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13 Weeks: Getting Animated

It takes a helluva lot of frames to make a movie.

by
Charlie Martin

Bio

March 30, 2013 - 11:02 am

Week 8 of my second 13 week season: low carb diet and more exercise, tracking my weight, blood glucose, and body fat. You can follow me at my 13 Weeks Facebook page for daily updates, and you can join Fitocracy (free!) and follow my daily exercise, and maybe even start tracking your own.

A few days ago, PJ Lifestyle ran an excerpt from Leonard Mosely’s book Disney’s World, in which Walt Disney, in a letter to his partner Ub Iwerks, expressed his frustration with the his first sound cartoon, the now-iconic Steamboat Willie.

He’s pretty depressed. he doesn’t like Hollywood, he doesn’t like being away from home, and he’s losing confidence in the still-unfinished film.  You can see why, when he was having trouble selling the idea, and animation is a frustrating process anyway.  This was in the days of the most primitive hand-drawn animation, where every frame of the film had to be hand drawn on clear acetate, with tiny changes from frame to frame. Twenty-four times for each second of film.  In this 7 minute 23 second film, that’s something like 10,600 frames.  He was tired, and he was bored, and he had trouble seeing any progress.

Why did this strike me, he asked rhetorically?  Well, it reminds me of my ongoing glucose/bodyfat/weight project.  Here I am, eight weeks into my second season, 147 days since I first started tracking this, and it’s a little frustrating and hard. I’ve been less diligent about the exercise, and I do find myself missing things I used to eat.  Like chocolate. And pasta. And bread.  And while I have lost some weight, it’s slow and the day to day variations make it hard to see.  It’s like Disney must have felt — another 24 frames, another day’s work, and what did he have? Another lousy second of film.  That no one wanted to distribute.  He was past the initial excitement and into the slog.

Right now, this project feels much the same.  I’m actually losing weight, and I can see changes — more muscle coming back to my arms, and to put it bluntly, my boobs are smaller.  I’ve lost six inches around my waist, and I can feel that every time I put on a pair of pants that were in the back of the closet because I hadn’t been able to wear them.  But at the same time, the progress is a little slow and hard to see, and it’s a little hard to explain why it should matter to anyone — especially me.

YouTube Preview Image

But then I got thinking, and a little Excel-fu got me this.  Here’s my actual weight, charted over the last sixty days, with a trend line.  This is very much like the other charts I’ve been posting.

My actual weight for the last 60 days.

Trend line is down. This is good. It’s not down very fast, and the added muscle certainly explains that — but also notice that individuual weights vary pretty wildly around that trend line. So here’s another chart.

Weight simulation assuming normally-distributed weights around the slope.

That chart is a simulation: I made a line that had the same rough slope as my weight loss, and then made synthetic data points around that line. The points are normally distributed — the famous bell curve beloved of statisticians — and the variance is around 5 pounds. Notice how similar they look?

And that’s the point. I am losing weight — and yes, my glucose is also dropping still, and the tape measure shows I’m losing body fat. Day to day, though, it’s hard to see — perfectly normal randomness is hiding it. It’s hard to see.

But then, I’ve only got 147 frames of this animation — a little over 6 seconds of film. It might be a little early to be discouraged.


Date 7 day Weight 7 day Glucose 7 day Bodyfat Sum Fitocracy Points Weekly Fitocracy Points
2013-02-01 272.50 116.43 33.1 447 447
2013-02-07 272.63 114.57 30.79% 1881 1881
2013-02-14 271.91 110.43 30.36% 2606 725
2013-02-21 273.79 115.29 29.16% 3775 1169
2013-02-28 274.44 104.00 30.00% 4929 1154
2013-03-07 273.11 115.86 30.24% 6022 1093
2013-03-14 269.86 101.86 30.10% 7233 1211
2013-03-14 272.08 112.25 30.64% 7681 448
2013-03-14 270.57 113.86 30.26% (??) 8180 499
Δ since 2-1 -1.93 -2.57 -2.88% N/A N/A

Charlie Martin writes on science, health, culture and technology for PJ Media. Follow his 13 week diet and exercise experiment on Facebook and at PJ Lifestyle

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All Comments   (5)
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From what I've read about latest research, and from my own experience at losing lots of weight (~100 lbs, and yeah, I gained it all back, twice), I'd say that exercise is for fitness (not a bad thing) and not about weight loss (homestasis appears, from studies, to cause compensating hunger). So I'm doing cardio (walking) and skipping the muscle building.

Also, recent research has shown several of things that are likely to be greatly helpful to future diabetics and dieters, but aren't quite ready for prime time unless you really are willing to go the extreme way:

(1) Gut bacteria are shown to have a significant impact on weight gain/loss, as shown by gut bacteria transplants in animals. New research, looks credible, but too soon to have any impact.

