Dr. Laurence Eyres
|
Laurence Eyres is the Technical and Development director for New Zealand Dairy Foods, a privately owned consumer goods company in Auckland. |
1 Introduction
This article is written from an Australasian perspective, but most of the information and comment is relevant to all developed countries. Over the last twenty five years there has been a concerted effort by medical practitioners, nutritionists and dieticians to combat the major diseases affecting the developed world. These diseases are predominantly cardiovascular disease and cancer, now being joined by diabetes.
Approaches have been mainly centred on the ‘lipid hypothesis’ whereby cholesterol and saturated fatty acids have been the main targeted ‘villains’ with polyunsaturated fatty acids seen as the ‘saviours’.
Although researchers never had any intention of simplifying the diagnosis and the cure, vested interests have ensured that the message remained simple and the nutritional changes required even more simplistic with respect to the role of lipids in the diet. These included eliminating trans fatty acids and, oxidised fat, and adding antioxidants, omega-3 fatty acids, dietary fibre and selenium.
2 Obesity
The increased incidence of obesity is perhaps the single biggest threat to a major segment of the world’s population. Our increasingly sedentary lifestyle and provision of plentiful and cheap fast food and sugary products has resulted in an alarming statistic showing that a significant percentage of people are overweight and many are obese.
To counter this trend in national diets, many people have climbed on the low-fat bandwagon with some influential people even suggesting the unworkable ‘fat-tax’. That this is not the route to pursue is illustrated by the fact that the percentage of obese persons in the USA is increasing alarmingly, despite low- fat mania and the fact that Mediterranean populations have average to high intakes of fat – predominantly monounsaturated oils. This would suggest that this view is too simplistic an approach.
Delany et al (2000), suggests that dietary fatty acids that are more prone to oxidation are the ones that are less likely to accumulate in body fat tissues. This research demonstrated that there was substantial variation in the proportion of the fatty acid which was found to be oxidised; stearate being far more slowly oxidised than linoleate. Delany et al concluded that in animal studies the rates of oxidation partially explained the differences in weight gain observed when the animals were fed different types of dietary fat and this mechanism may be a factor in human obesity. The trend toward the consumption of fast foods (predominantly deep-fried) high in energy and saturated fat is a likely link in the obesity epidemic and there are several solutions; one of which is to change the type of fat from saturated to monounsaturated and hydrogenated to monounsaturated, and the other is to provide tasty, economical nutritious alternatives to fried food. McDonalds did announce their intention to globally change to vegetable oils and to halve the trans fatty acid contents, but have subsequently delayed this change in some countries.
The use of oils containing polyunsaturated fatty acids in frying is not of great nutritional benefit because of their high susceptibility to oxidation and polymerisation.
NB The French limit linolenic acid to 3% in frying oils.
Back to top
3 Cholesterol
It was the controversial and much disputed epidemiological studies summarised and reviewed by Keys (1980) that showed that for some populations serum cholesterol levels were supposedly correlated with a high incidence of coronary heart disease. These studies were heavily flawed and have been much criticised by researchers in current years.
The whole topic has been shown to be much more complex than the simplistic approach taken by Keys. It is admirably reviewed by Gurr (1999).
It must be noted however that most General Practitioners in Australasia still use serum cholesterol and still advise patients to cut out saturated fats. It was also later shown that, contrary to earlier belief, serum `cholesterol is not closely related to dietary cholesterol intake, but is primarily related to the intake of saturated and trans fatty acids.
Nutritionists now accept that elevated total serum cholesterol levels are a just one risk factor for cardiovascular disease and levels above 5.5 mmol/L in adult men are seen by many doctors to indicate a moderate risk. Over the years there has been growing evidence that it is the oxidised low density cholesterol lipoprotein (LDL) that may be responsible for the build up of plaque in arterial walls, Kummerow (2000).
This area has been recently reviewed by Riemersma (2002) and merits further in-depth research.
4 Phytosterols
The plant kingdom, comprising cereal, vegetable seed oils, nuts and fruits, contains a number of sterols that differ from cholesterol by having ethyl or methyl groups or unsaturation in the side chain. The predominant ones are sitosterol, stigmasterol and campesterol which are present in diets rich in these food sources and contribute almost equally to the diet as cholesterol.
