13 Weeks: Week Nine — In Which We See Results
Starting on November 4th 2012, I began a 13 week experiment in changing my eating and exercise habits, for the best of all reasons: I didn’t want to die. I was chronically ill with stomach troubles, I was sleeping badly, and my average blood glucose was in the neighborhood of 150 mg/dL — well into the range of type II diabetes mellitus. For the experiment, I’ve cut my daily consumption of carbohydrates to a net of 30 grams a day and cut wheat out entirely, and I’ve added exercise following a Tabata Protocol, along with yoga, kettlebells, and (too rarely) weight lifting. I report my results here at PJ Media Lifestyle, and also on my 13 Weeks Facebook page.
If you’re been reading 13 Weeks since I started, you’ll remember that I had realized on about October 15 that I was 100 lbs or so overweight at 301.5; I was in chronic ill health with both gastric reflux disease and irritable bowel syndrome; and I had moved from pre-diabetic to flat-out diabetic in the span of about a year. At 57, I realized I was only 12 years younger than my father when he died, and only 20 years younger than my mother was when she died on January 11, 2012. Twenty years wasn’t enough, and twelve years was for damn sure not enough; something had to be done.
Now, after Week Nine, the effects of what I’ve done are starting to really show up. Here’s the chart I’ve been keeping to plot my progress. The plus signs are my weight in pounds, the x’s are my blood glucose as measured with a drugstore glucometer, and the lines are the linear best fit line to the data.
As you can see, the lines are headed down — which is the good direction. On Wednesday I went to the doctor, and got weight and my bloods done again. My weight’s down 30 lbs since October 19, 19 lbs since I started this November 4th. But I swore I wasn’t paying attention to the weight (gloat). Even if I lost a lot. (Gloat.) One of the blood tests I did was the glycosylated haemoglobin HbA1c test, which is a diabetes test. I’ll tell you my results below; before I do, however, I want to explain the test and why it’s important.
With diabetes, of course, we’re primarily concerned with the blood glucose level. When I was a kid, my “second mom” Julia Medina took care of us; Mrs. Medina was diabetic and dependent on insulin, but home glucometers weren’t available; the only real test diabetics had was to watch their urine for ketones using test strips, and the only real measure they had for control of diabetes was whether you tended to fall into a coma, either from low blood sugar, or from high. If your blood sugar stayed too high, you risked blindness, advancing neuropathy and pain, and kidney disease, hearth disease, or — worst of all from my point of view — creeping necrosis of the extremities. (Your fingers and toes die and become gangrenous; they’re amputated. The stumps become gangrenous; they’re amputated a little higher. Eventually you run out of pieces and you die. Don’t even google “diabetic necrosis”, you don’t want to look at those pictures.)
Luckily, Mrs. Medina was well-controlled; she lived a long life. A whole lot of diabetics didn’t. Three things, put together, improved the chances of a diabetic living a long life over the last 20-30 years. The first was inexpensive direct tests for blood glucose levels; the second was bio-engineered human insulin (before then, insulin extracted from the pancreases of hogs was used, but it doesn’t exactly match human insulin. It was better than nothing but still had problems.) The third was the wide availability of the glycosylated haemoglobin HbA1c test (which we’re going to just call the A1c from now on.) What the A1c let doctors do is infer what your average glucose had been over about the last three months.
As a red blood cell passes from erythropoiesis (birth) to eryptosis (death and recycling), the hemoglobin sometimes binds with glucose, a process called glycosylation.
Here’s how it works. Hemoglobin, the chemical component of the blood that carries oxygen and makes the blood red, can bind to glucose, forming glucose-bearing (or glycosylated) hemoglobin. The rate at which it binds is proportional to the concentration of glucose in the blood. It binds fairly slowly, so your hemoglobin doesn’t just suck up all the sugar right away. Instead, over the life of a red blood cell (an erythrocyte), which is about 100 days in the normal human, a fairly small percentage of the hemoglobin will glycosylate. At the end of the average 100-day lifespan of the red blood cell, it’s broken down by the body and it’s components recycled; part of that process separates iron from the hemoglobin, which also liberates the glucose.
