Thursday, September 8, 2016

How to Tell If Diet Mismatches Genetic Determined Metabolic Ability

Part 4 of “What Six Months of Soup Can Teach Me”

A few practical tips on doing this modified fasting diet are in order.  Timing this around what is going on in life can be helpful.  It gets harder during stressful times.  This made me appreciate how “stress eating” is a problem in the first place.  In contrast, this gets easier during times of high constructive activity.  It seems if we are meaningfully engaged, we don’t get as preoccupied with eating.  The moral is that controlling stress and being busy with meaningful activity is a poorly appreciated part of good dietary behavior.

On to the issues of what is happening with our eating behavior and why a modified fasting diet can be so helpful.  The real issue with the current Western diet for the majority of the U.S. population is that its composition places maximum stress on the portion of our metabolic machinery that is least adept at handling it.  Maximum stress on a weak area typically will cause failure, which in this case, is chronic metabolic disease.

That weak area is the broad group of enzymes used to manage a main end product of carbohydrate digestion - sugars.  There are many dozens of different enzymes involved in the process of trying to convert sugars into energy.  As we previously discussed, when the amounts of sugars exceed the need at the moment, it goes to the liver to be converted to the fat, triglyceride.  The triglycerides are then circulated destined for fat storage in the central (abdomen) portion of the body.  If carbohydrate/sugar intake chronically exceeds the need of the moment, triglyceride is increasingly produced and fat stores increase.

One of the primary features of the Paleo period genetic pattern is multiple SNPs of the genes involved in processing sugars to energy.  The 75-80% of westerners who have this pattern just cannot manage high amounts of carbohydrate/sugar under normal circumstances.

A great question to answer might be how much carbohydrate/sugar does one consume? 

The chart shows estimates of both the amount of energy or calories from carbohydrate as well as the factors regarding its quality.  The more refined the carbohydrate, the faster the sugars become available generating more metabolic stress.  Added refined sugars require no digestion before absorption so all of their energy is immediately available whether it is needed at that instant or not.

By all measures the amount of carbohydrate in the western diet has increased from 200-600%, yet the genetic ability to manage it has literally not changed.  The second and equally troublesome factor is the “glycemic load” of the western diet.  Glycemic load is a combination of how much and how fast a given carbohydrate will raise blood sugar.  Not all carbs are created equal.  Simple sugars and grains have a disproportionately high glycemic load compared to fruits and vegetables.  Simply put, they generate far more stress per gram on metabolism than other carb sources.

A great analogy might be a worker who can process 50 files very accurately in a 40-hour work week.  If you want to make this good worker make a lot of mistakes you can do it one or both of two ways. Have them try to process 200 files in the same week (increased amount of carbohydrate), or have them try to process the same 50 files but only working 2 hours a day for the 5 days (high glycemic load).  The western diet is like having that worker try to do both!

So how do we tell if we are in metabolic stress trying to manage carbohydrates?  The first sign is white adipose tissue or belly fat which is stored triglyceride. 

Typically, when triglyceride production stays high, more will be produced in the liver than can be quickly transferred to belly fat causing blood triglyceride levels to rise.  As fat stores become high, belly fat begins to produce inflammation which begins to injure insulin receptors which are needed to signal cells to take in and use blood sugar.  This fuels the whole triglyceride production cycle even further.

Additionally, when liver triglyceride production is high,  the production of HDL or “good cholesterol” drops and the production of a very small cholesterol molecule, VLDL, increases.  These VLDL particles are particularly worrisome as they become very small dense LDL which is the most dangerous regarding vascular disease risk.

The last step in this metabolic dysfunction cascade is that the insulin resistance so impairs the ability of cells to take in sugars to burn or convert to triglyceride that blood sugar rises.  At the first sign of this the diagnosis of “pre-diabetes” is made, and as it progresses it is eventually called diabetes.  Pre-diabetes is like calling the first trimester of pregnancy “pre-pregnancy”.  I think it should more appropriately be called simply early diabetes.

That was a lot so I’ll summarize.  The common order of problems showing up suggesting metabolic distress in handling carbohydrates is:
1)    Belly fat – excess triglyceride
2)    Increasing blood triglyceride - >125 mild concern, >150 real concern
3)    Decreased HDL - < 40-50.  A triglyceride/HDL >3 is a real concern
4)    VLDL cholesterol >30
5)    Increased small LDL particles – requires specialized testing called an NMR profile
6)    Increased blood sugar

The small LDL particle size needs a little explanation.  We generally make two sizes of LDL or “bad cholesterol”.  The size of the particles determines their ability to cause vascular disease with small, dense particles being more dangerous than large, fluffy ones.  We all make some of each but in varying ratios.  Genetics influence this ratio some, but diet also highly affects it.

The diagram shows 2 persons (“S” and “L”) with an identical LDL cholesterol value of 130 mg/dL.  This is the total weight of LDL in a fixed volume of blood. The small, dense particles are called apo B and the large, fluffy ones are apo A. 

While person “S” and person “L” have the same total weight of LDL, person “S” on the left side has many more small particles and therefore greater risk.

Some persons with “normal” LDL cholesterol levels develop vascular disease while others with relatively high LDL cholesterol never will.  The particle size and number variable is thought to be an important determinant of this contradictory risk.

The point of all of this is that before blood sugar inches up into abnormal range, the body has been firing warning shots across the bow for many years with the above changes in body and blood profile.  Diabetes is a late effect of chronic metabolic chaos. 

A minority in western populations can tolerate a greater percentage of carbohydrate and a somewhat higher glycemic load.  This is like the uncle someone has who smoked a pack of cigarettes and drank a quart of whiskey each day living to be relatively healthy until killed in a skydiving accident on his 90th birthday.  We all assume we are “that guy”, but they are very rare.  Most of us will need to give careful attention to matching our diet chemistry to our true metabolic ability.  Not doing so has led to the epidemic of metabolic disease which we are trying to beat down with drugs.  The food got us there, and it is the foundation for an effective solution.

So I continue with the modified, intermittent fasting to help reset my metabolism.  Starting with a normal body fat I still lost 7 lbs the first 2 weeks and 1 inch off my waist.  If you take the list of the problems that show up early indicating some metabolic stress, the modified, intermittent fasting does a “system restore” on it all.  The first indicator that that is happening is pulling triglycerides out of belly fat to burn for energy.  I choose not to curse my genetics but rather cheer the knowledge of a solution.

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