So in my physiology class, we're about to start the cardiovascular system. And my professor likes to put an emphasis on diseases since a majority of my class is pre-med. Every Fridays, we have a question & answer session and I'd love to ask some questions about saturated fat, PUFA oxidation, cholesterol, etc.
What are some good questions that I can ask, points that I can bring up (wouldn't mind being the smart-ass in class), or studies that I can show him that could potentially change his lectures and finally get the word out about why conventional wisdom about "why saturated fat is bad" is wrong?
Seriously guys, don't be afraid to have a field day with this.
asked byApril_S_ (10663)
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on March 21, 2012
at 04:53 AM
I asked my teacher if the ADA, who loves to promote 'evidenced based practice', ever reviews any current research about saturated fat, and whether we, as dietitians should consider changing our stance. I then sent her this, and she responded surprisingly well...
This paper combined the results of twenty-one studies that looked at associations between dietary saturated fat and cardiovascular disease (CVD). This included nearly 350,000 people over up to 23 years.
Conclusions: A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD.
This review looked at what happens what saturated fats are replaced with carbs.
It turns out that replacing dietary saturated fat with carbohydrates is associated with an increase in CVD risk (especially carbs with a high glycemic index), while replacing saturated fat with polyunsaturated fats is associated with reduced CVD risk. However, replacing a combination of saturated fat and trans fats with omega-6 fats (think vegetable oils) in controlled trials showed no indication of benefit and a signal toward increased coronary heart disease risk. This suggests that it is the omega-3 polyunsaturated fats that may be responsible for the protective association between total polyunsaturated fats and CVD.
High carbohydrate intake causes the liver to manufacture saturated fatty acids. This in turn causes chronic systemic inflammation. The authors conclude that avoidance of saturated fat accumulation by reducing the intake of carbohydrates with high glycemic index is more effective in the prevention of CVD than reducing saturated fat intake per se.
Investigators asked volunteers to weigh all food consumed at home for 1-2 weeks, and describe in detail all food consumed away from home. Compliance was good. This dietary accounting method was much more thorough than in most observational studies today. Animal fat intake ranged from 55 to 173 grams per day, and blood cholesterol ranged from 154 to 324 mg/dL, yet there was no relationship whatsoever between the two.
This was a large cardiovascular observational study conducted in Tecumseh, Michigan, which is often used as the basis for comparison for other cardiovascular studies in the literature. Using the 24 hour dietary recall method, including an analysis of saturated fat, the investigators found that: Cholesterol and triglyceride levels were unrelated to quality, quantity, or proportions of fat, carbohydrate or protein consumed in the 24-hr recall period.
This study found an association between saturated fat intake and blood cholesterol in middle-aged men in Chicago. However, the correlation was small, and there was no association between saturated fat intake and heart attack death.
The total to HDL cholesterol ratio did not change if carbohydrates replaced saturated fatty acids, but it decreased if cis unsaturated fatty acids replaced saturated fatty acids. The effect on total:HDL cholesterol of replacing trans fatty acids with a mix of carbohydrates and cis unsaturated fatty acids was almost twice as large as that of replacing saturated fatty acids. Lauric acid greatly increased total cholesterol, but much of its effect was on HDL cholesterol. Consequently, oils rich in lauric acid decreased the ratio of total to HDL cholesterol. Myristic and palmitic acids had little effect on the ratio, and stearic acid reduced the ratio slightly. Replacing fats with carbohydrates increased fasting triacylglycerol concentrations.