduction
Attaining an ideal weight and exercising regularly both help improve blood lipids (i.e. lower LDL and triglycerides). Regular exrercise alone can reduce total cholesterol by about six per cent and LDL cholesterol by about ten per cent. These topics are discussed in much more detail in the sections on Obesity and Physical Inactivity.
3. Reducing lipid levels by medication
Until recently, the National Heart Foundation (NHF) guidelines for commencing lipid lowering drug therapy related to both people’s lipid levels and their overall risk of coronary artery disease. This view has been changed and the NHF now recommends that the decision to recommend drug treatment should be based solely on the risk of developing coronary artery disease. An important reason for adopting this view is that the majority of people who develop coronary artery disease do not have markedly elevated blood lipid levels. Most heart attacks occur in people with a total cholesterol of about 5.5mmol/L. Thus, it is better to base drug treatment decisions on a person’s overall risk level rather than just on blood lipid levels.
Lipid lowering medication should be offered to all people at high risk of cardiovascular disease and to all people at moderate risk who have a total cholesterol greater than 4.5mmol/L. It has been shown that a 1.0mmol/L drop in total cholesterol equates to a 20 per cent reduction in the risk of symptomatic coronary artery disease, whether the person has had previous coronary artery disease or not.
Treatment targets for drug therapy are shown in the table above. As a general rule, the higher the risk level, the more aggressively raised total cholesterol and LDL need to be lowered. It is especially important to get lipid levels to target levels if the person already has established vascular disease.
As stated previously, dietary therapy to lower lipids should be tried first. Poor compliance is the main reason that diet fails to lower cholesterol and people need to give diet a proper chance; otherwise dieters will never know if whether diet works. And diet is a much cheaper option than medication. It also has no side effects.
If diet therapy does not achieve target lipid levels, then drug therapy needs to be commenced. The exception to this rule is people who have already had coronary artery disease and have a total cholesterol greater than 4.0 mmol/L. These people are at a much greater risk and should be commenced on drug and dietary therapy at the same time.
Unfortunately, the number of people in the higher risk groups is large and, due to cost considerations, not all people in these groups qualify for subsidised drug treatment.
Drug therapy is not recommended for people under 18 years of age and for young adults its use is usually restricted to males with severely raised lipids. For the aged, lipid lowering therapy is warranted in all patients with evidence of coronary artery disease and a reasonable life expectancy. It is probably not necessary in those over 75 years with no evidence of vascular disease.
Achieving optimum medication use in people at high cardiovacular disease riskPrescribing: A recent Australian study (2009) found that 47% of people at high risk of cardiovascular disease due to a past / present history of cardiovascular disease were undertreated regarding appropriate medication therapy. This was a significantly greater problem with regard to the use of cholesterol lowering medication than it was with the use of blood pressure lowering medication. (The figures were even worse when all categories of high risk patients were considered together.) Patient compliance with medication: A recent study of people commenced on lipid-lowering medication showed that a significant minority had stopped taking their drug after only six months. Those most likely to stop were people under the age of 65 years and those living outside capital cities. The most common reasons for ceasing medication were being uncertain regarding the need for treatment and poor response to medication. It is very important to stress that cholesterol lowering medication needs to be taken for life if it is to be of value. Do not just stop if there is a problem. Discuss the problem with a GP. |
Drug selection
Before drug therapy is commenced, it is necessary to categorise the type of lipid problem present as different problems require different medications. The three categories are:
- raised cholesterol alone
- raised triglycerides alone and
- a combination of raised cholesterol and raised triglycerides alone.
Detailed discussion regarding selecting the most appropriate drug should be done in consultation with a medical practitioners. As the vast majority of patients use statin drugs, they are discussed below.
Statin medications
Statin drugs account for 90 per cent of lipid-lowering medications prescribed in Australia. This is because they:
- achieve target LDL levels in most people
- significantly reduce coronary artery disease
- work well in lowering moderately elevated triglycerides (between 2mmol/L and 4mmol / L)
- have few side effects (especially in lower doses)
- have not been shown to have any significant long term adverse effects
- are are easy to take (once per day).
They are the first line therapy for all lipid abnormatities other than when triglycerides are greater than 4.5mmol/L and isolated low HDL (less than 1.0mmol/L) levels, when fibrates are generally the preferred initial choice.
For every 1.0mmol/L drop in LDL, there is a 25% drop in the incidence of major coronary events (i.e. heart attacks) and a 21% drop in the incidence of other major vascular disease events (such as strokes) over a five year period.
