The raison d'etre of this website is to provide you with hard scientific information which may help you make informed decisions in your quest for health (so far I have blogged concise summaries of over 1,500 scientific studies and have had three books published).

My research is mainly focused on the effects of cholesterol, saturated fat and statin drugs on health. If you know anyone who is worried about their cholesterol levels and heart disease, or has been told to take statin drugs you could send them a link to this website, and to my statin or cholesterol or heart disease books.

David Evans

Independent Health Researcher

Thursday 8 April 2010

How the beneficial HDL cholesterol may be increased by a high fat diet

This study was Published in the Journal of Clinical Investigation 91(4): 1665-1671 (1993)

Study title and authors:
Dietary fat increases high density lipoprotein (HDL) levels both by increasing the transport rates and decreasing the fractional catabolic rates of HDL cholesterol ester and apolipoprotein (Apo) A-I. Presentation of a new animal model and mechanistic studies in human Apo A-I transgenic and control mice.
T Hayek, Y Ito, N Azrolan, R B Verdery, K Aalto-Setälä, A Walsh and J L Breslow
Laboratory of Biochemical Genetics and Metabolism, Rockefeller University, New York 10021-6399.

This paper can be accessed at:
http://www.jci.org/articles/view/116375

This study shows the possible mechanism of how eating a high fat diet may cause a rise in beneficial HDL cholesterol.

Hayek notes that in humans, diets high in saturated fat and cholesterol raise HDL-cholesterol levels.

To explore the mechanism, the investigators devised a mouse model that mimics the human situation. In this model, mice were studied on low fat (9% cal)-low cholesterol (57 mg/1,000 kcal) (chow) and high fat (41% cal)-high cholesterol (437 mg/1,000 kcal) (milk-fat based) diets.

(i) The mice responded to increased dietary fat by increasing both HDL-C and apo A-I levels, with a greater increase in HDL-C levels. This was compatible with an increase in observed HDL size.
(ii) Dietary fat both increased the transport rate and decreased the fractional catabolic rate of HDL cholesterol ester and apo A-I.
(iii) The latter suggested that dietary fat increases reverse cholesterol transport through the HDL pathway.
(iv) The increase in apo A-I transport rate by dietary fat was confirmed by experiments showing increased apo A-I secretion from primary hepatocytes isolated from animals on the high fat diet.
(v) The increased apo A-I production was not associated with any increase in hepatic or intestinal apo A-I mRNA, suggesting that the mechanism of the dietary fat effect was posttranscriptional, involving either increased translatability of the apo A-I mRNA or less intracellular apo A-I degradation.

Hayek concludes: "In summary, a mouse model has been developed and experiments performed to better understand the paradoxical HDL-raising effect of a high fat diet".