There are thousands of lipid species in our bodies that represent 6 categories, but we only usually hear about the subcategories of cholesterol and triglycerides. We don’t yet understand how they are all altered in response to various nutrients, dietary and lifestyle patterns and so on. Recent advancements have made it possible to analyze a large number of lipid species from work by the LIPID MAPS Consortium, which is:
LIPID Metabolites And Pathways Strategy (LIPID MAPS) is a multi-institutional effort created in 2003 to identify and quantitate, using a systems biology approach and sophisticated mass spectrometers, all of the major — and many minor — lipid species in mammalian cells, as well as to quantitate the changes in these species in response to perturbation.
The ultimate goal of our research is to better understand lipid metabolism and the active role lipids play in diabetes, stroke, cancer, arthritis, Alzheimer’s and other lipid-based diseases in order to facilitate development of more effective treatments.
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Earlier this week, I caught an article in the New York Times covering a rare occurrence: 24 members of a high school football team in Oregon developed rhabdomyolysis (muscle breakdown) from an intense workout with limited water in very hot temperatures. Rhabdomyolysis is characterized by an increase in the enzyme creatine kinase, which is maybe one reason why reports erroneously seem to jump on the following dogma:
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Last week, Yoni Freedhoff highlighted a great JAMA editorial by Dariush Mozaffarian and David Ludwig entitled “Dietary Guidelines in the 21st Century-a Time for Food.” (1). It is a short but smart commentary by 2 researchers who clearly see the big picture (and have contributed research to support it): that we should be promoting whole foods, not specific nutrients which push consumers toward processed products. Yoni has reprinted most of it on his blog, so I will make a very short summary here:
- Nutritional science began by preventing many deficiency diseases, and in that has been a great success.
- RDAs were eventually created to prevent nutrient deficiencies.
- The last few decades of the last century saw an increase in many diseases of modernity, and along with them recommendations for specific nutrients to attempt to mitigate disease risks.
- RDAs are inadequate and irrelevant for the purpose of “dietary optimization.”
- Saturated fat per se doesn’t seem to be related to heart disease, individual nutrients largely fail to have measurable effects in clinical studies, and dietary guidelines recommend a diet of mostly carbohydrate, which is not only unnecessary in human diets, but carbohydrate qualities and sources vary dramatically.
- Information on food labels “nutrition facts” does not generally help consumers choose foods for good health- the real foods (fruits, vegetables, real meats and so on) tend not to have nutrition facts anyway.
- Specific foods and dietary patterns, unlike individual nutrients, do correlate consistently with reduced disease risks, which likely reflects a complex synergy of structure, preparation methods, and the thousands of nutrients in real foods.
- Marketing and fortification has given health halos to certain processed foods, skewing public perception of what is a healthy food.
- We should move toward food-based instead of nutrient-based dietary guidelines.
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Previous studies have indicated that after resistance training and subsequent refrainment for varying time periods, we regain muscle force and mass more quickly in response to training compared to how long it took intially. In fact, after discontinuing training for up to 2 years in one study, muscles remained at a greater hypertrophic status and retained a greater force compared to their untrained levels. This phenomenon of “muscle memory” is often suggested to be from neural adaptations to exercise, but this cannot explain the hypertrophic differences after disuse. A new study suggests that the nuclei in muscle cells may be the major memory mechanism and explain these findings.
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I am constantly on the lookout for studies on how biochemical mechanisms shift with age, the significance of these changes and how nutrition and lifestyle interact with them to potentially affect health. Ageing itself is clearly an immensely complex process, and teasing out changes caused from ageing itself rather than known variables that effect health is difficult.
A recent paper by Francine Einstein et al. (1) examined how age influences susceptibility to free fatty acid (FFA) induced insulin resistance independent of phenotype in an animal model. Rodents and humans experience an increase in FFA with age, and FFA elevation is a characteristic of visceral adiposity that often accompanies obesity. This can trigger an increased secretion of cytokines, leading to a proinflammatory milieu and insulin resistance. But does the ageing process alter some of these pathways itself?
