13 Weeks: The Thirteen Weeks Method
Okay, so back to work.
I’ve now completed the first week of my second 13 week program, which is like the first 13 week program with more cowbell exercise. I’ve also been thinking a lot about something that had been in the back of my mind for awhile: that this notion of thirteen week “programs” was applicable to lots more than lowering blood sugar. Dave Swindle noticed the same thing, and mentioned it in one of his own self-improvement pieces.
So let’s think about this in more general terms. My first, unformed, thoughts went like this: If I don’t do something about the diabetes I’m going to die, and I don’t want to die. But I’ve been on a million zillion diets and they’ve always been heartbreakers, appealing and attractive and exciting and then after a while leaving me flat. So I decided to try something I’d had some success with in the past, a low-carb diet informed by Gary Taubes books. Somewhat coincidentally, going low-carb meant not eating much wheat, and about the same time I read Wheat Belly, and realized my lifetime stomach problems might have something to do with wheat. But then I thought “I’ll never eat chocolate and pasta and bread again?” and wanted to shoot myself.
Which would really screw up the “I don’t want to die” part.
So I decided to make it an experiment. Limited time, limited goals, just doing something that I supposed would be helpful and seeing what happened. How long? It had to be long enough to see some real differences, but not so long that it seemed endless. I narrowed down to thirteen weeks sort of by intuition, based on liking the number 13, but thirteen weeks turns out to be 91 days. It’s basically one meteorological season, and when I was a kid at least it was a TV season — would Batman get picked up for another 13 episodes? There are four 13-week periods in a year, with a a day or two days change.
And it worked — I’ve lost 30 pounds, my blood sugar is back into more or less normal range, and as a side effect my stomach troubles are much much better.
By accident, however, I’d noticed a process, or pattern.
- Decide there’s something you want to change.
- Find ways to measure your progress.
- Decide on some small unthreatening things you can do that should affect those measures.
- Track the results for 13 weeks and see what happens. It helps to pick appropriate tools and techniques for that tracking, but something as simple as a Seinfeld calendar, where you just draw an X on a calendar for every day you do something can be very powerful.
I also, over this thirteen weeks, have realized there are some things that have been key insights for me.
First, “the goal of no goals” — I purposefully didn’t say “I want to lose 50 pounds” or “I want my blood sugar every morning before breakfast down to 90.” Instead, I said “I would like my weight to go down, and my blood sugar to go down, and I’m interested in how they respond for the next 13 weeks.”
The thing is, when you set a goal, you can fail at a goal: if I’d have said “I want to lose 50 pounds”, my 30 pounds would have been a failure. As it is, emotionally, I can say “cool! I lost 30 pounds!” instead of feeling guilt or shame.
In Buddhism, we talk about “establishing a Buddhist practice”; by refusing to set goals, I’m saying “this is a practice. I’m going to perform this practice. I’ll see what happens.” This is always what I’ve told people about meditation too: just do it for a while and see if it’s productive for you. So it took me 40 years to figure out it didn’t apply just to meditation.
Second, I made myself accountable by announcing it to people. Me, I’m a writer, and tend to be a fairly personal writer, so I announced it to thousands and thousands of my closest friends on Facebook and at PJ Media. (It didn’t hurt that I was hoping to write a book about my experiences.) But I think it would be just as effective if you only make yourself accountable to your partner, or your lover, or maybe even your cat. In fact, though, I think whoever you make yourself accountable to has to be able to be uniformly supportive. At least with me, if I had a girlfriend tracking this and nagging me about noncompliant days, I’d begin to resent it pretty quickly.
Third, I had to learn to keep a very special attitude. On the one hand, I had to learn to focus on the instant: if I had gained weight this morning, or I had eaten wheat the day before, it was in the past, it was no longer important. What is important is right now.
At the same time, however, each instant itself isn’t very important. Instants are like streetcars: wait a little while and another one will come by. And when you’re setting a limited time, this is much easier — no more “omigod, this for the foreseeable future”. I replaced it with “If I’m not happy with this by February, I can quit or change what I’m doing.”
Any progress over that 13 weeks was acceptable progress, and if I wasn’t happy with the progress after 13 weeks I’d just try something else. Three months was no big loss.
