Trinity College and St Hughs College

Oxford, United Kingdom

Trinity College and St Hughs College

Oxford, United Kingdom

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The evidence for beneficial effects of very long chain (VLC) n-3 polyunsaturated fatty acids (PUFA) on cardiovascular disease (CVD) is strong because it is based on the results of adequately powered intervention trials with disease endpoints. This contrasts with the evidence for a detrimental effect of saturated fat on CVD which is weak because such studies have not been carried out. Accordingly, any set of dietary recommendations which attaches more importance to saturated fat intakes than VLC n-3 PUFA intakes can be questioned. Despite the strength of the evidence there are practical difficulties associated with implementing the recommendation to increase intake of VLC n-3 PUFA to 1g per day which need to be overcome. These include the acceptability of fatty fish consumption, the presence of methyl mercury in fish at the top of the food chain and declining global fish stocks. © 2010 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.


Stanley J.,Trinity College and St Hughs College | Stanley J.,The-Edge
Lipid Technology | Year: 2010

The evidence for the lipid hypothesis is weak. After 20 years of follow-up, the Nurses Health Study, a prospective cohort study, was no longer able to demonstrate an association between intakes of saturated fat and risk of developing coronary heart disease. Randomised controlled trials with statins have shown that lowering LDL-cholesterol levels by 23% can reduce the risk of developing cardiovascular disease but reducing saturated fat can only reduce cholesterol levels by 10%. This issue can only be resolved by carrying out randomised controlled dietary trials with CVD endpoints. Although there are scientific difficulties standing in the way of such trials, it is the opinion of this author that these can be overcome. Whether there is the political will to fund them is another matter although some of the money currently spent on prospective cohort studies would be far better spent on randomised controlled trials. © 2010 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.


Stanley J.,Trinity College and St Hughs College | Stanley J.,The-Edge
Lipid Technology | Year: 2010

Age-related macular degeneration (AMD) is the leading cause of visual loss in the Western World. It is a disease of the retina probably initiated by the highly oxidising environment of this tissue. The Age-Related Eye Disease Study (AREDS) demonstrated in 2001 that a supplement of the antioxidants β-carotene, vitamin E, vitamin C and the minerals zinc and copper can slow down the progression of AMD. The use of this supplement should be standard practice in all countries. It is known that the carotenoids lutein and zeaxanthin and the very long chain n-3 polyunsaturated fatty acid docosahexaenoic acid (DHA) play special roles in protecting the retina against oxidative damage and there is some evidence from epidemiological studies that these nutrients slow down the progression of AMD. AREDS 2 a randomised controlled trial is testing the ability of DHA, lutein and zeaxanthin to slow down the progression of AMD. Until this study is complete in 2012 AMD patients should consider taking a supplement corresponding to the AREDS 2 formulation as a precaution. © 2010 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.


Stanley J.,Trinity College and St Hughs College | Stanley J.,The-Edge
Lipid Technology | Year: 2012

It is widely accepted that the very long chain n-3 polyunsaturated fatty acids (VLC n-3 PUFA) characteristic of marine oils protect against the development of cardiovascular disease (CVD). This idea is supported by a large body of consistent epidemiological studies showing favourable associations between intakes of VLC n-3 PUFA and CVD risk and more importantly by several large and lengthy dietary intervention trials showing favourable effects of VLC n-3 PUFA on the development of CVD. The effects of VLC n-3 PUFA on sudden death and on survival from a heart attack demonstrated in these trials could be explained if they have anti-arrhythmic effects. Recent meta-analyses of the available dietary intervention trials suggest that neither ventricular nor atrial arrhythmias are influenced by VLC n-3 PUFA intakes. Hence a convincing mechanism of action of VLC n-3 PUFA on CVD has yet to emerge. © 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.


Stanley J.,Trinity College and St Hughs College | Stanley J.,The-Edge
Lipid Technology | Year: 2013

The accumulation of triacylglycerols in the liver or steatosis can evolve into more destructive pathological conditions. Understanding how the metabolic pathways of triacylglycerol production and utilisation are balanced and how this balance is lost in insulin resistant states characterised by steatosis is crucial to understanding non-alcoholic fatty liver disease (NAFLD). Available evidence suggests that oversupply of fatty acids to the liver probably from de novo lipogenesis in the liver itself accounts for steatosis. In addition, steatosis can stimulate de novo lipogenesis by the same mechanism as insulin setting up a vicious circle which may be very hard to break. More research is needed to determine how this vicious circle is initiated. © 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.


Stanley J.,Trinity College and St Hughs College
Lipid Technology | Year: 2011

Obesity is associated with an increased risk of developing co-morbidities such as cardiovascular disease and type 2 diabetes. However, not all obese subjects have an increased risk of developing these co-morbidities. It has been suggested that triacylglycerols stored in subcutaneous adipose tissue protect the body against the accumulation of triacylglycerols in other tissues such as heart, skeletal muscle, liver and the β-cells of the endocrine pancreas which would impair their function. This phenomenon of lipotoxicity probably explains the defects in insulin action and insulin secretion seen in type 2 diabetes and perhaps impaired diastolic function of the heart. A distinction needs to be drawn between this 'unhealthy' ectopic body fat which is detrimental to human health and 'healthy' subcutaneous body fat which may protect it. © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

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