Remember, though, that the rate at which the glucose binds is dependent on the concentration – the more glucose, the more it binds to the hemoglobin, and once bound it stays bound until the red blood cell dies. The result is that the percentage of cells with glycolated hemoglobin in the blood is proportional to the average blood glucose level for the last several weeks.
Still with me? We’re getting to the payoff. From my blood glucose readings, I’d known things were improving.
In October, A1c was 7.5 percent. You can compute the equivalent average blood glucose, which comes out to be about 170 mg/dL. An A1c of 6.5 percent or more is diabetes.
Yesterday, my A1c was 6.2 percent, or an average of around 130 mg/dL. An A1c of between 5.7 percent and 6.4 percent is considered enough for a diagnosis of pre-diabetes.
Or, in my case, post-diabetes. By blood sugar is controlled now, down to healthy levels — and I’m only about two-thirds of the way through the life span of red blood cells that were new when I started this; I can expect the A1c to go down. If it keeps declining at the rate it has been, it might be as low as 5.5 percent by the end of this 13 weeks.
That would be normal.
One more thing I want to mention. A dear young friend of mine has decided she wants to enter the military, but to do so she needs to lose ten pounds, and wants to get in better shape. As a result, she’s started a blog of her own, 14 Weeks for Freedom, where she’s making her own open commitment to some life changes.
I am extremely proud of her; please drop over to the blog and give her your support.
That is an awesome A1c change. When my daughter was diagnosed Type 1 two years ago the dietician said ‘you can still eat whatever you want’. I quickly realized this was a crock – and had to break it to my then 9 year old daughter. I will NOT join the ADA until they change their recommendations for the amount of carbs that diabetics should eat. They are part of the problem, not the solution!
What great news, charlie.
Charlie: Inspired by your example, I started a Taubes regimen New Year’s Day. I still miss sugar in my tea and I’ve had some “Atkins flu” off and on, but otherwise it’s a relief not to crave sugar, flour and starch, and I’m surprised how tasty vegetables can be when my tastes buds aren’t jammed for sweet.
I’m 61 and would like to lose 40 lbs to get back to my thirty-something weight. I’d about given up, because regular diets take so much willpower and, if I stop paying attention, I lose my gains in a heartbeat. Happily, I find this diet and satisfying and no burden at all. I believe I can eat this way long-term.
At an intellectual level, I’m also enjoying Taubes’ crusade to take on low-fat diets, calorie-in/calorie-out thinking and the new Food Pyramid. It’s a fascinating debate and Taubes is such a good writer.
Congratulations, Charlie!
Taubes emphasizes that conventional wisdom from the mid-nineteenth century and the mid-twentieth century was that sugar, flour, and starches made you fat. Then the “experts” proclaimed that low-fat was the way to go. And, of course, during the last few decades we, as a nation, have become fat, our cholesterol has sky-rocketed, and many have flirted with or have embraced heart disease and diabetes.
Returning to a low carbohydrate, high protein, and high fat diet seems to me to be just the ticket!
Great news. You deserve credit for dedication and hard work to get this far this fast. I’m amazed that low carb/weight loss/exercise can make such a significant improvement in people’s health. I’ve seen it in my own life, having lost almost 40 pounds since August. It’s a shame that the medical community, government and food industry can’t tell us the truth about obesity and how to prevent it.
Mr. Martin, I’ve read some of your posts, especially this one and your account of post-Thanksgiving hell. Has you been checked for celaic disease or gluten intolerance? You don’t get headaches, bloating, etc. from just eating a big meal. That sounds exactly like a celiac getting glutened. If your doctor has not checked you for this very, very common affliction you should fire him immediately and get your butt to an allergist before you get colon cancer.
Wow. I should have proofread that before post. Oh, well. Here’s a link to the U. of Chicago celiac information page:
http://www.cureceliacdisease.org/living-with-celiac/guide/fact-sheets
Fred, I’ve been tested for celiac sprue and it didn’t show up, and I just had a colonoscopy where I discussed the wheat thing beforehand with the doc, and he didn’t see any signs of celiac-related changes. I do think, however, that there may be a spectrum of wheat sensitivities beyond true celiac.
