Mastering Nutrition

Hi, I'm Chris Masterjohn and I have a PhD in Nutritional Sciences. I am an entrepreneur in all things fitness, health, and nutrition. In this show I combine my scientific expertise with my out-of-the-box thinking to translate complex science into new, practical ideas that you can use to help yourself on your journey to vibrant health. This show will allow you to master the science of nutrition and apply it to your own life like a pro.
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Mastering Nutrition



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Now displaying: October, 2016
Oct 8, 2016

In episode 25, Insulin Resistance Isn't All About Carbs and Insulin, I explained why an individual cell would "decide" to stop taking up energy. Here in episode 26, I explain tissue-level energy overload, focusing on adipose tissue and liver.

At adipose tissue, the problem with fatness isn't the amount of fat. It's that we've reached the point where we can't get any fatter. Well, we can, but we can no longer do so while maintaining a healthy organizational structure within adipose tissue that allows blood, oxygen, and nutrients to get to where they need to go. Surprisingly, some of the things that enable proper expansion, and thus protect our metabolic health, are things that we usually think of as "bad," such as inflammation. In fact, the pro-inflammatory changes in the gut microbiome in response to an obesogenic diet provide information to adipose tissue that it needs to prepare for healthy expansion.  And adipose expansion is most protective at the site of the "bad" body fat: visceral fat in the abdomen.

At liver, the problem is fat gets trapped in the liver, flattening out everything in the cell and hogging the space needed for glycogen storage, and this can happen even in a lean person.

I conclude with some practical recommendations about body composition and nutrient density.

In this episode, you will find all of the following and more:

How adipose tissue expands (triglyceride and lipid droplet formation, extracellular matrix reorganization, capillary bed growth and reorganization); consequences of poor adipose tissue expansion (liver spillover into ectopic deposition in tissues like liver, skeletal muscle, and pancreas, internal oxidative and endoplasmic reticulum stress, hypoxia); providing more glycerol for greater triglyceride formation (via genetic manipulation of PEPCK to allow greater glyceroneogenesis) protects against metabolic dysfunction (which may indicate a protective role of carbohydrate, which provides the glycerol on a mixed diet); deletion of genes involved in lipid droplet formation exacerbates metabolic dysfunction; allowing matrix metallopproteinases (MMPs) to reorganize the collagen-based extracellular matrix known as septa protects against metabolic dysfunction; expression of hypoxia-inducible factor 1-alph (HIF1alpha) contributes to metabolic dysfunction; inflammation (tumor necrosis factor alpha or TNF-alpha, interleukins or ILs, toll-like receptors or TLRs) is necessary to allow proper extracellular matrix (ECM) reorganization and capillary bed reorganization; visceral abdominal fat expansion is most protective because visceral fat drains directly into the liver via the portal vein, and releases more fat into the liver when it cannot expand further; ectopic fat deposition at the liver is central because the liver is the metabolic hub of fat and carbohydrate metabolism; fat accumulation in liver likely directly compromises glycogen storage; sources of liver fat: include adipose and dietary fat; de novo lipogenesis (DNL) from carbohydrate is a minor source of liver fat; oxidative stress and poor choline status are major factors governing triglyceride export; the choline requirement is increased more by fat than other macronutrients and more by long-chain saturated fats than other fats; practical strategies: body composition is king, but it might not be the right time to lose fat; a well rounded, nutrient-dense diet is low-hanging fruit at any time; additional strategies require nutritional analysis with help of health care professional and data generation and interpretation.