The thing is, none of this is just about weight or blood sugar. It could be applied to anything you want to change, anything you want to do.
Need to stop drinking? AA already has the idea of 90 meetings in 90 days.
Want to lose weight? Find a sustainable, confortable diet for yourself, try it for thirteen weeks and see what happens. Or plan to walk at least 20 minutes a day every day, or make sure you take 10,000 steps a day, for 13 weeks, and see what happens.
Writing a screenplay? A page a day for 13 weeks is a 90 minute screenplay.
Want to have a baby? Be pregnant for … okay, maybe it doesn’t apply to everything.
Speaking of accountability, here’s where I am this week. You’ll recall that in this season I’m continuing to track wight and blood sugar, but adding to that by body fat and amount of exercise. Right now I’m reporting Fitocracy points as an easy measure, and I’ll report the total points accumulated that week.
Weight 272.63, Glucose 114.57, body fat 30.79% (by Withings scale.) All of these are the 7 day moving average of my regular measurements. Total Fitocracy points: 1881.
Next week, more reports on progress, and I’ll start talking about the tools you can use to measure your progress.
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Images courtesy shutterstock / catlook / Bertold Werkmann
Previously from Charlie Martin:
Nicely done, Charlie. Last week was my favorite article of all time, this one is second. It conveys the important messages in the experiment.
Thanks again for being awesome!
I love this article. Very inspiring to someone who puts off doing things because the goal seems too overwhelming. Thanks Charlie.
Good job!
Great article Charlie, I started last week and convinced my husband to join me for ‘a month’ but I think I like the 13 weeks concept better. It is totally doable and yet you don’t see yourself never being able to have a slice of bread again. So I am noticing much less joint pain within a few days after eliminating wheat and sugar from my diet. Do they cause inflamation? In my case it would seem one or the other affect me that way. My husband’s blood sugar has stayed in normal ranges since he began and for the past week has only had to take his tablets, so no insulin shots this week. Thank you for sharing i have checked in on you every now and again over the 13 weeks to view your progress. By the way, I am a pretty visual type, in case you are as well, stack 3 10lbs bags of potatoes in your cart the next time you are in the grocery store, and look at them. 30 pounds is pretty impressive when you can see what it represents. Best wishes for your continued success.
Thanks. I’ve been thinking about it in terms of water bottles. I buy water in 1.5 litre bottles. Basically I’m not carrying 9 bottles I was carrying in October.
I’ve got after pictures coming next week — I wasn’t sufficiently organized to get them taken by deadline this week.
So I am noticing much less joint pain within a few days after eliminating wheat and sugar from my diet. Do they cause inflamation?
The short answer is “no one knows for sure” but there is a lot of anecdotal information about this. It has certainly been my experience that my chronic stomach troubles are much abated — in fact, I realized the other day that I’d forgotten to take my nighttime omeprazole for several days and hadn’t noticed. This is kind of unheard of.
Fish oil is also supposed to ease inflammation.
poppycock.
time-based fad diets are some of the least successful and most dangerous.
try making permanent changes to your lifestyle.
Do you find being an idiot and not reading the articles contributes to your life?
Pardon my last week late comment’s running error.
I should have caught where repeatedly wrote “LPL lipo-lysis” & edited phrase to correctly read refrain as “non-LPL lipo-lysis”.
If just drop out the word “LPL” & keep the word “lypo-lysis” the comment is good.
(From where was composing comments I mixed up & dropped the explanation segue from leading sentences about LPL on to subject of non-LPL.)
Sorry for belated correction & confusing anyone.
13 weeks was also USMC Boot Camp for me back in the 50′s – I was too skinny – others were too fat. We all leveled out in 13 wks
Yeah, it’s funny how often this works out. 13 weeks is about 90 days (P90x) is a little more than 12 weeks (Artist’s Way, Body for Life) is a little less than the 100 days a lot of people are using for, say, 100 pushups.
One needs to look beyond the fat cell (adipocyte) to the cells making up the adipose tissue (mostly leucocytes, lymphocytes, macrophages with some pre-adipocytes, fibroblasts & collagen ). It has mostly immune cells designed to perform immuno-modulation .
