A Year of 13 Weeks
And what have I learned? It's complicated.
October 19, 2013 - 3:00 pm
Today is 19 October. Yeah, I know, you can see it at the top of the article, but that’s an important date, because it’s now exactly a year since I determined I had to take some actions about my weight and glucose. (I came out about it in my first 13 Weeks post, “A Fat Nerd Does Diet,” on 28 October last year.)
The results overall have been good. I had several different issues when I started.
- I weighed 301.5 on the 19th.
- My A1c was 7.5. Although I struggled with admitting it, that’s real no-kidding diabetes mellitus. For me it appears to be type 2, (T2DM) characterized by lowered sensitivity to insulin. That was on a pretty much maximum dose of metformin, 2500 mg/day; if I were depending on drug treatment alone, I was heading for insulin.
- I had a long-term problem with gastric reflux (GERD) and irritable bowel syndrome (IBS); I was on omeprazole every day and had been since a severe esophageal spasm and put me into the ER with chest pain two years before.
- My total lipids were reasonable on 20mg/day of simvastatin but my high-density lipoproteins (HDL) were low, and my low-density (LDL) were high.
- I also had a long-term problem with depression, although I hadn’t had a really acute episode in some years.
Now, a year later:
- I’m down nearly 40 pounds; my recent low was 264.
- My A1c is been between 5.9 and 6.4. The T2DM appears to be under control. I’m down to 1000 mg/day of metformin, and did a long stretch at 500 mg/day.
- My lipids are enough better that I’m off statins, at least for this 13 week period.
- The IBS no longer troubles me — I can’t say it’s completely resolved because, frankly, how would I know? But I haven’t had a painful episode in certainly almost a year. The GERD is also considerably better, and I’m slowly weaning myself off the omeprazole.
- I think I can say the depression is significantly better. I haven’t had an acute episode this year, but then I hadn’t had a really acute episode in some years. But I had also been chronically dysthymic, which in combination with acute depression is called “double depression.” I really feel like that’s significantly better. I plan to write more about depression in the coming months; there are interesting suggestions that there may be some physiology that connects depression, obesity, and T2DM.
What did I do?
- I’ve adopted a consistently low-carb, high-fat diet. I’ve played around with variants, and right now I’m around 50g carbs a day, with most of the carbs coming from fruits and yoghurt.
- I’ve nearly completely eliminated wheat. Occasionally eating wheat seems to result in immediate exacerbation of the GERD and possibly of the IBS.
- I’ve experimented with high-intensity interval training and high-intensity strength training, although I’ve had trouble making that a consistent practice.
- I recently tried a broad-spectrum probiotic, which seems to have had very good effects.
- I’ve largely structured these changes into a series of 13 week long experiments, which appears to be a sufficiently powerful model that a number of other people have adopted it for their own changes.
What have I learned in this year? It’s complicated.
No, seriously, that’s what I’ve learned — that it’s complicated.
Let’s talk about the weight issue first. I lost about 25 pounds very quickly on the severely carb-restricted diet and then plateaued hard, losing only about another 5 pounds over the next 20 or so weeks.
During the plateau, I started having hypoglycemic episodes. One of those was while I was driving, which was unpleasant. I’ve added some “slow” carbs — that is, low glycemic index — and hadn’t been having the hypoglycemic episodes any longer. That diet didn’t seem to make a whole lot of difference on the weight either, though.
Adding the probiotic seems to have made a significant difference, reducing the remaining GERD and IBS symptoms, reducing my blood sugar, and resulting in losing another 8 or so pounds.
I’ve also had a number of readers who have tried some of these same techniques, or reported their results having done similar changes. Some of them had very good results, some have had good results followed by a plateau, and some haven’t seen any significant changes at all.
I’ve been thinking about these various results, and as I say, I’ve come to the conclusion it’s complicated. Thinking about the physiology, though, I think it is a mistake to ever think it was simple.
Now, cue the people who are undoubtedly going to comment “Of course it’s simple; eat less, exercise more.” They’re right, that is simple. Unfortunately, for a very large population, it also just doesn’t damn work. It turns out that regulation of weight and body fat is complicated, with many different mechanisms involved.
In an appendix to this article, I’ve listed a lot of them — not all of them! — but the list got long and I thought it might be boring to anyone who doesn’t want to geek out about physiology. I’m going to mention some things I actually define in that appendix; if you’re unfamiliar with a term, look down there.
Here’s the point, though — the regulation of body fat and weight has lots of knobs, and changing the “setting” on any of several of those knobs can lead to excessive weight gain. All of them are involved in homeostatic mechanisms that in general have the effect of making it hard to lose weight.
Globally, it’s as if the body has a general idea: “You want to lose weight? What are you, nuts?!” So, although there are regulatory mechanisms that inhibit gaining weight, there are also very stubborn regulatory mechanisms that inhibit losing weight.
The result is what I’ve talked about before: losing weight is hard.
With that many knobs to adjust, though, I think it’s likely that there are actually a bunch of things that can lead to gaining weight; obesity isn’t one pathology, it’s a syndrome brought on by several different pathologies.
- insulin resistance, leading to increased insulin levels and “metabolic syndrome” with fat being stored in white adipose tissue.
- leptin resistance, where (genetically) some people basically don’t feel full as quickly. This may also go with ghrelin sensitivity, which would mean some people feel hungrier.