The most prominent is beta-sitosterol which differs from cholesterol in that it has an ethyl group at carbon 24 of the side chain.
In the early 1950s it was noted that the addition of sitosterol to the diet of cholesterol-fed chickens or rabbits lowered cholesterol levels in both species and inhibited atherogenesis., Tthis work was extended to humans by Miettinen (1994). Sitosterols were also studied extensively as cholesterol lowering agents by Lees et al (1997) and no adverse nutritional effects at large dose levels have been observed.
Over the past few years we have seen the launch of many products containing hydrogenated and interesterified beta-sitosterol which are reported to lower serum cholesterol by between 10 and 20%. However, these products are expensive, and currently hold a low market share.
Because of the expense and the reduction in yellow fat consumption, it would be advisable to have phytosterols included in selected food products such as dressings and baked goods, despite current nutritionists’ opposition to such widening of the scope for this effective nutritional change.
5 Changes in the Relative Intakes of Fatty Acids
A desirable balanced intake of fatty acids was calculated recently for the USA by Simopoulos (1999) and is compared with this author’s estimate for current New Zealand intake, Eyres (2000), as shown in Table 1.
Table 1. Fatty Acid Intake desirable for an 8400 kJoules diet
| Fatty Acid |
Latest target composition
|
Estimated NZ intake
|
|
|
% energy
|
g/day
|
g/day
|
|
| Saturated |
< 8
|
<17.8
|
40
|
| Trans |
< 1
|
<2.0
|
5
|
| Monounsaturated |
~ 20.0
|
48
|
38
|
| Linoleic (w-6) |
3.0
|
6.7
|
15
|
| Linolenic (w-3) |
1.0
|
2.2
|
1.5
|
| EPA. + DHA (w-3) |
0.3
|
0.7
|
<0.2
|
| Totals |
33
|
78
|
100
|
The implications for the Australasian diet is a recommended reduction in total saturated and trans fatty acid intake with a major increase in monounsaturated and Omega-3 fatty acids.
Table 2 shows a selection of new culinary oils which could contribute to modifying the above fatty acid intake.
Table 2. Fatty acid compositions of some new culinary oils
| Oil |
16:0
|
16:1
|
18:0
|
18:1
|
18:2
|
18:3
|
Other
|
| Avocado Oil (NZ) |
12.5
|
4.5
|
0.4
|
72
|
9.5
|
0.5
|
0.6
|
| Olive Oil (Australasian) |
8.5
|
0.4
|
1.1
|
84.6
|
4.5
|
0.3
|
0.6
|
| Macadamia (Australia) |
8
|
11
|
1.0
|
66.5
|
1.5
|
1.0
|
|
| Flax Seed Oil (NZ) |
5.9
|
-
|
2.7
|
15.5
|
16.6
|
59.0
|
0.3
|
| Omega Plus Blend |
12.1
|
1.3
|
1.5
|
71
|
8.3
|
3.6
|
2.2
|
The Omega Plus Blend is a new blend of avocado oil, olive oil and flaxseed oil available in Australasian markets and soon to be launched in the USA and UK.
6 Trans Fatty Acids
Trans fatty acids occur naturally in the depot and milk fats of ruminants. They are also produced during the hydrogenation of liquid unsaturated fish and vegetable oils.
Hydrogenation is used to produce solid and more stable fats for food manufacture. The major controversy over these fatty acids revolves around the claim that they were even more cholesterol- elevating than saturated fatty acids, and also increased LDL levels at the expense of HDL levels (Mensink et al, 1990).
Levels of trans acids in the US and European diets have been estimated to have come down from around 10-20g per day to about the same as Australasia, where the intake is now approximately 4-5g per day, Lake (1995).
In my opinion, the trans acids should be counted and added to the saturated fat content of a food. The controversy, which surfaces from time to time, illustrates that data from one country cannot be extrapolated to another.
The British Nutrition Foundation task force concluded that while levels around 4-5g per day posed no significant risk to the consumer, it would be prudent to discourage a rise in the average intake of trans fatty acids, by encouraging good food manufacturers to eliminate partially hydrogenated fats from oils and fat products.
Similar to Table 1 above, they also recommended that trans fatty acids should not account for more than 1-2% of energy intake.
