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13 Weeks: Tool Time

One of the quantities I've been measuring in this 13 week experiment has been body fat. And therein lies a tale.

by
Charlie Martin

Bio

April 6, 2013 - 9:38 am

MyoTape Measuring Tape

Measurements are fairly straightforward. I bought a MyoTape measuring tape, which is supposed to make it easier to take the measurements for yourself. It’s a white plastic object with a spring-loaded measuring tape. You wrap the tape around yourself, hook the end of the tape back into the plastic body, and then pull it tight. In theory, then you unhook the tape and read it.

In my arrogant opinion, this device basically sucks. The problem is that when you release the tape, the spring loading pulls in the tape until it catches a ratchet of some sort. This can be anything from a half inch to an inch. You’re better off with an old-fashioned sewing tape. Amazon has a bunch of them — in fact if you have eleven friends, you can buy twelve of them for about 50 cents each.

Skinfold Calipers

Skinfold calipers are supposed to be a good method. You pinch up a fold of skin and measure its thickness, then use a chart (or compute a somewhat complicated formula) to get your percent body fat.  I got one from Amazon for about $15.

But here’s the problem: it’s almost impossible to do yourself. One of the measurements you should take is on your back around your shoulder blade, and I defy anyone but a stage magician or a contortionist from a Chinese circus to do that for themselves, and I have completely failed to teach my cats to do it for me.

Impedance

So that leaves the bio-impedance method. There are lots of devices for this; I bought a Withings scale. It basically runs the current from one foot to the other while weighing you, then connects to your wireless network and sends the data home, where you can look at it on the web.