One gastroenterologist told me that upper endoscopy results were suspect because they can only go a short distance into the small intestine. On another note, there is also gluten intolerance which will test negative but still have celiac-like symptoms. Do you react badly to barley and rye?
Don’t know: at 10 g/day effective carbs — my score yesterday — I’m not getting much of *any* grains.
See if Heinz malt vinegar wrecks your day. No carbs.
Good thought. I’ll give it a try.
Hm. Come to think of it, I use soy sauce with no apparent troubles.
All the same, considering your reaction to T-Day dinner I would find a doctor who really understands celiac and gluten intolerance. From what I can tell allergists are more likely to know what’s going on than a gastro, especially an older gastro. I suffered, progressively getting worse until the age of 35 when I discovered the source of my problem and I can tell you that most medical professionals have no clue about these issues. Celiac by itself is 10x more common than Crohn’s disease and many times more common than type 1 diabetes. 98% are undiagnosed. I can say from my own experience that the amount and type of gluten ingested makes a difference. Liquid gluten like beer is probably the worst. Some people don’t react immediately, either. Some have a gluten response that builds and fades over a week or more. You need to sit down and have a long chat with someone who really knows this. Seriously.
I have read the Taubes books, and the book Wheat Belly, and Dr. Berenstein’s book The Diabetes Solution, and had just enough college chemistry and nutrition courses to understand a bit of the science described by these and other authors.
I once managed to lose 100 pounds with Atkins. Over the intervening decade of two pregnancies and eating healthy but not necessarily low carb (my beloved husband is a healthy mixed veggies and salads nut! and he has been very good for my eating habits), so I gained back about half–but half stayed off!! It is the only diet where I kept off anything.
So I went back to low carb, with all the new books out to encourage me, and the support of family. A week into it, I am down 5 pounds. In a month I will repeat my measurements and see if I dropped any inches.
My experience has been that while other diets can take off some weight (I followed Dr. Furhman’s book, Eat To Live, at one point and lost weight but it returned nearly instantly when I went off), low carb seems to reset my metabolism and I keep it off much longer, and if I stuck to it, I suspect I would keep it off forever.
Thank you for sharing, it helps me to stick to my plans to see others doing well!
The fourth big diabetes advancement was the pump. People don’t inject anymore, they walk around piped to a portable pump. That makes regulation much better.
They’re currently testing continuous glucose analyzers which will allow these pumps to be automatically controlled in real time. When this becomes widespread, it will be another huge advancement.
Hmmm, 9 weeks and food made me think of this..
http://www.youtube.com/watch?v=3vLBMEWexoI&feature=youtube_gdata_player
Yeah, I wish I had that help with my diet.
One theory as to why diabetes causes so much damage is that glucose binds to various proteins and body tissues, impairing proper function. So it’s not just hemoglobin involved. Read about advanced glycation end-products (AGEs) for details.
Excellent progress, Mr. Martin.
-Steve
Thanks, and thanks to gringojay as well. I’ve just gotten a half dozen papers to read,
God Bless Mr. Martin. Fight the good fight…too much to live for.
Most welcome news and thank you for the science behind the a1c test. Good to see the Taubesian approach in action.
Great work, dude. Keep going. So, physically, how do you feel?
Good, thanks. Thirty pounds (I’m actually at about -31 lbs now) seems to have been around the threshold where even my difficult relationship with body image can’t hold out — I feel significantly skinnier. With any luck at all, I’m about to get a new lifting partner, which will mean being able to do all those things that need a spot that I’ve been avoiding, and will be some additional motivation. The 13 Weeks runs out in February, and I plan to continue for another 13 weeks, with greater concentration on the exercise component.