Statins work in a number of different ways. Some of their effect comes from reducing cholesterol. They do this by inhibiting an enzyme called HMGCoA Reductase, which is important in cholesterol synthesis in the body, including the liver. (It mediates the conversion of HMGCoA to mevalonic acid, a precursor of cholesterol.) The resultant reduction in cholesterol synthesis in the liver causes a reduction in the production of the precursors of LDL in the liver and thus reduces their release into the blood.) It also causes an increase in liver uptake of blood LDL by increasing the number of liver LDL receptors. Thus blood LDL levels are lowered. Other important effects include stabilising fatty lesions in vessel walls (fatty plaques), partly through reducing the amount of inflammation (irritation and swelling) present, and reducing clotting through effects on platelets. (Mevalonic acid is converted to a variety of compounds as well as cholesterol. These other products are thought to influence clotting and inflamation and their ability to do this is altered by a reduction in mevalonic acid production caused by statin drugs. Interestingly, as well as influencing clotting, they also affect the immune system and people taking statins have been noted to have enhanced immunity, including enhanced transplant survival.)
There are a variety of statins on the market and newer, more potent ones are on the way. The main selection criteria is the severity of the LDL elevation. Statins vary in their potency as follows (in descending order of potency) – rosuvastatin (the most potent), atorvastatin, simvastatinand pravastatin (the least potent). Patients with moderately to severely raised LDL may require the more potent drugs or higher doses of less potent drugs. Generally speaking, doubling the dose of a statin already being taken can be expected to lower LDL by a further 6%.
Unfortunately, cholesterol levels in people taking statins do tend to gradually increase while on the medication and this means that the dosage often needs to increase with as time passes; or a more potent drug needs to be substituted. (For this reason it is important that cholesterol levels are regularly monitored while people are on lipid-lowering medication.)
Drug interactions and side effects, which vary with different statins, are also a consideration in choice. These need to be discussed with the prescribing medical practitioner.
Statins also work well in lowering moderately elevated triglycerides (between 2.0 and 4.0 mmol/L). Where triglycerides are above this level, the statins do not work as well and a better choice is a member of the fibrate group of drugs (such as gemfibrozil or fenofibrate) alone where triglycerides alone are raised or with a statin if triglycerides and cholesterol are raised. (The use of a fibrate in combination with a statin requires special care as significant muscle side effects are much more likely. Fenofibrate is less of a problem in this regard than gemfibrozil.) It is important to treat other causes of raised triglycerides at the same time, such as excess alcohol intake and diabetes.
Statins should usually be taken once a day at night.
Excretion of statins by the body: Statins vary in the way they are disposed of by the body. Pravastatin and rosuvastatin are excreted by the kidney and lower initial doses of these drugs should prescribed in people with kidney disease; or an alternate drug used. Atorvastatin, simvastatin and fluvastatin are mostly broken down in the liver. As all statins can adversely affect the liver, people with significant liver disease should not take them. (This is even more imperative with respect to statins that are mainly degraded in the liver.)
Contraindications: Statins should not be used in
- pregnant or lactating women
- women likely to become pregnant
- people with active liver disease
- people who have significant side effects (see below)
Side effects of statins:
Statins are usually well tolerated and safe to use, with significant adverse reactions occurring in only about two to ten per cent of people. (Statins are available over-the-counter in the United Kingdom.) Muscle pain and liver abnormalities are the most common and people with significant muscle or liver disease may not be suitable for statin therapy. Before commencing therapy doctors should document the base-line incidence of muscle aches the patient suffers and check blood levels of creatine kinase (CK) (a muscle enzyme that acts as a marker for muscle damage that statins can cause) and liver transaminases (liver enzymes that acts as a markers for liver damage that statins can cause). These tests should be repeated 2 to 3 months after therapy starts or the dosage has been increased (or sooner if significant symptoms occur) to see if statins are causing any adverse effect.
Developing diabetes: Statin therapy increases the risk of developing diabetes by about 9%. The consequences of this side effect are far outweighed by the advantages in lowering cardiovascular risk. The problem is more common in older people, in people who are overweight ad in people with high blood pressure.