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All Comments   (19)
All Comments   (19)
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You could have spared me the 'nipples' thing
Corwin
1 year ago
1 year ago Link To Comment
Oh, don't be a big baby.
1 year ago
1 year ago Link To Comment
Charlie,
I have an old impedance machine in storage.DO you want it?And,what is your waistline ? Corwin
1 year ago
1 year ago Link To Comment
Sure! I'll email you address. Waistline is 42 inches, chest at nipples is 53.
1 year ago
1 year ago Link To Comment
Charlie - You're winding up series & I'm due for going walk-about as the gringo again. So thought to write my presumption for the genetic component of your Type 2 diabetic fasting glucose.
The hexo-kinase group's gluco-kinase is rate limiter for liver to make glucose into glucose storage molecule glycogen. Gluco-kinase acts to phosphor-ylate our internally processed 6 carbon intermediate molecule (glucose-6-phosphate) that is derived from glucose. Then this intermediate 6-carbon "sugar" can proceed into pathway leading to glycogen synthesis.
To work in the liver gluco-kinase needs it's promoter the post-translational regulator gluco-kinase regulatory protein (GCKR). When there is lots of the GCKR in the liver then the liver adapts to capability & liver puts out lots of gluco-kinase.
The tie in between circulating insulin is,that, when insulin is low then gluco-kinase in the liver is low. Since "normally" when insulin isn't high it's because blood sugar/glucose is no longer high & body wants available glucose. Thus insulin being low is the signal to shut off the expression of most gluco-kinase to stop that rate limiting enzyme from diverting glucose in glycogen storeage . Conversely, high insulin signals that glucose abundant so ideal to store some in glycogen & to do so requires more gluco-kinase activity.
Type 2 diabetics who go on to eventually develop the need for insulin therapy get better blood sugar control because they have more insulin in circulation to make the gluco-kinase level rise & then make more glycogen to take glucose out of circulation.
But, Type 2 diabetics usually are still making insulin & have high fasting insulin. Those who still have high fasting glucose (even when eating a very low carb diet) should consider their genetics. Their problem most likely is not due to genetics improperly forming gluco-kinase enzyme, since the same enzyme (used for different function) is found in the pancreatic beta-cells & (in this diabetic stage) there's evidence insulin can be made (which indicates genetics allow proper gluco-kinase molecules can be made). Note: in maturity onset diabetes of the young,called MODY, then the genetics more directly involve abnormal gluco-kinase enzyme.
Fasting hyper-glycemia is more likely traceable to the genetics of the enzyme's post-translational regulator (gluco-kinase regulatory protein, GCKR). What is missing is there is not enough expression (or faulty composition) of GCKR to let the GCK level rise to match the amount of overnight gluco-neo-genesis (ie: can't make it into glycogen & awake with excess "blood sugar"). The excess fasting insulin is not effective to push GCK to get busy - because post-translational GCKR genetics dominate.
The unanswered question is why some apparently have a GCKR problem show up early & yet in other individuals is it something that can develop. GCKR is a protein & the endoplasmic reticulum rules protein folding; therefore, my surmise is that one can incur endoplasmic reticulum "stress" leading to progressive improper folding of GCKR. That sets up the complication that when GCKR loose inside the cell it doesn't unfold 100% correctly & is targeted for degradation.
With a shortened life-span (rather than genetic foible) GCKR with it's duration of half-life it (GCKR) is only half as effective on dealing with gluco-neo-genesis rate. And the wild card nightly playing is that if the rate of gluco-neo-genesis is elevated (see comments below concerning metaformin) then the GCKR is that much more overwhelmed.
...for technical orientation try full free text (2009) "Molecular Physiology of Mammalian Glucokinase" http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2780631/
1 year ago
1 year ago Link To Comment
Hey Charlie! I think I need a PhD to comment here. Where is Teresa? I always understand her.
1 year ago
1 year ago Link To Comment
Sally,
I apologize for my fogginess.What we are discussing is mainly insulin resistance.when I lecture, I try to describe it as 4 tires going slowly flat on your car. Yo can either re fill the tires or plug the leaks.(That's waht I try to do by lypolysis of mid section fat,and weight loss. Ralph DeFranzo,one of the bst diabetologists in the country has an "awful octet" of fat secreted substances ,that 'weaken' insulin.
I had a patient who we took off 200 units insulin over 5 motnhs -and decreased his sugar to normal. (This was using Byetta a f\different GLP and some other stuff So,plug the holes,fix the biochemistry
1 year ago
1 year ago Link To Comment
I didn't mean to LIKE my own comment lol.
1 year ago
1 year ago Link To Comment
GLP is glucagon like peptide our intestine puts out to incrementally (GLP is called an "incretin") slow absorbed food so our insulin can deal with it. For Type 2 diabetics, with their impaired 1st release of stored insulin, it buys them time as ramp up our naturally time lagged 2nd insulin response.
Metaformin's use for weight loss is mostly tied to how it decreases total food consumption. It's prescribed mainly for those with high fasting blood sugar (glucose) it's effect of reducing liver's use of lactate alters dynamics that lead to less self-made glucose (gluco- neo-genesis). Charlie's doctor happily cut metaformin dose because some people can build up lactate in kidney's to the level of risky lactate acidosis.