Congratulations Charlie and keep it up. Another thing that I’ve recently learned about that’s made a difference is the importance of glutathione levels. Whether you like Dr. Oz or not, he does a good job of laying it out here.
http://www.youtube.com/watch?v=Y62MFMymuus&feature=related
Great series, congrats on your progress. Interesting how differently our bodies react to dietary changes. About two years ago I read Primal Blueprint (Sisson) and began lazily cutting down on carbs and sugar, mostly focusing on eliminating wheat and increasing my “good” fat intake. No other significant changes to my modestly active lifestyle, and the weight simply flew off. I went from 180 to 155 in about six months, with commensurate improvements in basic biometric measures. None of these were far out of range to begin with. Two years later the dietary choices have become habit, and the weight has been absolutely stable. Some of the overall health puzzle is clearly good choices and self discipline, but I am thinking now that a lot more has to do with our individual genetic composition which impacts the ability to make different/better choices (diet and exercise), and the general body response to the same.
Advanced glycation end products’ action is more associated with complications of diabetes/metabolic syndrome – rather than being their sole cause. HbA1c can be 47-59% genetically influenced (an ex: individual’s turnover rate of the hemoglobin molecule; if slower has more time circulating to get more glycated).
By going very low-carb (~30 gr.) that makes for an after meal (post-prandial) low levels of glucose, which then influences the way internal fat (lipid, ex: triglycerides) molecules are processed. This is mainly a direct result of the low glucose causing a partitioning of a cell’s lipid molecule goes inside that cell.
Low glucose causes a shunting of lipid (fat) insidea cell to that cell’s endoplasmic reticulum – instead of that same cell’s lipid shifting (or holding steady) into that cell’s general cytoplasm area. Then exposure of some of internal cell’s lipid to the processing capabilities of the endoplasmic reticulum let that cell lipids be cobbled to distinct lipo-protein molecules (ex: ApoB, ApoA), which then physically lets that cell export out some fat (lipid).
Of course cells in different tissue groups make the dynamic a bit more complex. An essential point is that high blood glucose (hyper-glycemia) makes it so hard to mobilize stored fat (lipid) because it keeps so much of a cell’s lipids lingering inside that cell’s cytoplasm & not moving over to that cell’s endoplasmic reticulum for processing into form that can be sent out of that cell.
(This lipid turnover is not to be confused with the actual physical formation of lipid molecules – we naturally must make lipids & even when lose weight are going to make lipid molecules like triglycerides. A high fat diet makes for plenty of lipids forming. It is the rate of lipid turnover that modulates insulin sensitivity..)
Internal fat (lipid) is not just a glob inside a cell, like water in a balloon. The internal cell’s lipid mass takes on the characteristic of a droplet, yet on it’s surface inside a cell the droplet is covered with up to 105 distinct protein molecules.
One enzyme (protein) on a lipid droplet modulates how much lipid (ex: triglyceride) goes out of a cell. This relates to “sex” hormones estrogen (comprising estradiol, it’s inactived form estrone, & estriol) and testosterone (whose inactivated form is andro-stenedione).
This “sex” steroid enzyme, 17beta hydroxysteroid dehydrogenase 2, takes estrogen form estradiol & inactivates it; as well as taking testosterone & inactivating it. When this “sex” steroid processing enzyme on the lipid droplet is less active (due to genetics &/or metabolic influences) that enzyme will be doing less “sex” hormone inactivation. And then the amount of lipid (ex: triglyceride) being sent out from that cell will be higher.
Conversely, when the 17beta hydroxysteroid dehydrogenase 2 on a lipid droplet is over-active there is less amount of lipid turnover (less triglycerides mobilize from that lipid droplet out of that cell). This has nothing to do with the amount of lipid triglycerides being formed. A high fat diet forming up one’s lipids internally is distinct from the amount of lipid turnover & previous comment’s rate of lipid turnover.
Increasing the amount of testosterone blunts the effect of the aforementioned “sex” steroid enzyme – it (active testosterone) lets more lipid be sent out of cell. The ratio of testosterone to 17beta hydroxysteroid dehydrogenase 2 enzyme on an individual lipid droplet inside a cell helps regulate how much lipid can be sent out.
Unfortunately, by raising levels of active estrogen estradiol the above effect on amount of lipid secretion is not altered. More active estrogen, unlike more testosterone, doesn’t help in more lipid secretion – having high levels of the “sex” steroid enzyme on a lipid droplet will still cause less lipid amounts going out of the cell.