(2) Gastric bypass knocks out insulin resistance (resolves many cases of Type II diabetes) within days of the surgery - far sooner than can be explained by the weight loss that should follow. I first heard about this from my Mayo GI Doc, who was amazed at what they were seeing. This is so significant that there are now places that offer gastric bypass for Type II Diabetes treatment rather than just for morbid obesity. This indicates something is badly lacking in the understanding of insulin resistance.

(3) It appears that a duodenal-jejunal bypass sleeve has benefit similar to gastric bypass surgery, but is far less drastic (endoscopic emplacement, no cutting and re-plumbing) - both for Type II Diabetes and weight loss. Again, it results in the "cure" of Type II ( http://www.soard.org/article/S1550-7289%2813%2900034-8/abstract ).

As I diet and exercise along with you, all I can do about #1 & #3 is echo the great Glenn Reynolds and say "Faster Please!"
1 year ago
1 year ago Link To Comment
"I gained it all back, twice"

As they say in AA, relapse is part of recovery.

You're absolutely right about your three points, too. Basically, the naive thermodynamic model of weight loss, and the insistence on it by the medical establishment, has kept things like low-carb diets and research into the actual causes of obesity from being funded or pursued.

1 year ago
1 year ago Link To Comment
Insulin resistance affects weight, as broached last week.
Palmitate "fat" is made into ceramides, which go on to work against insulin in skeletal muscle & there increase insulin resistance. Muscle ceramides are mostly synthesized from dietary lipid fat.
In skeletal muscle the high palmitate intake forms stearoyl-ceramide (C18-Cer) & this adds to sustained post-prandial high circulating insulin. However the ceramide C16- Cer, palmitoyl-ceramide, is made more from de-novo lipo-genesis that the liver performs. So for those with normal liver insulin signalling they may none-the-less have their peripheral (muscle) insulin signalling antagonized by palmitate derilvative.
The so-called "ketogenic" amino acids, leucine, isoleucine, valine, lysine & theronine in the diet help reduce the level of ceramide (& di-acyl-glycerol) production; resulting in better peripheral insulin sensitivity. These amino acids limit the flux of dietary fat through the enzymatic de-satur-ase pathway & shunt dietary fat into the enzymatic elong-ase pathway (in practical terms this means post-prandial load of fatty acids are less cobbled into triglycerides in the liver).
Leucine, in particular, notably helps give better insulin signalling. Casein is ~9% leucine by weight & merits consideration consuming in the form of low-fat "quark" (drained low fat yogurt/kefir). Beef is 8% leucine, but it's fat has notable amounts of palmitate. (Note closing paragraph.)
Casein has ~27 glutamate residues per each molecule of casein & cells use glutamate to make alpha-keto-glutarate generating NADH as a phase of a cell's tri-carb-oxylic acid cycle (TCA). The NADH level keeps cell driving oxygen into the pathway whereby acetyl-CoA is oxidized so one's exercise program's exertion can be sustained .)
As for liver insulin sensitivity, it is more complex than the skeletal muscle pattern of chronic (or incident) insulin resistance. (On an individual scale adipose tissue retains it's insulin sensitivity longer than both liver or muscle in stages of metabolic syndrome, unlike Type 2 diabetics.) Palmitate complicates the insulin response of liver cells' Akt (simplified significance is an Akt molecule under-going phosphor-ylation is part of core insulin signal cascade inside a cell ).
Excessive palmitate causes less total (& also more selective which residue) Akt phospho-rylation to go forward - even though palmitate does not totally stop Akt phospho-rylation. There is a paradox where Type 2 diabetics actually have higher levels of liver Akt (since not getting used-up, so to speak) yet less sensitivity to insulin in the liver.
(Thus, even in Type 2 diabetics & metabolic syndrome insulin is still able to play it's anabolic role of driving triglyceride output. This lipo-genesis is due to insulin up-regulating transcriptor sterol regulatory element binding protein or Srebp1c, which leads to elevated activity of enzymes fatty acid synthase, acetyl-CoA carboxylase, glucokinase, glycerol-3-phosphate acyltransferase & diacylglycerol aceyltransferase-2.)
Palmitate increases the liver expression of one of the assorted de-phosphorylation enzymes that removes the normal triggering phosphorus from an Akt molecule & interferes with normal insulin response. The problem is that under certain normal metabolic phases this is desirable, but for those with weight problems it's untimely.
One of these enzymes, protein phosphatase 2A, is up-regulated in response to excess palmitate by up to 30% higher levels in the liver - it strips the phosphorus off when it should be on Akt. Protein phosphatase 2A enzyme is also found in skeletal muscle & the adipose so there too can be over-expressed due to palmitate (& other free fatty acids).
High fat dieters who are stalled or have incidents where weight toggled upward have an alternative to palmitate in substituting as much coconut oil as their desired caloric fat intake plan requires. Unless medically (or genetic) contra-indicated adults can replace fatty meat with casein from low fat dairy & some fish to meet daily protein required. Those happy high fat dieters who managed to drop all the weight they want are not proof everyone is un-affected by changing levels of palmitate (whether from food or internal processes).

