I understand your frustration. Sometimes it's like a puzzle trying to figure this whole thing out.
Bloat will go away with fat loss it's not a big deal however uncomfortable it may seem now.
I believe that you are insulin resistant and have been for sometime now. At the same time, as the fat deposits grew larger it also impeded your body's ability to produce and use the right amount of hormones.
From that food breakdown you dont eat a lot. This tells me that cells inside your body are shut down to normal nutrient partitioning as you mentioned, and that is a big problem. Normally, t3 does have an effect on geting them moving but perhaps is just an worse case of cellular damage than other cases.
I understand your frustration. Sometimes it's like a puzzle trying to figure this whole thing out.
Bloat will go away with fat loss it's not a big deal however uncomfortable it may seem now.
I believe that you are insulin resistant and have been for sometime now. At the same time, as the fat deposits grew larger it also impeded your body's ability to produce and use the right amount of hormones.
From that food breakdown you dont eat a lot. This tells me that cells inside your body are shut down to normal nutrient partitioning as you mentioned, and that is a big problem. Normally, t3 does have an effect on geting them moving but perhaps is just an worse case of cellular damage than other cases.
Good assessment on all! Now we're getting somewhere. Into the real nuts and bolts.
Insulin resistance and behind it, leptin resistance, many of us have it. What exactly led you to think IR is a problem for me?
This is another reason why I'm on VLC paleo/keto, the best diet for IR/LR. I read up a lot from Jack Kruse, the expert on this. And yes, increased adipocytes = increased inflammation = hormone imbalance (i.e. estrogen dominance, etc.). But if my a1c and FBG are good as you have seen, my post-prandial BG never goes higher than 130 (unless I eat >50g carbs in one meal), both my fasting insulin and leptin are very low -then why would this still be a problem? BTW, if rHGH increases insulin resistance, that's a problem. I need to increase insulin sensitivity.
Becoming keto-adapted means that I've successfully replaced carbs with fat as my main source of fuel, and fat does not illicit an insulin response which is the key to remaining in ketosis. Perhaps eating too much protein? That will drive up insulin levels via gluconeogenesis.
The diet I previously outlined is about 1350-1400 cals. My RMR is about 1500 give or take. My TDEE is about 2200 according to a calorimetry test I recently had done. That test also said my metabolism is...FAST. Go figure. On some days, my calorie intake will go up to 1800, mostly from fat. That still should be at a deficit. Somewhere along the line, my numbers are OFF and I must be still eating at a SURPLUS.
When you're talking "cellular shutdown" or damage what exactly does that mean? Dysregulated nutrient partitioning? If we look at my not firing on all 8 cylinders, then we're talking about hypometabolism. Throw in chronic inflammation - which slows metabolism - and then that's a problem. My elevated CRP reflects some kind of chronic unknown inflammation we cannot identify, so this has also been an issue. Just read that the overall level of inflammation in the body is determined by the ratio of omega-6 to omega-3 fats in cell membranes. Due to regular fish oil supplementation, I have a surplus of n-3 EFAs (EPA./DHA) over n-6.
But talking strictly about my RMR and macronutrient synthesis, you'd think T3 would come to the rescue, but it didn't do much by way of lipolysis. And when I upped the dose, I got some short and long-term sides, the worst being two blood clots in both legs within the last year which I attribute to too much T3 (and studies will back me up on this since I have zero genetic tendencies for this). IF should definitely help with nutrient partitioning. I think it all comes down to IR and tendency toward metabolic syndrome.
Now, here's something else I should mention. And whether this factors into the equation even though my hormone levels fall within normal ranges is unknown. I was dx'd with ESS when I had an MRI of my brain done a few years back: ncbi.nlm.nih.gov/pubmedhealth/PMH0001389/ (add the www since I am unable to post links still).
All the docs I've talked to says it's not an issue unless the pituitary doesn't function. Mine functions fine, otherwise, I'd be hypogonadal, etc., but who knows.
On a side note, my diet when I was at my leanest in my med-20s was very similar in terms of types of foods, but consisted of a lot more carbs and calories than my current diet + I ate 3 meals then instead of 2 meals I'm doing now. Looks like I partitioned a lot better then than now.
As you can see, I'm doing everything possible to be in a lipolytic state as opposed to a lipogenic state.
Again, the only thing I have not done is consistently make sure my calories are under my RMR nor have I started a cycle of anything to this day. I lied. I tried Genotropin rhGH 10 years ago, but the dose was subpar (0.2mg) and all I recall it doing was cause localized lipolysis at the injection site. That's not even a cycle.
I think the key is this: The more insulin "sensitive" you are, the better nutrients are partitioned in your favor.
And you are right - this has been around a long time as evidenced by the dx of fatty liver (NAFLD) 3 years ago. It's going to take some time to reverse the damage. It is taking a lot longer than I though to purge all those FFAs from the liver than I thought. I'm hoping the T and GH will help escalate things in the right direction, however the insulin issue with GH is of concern.
My body looks as if I ate crap, lots of carbs, and hardly worked out - certainly not the case which is highly discouraging. Again, this wan't the case in my 20s in which my hard work showed.