Canibais e Reis

O Diabetes Update, que eu acompanho através dos cabeçalhos de notícias (rss) na coluna do lado direito deste blogue, traz-nos mais uma notícia sobre má ciência na investigação em diabetes, que é coisa que, pelos vistos, não escasseia neste universo da medicina e saúde. A notícia trazida por Jenny Ruhl intitula-se Even MORE Bad Science: Triglycerides Predict Neuropathy e fala-nos de um artigo investigando a correlação entre triglicéridos e a progressão de neuropatias diabéticas. O problema acontece quando os doutores afirmam que triglicéridos elevados são causados por "gorduras nocivas". E até já estamos a imaginar que gorduras nocivas são essas, não é?

Já agora, para esclarecimento, a elevação de triglicéridos no sangue é resultado directo do consumo de hidratos de carbono de alto índice glicémico, de preferência daqueles que constituem a base da pirâmide alimentar "saudável" e que, por regra, formam a base das dietas high-carb / low-fat falhadas, mas que as autoridades oficiais e os "especialistas", apesar de tudo, insistem em nos recomendar. Convém recordar que triglicéridos elevados são sinónimo de risco cardiovascular acrescido e, conforme se constata, de agravamento de complicações diabéticas.

A seguir alguns artigos que os autores do artigo Elevated Triglycerides Correlate with Progression of Diabetic Neuropathy deveriam ter lido antes de começarem a publicar.

Como reduzir drasticamente os seus triglicéridos, e com isso também o seu risco cardiovascular e diabético?
Low-carb, meus amigos, low-carb!

Effect of Dietary Carbohydrate on Triglyceride Metabolism in Humans (pdf)

Elizabeth J. Parks

Department of Food Science and Nutrition, University of Minnesota, Twin Cities, St. Paul, MN 55108-6099

When the content of dietary carbohydrate is elevated above the level typically consumed (>55% of energy), blood concentrations of triglycerides rise. This phenomenon, known as carbohydrate-induced hypertriglyceridemia, is paradoxical because the increase in dietary carbohydrate usually comes at the expense of dietary fat. Thus, when the content of the carbohydrate in the diet is increased, fat in the diet is reduced, but the content of fat (triglycerides) in the blood rises. The present article will review studies of carbohydrate-induced hypertriglyceridemia, highlighting data obtained in fasted subjects habituated to high carbohydrate diets, data obtained from subjects in the fed state, and metabolic studies investigating fatty acid and triglyceride synthesis in subjects consuming diets of different carbohydrate content. The available data have been recently expanded by new methodologies, such as the use of stable isotopes, to investigate the metabolism of sugars in humans in vivo. Given the significant increase in body weight observed in the American population over the past decade and the changing availability of carbohydrate in the food supply, future studies of carbohydrate-induced hypertriglyceridemia promise to provide important information of how the macronutrient composition of the diet can influence health.

 

Carbohydrate-Induced Hypertriglyceridemia: An Insight into the Link between Plasma Insulin and Triglyceride Concentrations (pdf)

T. McLaughlin, F. Abbasi, C. Lamendola, H. Yeni-Komshian and G. Reaven

Department of Medicine, Stanford University School of Medicine, Stanford, California 94305

This study was initiated to test the hypothesis that endogenous hypertriglyceridemia results from a defect in the ability of insulin to inhibit the release of very low-density lipoprotein-triglyceride (TG) from the liver. To accomplish this goal, plasma glucose, insulin, free fatty acid (FFA), and TG concentrations were compared in 12 healthy volunteers, in response to diets containing either 40% or 60% of total calories as carbohydrate (CHO). The protein content of the two diets was similar (15% of calories), and the fat content varied inversely with the amount of CHO (45% or 25%). The diets were consumed in random order, and measurements were made of plasma glucose, insulin, FFA, and TG concentrations at the end of each dietary period, fasting, and at hourly intervals following breakfast and lunch. The results indicated that the 60% CHO diet resulted in higher fasting plasma TG concentrations associated with higher day-long plasma insulin and TG concentrations, and lower FFA concentrations. These results do not support the view that hypertriglyceridemia is secondary to a failure of insulin to inhibit hepatic TG secretion.