1 year ago
1 year ago Link To Comment
Charlie's weekly fitocracy in 2 examples was 449 (fitocracy) when 7 day's glucose averaged 113 while a big 1,881 weekly fitocracy engendered 7 day's glucose of 114 (presumably data is for overnight fasting glucose). To see more of what is happening it's worth looking at liver insulin sensitivity more than skeletal muscle insulin action.
This will partly explain why daily, rather than weekly, glucose variation is relevant to weight due to insulin resistance incidents. And why averaging 7 day weight data masks the impact on daily weight (as Charlie plotted) from incidents of water retention when greater degree of insulin resistance occurs (as detailed last week).
Liver's normal response to insulin is Akt phoshor-ylation; one of whose function is phosphory-lation of the transcriptor FoxO1. The effect is to lower the level of FoxO1 (forkhead box protein-O1). If FoxO1 stays active it up-regulates the gluco-neo-genesis enzymes glucose-6-phospahtase and phospho-enol pyruvate carboxy kinase1 (Pepck). Their relevance here is regarding fasting glucose that Charlie tracks for a 7 day average glucose.
Type 2 diabetes & insulin resistant metabolic syndrome have elevated basal glucose & basal insulin. For them excessive palmitate lets their liver Akt phosphorylation by insulin go ahead, but not strongly. The side effect is it inadequately gets FoxO1 phosphor-ylated, which even though not needed lets liver keep making glucose. Overnight, in Type 2 diabetes & some metabolic syndrome, the basal level of insulin the liver is exposed to is not properly shutting off the FoxO1 driver of gluco-neo-genesis.
High palmitate containing fat diets in those with impaired liver insulin sensitivity or insulin resistance are confusing the liver. The circulating level of palmitate (which can be from &/or synthesized from adipose cells' leaking freed fatty acids is one way obesity perpetuates high fasting glucose ) just doesn't let Akt naturally shut down FoxO1. Many overweight individuals have too high levels of free fatty acids, insulin & blood glucose.
Simply put, those who get a robust liver Akt response to insulin (whether post-prandial or fasting overnight) will properly regulate their liver's amount of FoxO1 impelled glucose production & have normal fasting glucose. (Note: this is apart from glycogen, the glucose storage molecule, synthesis that is another pathway which normally goes forward via insulin activated Akt phoshory-lation of the glycogen synthase enzyme GSK-alpha.)
The individual variability of one's response to palmitate & free fatty acids is partly due to which of the structural sub-units of the protein phosphatase 2A enzyme are interacting as regulatory sub-units on which different parts of the Akt molecule. And the sub-units of that enzyme are vulnerable to genetic variability. Just because physical fitness is known to improve skeletal muscle insulin sensitivity that is not going to allay liver insulin resistance.
Furthermore, it may interest some that in regards to adipose tissue the same palmitate/free fatty acid excess leads to untimely degradation of phosphor-ylation from Akt by the enzyme protein phosphatase 2A. Which interferes with anabolic insulin function that normally can induce cell differentiation. In this context it means that pre-adipocytes can't readily synthesize their cell matrix tubules to form up.
In long term weight loss, after a few months there are more newly differentiated adipocytes & those are ideal with less of an individual lipid load in each of them. These lighter loaded adipocytes are ideal since they "leak" less free fatty acids & are more insulin sensitive than old super-sized with lipid load adipocytes that are insulin resistant.
Obesity does not respond uniformly to fatty acids (ex: palmitate). One can lose some weight on a high fat diet yet still get episodes of lipo-genesis &/or high overnight glucose depending on circumstances. There are other molecules & enzymes that can knock down Akt phosphor-ylation which are not detailed here.
Type 2 diabetics, in particular, have to deal with an excess of the phosphatase enzyme Phlpp1 (PH domain leucine-rich repeat protein phosphatase) which by de-phosphor-ylation interferes with ideal Akt 2 insulin signalling sequence & then inside that cell the transport of glucose is poor. This phosphatase also messes up normal mTOR dynamic (not detailed here).
1 year ago
1 year ago Link To Comment
You're less diligent about exercise because, like me, you're a human being. People will naturally be able to sustain an exercise over years that seems more natural, fun and less rigorous and disciplined.

That's why setting one's eyes on biking, walking, running and throwing wins out in the end. It's one thing to get out of bed and start the day with 20 push ups. It's another to go to a special space and do a specific activity with no flexibility in the program and for decades. I can bike, play catch or walk for decades, especially if I use a bike for transport. It's fun and different each time.
1 year ago
1 year ago Link To Comment
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