By about age 55 men will have a bit more estradiol than a ~ 55 year old women. Of course adipose tissue is also an estrogen stash & rising insulin promotes elevated estrogen. If your genetics/epi-genetics predisposes lots of the described “sex” steroid enzyme to be covering the lipid droplets inside the cells of a specific tissue group then having lots of estrogen (estradiol) will sustain a feedback loop to keep the “sex” steroid inactivating enzyme level up-regulated.
Obesity & Type 2 diabetes show reduced testosterone (both men & women make/use testosterone & estrogen). Over-training (as opposed to exercise) can lower testosterone levels, as does advancing age.
(Look at the testosterone steroid taking fellow’s body fat for an example indicating the amount of lipids they can send out of their cells, despite often eating plenty of food that makes internal lipid molecules. Zinc is well understood to be essential for testosterone formation; unfortunately some drugs/diets impair zinc absorption. Those who take zinc should be aware that > 30 mg Zinc daily can lower the HDL cholesterol levels & also that too much zinc risks too little copper – about 2 mg. copper balances 30 mg. zinc.)
Charlie’s history of irritable bowel implies a bit of “leaking” into the body of non-nutrient molecules from intestine occurs (or had). Possibly the best known rogue leaking in is molecule LPS, which is a certain bacterial lipid membrane component (but not the subject of this comment).
We accept the obese have distinct profiles of symbiotic intestinal bacteria from a standard lean individual. Experiments show taking gut bacteria from obese mammals & replacing it with gut bacteria from the lean resolves obesity. Humans altering their diet composition will, in time, alter their gut bacteria profile.
Gut bacteria are hosts in their own right & carry non-alive entities – akin to how we host viruses. When a gut bacteria cargo of phages, virions & viral like particles break free (lyse) this puts non-nutritive amino acids/peptide/proteins in our gut. These can “leak” into the cells of the intestine & enter our system; some not always becoming benign.
Viral molecular component proteins inside our body, like those lysed from their hosting gut bacteria in our gut , can cause the increase in expression of the above detailed 17beta hydroxysteroid dehydrogenase 2 enzyme on individual lipid droplets. This is sort of a spill over effect because that family of “sex” steroid enzymes (again simplifying greatly) which converts estrogen estadiol into inactive estrone also generate other metabolites, which are part of helping human cells neutralize the scrap viral protein. The relevance here, if confused, is that a factor beyond what one eats can be also cause the up-regulation beyond the ideal amount of an enzyme that unfortunately contributes to a decreased amount of lipid being secreted by a cell.
Roux-en-Y gastric bypass surgery follow ups show it’s obesity cure to be more than just mechanics of less food exposure. The key seems to be bypassing the digestion site where short chain amino acids are absorbed, although investigators have not parsed which short chain amino acids do what. It indicates (to me) there is a lot of influence from different specific forms of amino acids/peptide/proteins on the expression of the numerous protein molecules on the surface of lipid droplets that are integral to how one handles their “fat”.
Edit correction again(sorry, got rushed out door) of my last comment’s end, where deal with Roux-en-& gastric bypass surgery.
Should read “branched” amino acids & not the submitted “short chain” amino acids.
Honestly, I don’t understand how a superlow carb diet is sustainable to most people.
After all, two medium size potatoes would break the 30 gm of carb limit.
So would 3 large onions or 4 large carrots.
As for fruits, they have, by and large, more carbs per ounce than veggies.
I’m not finding it all that difficult, honestly. There are a couple aspects to it. First of all, how often do you actually eat two medium potatoes? That’s a pound of potatoes. Second, you need to look at effective or net carbs. Carrots get about half their carb value from fiber, which is essentially indigestible (although good for you in other ways, he noted in passing). Avocados have very high carb counts, but very low net carbs.
In fact, I just checked, and yesterday I had three meals and a total of only about 10 grams of net carbs.
Avoiding wheat is a little tougher, but luckily I’m not as sensitive to it as a true celiac patient would be — a tiny bit in a sauce doesn’t cause me any noticeable distress. I miss sandwiches and noodles. On the other hand, I’ve had trouble with reflux disease and irritable bowel since I was five years old and cutting out wheat has helped dramatically. That’s pretty good reinforcement.
