13 Weeks: Season 2, Week 3 — Homo What?
Homeostasis. This is our vocabulary word for today.
Homeostasis is “[t]he ability of the body or a cell to seek and maintain a condition of equilibrium or stability within its internal environment when dealing with external changes” (via Biology Online.) On any diet or exercise program, homeostatis may not seem to be your friend.
| 7-day weight | 7-day glucose | 7 day bodyfat | Weekly Fitocracy Points | |
| Start | 272.50 | 116.00 | 33.10% | |
| 2013-02-21 | 273.79 | 115.29 | 29.16% | 1169 |
| Delta | 1.29 | -0.71 | -3.94% | 1169 |
Certainly, for the last six weeks it hasn’t seemed to be mine. Above is a table of the current results of this second season (I’ll be running similar tables for comparison for the rest of this 13 week season.) I’ve been keeping to the diet pretty religiously, with a very few days in excess of my 30g carbs target. According to LoseIt!, I’ve run a total calorie deficit in the previous six weeks of roughly 42,000 kcals (Calories), or on average about 7000 kcals a week. It only requires the tiniest application of higher math to see that at 3500 kcal/pound, I should have lost 12 pounds, or should have been losing 2 pounds a week. While I’ve hit several new lows, including breaking 270 about ten days ago, I haven’t lost any weight, according to the 7-day running average, since the second season started. In fact, what has really happened in is that I’ve actually gained something like 1.3 pounds.
This could be depressing. Believe me. What this is, is a demonstration of my body trying to preserve homeostasis. Basically, bodies don’t want to change, and they have mechanisms to prevent it.
Luckily, this isn’t a weight-loss experiment, this is a better-health and better-glucose experiment. (Repeat after me….) And I’m doing much better there — my cholesterol is now great, my glucose is near normal (and it’s been ten days or so since I cut my metformin dose in half, with no apparent damage to the glucose level), and — here’s the kicker — my body fat has dropped from around 33 percent to just over 29 percent — which means I’ve changed my body composition fairly radically in these three weeks.
Now, part of this is another demonstration that the naive “calories out minus calories in” model of weight loss is once again breaking down. Of course, since that model is so entrenched in so many people’s minds, the usual doctor’s explanation would be “you must be cheating”, as I talked about in an earlier episode; presenting the food diary and such wouldn’t deter them.
Another possible explanation is that it’s water — just as when they tell you rapid weight loss early in a low-carb diet is “only water”. But just as when I was dropping weight quickly, we’re talking about a lot of water. “A pint’s a pound the world round”, and that means we’re talking about 12 pints, 6 quarts, a gallon and a half of water. Call me crazy, but I’m thinking an additional gallon and a half of water would be pretty obvious in edema and puffiness and heart failure and such.
But the body composition — and one other thing — are hints at what I think is actually happening. That other thing is that after weeks of little change, I’ve begun to have measurements changing. Specifically, I’ve lost 2 inches around my neck and 5 (!!) inches around my waist from when I started the first 13 weeks.
The third favorite explanation of this would be that I’m gaining muscle as well as losing fat, and that one I think is plausible. What’s more, you can do that even when you’re running a big calorie deficit, as I have been, because a pound of fat contains about twice as many calories as a pound of muscle. The explanation that makes sense is that I’ve lost fat at 3500 kcals a pound, and gained muscle at 1800-odd kcals a pound, leaving me slightly heavier, and a good bit skinnier.
I can live with that.
****
Related at PJ Lifestyle:
If I understand your numbers correctly, you body fat % has decreased by 4 points in six weeks. Given that your weight was basically stable, that means you have, in fact, lost 11 pounds of fat, very close to what your caloric deficit would predict. Weight change is much more complicated than just fat loss or gain, so probably everything you described has happened - fat loss, muscle gain, changes in water composition.
There are also many variables to body composition and weight, macronutrient intake being one of them. But that doesn't mean "calories in calories out" is not valid. It is another important variable in the equation. Since you have changed both variables, it is... (show more)
If I understand your numbers correctly, you body fat % has decreased by 4 points in six weeks. Given that your weight was basically stable, that means you have, in fact, lost 11 pounds of fat, very close to what your caloric deficit would predict. Weight change is much more complicated than just fat loss or gain, so probably everything you described has happened - fat loss, muscle gain, changes in water composition.
