Thursday, August 7, 2008

the rabbit hole - dietary fat vs. adipose fat

Dare you come down here with me?  It is all starting to come clear.  But it is a complicated picture.

Let's begin.  

There are 3 basic parts of our foods.  Fats, Carbs, Protein.  Today we talk fats.  

Fats.  Naturally occurring fats are perhaps our best friends in the food world.  It doesn't matter which kind we are talking about.  All fatty foods contain a combination, and all are useful/healthy in their own ways.  I wrote much more about that here.   Fats are responsible for most of our day to day metabolism.  

I.  Our dietary fat is initially metabolized into free fatty acids.  The flow of free fatty acids from our livers (where the acids begin) to the blood (then to the adipose tissue and all other cells of the body) is vital to proper energy management systemwide.  This flow is enabled by most of our endocrine hormones.  It is disabled by one only one, insulin.  If we increase insulin, we push fatty acids into adipose storage, if we decrease insulin, we release the mechanism for fat storage, and fatty acids are free to roam and provide energy.

So, to sum up this first part:  dietary fat is broken down, the liver then sends the resultant fatty acids out to the rest of the body.  Whether this fat gets stored as adipose tissue, or metabolized, is primarily due to 1) the level of insulin in the blood, and 2) the predisposition of each of our hormones to fat storage.  

Let me make sure to state what adipose tissue growth or reduction is NOT due to:  1) the amount of overall calories we eat, and 2) the amount of exercise we perform.

Why not?

II.  Fatty acids can become energy only if they stay in their free fatty acid state.  The body can instead turn them into Triglycerides which are either locked into adipose tissue (via insulin) or they clog up the blood stream (atherosclerosis, when in large quantities).  So how do free fatty acids triple up to become bulbous immovable triglyceride plaque?

The fatty acids must be joined together, this is accomplished by glycerol 3 phosphate.  Gly-3-p is a product of the metabolism of glucose and fructose (refined sugars).  It forms the backbone of the triglyceride.  The process is illustrated nicely by this table.

How then does that plaque become adipose tissue?
The triglycerides are snared by a protein called LPL which pulls triglycerides out of the blood stream, and into adipose storage.  Therefore, the regulation of LPL is vital to the development of adipose tissue.

{Edit:  I significantly simplified the science here.  Let me fix:  LPL actually breaks the triglycerides down first, then transports.  The free fatty acids either go to fat storage or processing for fuel.  The higher the insulin levels the more LPL action moves toward fat storage, the lower the insulin the more the LPL action moves toward muscle tissue for fuel production.}

How do we get fat?
The LPL activity is increased by insulin.  The more insulin, the more fat accumulation.  Insulin is increased most profoundly by refined sugars.  Particularly glucose.  

To sum up the second part:  Fatty acids become fat (adipose tissue) only when combined into triglyceride form and pushed into adipose accumulation.  This entire process is guided by Sugar, via its direct influence on insulin.

The last piece of the puzzle.
Some people get fat, some don't.  The last element seems to be a hormonal imbalance in those that become Obese.  They are especially prone, in the Hypothalamus, to the effects of insulin.  If the (ventromedial) hypothalamus cannot properly regulate insulin then we will fatten.  Fattening will make us hungry, as there will be more need for fuel, and the vicious cycle of obesity will begin.

So, the final sum-up:

Sugars and refined grains raise insulin levels quickly and dramatically, their metabolism produces a bi-product that builds triglycerides.  The heightened insulin raises the amount of triglycerides that get stored as adipose tissue, causing obesity.

Let me again state what does not cause obesity:  Perverse appetite and lack of exercise.

So I guess the only question left is:  Is obesity bad?  


So why eat fats?  Fatty foods are high in nutrients, and if properly raised/produced will have an excellent Omega 6:Omega 3 ratio (as close to 1:1 as possible is best).  This study shows the benefits of a lower ratio.  Beef alone (when raised properly!) contains all essential amino acids and all but 1 of the essential vitamins, C.  C is readily available in citrus, among other foods. (although it may not be as necessary as we think)  Fats also provide lasting energy, and the means for excellent cell communication through the free flowing adipose tissue.  They are also associated with higher HDL and (only slightly) overall cholesterol, but lower VLDL triglycerides in the blood.  This is the structure of health the western medical establishment has embraced.  

The fats to stay away from:  
* Do not cook with polyunsaturated vegetable oils.  They should only be used at room temperature, such as in salad dressings.  
* Eat fried foods infrequently.  I don't know enough about this yet.  If you fry, fry your foods in lard.  Never fry in polyunsaturated oils.  
* Trans fats.  These oxidizing fats became very popular with the villification of saturated fats in the 50's and 60's.  However they go back to 1911, when crisco was invented.  The reason?  The almighty need for greater shelf-life.  They are hydrogenated vegetable oils, and they are to be shunned.

The fats to eat:
All the others!  Chow down!  Get the image of eggs, milk, beef, fatty bacon and heart attacks gone from your minds.  But remember, you must be eating pasture eggs, meat and cheeses to get the proper benefits.  Cows that grew up on grains do not produce meat that is all that nourishing when compared to pasture cows eating mostly grass.  This holds true for all livestock.  Also, hit your fatty veggies, the great beans (NOT soy!) and your flax seed and oils.  Fish oil, fish, chicken, olive oil, this is the food of everlasting health.  

Lastly, don't listen to the establishment.  The american heart association is recommending to this day a diet that is low in saturated fats, cholesterol, both of which have been demonstrated to be associated with higher rates of obesity, diabetes, stroke, cancer, bowel disease, and overall mortality.  But the conventional wisdom is powerful, and the anti-quackery boys are always out in force.

Note on sources:  Most of my information is based on the work of Gary Taubes, from his book "Good Calories, Bad Calories.  Challenging the conventional wisdom on Diet, Weight Control and Disease".  His source material is vast, and I am sitting squarely on his shoulders as I write this.  To learn more about his theories, watch this video:


David Brown said...

Hi Luke, You wrote, "How then does that plaque become adipose tissue?"

You might want to do a little more research on plaque formation and rework this discussion.

Plaque does not become adipose tissue. Adipose tissue consists of fat cells that take up and release fatty acids. Under normal hormonal conditions, free fatty acids cycle into and out of fat cells continually and are utilized for energy in muscle tissue and brown fat tissue as needed.

You also wrote, "Fatty acids become fat (adipose tissue) only when combined into triglyceride form and pushed into adipose accumulation."

If memory serves, only free fatty acids can pass into and out of fat cells. They get locked up in fat cells in the triglyceride form. Triglycerides have to be dissociated from the glycerol group to be released into the blood stream.

I don't have my copy of "Good Calories, Bad Calories" on hand to refer to so I'll leave it to you to review the process so you can correct our explanation.

Luke Weiss said...

thanks for the comments! Let me take a second to address them:

I was using plaque (incorrectly, I know) euphemistically. As I have always heard triglycerides in the bloodstream described as "plaque", I figured I would throw the word in the mix.

The mechanism I was describing in terms of fat accumulation was that of LPL's, which Taubes describes in some detail. From what I read, the LPL's have receptors for triglycerides, which enable the triglycerides to 'slide' into adiposity. The free flow of fatty acids is therefore not at issue when LPL's are high, as LPL's can put triglycerides strait into adipose storage. When there is lower insulin, and lower LPL's and of course, lower glycerol groups, we have less triglyceride formation, movement and transfer, and free fatty acids are again released in and out of the bloodstream.

This is my understanding as of now, I will have to look very closely at the chapters in question of the Taubes.



Luke Weiss said...

nvm, you were right! I edited the post.