The obese trend toward immuno-pathological conditions in their adipose tissue (popularly alluded to as low level inflammation). The immunological component of adipose tissue are more significant than the acipocyte, since the adipocyte is subjected to what the local immune cells put out.
The “normal” type of adipose tissue macrophages in residence are called “M2″ & arise transformed from mono-cytes sent out from the bone marrow. In the lean, those heavier after eating sprees & the mildly obese this is not pathologically modulating local “fat” conditions. Severely obese, Type 2 diabetics & aged still have these M2s, but a disproportionate ratio of other macrophages.
The beneficial immuno-modulation of M2 macrophages includes generating the beneficial IL-10 (interleukin) & the enzyme Arginase. This keeps down the pro-inflammatory molecules (like IL-6, IL-1beta & TNFalpha). We normally get just enough immune defensive (pro-inflammatory) IL-6 from macrophages & other cells ( ie:leukocytes, mast cell, B cells) in the adipose tissue.
With age the normal increase in IL-6 is not adipose derived , but in obesity from diet there is too much IL-6 put out by the adipose. In Type 2 diabetes inflammation there’s too much IL-6 being cranked out by the adipose tissue “B”cells.
Exercise is relevant here because it up-regulates the arginase (Arg2) enzyme expression. Exercise also increases PPARgamma in adipose tissue; which plays a role in keeping one’s M2s being expressed (ie: PPARgamma induces less adipose inflammation by favoring M2s). Unfortunately with age we’ve less PPARgamma receptors, so naturally lose some ability to field M2s as the “resident” adipose tissue macrophage.
Buuut…
The obese & Type 2 diabetics end up with too little “M2″ macrophages, because they get a lot of other types of macrophages that are polarized differently than the M2 macrophage. Macrophages in adipose tissue can come in that are shift to include more variants (pheno-type).
((Technically: Adipose tissue immmune modulators come about when the “Naive” (primal) T immune cell reacts to something (antigen). One signaling molecule from a “naive” T cell’s is the cytokine IL-4 which generates Th helper 2 type molecular “helpers”.
((If the naive T cell wants to suppress inflammation it’s signalling molecule is TGFbeta which engenders the TGFbeta Treg (reg= regulator.) This is desirable in control of parasitic helminth infections & keeping immune system generated inflammation from destroying healthy tissue.
((Insulin, in the lean & insulin sensitive overweight, will increase one’s levels of beneficial IL-4. This IL-4 is put out by both Treg (regulator) cell & T cells which act on a macrophage to limit transcription molecule Foxo1 (an energy adjusting regulator) from trans-locating to that macrophage’s nucleus. Benefit of design’s normal purpose is when have less transcription factor (Foxo1) causing that macrophage nucleus to put out the receptor (Ccr2, chemo-kine receptor) there are less immunological cells infiltrating into adipose tissue.
((Obese adipose puts out more of the mono-cyte (macrophages are from mono-cytes) chemo-attractant protein (Mcp1, a.k.a. Ccl2 chemo-kine ligand – which the above mentioned Ccr2 is receptor for). This Ccl2 is a pro-inflammatory cytokine.
((The obese are putting out excessive attractant molecules & pulling more mono-cytes to their adipose tissue, where the “naive” T cell influences it.
Recall how metabolic syndrome (insulin resistance) & diabetes exhibits excessive reactive oxygen species (ROS).
((It is increased ROS hydrogen peroxide (H2O2) that gets more Foxo1 transcription factor moving into a mono-cyte’s nucleus to put out more receptors (Ccr2) for the signal (Ccl2) pulling mono-cytes to adipose tissue. Which consequently means more ROS is going to give one more macrophages infiltrating the adipose tissue.))— End of technical details.
The immunological switch from modulation to pro-inflammation is useful for dealing with bacteria & viral issues. What is detrimental is when the T helpers (Th1 & Th17)engender a immune-pathology when body not really under attack.
