Beruflich Dokumente
Kultur Dokumente
Australian adults should consume 500 mg per day* of omega-3 polyunsaturated fatty acids (marine
source) to lower their risk of coronary heart disease
* Australian adults with documented CHD should increase their intake to 1000 mg per day
The main risk factor for CHD is high circulating LDL cholesterol and triglyceride levels. The average blood
cholesterol levels of Australian adults in the past two decades has remained at consistently high levels.
Half of Australian adults have high cholesterol (5.5 mmol/L or more) and are at significant risk of developing
CHD (1999-2000 AusDiab study).The build-up of plaque can potentially prevent blood from reaching the
heart, resulting in myocardial infarction, angina or stroke (5).
How omega-3 PUFA can reduce cholesterol and triglyceride levels in the body
There is an increasing amount of evidence showing that consumption of omega-3 fatty acids contributes to
the reduction of LDL cholesterol and TG levels. EPA and DHA are the long chain metabolites of alpha
linolenic acids and are found only in marine sources. Intake of EPA and DHA through consumption of fish is
likely to be the most effective non-pharmacological intervention to tackling the onset of CHD.
The enrichment of EPA and DHA in cell membrane phospholipids has various effects on improving blood
lipid levels in the body.
- reduced TG and remnant lipoprotein levels
- increased HDL cholesterol levels
High doses of marine omega-3 PUFA supplementation have significant effectives in improving blood lipid
ratios. Supplementation of 1000-4000 mg/day has been shown to decrease TG levels by 25-35 per cent and
increase HDL cholesterol levels by 1-3 per cent (1 (24,25)).
Patients with severe hypertriglyceridaemia (TG concentration 5.65 22.60 mmol/L), EPA and DHA may reduce
TG concentration by 45 per cent. In patients with extremely high concentration of TG (> 22.60 mmol/L), EPA
and DHA may reduce TG concentration by 50 per cent or more. (3 (18))
A recent review of 21 trials that evaluated the effects of consumption of EPA and DHA on serum CVD risk
factors found strong evidence for reduced TG concentration levels. on improving lipid outcomes.
- EPA and DHA consumption resulted in reduced TG level by 0.3 mmol/L and increased HDL concentration
by 0.04 mmol/L and increased concentration of LDL by 0.15 mmol/L. Higher EPA and DHA dose and higher
baseline levels lead to greater reductions in TG concentrations. Marine omega-3 PUFA has a dose
dependent beneficial effect on TG concentration, particularly in individuals with high levels. (3 (19).
Marine n-3 PUFA can regulate TG metabolism through several nuclear receptors that influence various
aspects of lipoprotein metabolism. Activation of PPAR-alpha reduces TG levels mainly by decreasing
apolipoprotein CIII expression, which inhibits lipoprotein lipase, a key enzyme of TG catabolism. Marine n-3
PUFA and its eicosanoid metabolites are natural ligands with high affinity for binding to PPAR-alpha (3,160).
Marine n-3 PUFA significantly lowers chylomicron levels probably by decreasing secretion of VLDL
cholesterol from the liver. Marine n-3 PUFA also decreases chylomicron size, which increases clearance and
possibly increases lipoprotein lipase activity. DHA and EPA appear equally effective in improving chylomicron
clearance (3(161))
EPA and DHA also influences the activities of several enzymes involved in carbohydrate and lipid
metabolism (1(48,49)). These changes lead to reduced synthesis of TG (1(51)) and increased mitochondrial
beta-oxidation (1(52-54) with a subsequent decrease in formation of VLDL (1(55,56).
Currently, the intake of n-3 PUFA is substantially below the 500 mg/day recommended by the Heart
Foundation. The 1995 National Nutrition Survey estimated that less than 10 per cent of the population
consumed more than the Heart Foundation’s guideline of 500 mg/day of n-3 PUFA (marine source) (3 (50)).
A 2007 study showed that the average n-3 PUFA intake of Australians is estimated to only 246 mg/day
comprising of 75, 71 and 100 mg/day from EPA, DPA and DHA respectively (1 (39)). The problem is that the
typical western diet is characterised by high intakes of saturated, omega-6 PUFA and trans fatty acids and a
low intake of n-3 PUFA (3 (57)).
Evidence
The following section explains what evidence behind these claims.
Two large scale trials where the population was followed for an number of years shows the relationship
between fish oil, lipid profile and reduced CHD risk....
