Thursday, February 9, 2012

Optimized Fat Metabolism (OFM) Part 3: Crisis Management 101

This is post #3 of the OFM series. If you have not done so already, I recommend reading Optimized Fat Metabolism (OFM) - Introduction and Optimized Fat Metabolism (OFM): Variability before reading this post. - Trish

From Peter:
Glucose Partitioning & The High Carbohydrate Diet
To gain insight into how OFM works and why our bodies actually prefer to metabolize fat for energy it is first necessary to have a basic understanding of what really happens to all those carbs you are consuming.  
While based upon basic physiology this post is a greatly simplified explanation for a number of complex and interconnected pathways.  As a starting point here are a few salient physiological facts to consider:
FACT #1: To begin it is vitally important to understand most of the carbohydrates a person consumes end up as the blood sugar, glucose. Thus, CARBS = SUGAR as far as the body is concerned. Most people know “SUGAR” is “BAD” but somehow there is a disconnect with carbs and that somehow carbs, especially “complex” or “Whole Grain” carbs or even a lot of carb calories derived from fresh fruit are “healthy” and should be consumed in copious quantities on a daily basis, often several times a day.  Once again; CARBS=SUGAR!
FACT #2: Human blood glucose levels are VERY tightly controlled! In the normal non-diabetic human body normal fasting blood sugar constitutes approximately 20 calories of free glucose in circulation, about 2 teaspoons of sugar (Jeff S. Volek, 2011) (link)
(For the sake of clarification, sugar, sucrose, is half glucose and half fructose so two teaspoons of sucrose is the same as a teaspoon of glucose)  The medical measurement used commonly for diabetics and pre-diabetics is mg/dl with 76-86 considered optimal, up to a 100 normal, above 125mg/dl as diabetic which represents a VERY narrow range!
FACT #3: Insulin is a hormone whose primary metabolic role is maintaining stable blood glucose level. It performs this regulation of glucose in a number of ways depending upon the circumstances and variables and is “just doing its job” under the circumstances.
FACT #4: Fructose, which is metabolized in the liver, while not insulin stimulating, does stimulate glucokinase synthesis. This further drives glucose metabolism since glucokinase (and also hexokinase), combined with glucose and ATP, begin phosphorylation. So a small amount of fructose accelerates complex carbohydrate metabolism and conversion of glycogen to glucose.
FACT #5: Variability.  The short post on Variability was and is important to keep in mind throughout this and future posts. It is clear there is a very wide range of individual tolerance to carbohydrates and this tolerance is due to how each individual’s body processes this macronutrient group. Keep this in mind as you read this and begin to see signs for where you may lie on the spectrum of variability to carb tolerance. These insights into your personal metabolic profile are key to tailoring your OFM program.
The reason for the title, Crisis Management 101, is because physiologically, this is what your body is doing when you ingest significant amounts of carbohydrates. Everything else stops to get glucose levels down . . . NOW!  Literally, your blood sugar levels are being flooded with glucose and unless you go out for, say, a brisk run or Crossfit workout right after your meal there is no fast way of bringing those levels down to normal.  Ask any T1 diabetic what happens if they eat a lot of carbs and not inject insulin……glucose becomes toxic. This being said, the body has a number of pathways it employs to maintain stable blood sugar.  Unlike vigorous exercise, each pathway cannot, by itself, metabolize a large amount of blood glucose (such as occurs when a high carbohydrate meal is consumed) to rapidly normalize blood sugar.  However, collectively, they can and do normalize blood sugar until something like insulin resistance occurs. We will examine some of the principle ones here.