Muscle pain: Muscle pain is the most common problem. It occurs as a vague ache in about 1% to 2% of patients in studies but in practice up to 10% are affected. It is more severe in about 0.5% of cases, where it also can cause muscle weakness. Mostly it occurs with higher doses and in people with a lower muscle mass, especially older people, especially older women. (The starting dose should be lower in these people.) People with an under-active thyroid are also more likely to get muscle symptoms and this is usually worth checking. Muscle symptoms will often disappear with a reduction in dose. Less commonly, muscle symptoms occur only with specific types of statins. Rarely, more severe muscle damage can occur. (aAbout 1 in 100,000 per year. There have very rarely in the past been deaths from this problem. This occurred mostly with ‘Cerivastatin’, which is no longer available.) As stated above, the degree of any pre-existing muscle soreness / pain should be quantified by checking the blood creatine kinase level and asking about any muscle symptoms before treatment commences in all patients. The CK level should then be rechecked 2 to 3 months after starting statin treatment (or sooner if symptoms occur). A significant rise indicates muscle damage may be occurring. If the CK level is greater than three times the upper limit of normal, statin therapy should be ceased and treatment reviewed. Less significant increases can be treated by reducing the dose and reviewing symptoms and the CK level in a few weeks. (Strategies such as changing the type of statin, permanent dosage reduction or use on alternate days, are often helpful strategies when dealing with a significant muscle problem in a patient who really needs the medication.) More severe muscle symptoms (incuding significant pain and any muscle weakness) are of serious concern and special care needs to be shown if statins are restarted. It is important that patients on statins report any muscle symptoms to a doctor without delay. Most people who cease their initiate course of statins because of mild muscle symptoms can be retried on the medication, usually on a different type of statin (or perhaps on a lower dose of the same medication); and most of these patients tolerate the medication at the second attempt.
Liver inflamation: Mildly elevated liver enzymes are not uncommon initially and only occasionally require ceasing of the drug. (People with active liver disease should not take statins.) As stated above, base-line liver transaminase levels should be measured prior to starting statins and then rechecked 2 to 3 months later. Stain therapy should be cease and the treatment reviewed if the liver transaminase enzyme levels increase to above three times the upper limit of normal. Alcohol use should be part of this review.
Other side effects: Other reactions include skin rashes, allergic reactions, headache, sleep disturbances and, uncommonly, fluid retention and raised blood glucose levels. If side effects are a problem but not serious, the patient should go off the statin for a few weeks and then go back on it at a much lower dose and carefully assess the response. If symptoms occur at the lower dose, a different type of statin may be worth trying. Obviously the above only applies to mild reactions. More significant reactions (especially allergic reactions) require permanent cessation of the medication. No long term side effects have been found to date and there is no evidence that it affects cognitive (thinking) ability.
Other lipid modifying medications
There are several other types of lipid modifying medications. The list here is not exhaustive.
Fibrates: These drugs are primarily used to reduce triglycerides. Their effect on LDL varies from a a significant reduction (up to 20%) to slight increase. They do also raise HLD. Generally, their overall beneficial effect is less than that of statins and they are most useful in people with significantly raised triglycerides (greater than 4.5mmol/L) and a low HDL, a combination that is common in people with type 2 diabetes. People who have high cholesterol and triglycerides may need a statin plus a fibrate. This is a potentially hazardous combination (especially in the case of the fibrate gemfibrozil) and should only be initiated by a specialist doctor involved in the treatment of lipid / cardiovascular problems.
Ezetimibe: This is a member of a newer class of drugs that acts by inhibiting the absorption of dietary cholesterol from the intestine. (It achieves this via a different mechanism to that used by plant sterols / stanols and thus, when used together, both provide benefit). The reduced cholesterol uptake from the intestine reduces the supply of chesterol to the liver which in turn makes the liver increase LDL uptake from the blood. It can reduce LDL by about 20% and is well tolerated with no known long term safety issues. it isusually added to statin therapy in patients who are on maximum stains doses without achieving desired LDL lowering and together they can lower LDL by up to 70%. (Adding ezetimibe to a statin is equivalent to trippling the dose of the statin.) It is also used alone in patients who cannot use statins. It must not be used with fenofibratem where gall bladder disease is present or with a stain in a pregnant / lactating woman or in a person with active liver disease.
Effectiveness of medication
The evidence to date indicates that statin drugs are very beneficial in reducing cardiovascular disease risk in the following situations.
- Patients with existing evidence of vascular disease (Grade IA evidence). This includes people who have had a heart attack or angina, a stroke or transient ischaemic attack, an aneurysm or peripheral vascular disease (claudication paion in the legs).
- Patients with specific vascular disease risk factors including diabetes and familial hypercholesterolaemia ('Grade IIB' evidence).
There is also less conclusive evidence ('Grade C' evidence) for benefit in reducing cardiovascular disease risk in other groups of people at high risk of vascular disease. There have been four major trials on the ability of statin drugs to lower cholesterol and reduce coronary artery disease. In summary, these trials show that statin drugs can be expected to reduce LDL by about 25 per cent and this has provided a 24 to 30 per cent reduction in the incidence of significant heart disease (heart attack or new angina) in these patients. This has been achieved in patients with and without pre-existing coronary artery disease. Statin drugs used immediately after having a heart attack can improve outcomes within as little as four weeks of treatment.
