High-Grain Diet May Increase Risk of Cardiovascular Disease
American Journal Clinical Nutrition January 2003 77: 43-50
When humans consume more carbohydrates than can be stored, the excess carbohydrate energy is converted to fat by the liver. This process may maintain blood sugar control and prevent diabetes in the short-term, however it may also increase triglyceride concentrations, which may increase the risk of cardiovascular disease.
In the last decade, researchers established that fat production by the liver varies depending on dietary habits and health status.
The typical Western diet has a high fat content, which means that only a limited amount of carbohydrates are available for liver fat production, and liver fat production tends to be very low among individuals who eat this type of diet. However, when too many carbohydrates were consumed, both liver fat and sugar production were increased.
A very low-fat (10 percent of energy) and very high-carbohydrate (75 percent of energy) diet also leads to increased liver fat production, with the increase being even more pronounced when more than half of the carbohydrate was consumed as simple sugars. This points to the importance of carbohydrate quality, as another study using 68 percent of energy from complex carbohydrate resulted in minimal liver fat production.
However, it was found that obese individuals with high insulin levels who consume a high-fat (40 percent of energy) diet had a liver fat production rate three to four times higher than that of lean individuals with normal insulin levels. But, both normal and high insulin groups had lower liver fat production on the high-fat diet than on a low-fat, high-carbohydrate diet.
Moreover, the low-fat, high-carbohydrate diet caused an increase in triglyceride concentrations, a risk factor for coronary heart disease, which was associated with the liver fat production in both normal and high-insulin individuals.
Researchers concluded that the low-fat, high-carbohydrate diet might not be ideal, as it can induce liver fat production and insulin resistance. This is especially true when most of the carbohydrate is in the form of simple sugars.
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1: Am J Clin Nutr 2003 Jan;77(1):43-50
Hepatic de novo lipogenesis in normoinsulinemic and hyperinsulinemic subjects consuming high-fat, low-carbohydrate and low-fat, high-carbohydrate isoenergetic diets.
Schwarz JM, Linfoot P, Dare D, Aghajanian K.
Department of Nutritional Sciences and Toxicology, University of California, Berkeley (J-MS and KA), and the Department of Medicine, University of California, San Francisco (J-MS, PL, and DD).
BACKGROUND: Hypertriglyceridemia is associated with increased risk of cardiovascular disease. Until recently, the importance of hepatic de novo lipogenesis (DNL) in contributing to hypertriglyceridemia was difficult to assess because of methodologic limitations. OBJECTIVE: We evaluated the extent of the contribution by DNL to different conditions associated with hypertriglyceridemia. DESIGN: After 5 d of an isoenergetic high-fat, low-carbohydrate diet, fasting DNL was measured in normoinsulinemic (</= 85 pmol/L) lean (n = 9) and obese (n = 6) and hyperinsulinemic (>/= 115 pmol/L) obese (n = 8) subjects. Fasting DNL was measured after a low-fat, high-carbohydrate diet in normoinsulinemic lean (n = 5) and hyperinsulinemic obese (n = 5) subjects. Mass isotopomer distribution analysis was used to measure the fraction of newly synthesized fatty acids in VLDL-triacylglycerol. RESULTS: With the high-fat, low-carbohydrate diet, hyperinsulinemic obese subjects had a 3.7-5.3-fold higher fractional DNL (8.5 +/- 0.7%) than did normoinsulinemic lean (1.6 +/- 0.5%) or obese (2.3 +/- 0.3%) subjects. With the low-fat, high-carbohydrate diet, normoinsulinemic lean and hyperinsulinemic obese subjects had similarly high fractional DNL (13 +/- 5.1% and 12.8 +/- 1.4%, respectively). Compared with baseline, consumption of the high-fat, low-carbohydrate diet did not affect triacylglycerol concentrations. However, after the low-fat, high-carbohydrate diet, triacylglycerols increased significantly and DNL was 5-6-fold higher than in normoinsulinemic subjects consuming a high-fat diet. The increase in triacylglycerol after the low-fat, high-carbohydrate diet was correlated with fractional DNL (P < 0.01), indicating that subjects with high DNL had the greatest increase in triacylglycerols. CONCLUSIONS: These results support the concept that both hyperinsulinemia and a low-fat diet increase DNL, and that DNL contributes to hypertriglyceridemia.
PMID: 12499321 [PubMed - in process]
http://www.ncbi.nlm.nih.gov/entrez/...1&dopt=Abstract
http://www.mercola.com/2003/jan/8/high_grain_diet.htm