Pathway #1: One of the biggest advantages endurance athletes have over relatively sedentary folks is conversion of glucose to its storable form, glycogen.   This is well studied and generally accepted. Due to this adaptation, glucose conversion to glycogen is one of the first pathways in which elevated levels of free glucose are taken out of circulation. It is because athletes, particularly endurance athletes are so well adapted that, compared to sedentary people, they can often, on the surface, remain lean and fit, and, as a group, demonstrate markedly better carbohydrate tolerance. Exercise is vital but we already know this.
Pathway #2:  Use of exogenous glucose sources for brain & nervous system energy requirements. When your glucose levels are elevated the brain burns glucose almost exclusively as another pathway to help get blood sugar down. Now this is a “like duh….” statement except when we consider the alternative ways our body produces energy for the brain & nervous system . . .
We have all heard “your brain needs glucose and cannot burn fat so you need carbs”.  This is a partial truth….. Yes, your brain and nervous system do not utilize fat as fuel and some glucose is necessary, however, the brain & nervous system run quite well on a mix of glucose and ketone bodies (which are synthesized from fats). Emerging research (link) suggests a mix of glucose and ketone bodies often approaching and even exceeding 50% as ketones may be superior to a fuel substrate made up of mostly or entirely glucose.
Contrary to the popular belief that dietary constant intake of carbs are necessary for  healthy brain and nervous system function, our body, via the liver,  makes both glucose (gluconeogenesis) and ketone bodies (ketosis) in ample amounts (under the right conditions) to fuel most of the athlete’s brain & nervous system needs under all but racing or long brick training conditions. These pathways, though more complex actually serve to stabilize blood sugar preventing the ups & downs in energy levels, mental focus and clarity, motor skills degradation, and fatigue.
The problem is this production of glucose and ketones is basically shut off when glucose levels are constantly elevated. The moderator is insulin and as long as insulin levels remain high the body, in an effort to reduce glucose levels, keeps the liver from producing ketone bodies. Interestingly enough though, gluconeogenesis may continue due to readily available glycogen stores in the liver and prompting from Fructose production of hepatic glucokinase…..this is a double edged sword….it can potentially have benefits during exercise, however, research also suggests as individuals develop insulin resistance, this fructose driven manifestation of gluconeogenesis maintains high glucose levels even during fasting, thus maintaining higher insulin levels.
Pathway #3:  “De novo Lipogenesis” . . .  While we are talking about the liver let’s segway into Pathways #3, de novo lipogenesis.  So, you have your conventional athletic high carb meal where say, 400-600 calories are derived from carbohydrate sources with more than half of those made up of starches (because the volume of veggies/salad etc. it would take to consume that many digestible calories is not practical),…
Via pathway #1, your liver is taking the easy route of converting glucose to glycogen as fast as it can (rate limited and possibly now the glycogen stores are topped off)
Via pathway #2, your brain & nervous system are running on glucose exclusively
Via pathway #3: De novo lipogenesis, latin for making “a fresh batch of fats”…and, (drum roll please!) guess what kind of fats are made from all those carbs when this occurs?...those Pattern B LDL’s (or VLDL’s) and Triglycerides which, when both are found in high levels, are generally accepted in the medical community as atherogenic (i.e. causing heart disease)…
This is where things start to get ugly, literally and metabolically.  This is because some of those carbs that are converted to fats wind up being deposited in first the liver, then in organs and tissue around the waistline creating “bellyfat” (or, as Dr. William Davis terms it “Wheatbelly” due to the particularly insidious glucose spike caused by wheat consumption) while the rest of those VLD’s and Triglycerides are spit out and circulating in the bloodstream and wind up on your blood panel! (more on this later). 
In short, de novo lipogenesis works. It gets blood sugar down by taking the glucose from the carbs we consume and converts them to fats. This is not bad because as stated, Glucose levels need to be normalized NOW! when elevated to the levels a high carb meal provokes.  However, long term, there are “unintended consequences” which are undesirable and avoidable. Unfortunately, most people (including athletes) do not understand when they reach for the carb laden, fat free foods found in the store that it is this process of de novo lipogenesis that is adding those extra pounds and inches to their waistline.
Pathway #4: Glycation. This is basically the haphazard attachment of excess free glucose to lipoproteins in the blood to lower elevated blood sugar.  This attachment is not a benign process since attachment of glucose to a lipoprotein makes it less stable and more susceptible to oxidation and even mutation.  So, if de novo lipogenesis did not scare you into re-considering the merits of the high carb diet then glycation will.  A simple Google search on Glycation and AGE’s (Advanced Glycated End Products) will explain more than you probably want to know. While little is known about the exact process (it is currently a hot area of investigation though) glycation is being implicated more and more as a major factor in several chronic illnesses like heart disease, cancer, and premature aging.  However, when blood sugar spikes with glucose reaching toxic levels and all the other pathways are at their rate limit glycation is an important contributor in managing the immediate crisis of bringing down blood sugar.
Pathway #5: At the same time the above glucose metabolic pathways are in full swing your body is also doing several things to inhibit fat metabolism . . . doing so clears the way for glucose to “cut to the front of the metabolic line” (this termed by Drs. Phinney & Volek). However, doing so makes our body much more dependent upon glucose as an energy source which is unsustainable.
With insulin as the mediator, metabolism of fatty acids in the muscles  is sharply inhibited in, the liver shuts down ketosis making the brain & nervous system entirely dependent upon exogenous intake of carbs and sporadic fructose induced gluconeogenesis, the liver is now making more triglycerides and LDL particles from carbs to add to the log-jam of fats that cannot be processed because the glucose “cut to the front of the line” ….worse yet, if a person is not carbohydrate tolerant and/or once a person’s other hormones begin to wane and they begin to lose insulin sensitivity the elevated levels of insulin continue to prevent fat metabolism even after blood glucose levels have fallen which means the body continues to be dependent upon glucose for fuel leading to hypoglycemia (i.e. low blod sugar, “Bonking” or “hitting the wall”). 
Pathway #6: At the same time insulin is busy at the fat cells facilitating storage of fats (triglycerides) while, at the same time sharply inhibiting the release of fat into the blood stream, again, forcing the body to be even more dependent upon insulin.  
Now all of these pathways are not “bad” in and of themselves. They are part of the body’s systems for maintaining homeostasis. In fact, they are well adapted mechanisms which, when understood in the context of the larger picture, can help an athlete utilize them to improve performance, recovery and health.
As an example, geese eat a quantity of carbohydrate laden foods in the late summer and early fall which causes deposition of fat including a large deposition of liver fat and glycogen, however, when they begin their migration this carb rich diet pretty much ceases as they spend most of their day flying in migration. Not only do these geese utilize fat as fuel for muscle metabolism but their liver fat stores become a readily available and concentrated substrate for conversion to ketone bodies and glucose.  Ironically, domestic geese producers have utilized the principles of Pathway #3:, De novo lipogenesis, as a way to make what is considered the best goose liver pates!
Again, let me remind you this is a simplified version of a series of very complex and interrelated metabolic processes.
Crisis Management 101: Take care of the immediate problem because it is so threatening yet ignore the consequences of the actions one has to take.
There has to be a better way . . . and there is: OFM Optimizing Fat Metabolism.