Insulin and Inflammation: Making a Data Dashboard

November 19, 2012

Insulin and Inflammation: Making a Data Dashboard 

 Reference:  Scientific American  Dec 16 2009 

 Last week we talked about making glucose an important part of our “data dashboard” as we learn how to manage our own chronic risks.   This week, it’s insulin. What is insulin?  I’ve been taught my entire life that insulin is the hormone that controls your blood sugar.   If you look up insulin in Wikipedia, you will see the emphasis on insulin being your blood glucose controlling hormone.   

I’m going to hypothesize that explanation is too simplistic.  Yes, it does control your blood glucose.   But what’s happening when you lower your blood glucose?  You are putting glucose into storage.  That’s called fat.  In nature, we want to store fat when we need to prepare for a long season coming ahead in which we will be starving.  That’s called Winter.   So, I’m going to offer a different explanation.  

I would suggest that insulin is your STORAGE hormone.  It accomplishes that by having an effect on glucose.  It is released when you eat foods that are high in easily released glucose: fruits and grains.  Those foods ripen in late summer, early autumn, just before winter.  I would posit that insulin becomes the hormone that accomplishes the need to put on fat to store against lean times coming. 

 The only problem of modern civilization is that we never have the "lean times" biochemically, aka, with lack of glucose.  Nor do we ever have a natural break in the rhythm of our lives and not have foods that make us release insulin.  Our bodies live in a constant state of “late summer”, thinking they have to store calories for the coming winter season.   Because our food supply is made up of what we like, instead of what is available by season, we eat foods every day that are high in free glucose.  Hence, we are always in storage mode.  So, we get fat. 

 But that’s not the whole story with insulin.  The dark side of insulin is that it is also intimately tied up with inflammation.    We have known for about a decade now that becoming overweight makes our fat cells release chemicals called cytokines.  TNF-alpha is a prime example.  Those cytokines suppress insulin-signaling pathways, making our bodies more insulin resistant.   As you become insulin resistant, you can no longer suppress FOXO-1.  FOXO-1 is the master switch to turning on interleukin 1-beta, which also suppresses insulin.   

Confused?  Round and round we go.  Fat cells get so big, they die.  That causes more inflammation.   Which comes first, inflammation or insulin resistance?  No one is quite sure, yet.  The “common soil” hypothesis suggests that both processes arise out of the same origins.   And that’s the final conundrum.  Most of our illnesses of the modern era have inflammation as part of what makes them occur.   Hence, they are all associated with adult diabetes and obesity.  Being overweight is a high risk for Alzheimer’s, heart disease, cancer, and diabetes. If I’m to manage my life, I want to know my insulin level.  It often rises before glucose and driving it back to normal should be one of my goals.   What’s normal?  In America, we call 2-22 the normal range for insulin.  The slender, physically fit folks have levels below 5.  Overweight folks have levels much higher. 

 WWW.  What will work for me?   I want an insulin level below 5.  To do that, I need to be slender.   Hmmm.  Back to this weight loss thing.  Got any suggestions with Thanksgiving around the corner?   I’m going for the vegetables.    And muttering against the tyranny of FOXO-1.

Written by John Whitcomb, MD Brookfield Longevity and Healthy Living Clinic, 262 -784-5300 17585 W North Avenue, Suite 160.