Denmark has recently taken steps to limit the amount of trans fat in processed food to a maximum of 2% (of total fat). It is likely that the rest of Europe will follow and several food manufacturers have quickly adopted the new recommendations.
7 Polyunsaturated Fatty Acids
When the term polyunsaturates was starting to become well known in the early 1970s, most technologists and nutritionists equated this with linoleic acid (omega-6) while linolenic acid (omega-3) was ignored.
The soft polyunsaturated margarines which emerged onto the market in Australasia and elsewhere had linoleic acid levels in excess of 40% and saturated fatty acid levels less than 20%.
It is thought that our ancestral diet before the Industrial Revolution had dietary levels of omega-3 and omega-6 in an equal ratio. These essential fatty acids are necessary but current research suggests that we should reduce our intake of linoleic acid to less than 7g per day and increase our linolenic acid (from canola, flaxseed and other sources) to approximately 2g per day i.e. A a ratio of around 3-4:1 of linoleic to linolenic is desirable, not the current ratio of approximately 15:1, Simopoulos (1999).
There are concerns that excessive amounts of linoleic acid may increase the susceptibility to oxidation of the atherogenic lipoproteins, especially with low antioxidant intakes (Louheranta et al, 1996). Flaxseed oil is now being commonly used in salad oils and in spreadable margarines in order to achieve a balanced ratio of omega-6 to omega-3 fatty acids.
8 Long Chain PUFA and Fish
The long chain PUFA from fish oils are sadly lacking in many Westerners’ diets. High price and unavailability of quality fish are often cited as the main reasons for this.
In Australasia, This is an urban myth and quality fish can be sourced economically and utilised in a variety of “healthy” recipes for most families.
Fish and chips, whilst an acceptable meal for most families is nutritionally balanced when it is not overloaded with saturated fat and oxidised cholesterol from heat-abused animal-fat-based frying media.
Tinned salmon and tuna in brine (not vegetable oil) provide an adequate source of long chain PUFA. There are concerns that the supply of fish in Europe and North America is not sustainable and that fresh fish is becoming scarce. The source of long chain Omega-3 may therefore have to be from algal or microbial sources.
9 Monounsaturated Fatty Acids
The Mediterranean diet has often been cited as the preferred diet and the Lyon Study verified that intervention groups showed a significant reduction in the death rate from CHD with also a reduction in related risk factors such as LDL-cholesterol. (Lorgeril, 1999).
Interestingly, the total serum cholesterol of the intervention and control groups showed no significant differences.
The monounsaturated fatty acid, oleic acid, is the major component in olive oil and avocado oil yet the beneficial influence of these oils may not be solely due to their fatty acid compositions, but may also involve the other minor components such as beta-sitosterol, tocopherols and other antioxidants. Observers of the literature have also noted that there is no distinct difference in mortality rates between the Mediterranean countries and the USA and Northern European countries.
There have been several new generation high-oleic oils developed over the last few years and these were recently reviewed by Kristott (2003). These include high-oleic versions of rapeseed, safflower and soybean adding to the well-developed business for high-oleic sunflowerseed oil. These oils when tested for their performance in frying, did not show a direct correlation between their fatty acid composition and frying stability. Tocopherols and other antioxidants play a part in the frying behaviour and probably their nutritional behaviour.
10 Fast Food
The last twenty five years has seen a massive change with respect to the role of meals not consumed at home. There has been prolific growth in fast food chains and they have one main item in common: their use of stable and economic frying fats.
These refined and deodorised fats are stable, economical and are refined to a low FFA. Foods fried in these fats tend to have a high energy content and be carriers of oxidised lipids which destroy natural antioxidants and leave the consumer satiated. They tend to be marketed towards the younger generation.
There is a suggestion from nutritionists that we should revert back to ‘slow food’ where the whole family sits down and takes time to enjoy and digest a balanced blend of fresh, well-cooked, food (with the correct lipid concentration of course).
11 Frying Fats
Frying is a complex process. The reactions taking place are not simple oxidation reactions and their rate is fast at temperatures between 180-190°C.
New Zealanders and Australians consume large amounts of fried food. Sausages, fish, chicken and potatoes are the common ingredients which tend to be cooked in processed animal depot fats, beef and mutton tallows.
Exchange of lipids occurs between the food and the fat. The processors require a stable, cheap and quality frying fat and common frying fats vary globally from tallow to palm olein and partially hydrogenated rapeseed oil (15% trans).