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When you consider how highly complex food systems interact with highly complex human systems, it is a bit overwhelming. Then consider the thousands of different food species, nutrients, dietary patterns and combinations, how these interact with differing activities and other environmental variables, and elucidating an ideal diet seems an impossible task. Though we know a lot about some aspects of food, we are more confused than ever on others. I think this reflects a limited cognitive capacity to account for all of these variables (the human tendency is to look at few variables at a time and discount the importance of others), and human cognitive bias’ that push us toward seeing patterns that might not be there, or misinterpreting data in in the wrong context.
Existing nutritional research is often difficult to interpret and seemingly contradicting, until you meticulously consider design and potential residual confounders that are so difficult to mathematically account for.
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Last week I ranted about the ADA and its corporate sponsors after hearing about the latest sponsorship by Hershey.
Fooducate also commented about this, took the initiative to contact the ADA, and posted some of the statements along with some great comments.
They found that in 2009, less than 9% of ADA’s revenue comes from corporate sponsorships. Of ~$33 million, sponsors provided ~$2.9 million. From the Annual Report, I found that there are approximately 70,000 members. Membership fees bring in about $10.8 million. Membership fees vary significantly from students ($50) to returning active members (see screenshot below), but averaging $10.8 million by 70,000 members gives ~$154.00. To reach $2.9 million more, an average of ~$41 per member could make up the $2.9 million to rid the sponsors.
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Last week, the American Dietetic Association announced a new corporate sponsor: The Hershey Center for Health & Nutrition. The press release is vague but states that they:
“…will collaborate with ADA on consumer and health professional initiatives including an innovative, national consumer-focused nutrition education campaign.”
Whatever that means. But the goals of these partnerships are always primarily to improve brand image so more people will include their products in a “healthy” diet, or at least reduce negative perceptions of the brand. Hey, if the ADA allows them to sponsor, their products must be ok to eat, right? That is what I might think, or at least subconsciously perceive, if I didn’t study nutrition.
While clearly moderation does seem to be a good rule in most cases for food products, this is moving in the wrong direction. The evidence clearly suggests that whole foods should be priority. But people hardly understand the boundaries of a healthy diet, and partnerships with food companies that influence public perceptions may blur the lines even further.
This sponsorship adds to the growing list that also includes companies such as: Coca-Cola, PepsiCo, the National Dairy Council, General Mills, Kellogg’s, Mars, Soyjoy, and Unilever.
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Last year, I described a study that found an epigenetic mechanism of peripheral insulin resistance through methylation of the PGC-1alpha promoter. Recently, Chang et al. explored an epigenetic mechanism in non-alcoholic fatty liver.
Fatty liver is closely linked with insulin resistance and diabetes as well as obesity. As it is not yet fully understood, the only effective treatment is lifestyle intervention (exercise and weight loss). However, one compound that has potential, Berberine, is a natural alkaloid that is sold as a dietary supplement in the U.S. It has been studied in animal and human models in which it ameliorates metabolic problems like dyslipidemia and insulin insensitivity. The authors also note that it has been found to reduce serum cholesterol and LDL-cholesterol by increasing hepatic LDL-receptor expression. I have written previously a little about some of these biomarkers- I don’t think (in general) they are good representations for disease, at least yet. Berberine does reduce fatty liver in some genetically altered mice, but these do not represent a normal milieu. If berberine can improve the aforementioned dysfunctions and fatty liver in a normal mouse model, it has potential to go on to human trials and possibly be used therapeutically, or its structure used to develop more potent drugs for fatty liver.
So the authors tested this, and elucidated an epigenetic mechanism in which it develops. A short summary is available at the end. Continue reading →
I have often wondered why, when buying coffee from the same establishment on different days, or the same size from different establishments- they do not have an equal effect on my subjective alertness. It probably has a lot to do with internal milieu- hormones, neurotransmitters and the like, but I came across another reason: the amount of caffeine in coffee can vary quite a bit, even when bought at the same place on different days. If fact it was pretty shocking to me, so I thought I would report it here for those who may not know. There are also health concerns- if you are expecting a certain dose and it is actually well above it, it may cause anxiety in those prone to it, interact with medications, or negatively effect the cardiovascular system.
Prior to the study by McCusker et al. (1), it was established that preparation of coffee and the source of the coffee bean influences caffeine content dramatically. The average value in a 150mL/5oz cup is approximately 85 mg. But McCuster and colleagues tested specialty coffees to see how much they differed.
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