Obese can get this when “naive” immune T cells shift into pro-inflammatory modes driving adipose tissue macrophages into differently polarized macrophage phenotypes. Lean can get these non-M2s as well (ex: thin women with poly-cystic ovaries) & for that matter so do many with advancing age irregardless of weight. Aged have more Treg cells in adipose & get more subcutaneous adipose macrophages.
What goes awry:
When T cell helpers in the adipose tissue (not the adipo-cyte) put out paracrine factors (for Th1 = TNFalpha, IFNgamma & for Th17=TNFalpha, IL-6, IL-17) that make mono-cytes turn into adipose macrophages that are not the normal resident M2 type. Obesity, Type 2 diabetes & aging engender different sub-sets of T cells outside of the adipocyte itself.
Instead of pre-dominant M2 adipose tissue macrophages the ratio of M2s lessens & a different polarized macrophages, like the M1 comes on the scene. This M2 vs M1 paradigm is not absolute, because there are hybrid M1/M2 macrophages & also the so called DN (double negative) polarized macrophage.
As M1 gains representation the adipocyte cells in that adipose tissue hyper-trophies (bulks up), since M1 inhibits adipo-genesis – which leaves old adipocyte more vulnerable to necrosis. This is in contrast to “normal” M2 macrophage where adipo-genesis readily goes on & enjoy less adipocyte hyper-trophy.
So, with mild obesity there are still M2 macrophages, but M1 types starting to come active. It is hard to quantify because we have different sub-sets of molecules (antigens) being related to by our “naive” T cells.
Anyway, the person is still insulin sensitive at this stage; even though putting out extra pro-inflammatoryu IL-6, TNFalpha & less IL-10 (good chemo-kine). But drastic obesity is usually when adipose tissue macrophages put out excessive IL-6, TNFalpha & iNOS (inducible nitric oxide synthase).
The effect of these macrophage phenotypic molecular storms is then on the local adipocyte itself. It is under this immuno-pathological paradigm (unrelenting IL-6, TNFalpha & iNOS ) that the adipocyte becomes insulin resistant .
Severe obesity is where usually get more of the DN macrophages; which are capable of forming crown-like structures & kicking out the level of Ccr2 (chemo-kine receptor) to get inflamatory cytokines IL-6, TNFalpha & iNOS to the level where insulin resistance occurs.
In age the DN macrophage phenotype increases; while M1s that stick around are what provokes age diminished insulin driven uptake of glucose even though old may not be clinically obese. Iin age only M2s decrease, yet they are not necessarily exhibiting the risky Ccr2 (Cc is a chemo-kine motif) level of immuno-modulatory expression seen in younger/adult obesity. The aged’s more DN polarized macrophages doesn’t always lead to an increase in crown-like structures & perhaps this is why obesity in the old is not associated with a shorter life span.
About that diet….
It is lipo-lysis from visceral adipose, & not subcutaneous adopose, that drives how much of a macrophage build up occurs in adipose tissue. When one starts to lose weight or starts starving (restricted calorie intake) they have used up glycogen energy stored reserve.
Then adipocyte cells do lipo-lysis to release “fat” lipids. The local M2 macrophages among the adipose tissue take up (phago-cytise) some of that lipid load stashing fatty acids right there to dole out.
The quirk is more M2 come into adipose tissue at first (an innate starvation strategic program). But if one is actually losing weight the deficit of calories makes body not need to dole out “fat” lipids from M2 stash, since it needs them in real time.
So in due course the visceral adipose tissue M2s are going to pass on redundancy & going to be less numerous. In time the reduced number of adipose macrophages allows conditions that favor up-regulation of the non-LPL lipo-lysis enzyme ATL or adipose triglyceride lipase.(As for the other non-LPL lipo-lysis enzyme, HSL or hormone sensitive lipase, it is less responsive to caloric deficit & beocmes activated more when body has endured prolonged caloric deficit.)
Dieters want to reach this is stage where an adipose cell has to break free “fat” as the body demands free fatty acids’ carbon. For the vanity weight loss it is easy, but the obese & Type 2 diabetic can’t catch a break.
Obese tend to have larger sized adipocytes, perform more lipo-lysis, have more macrophages & complicated macrophage pheno-types (M1,hybrid M1/M2 & DNs) among their adipose tissue. Their macrophages can hold more than 1 lipid droplet or have more than 1 nucleus while holding 1 huge lipid droplet.
