Hal:

Except in certain rare pathologies, fat floats around in the bloodstream for a while (not by itself in any significant quantity -- it's packaged into lipoproteins, because oil and water don't mix), after which it gets either burned or reabsorbed by your fat cells.

Fat is not a passive storage vault!  Adipocytes are continually releasing fat into circulation and taking it up from circulation.

Lack of met flex has little to do with your absolute amount of bodyfat.  (It's a lot easier to accumulate more bodyfat if you're metabolically inflexible, but the fat didn't cause the dysfunction.)  The best way I've found to address it is to get regular exercise, both aerobic and resistance, stop snacking, and eat like a predator.  

Note that I used to be the guy you had to feed every three hours or I got cranky with everyone -- and this was with daily exercise!

pam:

You can even get "peri-workout" shakes now -- so you can eat DURING your workout, too.  Pretty soon we'll just be walking around with IV glucose drips.

I'm glad you like the shirt!  I don't want to overload my fans with nerga, but I'll look into other potentially useful stuff.  

(Yes, I could open a Cafepress/Zazzle/etc. store...the problem is that they charge so much for what they make that it's not worth my time to sell them to anyone!)

JS

Jack:

I highly suspect it's due to the same dietary trends we've seen in the USA.  As to the mechanisms involved, I'm working on that, and it'll be the subject of this year's AHS presentation!

JS

tam:

Most of the citations in my bibliography showing improved met flex are via exercise done indoors -- so while I've always encouraged outdoor exercise and being outdoors in general, it's not the mechanism by which exercise improves met flex.

That said, there are many benefits to sunlight exposure!  However, interpret that article with caution, as it's a small associational study, with all the confounders you'd expect.  

JS

If you want to build muscle, it's important to make sure you have protein in your system soon after a heavy weight workout. Protein powder is one way to do this, and it's quite convenient! However, there are both alternatives and caveats to this.

Caveats:
1. Most commercial "protein drinks" or "protein bars" have very little protein and a lot of sugar (or artificial sweetener)...and oftentimes it's soy protein or some other Frankenfood. (*cough* Muscle Milk *cough) I don't recommend anything but pure whey isolate for this reason (see below for my recommendation).

2. Because of all the filler, they're also very expensive *per gram of protein*. Someone pays for all that advertising. Hint: it's you.

3. If you're not consuming enough energy ("calories"), it doesn't matter how much protein you consume or you won't get any bigger...especially if you're trying to do endurance exercise, like soccer, at the same time.

4. If you really want to Get Big you've pretty much got to give up on cardio and just start eating and full-body working out. No "bodypart splits"...just the basic compound movements. Squats, deads, power cleans, presses, pulls (chins and rows), loaded carries. The assistance exercises come in when you need sport-specific training or aren't satisfied with what you get after all that! I refer you all to the work of Dan John (danjohn.net)..."Mass Made Simple", "Even Easier Strength", etc.

Alternatives:
1. EAT FOOD. Cans of tuna are cheap, portable, and a lot better for you than "ProMax 36000 Muscle Fuel Deluxe Gainer (blueberry donut flavor)". Leave a can opener in your kit and suck one down right after lifting.

2. So long as you eat a protein-heavy meal within perhaps 30 minutes after lifting, you're still fine. Skip the post-workout fluff: just head home and eat. You can foam roll at home and do bosu ball stuff never.

3. I think of "protein powder" as a bridge between PWO and getting real food. As such, half a scoop (15g) is fine and it will last you forever at that rate. The only "protein powder" product I consume is unflavored whey isolate from NOW Foods, because it's basically 100% whey and zero fillers. Get a 10# bag of that, take 15g (half a scoop) at a time as a bridge between PWO and dinner, and the bag will last you about forever. No, it doesn't taste like a blueberry donut. Suck it up, princess!

JS

Hal

I'm glad you find my work illuminating!

It is indeed possible for a primary HPTA axis disorder to cause mitochondrial damage and impaired metabolic flexibility as a consequence -- but these cases (e.g. Cushing's, Hashimoto's, certain cancers) are rare compared to those caused at the mitochondrial level by species-inappropriate diet and lack of exercise. Exogenous T3 isn't solving the obesity epidemic! That being said:

Even though variability of metabolic function is preserved when cells are separated from their endocrine environment, metabolically healthy cells would surely lose some of their function when exposed long enough to an especially destructive one?

I agree: it is very likely that once your higher-level systems like HPTA are no longer able to compensate for broken mitochondria and start breaking, the resulting neural, hormonal, and biochemical environment ("milieu interieur", if you're trying to impress people) is indeed disruptive to mitochondrial health -- resulting in further impaired met flex --> impaired glucose tolerance and fat oxidation. Like many situations, it's a positive feedback loop that only ends once your body settles into a stable disease state, usually Type 2 diabetes.

Meanwhile, while it's often beneficial to treat side effects, it's important to keep the first cause in mind -- because most treatments are either wholly ineffective, or they focus on "fixing" side effects like impaired glucose tolerance, and thus can never fix the underlying mitochondrial problem to pull you out of the disease state into health. (Remember, weight loss alone does not and cannot improve fat oxidation.)

(Note that depending on how long you've been Type 2 diabetic, and especially if you have inherited broken mitochondrial from a diabetic mother, you may be stuck for life with palliative measures like metformin and low-carb diets. This is consonant with the empirical evidence that the longer you've been T2D, the less likely you are to be able to recover from it.)

That's actually a good series of questions: thank you for asking them!

JS

Patricia:

The endocrine disruptor hypothesis is plausible. I suspect that it does indeed contribute to the problem -- but without good historical statistics on both the use of such chemicals and the levels of them found in human blood/tissue, I don't have a good way to evaluate or quantify the contribution. If you know of anyone who's done that, or tried, do let me know!

JS