Adiponectin is one variety of adipose "adipo-kine"; some are undesirable due to being pro-inflammatory & yet adiponectin is desirable because it is anti-inflammatory. Type 2 diabetics, as well as many overweight classified as obese, have undesirably low adiponectin. Dr. Corwin pointed out that adiponectin is part of improving the insulin sensitivity dynamic.
1 year ago
1 year ago Link To Comment
GJ,
The worries about lactic acidosis are for 65 or greater yo. I've never seen it in real life,but I agree with your comments.Andre' the daily GLPs Byetta does much better with the post prandial insulin-I think Check out the part in the four hour body re' adiponectin
1 year ago
1 year ago Link To Comment
GJ,
I do enjoy your comments,but fasting insulin levels are expensive(I had mine atv Atkins' clinic years ago ) and I don't see the need.Remember anything that increases adiponectin,decreases insulin resistance,Charlie is doing this on a minimum of 'scripted meds,and these are the most potent.
I'm more intterested in waist size.And,as much as I like metformin,it doesn't budge adiponectin.Let's give Charlie a little more time and see what happens. The biggest wt loss I've seen with a patient (150-well,`147 #0 had an awful lot of diuresis -since the GLPs knock down Pulmonary htn so much- it's hard to measure adipose loss with just a treadmill.
(I'mpretty worried about mainteance sincehe's not getting samples and even low dose GLPs are expensive.)
1 year ago
1 year ago Link To Comment
Adiponectin increased avg. 59% in Asian male Type 2 diabetics given cholesterol lowering drug (simvastatin) for 3 months.... see 2009 http://dvr.sagepub.com/content/6/4/262.long ("Anti-inflammatory effects of simvastatin on adipokines in type 2 diabetic patients with carotid atherosclerosis"). My suggested non-drug tactic regarding dietary cholesterol restriction might, if the correlation carries over, elevate adiponectin.
1 year ago
1 year ago Link To Comment
Charlie,
Last week sparse fitocracy, sparse glucose yet ~10% heavier than previous week with double fitocracy & higher glucose. You've demonstrated the differences long term Type 2 diabetics have with other dieters using low carb high fat/protein weight loss regimens. The exercise protocol you pursue is good for muscle insulin sensitivity, the low carb improves dynamics associated with liver insulin sensitivity & of course any metaformin dosage is medically supervised.
Adipose tissue/cells' insulin sensitivity is your wild card if wish to notably lose more body weight. No one can account for their precise genetic quirks contributing to being overweight, nor exactly how an individual wth Type 2 diabetes plays out. You've not given any fasting insulin measurements so
hard to analyze that.
The current experiment paradigm is set to finish it's 13 week trial & maybe after your deadline you can tweak your low carb diet for greater weight loss given you are Type 2 diabetic. It will be good having 26 weeks data to take off from for comparison. There have been errors in my comments which haven't been edited for correction - so you may be dubious about input.
1 year ago
1 year ago Link To Comment
Jay, from 270.57 to 271.31 is hardly 10 percent heavier. As I showed last week, the weight -- even on a time scale of a week -- is nearly indistinguishable from being simply random. That said, I've been whining on facebook about the exercise -- my knees have been giving me fits for two weeks and I've been overworking, both of which have made the exercise thing harder. However, tomorrow I have an appointment with a trainer at the new gym....
1 year ago
1 year ago Link To Comment
Comment should've read "... glucose ...~ 10% greater ...." Wish edit function existed here & an expanded comment composition box to scan. I blame all botched writings on the dog!
1 year ago
1 year ago Link To Comment
Actually, the glucose variance is high too, so I'm not sure the seven-day average has that much information. The trendline fit is stile distinctly down. Sigh, I see some R programming in my future...
1 year ago
1 year ago Link To Comment
Fasting (overnight's) morning blood glucose involves self made glucose (gluco-neo-genesis) more than after meal (post-prandial) blood glucose. When cut metaformin dose the drugs inhibition of gluco-neo-genesis is less & the modulating action of low carb intake on post-prandial blood glucose is not consistent.
Metaformin working on the mitochondria counter-intuitively lessens mitochondrial "oxidative respiration" (one way to make ATP) by stalling the mitochondria Complex I function by up to ~53%, depending on dose. This inhibition changes the ratio of molecules NADH, H+/NAD+ (factors of "re-dox potential") that normally let the oxygen involved be handled for an ATP outcome.
This makes the potential fuel carbon that starts as glucose unsuitable for the way mitochondria Complex I needs to work with intermediaries 100% derived from glucose. Since we have redundant energy pathways that cell shifts to use the ATP production tactic that relies less on Complex I.
The result is potential fuel carbon for mitochondria to make into ATP becomes focused on fatty acids, since metaformin becomes involved with signals by up-regulating AMP-activated protein kinase (AMPK). Fortunately metaformin's affect on mitochondrial Complex I only impairs fatty acid oxidation by up to ~10% (this side effect is from too much NAD+, which inhibits the re-oxygenation of an intermediate molecule via NADH in order to keep driving fatty acid oxidation).
With metaformin the ratio of lactate to ketone changes, which increases the pool of Acetyl-CoA that can be put into fatty acid ATP production. Yet, more significantly, the elevated Acetyl-CoA also increases the acetyl-ation of a genetic player, the histone.
When an acetyl tags onto a histone that makes the targeted gene DNA move away from the histone so it can transcribe for action.
