Pardon the delay in posting and responding to comments. I was on Dauphin Island off the coast of Alabama for a wedding last week. I couldn’t ask The Older Brother to sit in, since it was his Middle Son getting married.
Anyway … in my last post, I commented briefly on a video presentation of a study that, in some people’s minds, nailed the coffin-lid shut on the Carb-Insulin hypothesis. I replied that I don’t believe the hypothesis is dead, but needs some revising. Based on personal experience, lots of reading and listening to podcasts, conversations with other people and so forth, I’ve been slowly revising it my own head for years. So let me reach up there between my ears and pluck out some thoughts, then see if I can work them into a coherent post.
More Carbohydrates => Higher Insulin => Fat Storage
That’s the Carbohydrate-Insulin hypothesis in a nutshell. The more carbohydrates you eat, the more insulin you produce, and the more insulin you produce, the fatter you become. Or to express it in reverse for those trying to lose weight: the fewer carbohydrates you eat, the less insulin you produce, and the less insulin you produce, the leaner you become.
Simple is certainly appealing. But I happen to know the linear equation of more carbs = more body fat isn’t true in my case.
But wait … didn’t you finally lose weight after going low-carb?!
Why, yes, I did. And it was easy. Unlike when I tried low-fat/low-calorie diets based on cereals, pasta, bread and rice, I dropped the pounds fairly quickly and wasn’t hungry. Like a lot of people, I figured if low is good, lower is better. So I stayed on a very-low-carb diet for a long time.
But after reading The Perfect Health Diet, I put real-food starches like potatoes and squashes back into my diet. After listening to Jimmy Moore’s podcast with the guys who designed the Carb Nite protocol, I started enjoying a high-carb Saturday night (but with a Mexican dinner, not donuts). After reading about the gut microbiome, I started eating tiger nuts for the fiber and resistant starch. After reading a book called Natural Hormone Enhancement, I decided to mix things up even more. Some days my diet resembles The Perfect Health Diet. Some days it resembles an Atkins induction diet, all meats and eggs and green vegetables. Some days I skip breakfast. Some days I fast until dinner. Saturday is still the high-carb night.
I average more carbs per day now than I did a few years ago, but haven’t gotten any fatter. So more carbs = more body fat clearly isn’t true for me, at least not as a linear relationship.
Does that mean insulin doesn’t drive fat accumulation? Nope, not at all. I don’t think we’ve seen the final word on the research, but let’s just say I’ll be stunned if turns out insulin has little to do with gaining weight.
Insulin inhibits lipolysis — the breakdown and release of fat from fat cells. Any book on metabolism will tell you so. That’s one of insulin’s many jobs, and it’s a crucial one. When you eat a meal that raises your blood sugar, insulin brings the blood sugar down partly by storing fat and keeping it stored. That way your cells burn the glucose first.
Take a look at this graph from a study by Dr. Jeff Volek. It shows the relationship between the concentration of insulin in our blood and the ability to release fat.
Here’s a quote from text accompanying the graph in the Volek paper:
Adipose tissue lipolysis is exquisitely sensitive to changes in insulin within the physiological range of concentrations. Small to moderate decreases in insulin can increase lipolysis several-fold, the response being virtually immediate. Insulin also stimulates lipogenesis [creating new body fat] by increasing glucose uptake and activating lipogenic and glycolytic enzymes. Small reductions in insulin levels, such as that easily achieved with dietary carbohydrate restriction, remove the normal inhibition on fat breakdown.
I’ve seen several studies in which giving diabetics higher concentrations of insulin made them fatter. In a study of the effects of obesity on rats, the researchers stated matter-of-factly that they made the rats obese by pumping them full of insulin. When they stopped pumping the rats full of insulin, the rats returned to their normal weights. So yes, high insulin levels encourage fat accumulation and inhibit fat breakdown. And yes, your body releases insulin when you eat carbs.
But it’s not the temporary spike in insulin after a meal that makes you fat. That’s when insulin is doing exactly what it’s supposed to do: partitioning nutrients, shuttling glucose into cells, storing fat so glucose is burned first when glucose is high, etc. Later, insulin is supposed to drop and allow fat to flow from the fat cells. Lower insulin also allows glycogen to be converted to glucose. It’s all about keeping glucose within a safe range.
