Male, white, 52 5-7 170lbs approx. 130lbs fat-free mass Bodyfat: approx. 19%
GOAL: <10% bf using a LC PaIeo diet combined with Intermittent Fasting which means I must lose at least 17lbs of bf, both subcutaneous and visceral.
Resistance train 4xs/week Cardio interval train 2-3xs/week
I was dx'd via ultrasound with non-alcoholic fatty liver disease (NAFLD) two years ago. It is indeterminate how long I've had it. Liver enzymes continue to remain within normal range and I notice no symptoms
I am hypothyroid and have been taking 75mcg of sustained-release T3. My latest thyroid numbers are posted in the link below [p2, 3, 10].
TSH has improvement over last labs. Both T4 and T3 show depressed, however, I was fasting for nearly 20 hours on the first day. rT3 is less this time, which is a good thing.
Have been on LC Paleo diet for last three months and doing between a Lean Gains [ http://www.leangains.com/2010/04/leangains-guide.html ] 16/8 IF protocol to as much as 20/4 IF protocol. I do mini-carb refeeds (about 50-60g) on my workout days only. If I increase carbs more than this, my post-prandial BG will exceed 125.
What's freaking me out are my latest lipid tests. I had the top three done in a matter of two consecutive days [p2, 5, 11-14].
If we’re clearing lipids from the liver, then this is a good thing, but HOW CAN I DETERMINE THAT IT'S THIS AND NOT FROM THE DIET ITSELF?
In other words, is the increase due to CREATION or CLEARANCE (resolution of NAFLD)?
I have not changed any macros in my diet, maybe slightly more lean grass-fed animal protein, but saturated fat intake has remained constant throughout. And most of the saturated fat is drained because I steam all my meats, so how can it be CREATION?
The only other fats I eat with frequency are O3s (2-4g), coconut, flax, macadamia and olive oil.
What evidence supports this unconventional theory?
I understand that one of the key problems with fatty liver disease is that the lipids get stuck in the liver and they’re not being released into the bloodstream.
How could this be the case when taking liver support supplements like milk thistle, dessicated liver, choline, lecithin, etc.? Why wouldn't such intervention spur on the purge also?
Why wouldn't free fatty acids (FFAs) from stored subcutaneous fat be released into the bloodstream as well?
Could this explanation be the mechanism behind the clearance of FFAs: During fasting or starvation, free-fatty-acids are released during lipolysis into the liver and muscles to be burned as energy, this is called fat-oxidation. During the fed-state and especially while eating a starch-based-diet, fat-oxidation is inhibited and replaced with carbohydrate-oxidation, insulin is what mediates this shift. When carbohydrate-oxidation is taking place, fatty-acids are shuttled back and "locked away" in adipose-tissue... where they belong.
In addition to LC Paleo/IF, I also began taking 1g of choline nearly a month before the labs + 3mg methylfolate/day to help with a genetic methylation defect.
Could the above combination have created a mega-purge?
Could the answer be that the best predictor of fatty liver is obesity and insulin resistance?
Another thing: I have been on warfarin for 3 months and must remain on it for another 3 months. This was the only thing I could find on warfarin and its effects on blood lipids:
Coumadin binds to bile acids in the intestine leading to increased excretion of bile acid in the feces leading to increased oxidation of cholesterol to bile acids resulting in increased numbers of low density lipoprotein receptors with increased hepatic uptake of LDL and lower serum cholesterol levels source: http://www.flash-med.com/Side_Effects_Coumadin.asp
Anomalies to purge theory:
Why the decreased HDL when I was making nice progress before?
Lastly, I had been fasting for 18-20 hrs prior to my blood being drawn. My fasting insulin was only 5.2. Then why an elevation in HbA1c (5.8) and FBG (95)? Should've been in the low 80s, especially when fasting for LONGER periods AND on LC Paleo.
This even when on a broad range of BG-lowering natural agents including corosilic acid, chromium, cinammon, etc.
So, why is my insulin sensitivity is taking a nosedive during this so-called healing crisis as well [see Insulin Resistance Score - p12, 14]?
Can someone please interpret my lipid profiles, especially the NMR LipoProfile and tell me what is going on?