20 de Junho, 2009
Documento da Fundação Nacional do Coração da Austrália parece reconhecer inexistência de relação entre nível de colesterol total e risco de AVC
Do documento Dietary fats and dietary cholesterol for cardiovascular health (2009), publicado pela National Heart Foundation of Australia este ano, e cujo objectivo foi compilar toda a evidência relativa à relação entre consumo de gorduras e de colesterol com as doenças cardiovasculares, constam algumas conclusões importantes, das quais eu destacaria estas a seguir:
Saturated FA (SFA):
SFA intake is associated with CHD
Replacing SFA with cis-unsaturated FA has a greater positive influence on CHD risk than replacing SFA with carbohydrates (CHO)
Replacing SFA with n-6 PUFA to achieve a ratio of PUFA to SFA of greater than one will reduce the risk of CHD
Replacing SFA with monounsaturated FA (MUFA) lowers total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C), although not to the same extent as PUFA
Increasing SFA intake results in an increase in TC and LDL-C compared to CHO, PUFA and MUFA
Myristic, palmitic acids and lauric acids are associated with elevated LDL-C
Stearic acid has a negligible effect on LDL-C
Lauric, myristic and palmitic acids are associated with an increase in HDL-C compared to CHO. Lauric acid increase of high-density lipoprotein cholesterol (HDL-C) is greater than other individual SFA
Lowering dietary SFA to <7% of energy intake with restricted dietary cholesterol results in further LDL-C lowering than diets containing <10% of energy intake from SFA
Trans FA (tFA):
tFA intake increases LDL-C, decreases HDL-C, increases Lp(a) and increases the concentration of fasting serum triglycerides (TG)
tFA intake is associated with increased CHD incidence and risk of CHD
tFA intake is associated with an increased risk of non-fatal and fatal MI
tFA intake has little effect on haemostatic factors, the susceptibility of LDL-C to oxidation, or blood pressure, but may have an adverse effect on postprandial lipids and endothelial function
Ruminant tFA have a similar effect on LDL-C and HDL-C as industrially produced tFA
Replacing partially hydrogenated oils (PHO) with oils high in cis-unsaturated FA improves the lipid profile
n-6 PUFA:
n-6 PUFA intake lowers LDL-C
The CVH benefits of n-3 PUFA are not influenced by background n-6 PUFA
n-3 PUFA:
In secondary prevention, a diet with 2 g/day of ALA decreases the risk of CHD
In secondary prevention 850 mg/day marine n-3 PUFA supplementation reduces the risk of CHD mortality, and 1,800 mg/day reduces major coronary events
In secondary prevention, there is conflicting evidence about the effect of marine n-3 PUFA supplementation on the risk of sudden death in patients
Marine n-3 PUFA supplementation of 1,000-4,000 mg/day decreases TG levels by 25–30% and increases HDL-C levels by 1–3%. A dose relationship exists between the intake of marine n-3 PUFA and decreased TG levels
Marine n-3 PUFA has an additive effect to statin therapy in decreasing TG levels and increasing HDL-C
Total fat:
An increase in the consumption of SFA and tFA, rather than total fat, increases the risk of CHD
Dietary cholesterol:
There is little evidence of a relationship between serum cholesterol and stroke
Dietary cholesterol increases TC and LDL-C, but substantially less so than SFA and tFA
HDL-C and TC:HDL-C:
Higher HDL-C may reduce the risk of CHD
TC:HDL-C is an informative predictor of CHD mortality
Specific foods:
Consuming up to six eggs/week in a diet low in SFA is not associated with adverse CVD outcomes. Increased egg consumption may increase CHD risk in people with diabetes
Individuals with a higher intake of fish have a lower risk of CHD mortality, total CHD and total stroke (from Fish, fish oils, n-3 polyunsaturated fatty acids and cardiovascular health)
Consuming fish at least once a week is associated with a lower risk of total stroke and CHD mortality in the general population and post- MI patients (from Fish, fish oils, n-3 polyunsaturated fatty acids and cardiovascular health)
Consuming nuts improves the lipid profile
Fonte: National Heart Foundation of Australia (2009).
A vermelho estão assinaladas duas afirmações. A primeira acaba por ser um contra-senso, pelo simplismo que encerra. As gorduras saturadas não são todas iguais. Por exemplo, as gorduras saturadas da carne são, essencialmente, ácido esteárico, as quais este mesmo documento da NHFA reconhece terem um efeito negligenciável no LDL-C. No que respeita à segunda afirmação, era o que seria de esperar. No entanto, este documento não é suficientemente claro a este respeito, sugerindo no início que níveis elevados de colesterol representam risco de AVC. De qualquer forma, há um mega-estudo muito recente que confirma isto mesmo ("The absence of an independent positive association of cholesterol with stroke mortality, especially at older ages or higher blood pressures, is unexplained, and invites further research."), o que deixa os "especialistas" à rasca!