Some manufacturers have turned to canola oil, cottonseed oil, and palm oil but change is slow and none of these products are ideal from a technological point of view. High-oleic sunflowerseed oil, a relatively recent vegetable oil is an ideal product for frying. It is high in monounsaturates (80%), contains no cholesterol and contains tocopherols. However it is expensive and this is delaying its successful large scale introduction into the market.
12 Oxidised Lipids
Most nutritionists have been very concerned about the ingestion of oxidised lipids for many years, but this was based on theory and with little scientific evidence that rancid fats or oxidised lipids of any form were directly involved in diseases such as cardiovascular disease or cancer.
Despite this, however, there is circumstantial evidence and examination of certain biomarkers suggest that oxidation of all lipids is a logical and plausible source of high risk factors for cardiovascular disease and other inflammatory diseases (Steinberg 1997).
There is great interest in this area particularly relating to the molecular mechanisms that lead to atherosclerotic plaque formation and the protective effects of natural antioxidants. The key questions to resolve are:
· whether peroxidised lipoproteins exist in plasma and if they are elevated in subjects at higher risk to cardiovascular disease;
· what is the source of the peroxides.
Some researchers believe the case is proven and cite experimental evidence from studies of atherosclerosis in the LDL receptors in mice, Stapranset al (1999).
The table below shows some common sources of oxidised lipids from typical foodstuffs such as aged nuts and aged vegetable oils (particularly those in clear plastic on supermarket shelves).
Table 3. Sources of Oxidised Lipids in the diet
| Common Oil Source | Intermediate Oxygen Species | Likely Products |
| Vegetable oils in clear plastic bottles | Peroxidised linoleic acid | Aldehydes, hydroperoxides |
| Rancid nuts | Oxidised triglycerides | Polar material |
| Grilled pizza cheese | Oxidised cholesterol | |
| Fried chicken/sausages/shell fish | Oxidised cholesterol and long-chain PUFA | Polar material, dimers, aldehydes, oxidised fatty acids |
| Barbecued meat | Pyrolysed fatty acids and oxidised cholesterol | Aldehydes, polymers, benzpyrene |
| Fish Oil supplements | Oxidised PUFA | Aldehydes |
13 Antioxidants
The classical mechanism of lipid oxidation via free radicals has been established for many years. The protection of lipids by hindered phenols such as tocopherols has also been documented, investigated and utilised in food manufacture.
Again, original approaches of supplementing diets with pure derivatives of alpha tocopherol or in some cases beta-carotene is not ideal for human nutrition. Oxidation and antioxidant defence within the body is complex and it appears that we may need a cocktail of different antioxidants as suggested below (author’s proposal). One of these essential elements is selenium known to be deficient in many diets.
Selenium is relatively easily added to the everyday diet and we should possibly emulate the Finnish authorities who decided in 1984 to ensure an average minimum intake of 25 micrograms per day via fertilisers. The whole area of selenium in food is admirably reviewed by Combs (1986).
Suggested Antioxidant Cocktail (per day), Vitamins A, C, and E together with selenium:
• Vitamin E 200-1200 iu/day
• Vitamin C 100-250 mg/day
• Vitamin A 750 µg retinol/day
• Selenium 50-200 µg/day
These nutrients are best taken as part of our food supply and not as pills or capsules.
Recent research has shown that selenium may be synergistic with sulphoraphane from brassica. The habit of drizzling extra virgin olive oils on salads and vegetables provides a source of many different anti-oxidants.
Inconclusive work on vitamin E may have been as a result of using dl-a-tocopherol in the trials instead of a mixture of the eight naturally occurring isomers.
However, feeding one antioxidant in isolation is possibly too simplistic an approach. The oxidation mechanisms in vivo are extremely complex and there are several layers of defence mechanisms involving vitamin E, vitamin C, carotenoids (not just beta-carotene) and selenium.
The natural flavanoids in berry fruits, coloured vegetables, red wine, olive oil, avocado oil and green tea are receiving world-wide attention. In most Western countries it is probably safe to say that our dietary intake of these natural foodstuffs has been low and we should endeavour actively to increase it by food intake and not by individual agents in supplements.