Omega-3 fatty acids have been found to be one of the most effective lipid-lowering intervention to reduce
overall morality risk from CHD. It came a close second behind statins, and out performed other
pharmacological agents such as resins and fibrates. Compared with control groups, the mortality risk rate
was 0.87 for statins and 0.77 for EPA and DHA. (3(137)). It is recommended that pharmacological means
should only be used if dietary measures like omega-3 supplementation fail after 3 - 6 months trial. (4,
RACGP - Diabetes mgmt in GP 5th ed 2009/10)
There are many large-scale, prospective population studies of the association between plasma total (and
LDL) cholesterol levels and the future risk of developing CHD. These include the Multiple Risk Factor
Intervention Trial (MRFIT),6-8 the Framingham Heart Study9 and the Prospective Cardiovascular Munster
(PROCAM) Study.10 The Multiple Risk Factor Intervention Trial (MRFIT),6-8 a prospective study of more than
360000 men, with follow-up now more than 10 years, shows a continuous positive curvilinear relationship
between plasma cholesterol concentration and rates of death from CHD (see Box 3).
1-2 servings per week of 170 g of fish high in EPA and DHA resulted in decreased risk of coronary death by
36 per cent. It is estimated that an intake of 250 mg/day of EPA and DHA is sufficient for primary prevention
(3 (30)).
Studies reveal the potent ability of EPA and DHA to significantly reduce circulating levels of blood TG. Within
2-3 weeks of EPA and DHA supplementation, significant reduced blood TG levels within an approximate
reduction of 6-8 per cent or more per gram of EPA and DHA consumed (6(20)).
In a placebo controlled, double blind trial, a 26 per cent lowering in fasting TG levels in post menopausal
women receiving 4 g EPA and DHA daily over 28 days was demonstrated. (6 (22)).
GISSI Prevenzione Trial (7 (58)) found a small reduction in triglyceride concentrations in patients receiving
EPA and DHA. A large scale study where 5,500 post myocardial infarction patients received 1 g of EPA and
DHA a s fish oil and a smilar number of patients served as controls. After 3.5 yeasr, treated patients had a
significant reduciton in CV mortality, from 6.2 per cent to 5.1 per cent.
Practical steps
The inclusion of 1-2 servings of fish per day is important in ensuring that the Australian adult receives
sufficient quantities of EPA and DHA to protect against CHD. These LCPUFA are only found in marine
sources and the body’s rate of conversion of ALA into its LCPUCA metabolites is extremely low at about 10
per cent (6((7,8)). Modern consumption patterns in industrialised societies also reflects a higher consumption
of omega-6 PUFA (mostly from common vegetable oils) compared to omega-3 PUFA. This is a concern as
the competitive influence of high LA intakes further reduces the body’s already limited ability to metabolise
ALA to EPA and DHA (6).
You can achieve this by eating a combination of two to three 150 gram serves of oily fish every
week (state what is oily fish in a txt box) and by supplementing your intake with fish oil
supplements (capsules or oil) and omega-3 enriched food and drinks. Aim to consume about 3500
milligrams of EPA and DPA over the whole week.
Good sources of marine omega-3 include: Atlantic and Australian salmon (fresh or canned),
gemfish, blue-eye trevalla, blue mackerel, oysters, arrow squid, canned sardines and some
varieties of canned tuna.
(5) Australian Institute of Health and Welfare 2008. Australia's health 2008. Canberra: Australian Institute of
Health and Welfare. PDF, viewed 5 April 2010, <http://www.aihw.gov.au/publications/aus/ah08/ah08.pdf>.
(1 (24,25))
24. Milte C, Coates A, Buckley J, Hill A and Howe P: Dose-dependent effects of docosahexaenoic acid-rich
fish oil on erythrocyte docosahexaenoic acid and blood lipid levels. Br J Nutr. Oct 31: 1-6, 2007.
25. Balk EM, Lichtenstein AH, Chung M, Kupelnick B, Chew P and Lau J: Effects of omega-3 fatty acids on
serum markers of cardiovascular disease risk: a systematic review. Atherosclerosis. 189: 19-30, 2006.
(3 (18))
18. Milte C, Coates A, Buckley J, Hill A and Howe P: Dose-dependent effects of
docosahexaenoic acid-rich fish oil on erythrocyte docosahexaenoic acid and
blood lipid levels. Br J Nutr. Oct 31: 1-6, 2007.
(3 (19).
19. Balk EM, Lichtenstein AH, Chung M, Kupelnick B, Chew P and Lau J: Effects
of omega-3 fatty acids on serum markers of cardiovascular disease risk: a
systematic review. Atherosclerosis. 189: 19-30, 2006.
(3(160))
160. Krey G, Braissant O, L'Horset F, Kalkhoven E, Perroud M, Parker MG and
Wahli W: Fatty acids, eicosanoids, and hypolipidemic agents identified as
ligands of peroxisome proliferator-activated receptors by coactivator-
dependent receptor ligand assay. Mol Endocrinol. 11: 779-91, 1997.
(3(161))
161. Park Y and Harris WS: Omega-3 fatty acid supplementation accelerates
chylomicron triglyceride clearance. J Lipid Res. 44: 455-63, 2003.
(1(48,49))
48. Jump DB and Clarke SD: Regulation of gene expression by dietary fat. Annu
Rev Nutr. 19: 63-90, 1999.
