The main explanation for the relatively low increase of blood fat levels with butter is that about 20 percent of the fat in butter consists of short and medium-length fatty acids. These are used directly as energy and therefore never affect the blood fat level to any great extent. Health care uses these fatty acids with patients who have difficulty taking up nutrition in other words, they are good fatty acids.

“A further explanation, which we are speculating about, is that intestinal cells prefer to store butter fat rather than long-chain fatty acids from vegetable oils. However, butter leads to a slightly higher content of free fatty acids in the blood, which is a burden on the body,” explains Julia Svensson, a doctoral candidate in Biotechnology and Nutrition at Lund University.

The greater difference in men is due to, among other things, hormones, the size of fat stores, and fundamental differences in metabolism between men and women, which was previously known. This situation complicates the testing of women, since they need to be tested during the same period in the menstruation cycle each time in order to yield reliable results.

“The findings provide a more nuanced picture of various dietary fats. Olive oil has been studied very thoroughly, and its benefits are often extolled. The fact that butter raises blood cholesterol in the long term is well known, whereas its short-term effects are not as well investigated. Olive oil is good, to be sure, but our findings indicate that different food fats can have different advantages,” emphasizes Julia Svensson.

“Finally, all fats have high energy content, and if you don’t burn what you ingest, your weight will go up, as will your risk of developing diseases in the long run,” she reminds us.

Here’s how the test was done: 19 women and 28 men participated in the study. Each individual ate three test meals containing canola-flaxseed oil, butter, or olive oil. The day before the test they had to fast after 9 p.m. The following morning a fasting blood sample was drawn to check their health status and all blood fats. The test meal consisted of the test fat mixed into hot cream of wheat, 1.5-% milk, blackberry jam, and a slice of bread with ham. The meal contained 35 g of test fat and about 810 Kcal. Blood samples were then drawn 1, 3, 5, and 7 h after the meal, and all blood fats were analyzed. The participants fasted during the day.

Julia Svensson is on parental leave until April. When she returns she will primarily finish studying how women react to various fats.

She and her colleagues will also be studying whether fats lead to varying degrees of satiety. What’s more, they will be evaluating parameters such as hormone status, exercise, waist measurement, and how the daily diet otherwise affects how the body takes up fat after a meal.

Source: Expertanswer

The study was the work of Dr Pia R Kamstrup, of Herlev Hospital, Copenhagen University Hospital in Herlev, Denmark, and colleagues, and is published in the 10 June issue of the Journal of the American Medical Association, JAMA.

Despite the fact that statins are now routinely used to lower levels of low-density lipoprotein (LDL, or “bad” cholesterol), myocardial infarction (MI or heart attack) remains a leading cause of illness and death, wrote the authors.

There is a need to identify other risk factors as targets for treatment they said. Lipoprotein (a), a cholesterol that is not included in routine cholesterol screening, has been suggested as a potential candidate, but there is not enough evidence of how closely it is linked to heart attack risk.

Lipoprotein (a) levels vary from person to person, sometimes the level in one person can be thousands of times higher or lower than the level in another person, the range is so vast. This is partly determined by genetics, and the variations in one gene in particular, known as the “Lipoprotein (a) kringle IV type 2 (LPA KIV-2) size polymorphism genotype”. The authors wrote in their background information that the number of KIV-2 repeats is already known to correlate inversely with levels of lipoprotein(a).

For the study, Kamstrup and colleagues looked at whether genetically elevated levels of lipoprotein (a) were linked to increased risk of heart attack (MI) in three studies covering about 45,000 white individuals from Copenhagen who started giving samples in 1976 until 2007.

The researchers found that risk of MI increased with increasing levels of lipoprotein (a), and with “decreasing numbers of lipoprotein(a) KIV-2 repeats associated with elevated levels of lipoprotein(a)”.

They saw a consistent increase in MI risk linked to genetically elevated levels of lipoprotein (a) in all three studies, and noted that the KIV-2 genotype explained 21 per cent and 27 per cent of the total lipoprotein (a) concentrations in two of the three studies.

Kamstrup and colleagues wrote that:

“Instrumental variable analysis (in which the increase in lipoprotein (a) levels explained by the KIV-2 genotype was related to MI) directly demonstrated that genetically elevated lipoprotein (a) is associated with increased risk of MI, like elevations in plasma lipoprotein (a).”

They suggested that while the findings appear strong enough to show that the higher levels of lipoprotein (a) probably caused the increased risk of MI, final proof should still be sought using randomized clinical trials that show MI risk going down in response to therapies that lower lipoprotein (a).

In an accompanying editorial, Drs George Thanassoulis and Christopher J. O’Donnell of the National Heart, Lung and Blood Institute’s Framingham Heart Study, commented that although Kamstrup and colleagues revealed some “interesting mechanistic insights” into the biological link between lipoprotein (a) and MI, and put forward evidence that there might be potential benefit in reducing lipoprotein (a) early in life, the “clinical implications are quite limited”.

“These results do not provide the necessary evidence that genetic testing of the LPA locus or measurements of plasma lipoprotein(a) have a role in cardiovascular risk stratification or decisions regarding lipid-lowering therapy,” they wrote, agreeing with the authors in that “ultimately, despite nature’s best efforts to provide causal evidence for lipoprotein(a), only a true randomized controlled trial demonstrating reductions in MI with targeted lipoprotein(a)-lowering therapy can provide the evidence for benefits and risks of an lipoprotein(a)-lowering strategy”.

“Genetically Elevated Lipoprotein(a) and Increased Risk of Myocardial Infarction.”
Pia R. Kamstrup; Anne Tybjaerg-Hansen; Rolf Steffensen; Borge G. Nordestgaard.
JAMA, 2009;301(22):2331-2339.
Vol. 301 No. 22, June 10, 2009

Written by: Catharine Paddock, PhD
Copyright: Medical News Today