There are also many variables to body composition and weight, macronutrient intake being one of them. But that doesn't mean "calories in calories out" is not valid. It is another important variable in the equation. Since you have changed both variables, it is impossible to conclude which one has had the intended effect just from your own experience. (show less)
I recently ran across Paul Jaminet's great blog; he noted that glucose does pay a role in the creation of some structures: collagen, mucus, etc. While glucose is available through glucogenesis, this is a more difficult (i.e., stressful) way to acquire this molecule in our cells.
I am amused by the "calorie is a calorie" conversation -- and how the Coca Cola company is valiantly striving to promote this... (show more)
I recently ran across Paul Jaminet's great blog; he noted that glucose does pay a role in the creation of some structures: collagen, mucus, etc. While glucose is available through glucogenesis, this is a more difficult (i.e., stressful) way to acquire this molecule in our cells.
I am amused by the "calorie is a calorie" conversation -- and how the Coca Cola company is valiantly striving to promote this disinformation. Their "Be OK" and "Coming Together" videos on YouTube are clearly targeted along these lines; they are not getting a favorable response in the comment chains of those videos. I'm surprised they didn't disable comments... (show less)
Anyway, cravings have been very rare. I crave chocolate every now and then, but something like a dozen peanut M&Ms will satisfy that at a cost of about 10g net carbs. I sort of "pseudo-crave" bread because sandwiches are so convenient.
I've finally gotten the Jaminets' book after ridiculous struggles with Amazon.
Anyway, cravings have been very rare. I crave chocolate every now and then, but something like a dozen peanut M&Ms will satisfy that at a cost of about 10g net carbs. I sort of "pseudo-crave" bread because sandwiches are so convenient.
I've finally gotten the Jaminets' book after ridiculous struggles with Amazon.
An excess stash of "fat" in short-lived chylo-microns is often taken up by the tissue macrophages. Regular exercise knocks down the number of macrophages in muscle tissue so here it is primarly adipose tissue macrophages that internalize post-prandial chylo-micron "fat". (Macrophage immunological complications detailed previously.)
ApoA-IV (even more so than liver generated apoA-I in HDL) stimulates the secretion... (show more)
An excess stash of "fat" in short-lived chylo-microns is often taken up by the tissue macrophages. Regular exercise knocks down the number of macrophages in muscle tissue so here it is primarly adipose tissue macrophages that internalize post-prandial chylo-micron "fat". (Macrophage immunological complications detailed previously.)
ApoA-IV (even more so than liver generated apoA-I in HDL) stimulates the secretion of insulin. Look at the sharp post-prandial insulin spike from butter. ApoA-IV is the only lipo-protein increased specifically in response to dietary fat - it is our natural "Homo what" gives response to eating a big fat portion.
Insulin acts to stop (inhibit) lipo-lysis from breaking out "fat" from an adipocyte; which means eating fat is not the same as losing "fat". Obese/MetS/Type 2 diabetics often lack the 1st phase insulin release, so for them high fat's engendered apoA-IV triggered post-prandial insulin spike is about more than just how it inhibits lipo-lysis.
High fat diet does limit the dynamic arising from carb based diet's post-prandial high blood sugar state (ie: excess carbs induces liver to make extra triglycerides, liver makes more VLDL cholesterol to carry all those triglycerides out, more VLDL leads to HDL coming back with so much triglycerides that HDL degrades too quickly, amount of HDL becomes low & carb engendered triglycerides begin to stay out of the liver to be stored as "fat"). The chylo-micron "fat" implications are a bit different; but an incident of big fat intake can post-prandially also lead to stashing excess "fat" in the liver.
