Community

Table of Contents

The following work is intended to bridge between research activities of our laboratory and broader interests of our community.
U of I study: Lack of omega-3 fatty acid linked to male infertility Press release, April 2010
U of I study: Lack of omega-6 fatty acid linked to severe dermatitis Press release, April 2010
U of I Study: Fructose Metabolism More Complicated than Was Thought Press Release, December 2008
Essentials for Eaters and Dieters A James Scholar Honors Program Research Project. A website of concise advice for building healthy and sustainable eating habits and for effective weight loss. 2005, 2006, 2007
A Minute With KFC removes trans fats – will other fast food chains follow? November 2006
Take-Home Message of Super Size Me by Chad Stroud. After taking detailed notes by watching DVD, Chad, a PhD student of our group, wrote a comment on the movie “Super Size Me”. Find what Chad has to tell you about the movie. March 2005
Atkins-Diet Studies by Mani Nakamura. Comments on studies published in New England Journal of Medicine. June 2003
Non-Technical Summary of Delta-6 Desaturase Research by Mani Nakamura. Summary of research conducted by our group and funded by American Heart Association. January 2003

Take-Home Message of Super Size Me

Chad Stroud, March 2005

Some people have asked me about my thoughts on the documentary, Super Size Me, by Morgan Spurlock that was released in 2004 and received an Oscar nomination for Best Documentary. Many people seem to make incorrect inferences about the causes of Morgan’s health deterioration. I will try to provide an explanation to the health effects observed in the movie.

• First, let’s look at those changes that occurred over the 30 days.
• He experienced a weight gain of 24.5 pounds.
• His total cholesterol increased from 168 to 230 mg/dL.
• His body fat went from 11% to 18%.
• His triglyceride levels (a measure of the fat level in blood) were varied and went up and down throughout the 30 days.
• He experienced other effects, such as increased uric acid levels and altered liver enzymes.

The increase in weight (and the increase in fat) can be directly attributed to increased caloric intake. The dietician he met with throughout his 30 day diet advised him to consume ~2500 Calories per day. On the subsequent two visits to the dietician, she warned him that he was consuming twice as many Calories as needed, approximately 5000 per day. Using simple arithmetic, we can calculate the approximate weight gain based on the extra 2500 Calories per day. 2500 Calories/day x 1 pound (fat)/3600 Calories x 30 days = ~21 pounds. This closely matches the ~25 pounds he gained. The weight gain was due to the extra Calories coming from extra fat, protein and carbohydrates. This is sometimes confusing for the general public. Excess sugar can and does turn into fat in our bodies. I don’t necessarily want to defend McDonalds, but the weight gain could have been avoided by meeting his caloric needs as the dietician recommended. If he had limited his choices to ~2500 Calories, he wouldn’t have seen the weight gain. Morgan did not release his actual food consumption for the 30 days, so it’s impossible to calculate exactly what he was getting. At several meals though, I noticed that he was eating more food than would comprise a normal balanced meal. For example, at one point, he had a dinner sandwich, supersize fries, 5 coffee creamers, large coffee, quart of soda (or shake), chocolate sundae and 2 pies (roughly 2300 Calories). I can’t say I’ve ever seen anyone actually eat that much at one sitting at McDonalds or any other fast food restaurant.

On the other hand, most of the food at McDonalds has a high energy density, which means it’s easier to over consume Calories, especially if you eat the above meal 3 times daily. The excess fat is being stored in adipose (fat) tissue, the extra protein and carbohydrates are being converted to triglycerides (fat) and then stored in adipose tissue. This also explains why he was experiencing liver problems. The liver is the key metabolic organ and is central to the conversion of protein and carbohydrates to fat. When overeating carbohydrates (sugars and starches) the liver is working full-time to convert that excess to fat to be stored. It is possible to then develop fatty liver caused by this over consumption and can lead to liver toxicity if continued. These same effects would be seen by someone overeating regardless of whether the food came from McDonalds. Eating home cooked foods can cause the same problem if you continually eat lots of high-energy dense foods.

Blood cholesterol levels have been shown to be strongly correlated with increased risk of cardiovascular diseases. The increase in total cholesterol is probably due to the amount of saturated fat in his temporary diet. Saturated and trans-fat have been shown to increase the amount of blood cholesterol. Many McDonalds foods are high in saturated fats. They primarily come from animal fat. Trans-fat has gained a lot of press lately and has been shown to cause an increase in cholesterol, specifically raising the bad cholesterol (LDL) and lowering the good cholesterol (HDL). French fries are one of the largest sources of trans-fat. If he ate fries a couple of times per day, he was consuming far too much trans-fat. Trans-fat is often found in fried foods and foods containing vegetable shortening or partially-hydrogenated vegetable oil. It is found not only in French fries, but also the McNuggets and Filet-O-Fish as well as the biscuits and possibly the buns.