- differences in thermogenesis and basal metabolic rate regulation.
- differences in the proportion of brown and white adipose tissue.
And, again, I don’t think I’ve listed all of them.
This has one very clear implication, though: no one diet is going to lead to the same weight loss across a large population. For some people, especially people who are only slightly overweight, simple calorie restriction might do the job. For a lot of people, however, simple calorie restriction just isn’t going to be adequate.
People with T2DM or incipient T2DM — metabolic syndrome, syndrome X — seem to have good effects with carbohydrate restriction, possibly because that results in lower insulin levels because blood sugar is also lower. This would lead the body to store less fat.
But you know what? If overproduction of insulin isn’t the root cause, it’s just possible a low-carb diet won’t lead to major weight loss either.
Then there are the other possibilities. If you’re leptin resistant or naturally don’t produce enough leptin, or if you are ghrelin sensitive or produce too much ghrelin, the effect may be that your body just really does want to eat too much. This may well be a genetic component; certainly it’s known that some severe obesity is associated with a specific mutation affecting leptin levels.
There apparently are populations whose bodies are just really really good at down-regulating the basal metabolic rate. In fact, we know at least one such population, the Pima Indians in Arizona.
The conclusion, like all good research, is that more research is needed. But from the pragmatic standpoint, I think the conclusion is that if you try a diet and it doesn’t work over a reasonable length of time, then what you should do is not say “Oh, I can’t lose weight,” or it’s evil twin “I’m just a fat slob who doesn’t have any self control.”
Doctors need to learn this too. It’s complicated, and what they told you 30 years ago in medical school is largely wrong. A syndrome this stubborn is a real problem, not just self-indulgence; physiology this complicated isn’t going to have one and only one regulator.
So try another approach. A different diet. Different exercise. Different eating patterns, like intermittent fasting, or many small meals.
Don’t give up; even if you, like me, don’t lose as much weight as you want in the first stretch, you can do things that significantly improve your heath.
There are a whole lot of different physiological mechanisms that affect weight. Let’s look at some of them.
Basal Metabolic Rate regulation
It’s now well-known that calorie restriction leads the basal metabolic rate — the amount of energy your body uses just to keep going — to regulate down. In other words, independently of what you’re doing, eating fewer calories causes your body to adapt to use fewer calories. In some people, this adaptation can be very significant.
This doesn’t mean that if you cut calories severely for a long time, you won’t lose weight, although that is often presented as a straw man when this is pointed out. Cut down to 500 kcal/day and you’ll lose weight. In fact, you’ll eventually starve to death, and you’ll be pretty damn skinny when you die.
Maintaining that restricted a diet, however, is damn near impossible for most people outside of a concentration camp. What’s more, the down-regulation appears to persist: after an extended period of severe calorie restriction, the basal metabolic rate stays low. What would have been a maintenance level of caloric intake actually causes you to gain weight.
An important aspect of this BMR regulation is thermogenesis, that is the production of heat in the body. Of course we’re familiar with heat production by exercise, but there turn out to be two other mechanisms. In mammals, brown adipose tissue also produces heat, which naturally means expending more calories. White adipose tissue doesn’t do this, and it’s clear that different people have different proportions of brown and white adipose tissue.
Another component of the regulation of thermogenesis, it turns out, is food composition: different foods cause the body to generate more or less heat.
There are several hormones that are associated with appetite regulation: leptin, ghrelin, adiponectin, and resistin are four of them. (There are a lot of other ones.) They are produced by adipose tissue — fat-storing cells — and in the case of ghrelin, by the stomach.
The interaction of these, along with insulin and human growth hormone, is known to be different in obese people. Resistin seems to also be connected with insulin resistance; adiponectin with atherosclerosis and inflammation.
What is known is that in obese people, leptin levels are lower and sensitivity to leptin is reduced; the effect of reducing leptin is to increase appetite.
In other words, regulation of body fat. More body fat leads to higher leptin levels, which is part of how the body regulates body weight — as you add body fat, it reduces appetite.
Higher insulin levels lead adipose tissue to store more fats. Somatotropin — human growth hormone — stimulates the release of fats and increases their metabolism.
Glucose (blood sugar) regulation
The major hormone regulating blood sugar is insulin, which has a whole raft of different effects:
- it leads muscle tissue to absorb glucose for energy.
- it leads adipose tissue to convert glucose to triglycerides and store them as fat.
- it leads the liver to store glucose in the form of glycogen, and inhibits the liver from releasing glucose (gluconeogenesis).
- it enhances learning and memory.
- it increases stomach acidity.
There are several different disorders of insulin regulation. Of course, there’s type 1 diabetes, in which the pancreas just stops producing insulin. This is characterized by weight loss and extreme thirst and urination; the body can’t store glucose as fats, and then has to try to get rid of the excess glucose through the kidneys.
A second disorder is type 2 diabetes, where the body becomes insensitive to insulin, so more insulin is produced. This one leads to weight gain, as the adipose tissue responds to high insulin levels by doing their job — storing glucose as fat.
A not very well known third type is called latent autoimmune diabetes, sometimes called “diabetes type 1.5.” For unclear reasons, some people basically have the same syndrome as type 1, where the cells that produce insulin disappear, but this happens slowly and progressively, instead of acutely. This causes chronic mild high blood sugar, with a whole bunch of bad effects, but often goes misdiagnosed as type 2.