Chris M.'s lab work (fasting insulin also decreased ?) is showing good changes, yet has some weight gain/stalls despite very low carb & calorie cut back. Proteo-lysis (protein cleaving) in body is apparently elevated in obesity & Type 2 diabetes. Adipose tissue that is putting out pro-inflammatory molecules stimulates the production of anti-bodies which activate matrix metallo-proteinase (MMP) enzymes that add to proteo-lysis. Some of these type of enzymes (MMPs) increase the degradation of the protein-ase inhibitor anti-trypsin; this lets level of serine proteinase rise, which in turn degrades the protein components of insulin receptors showing on cells' membranes (ie: worsens insulin resistance). The same auto-immune glitch of MMP's dynamic also degrades collagen & shows up in joint problems associated with obesity. Similarly the destructive MMP-9 proteinase is relevant to cardio-vascular disease progression.
Subjectively, if one had joint pains & rheumatic arthritic symptoms that have completely disappeared on a high fat diet then that indication is one's adipose tissue macrophage pheno-type population is also shifting to a more normal "resident" profile (less pro-inflammatory with less MMP). In which case the "fat" weight is becoming more benign - one just can't see the beneficial changes going on in all the "fat" tissue by looking at the scale's weight records. A significant decrease in HbA1c is more indicative of less MMP proteinases' activity than fasting glucose.
(show less)
An excess stash of "fat" in short-lived chylo-microns is often taken up by the tissue macrophages. Regular exercise knocks down the number of macrophages in muscle tissue so here it is primarly adipose tissue macrophages that internalize post-prandial chylo-micron "fat". (Macrophage immunological complications detailed previously.)
ApoA-IV (even more so than liver generated apoA-I in HDL) stimulates the secretion... (show more)
An excess stash of "fat" in short-lived chylo-microns is often taken up by the tissue macrophages. Regular exercise knocks down the number of macrophages in muscle tissue so here it is primarly adipose tissue macrophages that internalize post-prandial chylo-micron "fat". (Macrophage immunological complications detailed previously.)
ApoA-IV (even more so than liver generated apoA-I in HDL) stimulates the secretion of insulin. Look at the sharp post-prandial insulin spike from butter. ApoA-IV is the only lipo-protein increased specifically in response to dietary fat - it is our natural "Homo what" gives response to eating a big fat portion.
Insulin acts to stop (inhibit) lipo-lysis from breaking out "fat" from an adipocyte; which means eating fat is not the same as losing "fat". Obese/MetS/Type 2 diabetics often lack the 1st phase insulin release, so for them high fat's engendered apoA-IV triggered post-prandial insulin spike is about more than just how it inhibits lipo-lysis.
High fat diet does limit the dynamic arising from carb based diet's post-prandial high blood sugar state (ie: excess carbs induces liver to make extra triglycerides, liver makes more VLDL cholesterol to carry all those triglycerides out, more VLDL leads to HDL coming back with so much triglycerides that HDL degrades too quickly, amount of HDL becomes low & carb engendered triglycerides begin to stay out of the liver to be stored as "fat"). The chylo-micron "fat" implications are a bit different; but an incident of big fat intake can post-prandially also lead to stashing excess "fat" in the liver.
Chris M.'s lab work (fasting insulin also decreased ?) is showing good changes, yet has some weight gain/stalls despite very low carb & calorie cut back. Proteo-lysis (protein cleaving) in body is apparently elevated in obesity & Type 2 diabetes. Adipose tissue that is putting out pro-inflammatory molecules stimulates the production of anti-bodies which activate matrix metallo-proteinase (MMP) enzymes that add to proteo-lysis. Some of these type of enzymes (MMPs) increase the degradation of the protein-ase inhibitor anti-trypsin; this lets level of serine proteinase rise, which in turn degrades the protein components of insulin receptors showing on cells' membranes (ie: worsens insulin resistance). The same auto-immune glitch of MMP's dynamic also degrades collagen & shows up in joint problems associated with obesity. Similarly the destructive MMP-9 proteinase is relevant to cardio-vascular disease progression.
Subjectively, if one had joint pains & rheumatic arthritic symptoms that have completely disappeared on a high fat diet then that indication is one's adipose tissue macrophage pheno-type population is also shifting to a more normal "resident" profile (less pro-inflammatory with less MMP). In which case the "fat" weight is becoming more benign - one just can't see the beneficial changes going on in all the "fat" tissue by looking at the scale's weight records. A significant decrease in HbA1c is more indicative of less MMP proteinases' activity than fasting glucose.
(show less)