In summary, the effects seen were the result of over consuming Calories. He demonstrated the effects that continual, unrestrained caloric consumption can cause. Eating less energy dense foods (fruits and vegetables) will allow you to eat more food (on a weight basis) while controlling caloric intake. One reason the US Dietary Guidelines recommend eating a large number of fruits and vegetables is that by doing so, you can limit Calories, while increasing content of other important nutrients. Eating fast foods (junk food) periodically, if balanced with low-energy dense foods, won’t necessarily cause a weight gain, or an increase in cholesterol levels.
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Comments on Recent Studies of the Atkins Diet

Manabu T. Nakamura, June 2003

Very-low-carbohydrate, Atkins-type diets showed more weight loss than high-carbohydrate diets, which performed poorly under minimal counseling (1, 2). Another study with stronger dietary guidance showed that a high-protein, moderately-low-carbohydrate diet resulted in better lean-body retention and higher comfort during dieting than a high-carbohydrate diet, while both groups lost weight successfully (3). These studies suggest that high-protein, low-carbohydrate diets may be better suited for weight loss, in which our body adapts its metabolism to a gluconeogenic and ketogenic state by altering gene expressions. High-protein, low-carbohydrate diets are gluconeogenic and fits well to this condition, whereas high-carbohydrate diets could disrupt this adaptation by stimulating glycolysis and lipogenesis. Furthermore, the better lean-body retention by a high-protein diet (3) suggests a higher protein requirement for weight loss. However, low-carbohydrate intake may have no advantage for weight maintenance. In fact, the subjects on the Atkins diet regained weight after 1 year (2). Nutrient balance and energy density would be more important for weight maintenance (4). In addition, a very-low-carbohydrate diet could be detrimental during weight maintenance because up-regulation of gluconeogenesis causes insulin resistance (5).

1. Samaha FF, Iqbal N, Seshadri P, et al. A low-carbohydrate as compared with a low-fat diet in severe obesity. N Engl J Med 2003; 348:2074-81.
2. Foster GD, Wyatt HR, Hill JO, et al. A randomized trial of a low-carbohydrate diet for obesity. N Engl J Med 2003; 348:2082-90.
3. Layman DK, Boileau RA, Erickson DJ, et al. A reduced ratio of dietary carbohydrate to protein improves body composition and blood lipid profiles during weight loss in adult women. J Nutr 2003; 133:411-7.
4. Stubbs RJ, Harbron CG, Murgatroyd PR, Prentice AM. Covert manipulation of dietary fat and energy density: effect on substrate flux and food intake in men eating ad libitum. Am J Clin Nutr 1995; 62:316-29.
5. Rossetti L, Rothman DL, DeFronzo RA, Shulman GI. Effect of dietary protein on in vivo insulin action and liver glycogen repletion. Am J Physiol 1989; 257:E212-9.

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Delta-6 Desaturase Regulation by SREBP-1 and PPAR-alpha: Nontechnical Summary of the Project

Manabu T. Nakamura, January 2003

What problem is addressed in this study?

Benefits of polyunsaturated fats for cardiovascular health have been known for long time and have been gaining more scientific ground. Polyunsaturated fats are converted to more unsaturated fats called highly unsaturated fats, which are essential for proper function of our body including regulation of blood pressure, blood clotting, blood cholesterol/triglyceride metabolism and heartbeat. Dietary polyunsaturated fats and hypolipidemic drugs affect the synthesis of highly unsaturated fats in our body. However, the regulatory mechanism of this synthetic pathway is poorly understood. Thus, the major problem addressed by this study is how the synthesis of highly unsaturated fats is controlled in our body.

What specific questions are we asking?

In this project, we investigate the control mechanism of highly unsaturated fat synthesis by studying the regulation of delta-6 desaturase, the key enzyme of this pathway. In our previous studies, we found that two proteins called sterol regulatory element binding protein-1 (SREBP-1) and peroxisome proliferator activated receptor-alpha (PPARa) are involved with the regulation of delta-6 desaturase. Therefore, the specific question we are asking in this project is how SREBP-1 and PPARa regulate delta-6 desaturase in response to polyunsaturated fat deficiency and hypolipidemic drug administration. We will approach this question using rats and mice as animal models. We will determine the role of SREBP-1 and PPARa by transiently introducing the animals a mutated gene that lacks a response to these proteins.

What is a long-term significance of the work for cardiovascular health?

Our long-term goal is to address the following unresolved questions: 1) optimal intake of n-6 linoleic acid and n-3 alpha-linolenic acid, 2) benefit of fish oil (n-3 EPA, DHA), 3) if so, what sub population.

Elucidating polyunsaturated fat metabolism has two long-term biomedical significances. As mentioned in the previous section, highly unsaturated fats are involved in many aspects of cardiovascular function. Thus, understanding the regulation of highly unsaturated fat synthesis will enable us to provide a better dietary recommendation and therapeutic intervention for optimal cardiovascular health. The knowledge in the effects of hypolipidemic drugs on highly unsaturated fat synthesis will be particularly beneficial for those who need to chronically take these drugs. Moreover, SREBP-1 and PPARa, the proteins that regulate highly unsaturated fat synthesis, are also involved in the regulation of the metabolism of other fats and cholesterol. Therefore, this line of studies will yield critical knowledge regarding how polyunsaturated fats affect metabolism of blood cholesterol and triglycerides, both of which are important factors for cardiovascular health.

This project was funded by:
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