I just finished my first week low carb and it wasn’t hard to cut out sugar, flour and starchy vegetables. I don’t feel deprived, like on other diets, when I can eat whenever I feel hungry and I can add previously forbidden items like bacon, butter, and sour cream.
Quitting sugar made spinach, broccoli and peppers taste vibrant. I still eat onions the way I always have: a slice at a time. I’m eating much more vegetables than I usually do and I’ve had some delicious meals.
It’s only the first week for me, so I’ll try not to get carried away, but this diet feels like coming home.
Bad news from a recent study in the New England Journal of Medicine. The paper described a trial in which 947 diabetic patients with ischaemic heart disease underwent surgery and 953 underwent angioplasty (there were no untreated controls). At five years, mortality in the angiolasty group was 16.3 percent as against 10.9 percent in the surgical group; in total 26.6 percent of those treated with angioplasty had either died or had had a stroke or heart attack, as against 18.7 percent of the surgical group.
These are disheartening matters for someone like me who has had an angioplasty and suffers from type II diabetes.
Another subject. I have the Taubes’s book “Good Calories, Bad Calories”. I don’t find any mention of the artificial sweetner Splenda in it however. Doesn’t anyone who had read Taubes’s later books know what he says about Splenda? Can I put it in my coffee or tea?
Atkins recommends it in his original diet book. I use it all the time with no apparent weight gain.
Paul, I use the ViSalus Body By Vi protein shakes (http://samanddawn.myvi.net/Resource/DbFile/?f=Vi-Shape_Ingredients.pdf) which are high protein, high fiber, low carb and low sodium. They’re basically sugar free and use the artificial sweetner, sucralose, which is just Splenda. I’ve been doing them since August 1st and I’ve lost over 50 lbs from my original weight of 285 lbs. There is no issue with increased appetite from the sucralose unlike some other sweeteners. I can’t answer what Taubes has to say, but like Atkins I can recommend it and say that I’ve seen no adverse harm on my efforts to lose the weight and get healthier. For more info on the Body By Vi program look here – http://theritterchallenge.com/
As for Charlie, I’m enjoying watching your success. Keep it up.
Charlie, thanks for sticking with this. You are inspiring both my wife and me.
Thank you! And thanks to everyone who has been so complimentary — I hate to go through and thank everyone individually and make half the comments on the thread be me.
Interesting how the cosmic spheres align at times. Channel surfing after the end of most of football and I come upon a half hour show on Discovery called the United States of Bacon. It has a rotund chef making the rounds of barbeque joints nationwide eating various bacon heavy dishes. You look at what he is pushing (and it all looks great) and quickly come to the conclusion that it is very carb friendly (as long as you stay away from sweet sauces, beans and breads) and looks wonderful. Might be a good avenue for additional exploration. Cheers -
Forgot the link: http://bacontoday.com/united-states-of-bacon-2/
Charlie,
Here’s link for 2012 “Early Origins of Adult Health Profile” by Netherland’s Gerthe Kerkhof. Chapter 4 is his team’s otherwise pay walled “Early Origin of the Metabolic Syndrome: Role of Small Birth Size, Early Postnatal Weight Gain and Adult IGF-1″.
Page 65, chapter 4, is a good starting point – pdf cover lots of issues.
The chapter’s gist is: when birth weight is low the modern capability/effort to rapidly boost up weight in 1st 3 months of infant’s life overtakes the infant’s normal growth rate in body length & this alters key developmental paradigms in ways that sets up more risk of person developing metabolic syndrome by age 21.
Free Netherland link to whole book=
http://repub.eur.nl/res/pub/32604/120619_Kerkhof,%20Gerthe%20Femke.pdf#page=1
Oh, now that’s interesting. I was significantly premature. Especially for 1955.
Charlie: I hope you choose to renew this project for another quarter. I’ll certainly read your posts with interest.
I think you’ve been wise to focus first on diet, while moving more slowly into exercise. I’ve been exercising most of my life and I’ve learned to be very careful about listening to the signals that may mean I’m close to injury, and I still go over the line now and then. I don’t know what it would be like to start exercising at 57 without much previous experience.