The macrophage having more than 1 nucleus (yet jumbo lipid droplet) is what snags (phago-cytose) an adipocyte that is dead/dying (necrotic). These pheno-type macrophages, instead of residing naturally between adipocytes, cluster around the necrotic adipocyte, like crusts of crown-like structures on that adipose cell.
Some dietary situations let LPS (lipo-poly-saccharide) of certain bacteria “leak” into the body. Modern dwarf wheat’s intestinal protein remnants let more LPS into body, as can saturated fat. Fish oil tightens up the intestine cells so less leaks in & poly-unsaturated fat shifts gut bacteria to types of bacteria shedding less LPS.
LPS acts of low grade inflammation trigger when it is recognized on a membrane Toll-like receptor (TLR); and also some fatty acids also trigger the TLR. What happens is the lipid ceramide (ceramide is made from sphingnomyelin) gets moving inside that cell.
Ceramide inside that cell encounters other receptors (Nod-like receptors, NLR) instigating changes in gene expression in that cell’s nucleus. In the adipose tissue this ceramide, like reactive oxygen species(ROS also trigger NLR) leads to a pro-inflammatory disposition & own immune function co-opted to become immuno-pathological.
Long term obese who are insulin resistant have a serious immunological hurdle to get past. The insulin resistant adipose, under ceramide’s bad influence, has nuclei up-regulating NFkappaB that then goes on to alter the profile of adipokines (ex: leptin) secreted.
Way to go Charlie! You’re an inspiration! To guys like me, for example, faced with same demons: pre-diabetic, overweight, plus off-the-charts triglycerides. So, I’m going with the So. Beach diet which is similar to Taubes with focus on carbs, blood sugar, etc. It’s fascinating to see the multi-faceted whole-body reaction to what we eat and how we eat it. Cut back the carbs, everybody – organs, heart, blood – they all go, “Yay!! Thanks, buddy!” I figure that having gotten me through 70 years, it’s the least I can do for them.
I like your 13 week approach. I’m doing 30 steps of 4 days each to see if I can lose about a pound every step or so. That would add up to 30 pounds in 120 days. But, if I even make 20 that will rank right up there on the human achievement level with… oh, I don’t know… inventing round manhole covers or something. But, you’re right. It’s not an ironclad goal rather a “let’s see what happens” approach. I like your take on goals.
So, good luck! Hang in there and never give up! It’s the work of a lifetime and, if you pull it off, it’ll really piss off the Moirae! That’s an added bonus.
Good job. I’m starting down the same path myself, although I’m not diabetic.
One thing you might want to change: Monitor A1c and blood sugar. A1c is a much better indicator for diabetics, since it measures your average blood sugar over the last 6-12 weeks. Checking it once a month or so would do. There are home testing machines available.
Yep. Here’s my week 9 article where I talked about A1c. http://pjmedia.com/lifestyle/2013/01/05/13-weeks-week-nine-in-which-we-see-results/
The exercise thing does seem to be significant in this new 13 weeks. My blood sugar seems to have dropped sort of precipitously, to the point where I’m seeing morning blood sugars some days in the 80s and I’ve been as low as the upper 70′s during the day — which is to say, even slightly hypoglycemic. I talk to the doctor on Wednesday about cutting my metformin (blood sugar meds).
Augh, that should read “morning blood sugar in the 90′s”.
One observation about goals: there are some goals you control and some you don’t, and I think it’s better/less crazy-making to set a goal that you control. A goal that deals with your behavior, not the desired result of behavior.
The classic example being weight: we can do various things that influence body weight, but it’s not something we control directly. So “losing N pounds” turns out to be a bad goal, because you can fail to achieve it without knowing why. The same applies to blood-glucose readings, arm strength, and similar.
On the other hand, “eating no more than 30 grams of carbohydrate a day” is something you have control over: it’s a behavior, not a hoped-for result, so you can tell whether you’re doing it or not. (It may or may not turn out to be a good goal, but the point is you have control over whether you do this. Control over your metabolism, not so much.)