Metaformin works on, among other things, the gene(s) influencing gluco-neo-genesis. When the liver lowers the ratio of lactate used to "x" level it, in proportion to that level, acts to shut down (either more or less of) overnight gluco-neo-genesis. Those with long standing Type 2 diabetes have complications to their gluco-neo-genesis which the merely obese do not have to overcome; thus lots of overweight people can just go low carb & normalize their fasting blood "sugar" glucose because they've stopped making excessive lactate (a byproduct of glucose carbon burning).
For Charlie's fasting glucose variability despite consistently eating very low carb it is a question of not always shutting down the mitochondrial Complex I to the same degree every night (now that metaformin dose lower). These episodes of resurgence are from more re-dox potential, more Complex I reactive oxygen (ROS) signalling, extra capacity for successful oxidative respiration is due to the amount of certain types of protein eaten lately.
It's impossible to surmise what Charlie may have for gluco-neo-genesis genetics. Here is a suggestion that may be another tweak to the idea "natural" is best or eat like a "paleo-lithic". I'm assuming he's eating lots of protein.
The molecule glutamate is a substrate for mitochondrial Complex I. Meat is usually pretty high in glutamate & so down the way boosts that Complex I acting. Metaformin, which Charlie cut back on, reduces glutamate use in Complex I - but it is dose dependent. Which leads me to say fasting glucose improvement from eating more of total protein in the form beans, like hummus made exclusively with olive oil, might be worth Type 2 diabetics consideration.
The reason "normally" we don't get messed up from nightly gluco-neo-genesis is because of night being the natural time for body's house keeping auto-phagy & mito-phagy (of mitochondria) recycling. A cell doing this uses the self-made glucose for ATP, exports the by-product of lactate, a cell nearby then takes that lactate up & uses lactate as an intermediary to push it's own Acetyl-CoA into mitochondrial TCA cycle to make ATP. Part of the lactate use is for more mitochondrial bio-genesis. But, for Type 2 diabetics not only is their autophagy impaired, nor are they replacing old mitochondria ideally, but they have lactate levels in liver cells that (as per above) lead to up-regulation of gluco-neo-genesis.
1 year ago
1 year ago Link To Comment
In order to limit pro-inflammatory macrophage activity in adipose tissue (elaborated weeks ago) consider phasing in diet replacements that have less cholesterol when there is long term adipose insulin resistance. This can be done by replacing meat with fish & switch from eggs to low/no-fat dairy clabber (casein without whey) with quality coconut oil added.
Post-prandial dietary fat & dietary cholesterol ingested is cobbled into several molecules, including chylomicrons. The chylomicron incorporates eaten "fat" derived lipids into triglycerides that it carries to inside abdomen adipose tissue cells (not subcutaneous white fat).
There (adipose) the chylomicrons are exposed to enzyme lipo-protein lipase that instigates some lipo-lysis at the adipose tissue. A number of chlyomicron remnants results & part of the postprandial cholesterol fraction being oxidized generates molecules of oxy-sterol.
The molecular conformation of the oxy-sterol interacts with immunological cells around the local adipose tissue. It sets in motion the accumulation of pro-inflammatory type of macrophages & leads to increased adipose tissue levels of TNFalpha that gets involved in insulin resistance.
Liver blood supply is (mostly) down-stream from the adipose tissue & can receive extra pro-inflammatory cytokines leading to a knock-on effect. Gut adipose insulin resistance (due to macrophage inflammation) is not measured well by CRP, since CRP is carbohydrate level sensitive.
A better blood indicator of increasing pro-inflammatory adipose tissue macrophage level is when liver reacts to put out more serum amyloid A with exported VLDL. This molecule snags on cell surface proteo-glycans & plays a role in perpetuating chemo-attraction for inflammatory molecules. Fish EPA oil oxidized in the liver congeals the apo-protein that gets built into VLDL which results in a deficit of building blocks to form VLDL & this reduces the VLDL put out by the liver.
Fish exchanged for meat/dairy fat still has cholesterol; yet there's a paradox making fish oil better for adipose insulin sensitivity. The EPA/DHA fats in fish oil lead to more un-esterified cholesterol going into the adipo-cyte cells. This ameliorates the level of cholesterol that otherwise promotes (detailed above) pro-inflammatory subsets of adipose tissue macrophages & TNFalpha.
Fish oil is not , by itself, going to systematically reduce the physical size of all adipo-cytes, nor automatically the total mass of adipose tissue, even though it improves local insulin signaling sensitivity. It does help adipo-cytes properly respond to insulin & then lets natural incidents of daily flux of "fat" lipids in & out of adipo-cytes go on when appropriate for moderate eaters.
Part of this modulation is due to the way that, in addition to relationships with dietary cholesterol, EPA/DHA alters the ratio of different lipid molecules that compose the "fat" let into intra-abdominal adipo-cytes. (From memory think that last year several hundred distinct lipid "fat" molecules were identified in mammals.) In order to end up losing "fat" weight from intra-abdominal adipocytes one needs to be able to mobilize them out when can actually use them up & stop futile "leaking" of free fatty acids.
1 year ago
1 year ago Link To Comment
I have given up on my Withings scale, but I didn't know it had been discontinued. This is a great article Charlie; I'm happy to see your sense of humor again. :)
1 year ago
1 year ago Link To Comment
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