It has also been shown that significantly lowering elevated triglycerides reduces coronary artery disease. The results from one large trial (Veterans Affairs High-Density Lipoprotein Cholesterol Intervention Trial) studied the effect of lowering triglycerides by the fibric acid group of drugs (fibrates) on secondary prevention of heart disease (i.e. its effect in reducing further heart disease incidence in patients with pre-existing heart disease). This trial showed that a 31 per cent lowering of triglycerides was accompanied by a 22 per cent lowering in coronary events (heart attack and new angina).
How much can diet and medication reduce cholesterol?
A diet low in saturated fat and the use of spreads containing plant sterols can each reduce LDL by 10 to 15 per cent and the use of medication should reduce LDL by a further 25 per cent. Additional reductions can be achieved by consuming a diet high in soluble fibre. For healthy Australians, the desired LDL cholesterol level is 3.5 mmol/L or less. Using the above figures, most people with an LDL of up to 4.0 should be able to achieve these optimum levels with diet and the use of sterols (if needed). The addition of medication should mean that those with LDL levels of 4.0 to 5.3mmol/L can also achieve this desired LDL level of 3.5 or less. Very few Australians have an LDL level of above 5.3mmol/L.
Any drop in cholesterol significantly reduces the risk from vascular disease. It has been estimated that each 1.0mmol/L drop in LDL cholesterol reduces the risk of dying from any cause by about 12 per cent, the risk of dying from a heart attack by 19 per cent and the risk of having a stroke by about 17 per cent. Importantly, this benefit occurs irrespective of age, sex, the presence or not of diabetes or high blood pressure, and the starting level of LDL cholesterol (i.e. the benefit continues with reductions of LDL to 2.0mmol/L).
With some effort, most Australians should be able to achieve a normal cholesterol level. It is therefore unfortunate that about 50 per cent of adults still have a total cholesterol over 5.5 mmol/L.
Medications in real life
It is important to remember that the impressive reduction in the risk of suffering from cardiovascular disease that has occurred with the use cholesterol lowering medication was achieved in well-conducted trials. In such trials, the patients are regularly monitored to make sure they are taking adequate medication to achieve their target blood cholesterol levels and also to ensure they stay on their medication. Often this does not happen in real life and many people on lipid-lowering medication do not achieve optimum benefit from their medication.
To ensure people gain maximum benefit from their medication, they need, with the help of their GP, to make sure that they;
- know the LDL-cholesterol level they should be aiming for
- do all that they can to ensure they achieve this level
- continue on their medication and regularly monitor its effectiveness. This means having their cholesterol checked every six to 12 months.
Reasons for non-compliance with long-term medical therapy |
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About 40 to 50 per cent of people who have been advised to take long-term medication therapy do not continue with this therapy for longer than 12 months, irrespective of the disease being treated. This non-compliance can adversely affect their health outcomes very significantly. The reasons for this non-compliance are detailed below. Many relate to more time spent in patient education. This is the responsibility of both the doctor AND the patient. |
|
Reason |
Solution |
| Where treatment is preventative in nature, the absence of symptoms means there is no immediate advantage gained. | More time spent in patient education. |
| Lack of knowledge about disease | |
| Denial of illness | |
| Disagreement about the need for treatment with medication | Achieve compromise between doctor and patient. |
| Illness affecting attitude to medication e.g. mental illness, especially depression and dementia | Awareness by GP and other family members |
| Lack of support from other family members | Counselling by GP |
| Complicated / inconvenient administration due to multiple medications, frequent dosages | Help from family Change in medication administration |
| Medication side effects | Change medication or change dosage |
Cost of medication |
Try cheaper option. |
Cost of follow up |
Discuss issue with patient |
Who needs referral to a specialist in lipid therapy?
Achieving target levels can be diffucilt in some people and some people react adversely to medication. Situations that are best dealt with by a specialist include:
- People who are unable to achieve target levels, especially those at high risk
- Those requiring combination lipid-lowering therapies, especially those needing statins and fibrates.
- People who develop significant side effects to therapy.
- People with conditions that are difficult to treat, especially people with very higgh levels of LDL and triglycerides, especially if they are due to hereditary conditions such as Familial Hypercholesterolaemia and isolated low HDL
- People with other disease contributing to their cardiovascvular risk, such as diabetes, high blood presure that is difficult to control, chronic kidney disease and excessive alcohol intake.