In a lecture I watched online, a biochemist described insulin rising as the building/storing phase and insulin dropping as the burning/using phase. Both phases are necessary for good health. The problem is that for metabolically damaged people, insulin stays high when it ought to be low. They spend too much time in the building/storing phase, and not enough time in the burning/using phase.
During his presentation on hyperinsulinemia on the cruise, Dr. Ted Naiman showed a chart of the insulin responses of normal vs. obese/insulin-resistant people to the same meal. The obese people not only had a much higher initial insulin spike, their insulin levels stayed higher for several hours. Take another look at Dr. Volek’s graph. It doesn’t take much extra insulin to inhibit lipolysis rather dramatically.
But those are metabolically damaged people. (We’ll get to what I believe causes the damage shortly.) For metabolically healthy people, a high-carb meal will certainly raise insulin temporarily — as it should — but that doesn’t necessarily mean insulin will stay high. When I first started hearing from paleo types that tubers have been part of the human diet for eons and are perfectly fine foods, they usually pointed to the Kitavans – native people who live on a high-carb diet (mostly sweet potatoes), but aren’t fat or diabetic.
So I looked up some articles and a study of the Kitavans. Yup, they eat a lot of sweet potatoes and they’re not fat or diabetic. But here’s the interesting part: their average insulin level is 24 pmol/L. If you check Volek’s chart, you’ll see that’s down in the range where fat breakdown occurs. (By contrast, one study puts the average insulin level for American adults at around 60 pmol/L.) So for the Kitavans at least, a high-carb diet of whole unprocessed foods doesn’t lead to high insulin levels throughout the day. In other words, they don’t become insulin resistant. I’m sure we could find plenty of other paleo people who ate natural starches without becoming fat and diabetic. Quite a few Native Americans, for example, grew squashes and beans.
No doubt the potatoes and other starches I eat now temporarily spike my insulin. So why haven’t I gotten any fatter? Well, I don’t have any way of checking my fasting insulin level at home, but I’d wager a large sum it’s no higher now than it was a few years ago, when I rarely ate starch. I’d also wager a large sum that when I was living on low-fat cereals, low-fat pasta, whole-wheat bread with margarine and other vegetarian delights, my fasting insulin was much higher.
So the first revision of the “alternative hypothesis” I carried around in my head looked something like this:
Damaging Diet => Chronically High Insulin (Insulin Resistance) => Fat Storage.
What is or isn’t a damaging diet certainly varies among individuals. Back in this post, I recounted a section from Denise Minger’s excellent book Death By Food Pyramid in which she wrote about the huge variations in how much amylase we produce. People who produce little amylase experience much more dramatic blood-sugar surges when they consume starch than people who produce a lot of amylase. The low-amylase producers are also eight times as likely to become obese.
I doubt that’s a coincidence. Excess glucose damages cells. It makes sense that cells would protect themselves against high-glucose assaults by developing resistance to the insulin that’s trying to shove glucose through the door. So perhaps for some people, it really is as simple as too many carbs => insulin resistance.
But having said that, I doubt many type II diabetics got that way by eating potatoes and fruit. I think it’s much more likely that the carb culprit was processed carbs. It isn’t just that they spike blood sugar (although they certainly do). These “acellular” carbohydrates also produce inflammation – and inflammation is a likely driver of insulin resistance.
Which brings us to a major non-carb culprit: the crap oils that have been displacing natural fats in our diets for decades. We didn’t just start eating more breads and cereals after the Food Pyramid came around. We also started replacing butter and lard with soybean oil, cottonseed oil and other industrial horrors that drive inflammation. If inflammation in turn drives insulin resistance, then the “heart healthy” diets people started adopting in the 1980s were a double whammy: too many processed carbs, combined with industrial oils. Pass the (ahem) “whole wheat” toast with margarine, please, because I’m being good to my heart.
The second revision of the “alternative hypothesis” I carry around in my head took it from this:
Damaging Diet => Chronically High Insulin (Insulin Resistance) => Fat Storage.
Damaging Diet => Hormonal Disruption => Fat Storage.
Yes, insulin resistance is a form of hormonal disruption, and yes, I believe chronically high insulin drives fat accumulation. But other hormonal disruptions can make us fat too. I’ve mentioned seeing a documentary called The Science of Obesity that featured a woman who’d been lean her entire life, then started blowing up. She cut her calories to 1500 per day and still got fatter. Doctor after doctor accused her of lying about her diet.