 

Effect of High-Carbohydrate Feeding on Triglyceride and Saturated Fatty Acid Synthesis (pdf)

Lisa C. Hudgins

The Rogosin Institute, Rockefeller University, New York, New York 10021

It has been known for decades that low-fat, high-carbohydrate diets can increase plasma triglyceride levels, but the mechanism for this effect has been uncertain. Recently, new isotopic and nonisotopic methods have been used to determine in vivo whether low-fat, high-carbohydrate diets increase triglyceride levels by stimulating fatty acid synthesis. The results of a series of studies in lean and obese weight-stable volunteers showed that very-low-fat (10%), high-carbohydrate diets enriched in simple sugars increased the fraction of newly synthesized fatty acids, along with a proportionate increase in the concentration of plasma triglyceride. Furthermore, the concentration of the saturated fatty acid, palmitate, increased and the concentration of the essential polyunsaturated fatty acid, linoleate, decreased in triglyceride and VLDL triglyceride. The magnitude of the increase in triglyceride varied considerably among subjects, was unrelated to sex, body mass index, or insulin levels, and was higher when fatty acid synthesis was constantly elevated rather than having a diurnal variation. It was notable that minimal stimulation of fatty acid synthesis occurred with higher fat diets (>30%) or with 10% fat diets enriched in complex carbohydrate. Public health recommendations to reduce dietary fat must take into account the distinct effects of different types of carbohydrate that may increase plasma triglycerides and fatty acid synthesis in a highly variable manner. The mediators and health consequences of this dietary effect deserve further study.

 

Introduction: Low-Saturated Fat, High-Carbohydrate Diets: Effects on Triglyceride and LDL Synthesis, the LDL Receptor, and Cardiovascular Disease Risk (pdf)

Robert H. Knopp

Northwest Lipid Research Clinic, University of Washington, Seattle, Washington 98104.

 

Fasting versus Nonfasting Triglycerides and the Prediction of Cardiovascular Risk: Do We Need to Revisit the Oral Triglyceride Tolerance Test? (pdf)

Paul M Ridker

Center for Cardiovascular Disease Prevention, Brigham and Women’s Hospital, Boston, MA.

Historically, triglycerides have been measured in the fasting state for 2 reasons. First, because of the marked increase in triglycerides after fat ingestion, the variability in triglyceride measurements is much smaller in the fasting state. Second, before the availability of direct assays for LDL cholesterol (LDL-C), estimation of LDL-C was performed in clinical practice almost exclusively by use of the Friedewald equation, which requires that both the HDL-C concentration and the fasting triglyceride concentration divided by 5 be subtracted from the total cholesterol concentration.

The recommendations to measure triglycerides in the fasting state did not, however, derive from a consistent set of prospective cohort studies showing that fasting concentrations were superior to nonfasting concentrations for the detection of cardiovascular risk. Instead, following screening guidelines, most epidemiologic investigations simply relied on fasting triglycerides. Taken as a whole, such studies indicate that fasting triglycerides are a univariate predictor of vascular disease. Controversy exists, however, regarding the clinical usefulness of fasting triglycerides as an independent predictor of risk, because adjustment for other covariates—in particular HDL-C—markedly decreases both the magnitude and significance of observed epidemiologic effects (1). The extent to which investigators have sought to avoid nonfasting triglycerides as a method for risk detection is evident in a recent metaanalysis that limited evaluation only to those epidemiologic studies that measured fasting triglycerides, specifically "to exclude the possibility of postprandial effects" (2).

Is it possible, then, that recommendations to measure triglycerides in the fasting state have systematically underestimated the impact of hypertriglyceridemia in clinical practice?