49. Dallongeville J, Bauge E, Tailleux A, Peters JM, Gonzalez FJ, Fruchart JC and
Staels B: Peroxisome proliferator-activated receptor alpha is not rate-limiting
for the lipoprotein-lowering action of fish oil. J Biol Chem. 276: 4634-9, 2001.
(1(51-56))
51. Weber P and Raederstorff D: Triglyceride-lowering effect of omega-3
LC-polyunsaturated fatty acids--a review. Nutr Metab Cardiovasc Dis. 10:
28-37, 2000.
52. Halminski MA, Marsh JB and Harrison EH: Differential effects of fish oil,
safflower oil and palm oil on fatty acid oxidation and glycerolipid synthesis in
rat liver. J Nutr. 121: 1554-61, 1991.
53. Gronn M, Christensen E, Hagve TA and Christophersen BO: Effects of dietary
purified eicosapentaenoic acid (20:5 (n-3)) and docosahexaenoic acid (22:6(n-
3)) on fatty acid desaturation and oxidation in isolated rat liver cells. Biochim
Biophys Acta. 1125: 35-43, 1992.
54. Willumsen N, Skorve J, Hexeberg S, Rustan AC and Berge RK: The
hypotriglyceridemic effect of eicosapentaenoic acid in rats is reflected in
increased mitochondrial fatty acid oxidation followed by diminished lipogenesis.
Lipids. 28: 683-90, 1993.
55. Nossen JO, Rustan AC, Gloppestad SH, Malbakken S and Drevon CA:
Eicosapentaenoic acid inhibits synthesis and secretion of triacylglycerols by
cultured rat hepatocytes. Biochim Biophys Acta. 879: 56-65, 1986.
56. Westphal S, Orth M, Ambrosch A, Osmundsen K and Luley C: Postprandial
chylomicrons and VLDLs in severe hypertriacylglycerolemia are lowered more
effectively than are chylomicron remnants after treatment with n-3 fatty acids.
Am J Clin Nutr. 71: 914-20, 2000.
(1(39)
39. Howe P, Meyer B, Record S and Baghurst K: Dietary intake of long-chain
omega-3 polyunsaturated fatty acids: contribution of meat sources. Nutrition.
22: 47-53, 2006.
(3 (57)).
57. de Lorgeril M and Salen P: Dietary prevention of coronary heart disease:
focus on omega-6/omega-3 essential fatty acid balance. World Rev Nutr Diet.
92: 57-73, 2003.
(3(137))
137. Studer M, Briel M, Leimenstoll B, Glass TR and Bucher HC: Effect of different
antilipidemic agents and diets on mortality: a systematic review. Arch Intern
Med. 165: 725-30, 2005.
(3 (30)).
30. Mozaffarian D and Rimm EB: Fish intake, contaminants, and human health:
evaluating the risks and the benefits. JAMA. 296: 1885-99, 2006.
(6(20)).
20. Harris WS. Fish oils and plasma lipid and lipoprotein metabolism in humans:
a critical review. J Lipid Res1989;30:785-807.
(6 (22)).
Study. Circulation1998;97:1029-36.
22. Stark KD, Park EJ, Maines VA, Holub BJ. Effect of a fish-oil concentrate on
serum lipids in postmenopausal women receiving and not receiving hormone
replacement therapy in a placebo-controlled, double-blind trial. Am J Clin
Nutr2000;72:389-94.
2002 WORKSHOP SCHEDULE
(7 (58))
58. Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after
myocardial infarction: results of the GISSI-Prevenzione trial. GISSI-Prevenzione
Investigators. Lancet 1999; 447: 447-455.
(6((7,8))
7. Raper NR, Cronin FJ, Exler J. Fatty acid content in the US food supply. J
Am Coll Nutr1992;11:304-8.
8. Kris-Etherton PM, Taylor DS, Yu-Poth S, Huth P, Moriarty K, Fishell
(6).
B. J. Holub Clinical nutrition: 4. Omega-3 fatty acids in cardiovascular care. Can. Med. Assoc. J., March
1, 2002; 166(5): 608 - 615.
are found predominantly in fish and fish oils. Although the body can convert ALA into
Summary of how omega 3 can reduce risk of CHD (then use sci evidence to back up these claims)
Effects of omega-3 fats - may help prevent blood clots from forming and inflammation
from affecting artery walls. Omega-3 fats also may reduce the
risk for heart rhythm problems and, at high doses, reduce
triglyceride levels. Studies have suggested that omega-3 fats
reduce the risk for heart attack and death from heart disease for
those who already have heart disease.
The baseline AusDiab study revealed that 66% of participants had dyslipidemia.
People who have high total cholesterol and triglyceride levels are at a significantly greater
risk of developing cardiovascular disease than those with normal blood lipid levels.
EPA and DHA are believed to reduce the impact of abnormalities in blood lipid levels which
cause CHD through the following mechanisms (1):