14 Conclusions and Recommendations
A significant proportion of the developed world’s population has paid no heed to the nutritional messages of the last twenty five years. The increasingly sedentary population consumes too much energy, too much saturated and trans fat, insufficient monounsaturated and omega-3 polyunsaturated fatty acids and has deficiencies in natural antioxidants and their co-activists which include tocopherols (vitamin E), vitamin A, vitamin C, flavanoids and selenium.
Most of these imbalances may be traced to current dietary practices, with the consumption of fast food, takeaways and high energy snacks dominating the diet together with a corresponding lack of intake of fruits, vegetables, fish and good quality plant oils.
There are economical ways of improving the daily diet and more notice should be taken to ensure that the lipids in our diet are free of oxidised species such as the peroxides of polyunsaturated fatty acids and the oxides of cholesterol. Perhaps it is now time to qualify the ‘no-fat’ dogma and to ensure we have a dietary regime comprising the right fatty acids in a pristine state.
Willet’s new food pyramid, which is indeed controversial, challenges the status quo on fats and oils and should provoke intense debate. (Willet, W.C (2001).
See Figure 1:
Nutrigenomics has started to examine the differences in diet response depending on the individuals genetic makeup. Heredity is well known to be major risk factor in CHD incidence followed by the self-inflicted risk factors such as smoking, obesity, lack of exercise, alcohol and drug abuse etc.
This review only covers this author’s opinion of a healthy lipid intake from an observation of the current and past literature and does not take into account the other risk factors.
Populations need to focus on the problem of insufficient exercise, obesity, overweight and diabetes. Researchers need to examine new biomarkers as indicators of incorrect nutrition. The role of oxidised lipids and in particularly cholesterol oxides needs to be clarified with respect to their relationship with inflammatory diseases such as heart disease. The presence of oxygen-containing species should be correlated with antioxidant states, particularly in people at risk.
There is a realisation that it is not fat which is bad for one, but it is excessive amounts of the wrong types of lipid and in the wrong oxidised state that results in the diseases that are prolific in the Western World. If we wish to significantly change the Western diet we must focus on areas of maximum impact such as the nature of frying fats in fast foods, the reduction of oxidised species by better food handling practices, and the analysis, identification and incorporation of the necessary antioxidants in our food supply.
References
1. Combs G F and Combs S B (1986) The role of selenium in Nutrition. Academic Press New York.
2. Delany J P, Windhauser M M, Champagne C M & Bray GA (2000) Differential Oxidation of individual dietary fatty acids in humans. American Journal of Clinical Nutrition, 72, 905-911.
3. Eyres L (2000) Fats, Fatty Acids and Cholesterol. The New Zealand Food Journal, 29(4), 143-146.
4. Kannel W.B, Wilson P.W (1992) Efficacy of lipid profiles in prediction of coronary heart disease. American Heart Journal, 124, 768-.
5. Kristott J (2003) High-oleic oils – how good are they for frying? Lipid Technology, March, 29-32.
6. Lees A M, Mok H Y I, Lees R S & McCluskey M A (1997). Plant sterols as cholesterol – lowering agents. Atherosclerosis, 28, 325-338.
7. Louheranta A M, Porkkala-Sarataho E K, Nyyssönen M K, Salonen R M & Salonen J T (1996) American Journal Clinical Nutrition, 63, 698-703.
8. Mensink R & Katan M B (1990) New England Journal of Medicine, 323, 439-445.
9. Reische D W, D A Lilliard & Eitenmuller R R (1997) Antioxidants, in Food Lipids, edited Simopoulos A P (1999) Workshop on essential fatty acids, NIH Maryland, USA.
10. Staprans I, Pan X M, Rapp J H, Grunfeld C & Feingold I C R (1999) Oxidised cholesterol in the diet accelerates the development of atherosclerosis in LDL receptor- and apolipoprotein E- deficient mice. Arteriosclerosis Thromb. Vasc. Bisl., 708.
11. Steinberg D (1997) The Journal of Biological Chemistry, 272(34), 20963.
12. Riemersma, R (2002) Lipid Technology, 14, 125-128.
13. Willet, W.C. (2001) Eat, Drink or be Healthy: The Harvard Medical School Guide to Healthy Eating. Fireside.
14. Weblink to the Food Pyramid; www.sciencefriday.com/pages/2003/Jan/pyramids.html.