But finally an endocrinologist ran some tests and found she had a small tumor on her brain. The tumor was preventing her brain from sensing the hormone leptin. Since leptin tells the brain how big our fat stores are, her brain concluded that she had no fat stores and needed to build them up. Fat stores are, after all, a crucial part of our fuel system. So each time she restricted her calories more, her body responded by slowing her metabolism more.
Few obese people have a brain tumor, but once again, a bad diet can lead to leptin resistance. Inflammation may cause leptin resistance directly, and chronically high insulin can block the leptin signal from reaching the brain. So we’re back to the same likely suspects: processed carbs and crap oils.
A baked potato with butter contains neither, which is one reason I now eat the occasional baked potato with butter. I may have surprised a few people on the low-carb cruise by eating the potato that came with my dinner on several nights. Then again, I saw others in our group doing likewise. Like I said, the low-carb movement is becoming more of a real-food movement, at least among the people I know.
But I don’t just eat the potato because I think I can get away with it. I eat the potato because I believe I’m better off with it than without it. Yup, you just heard me say that … er, write that.
Once again, the reason has to do with hormones. Going down to near-zero on the carbs and staying there can cause hormonal disruptions in some people. In the Natural Hormone Enhancement book I mentioned above, author Rob Faigin praised low-carb diets as a way to jump-start weight loss, but cautioned that going very-low-carb permanently can reduce testosterone and raise cortisol in men. He cited several studies to back up the point. Here’s one I just dug up.
He also cited evidence that going permanently low-carb can lead to a slower thyroid. I know Dr. Ron Rosedale insists the change in thyroid hormones is a healthy adaptation, but come on … if you’re trying to lose weight, do you really want a “healthy” slower thyroid?
Faigin’s solution is to mix it up: a VLC diet five days per week to promote weight loss, then high-carb (but not processed carbs) with reduced fat two days per week to prevent hormonal disruptions. The Carb Nite protocol is based on a similar idea. Paul Jaminet’s solution, of course, is to eat some “safe starches” daily while still keeping carbs on the lowish side overall. I can’t say if one solution is better than the other. It probably depends on the individual. Like I said, I mix things up and go with different diets on different days.
Having said all that, I would never encourage type II diabetics to run out and eat potatoes. During a Q & A session on a previous low-carb cruise, Denise Minger put it something like this: a low-carb diet is an effective treatment for type II diabetes, but that doesn’t mean metabolically healthy people have to give up fruit and potatoes to avoid diabetes. In other words, just because someone with a broken leg needs crutches, it doesn’t mean we must all use crutches to avoid breaking our legs. On the other hand, just because people can eat potatoes and fruit without becoming diabetic, it doesn’t mean diabetics should eat potatoes and fruit. In other words, just because walking without crutches won’t break your leg, it doesn’t mean people with broken legs don’t need crutches.
So to wrap up a very long post:
I don’t believe obesity is as simple as the more carbs we eat, the higher the insulin, and the higher the insulin, the more fat accumulation. Losing weight also isn’t as simple as the fewer carbs we eat, the lower the insulin, and the lower the insulin, the leaner we become. Cutting carbs can certainly promote weight loss (as it did for me), but when most of us go low-carb, we not only cut out the acellular processed carbs completely, we also embrace real fats and give up the crap oils. We eat bacon and fry our eggs in real butter. So I suspect the benefits are partly the result of reducing inflammation, which in turn reduces insulin resistance and perhaps leptin resistance.
To keep the benefits coming, it’s not necessary (or even advisable for many people) to stay at near-zero-carb levels permanently. For non-diabetics, I believe it’s better for overall hormonal health to mix it up, adding in some real-food starches, or cycling VLC days with higher-carb days.
To me, the golden nugget of the “alternative hypothesis” is that getting fat isn’t about calories; it’s about hormones. When our government told everyone to eat plenty of grains and cut the arterycloggingsaturatedfat!, following that advice created hormonal disruptions for many, many people. The cure is to 1) eat real, unprocessed food and 2) reduce the carbs to a level appropriate for your metabolism.
If you enjoy my posts, please consider a small donation to the Fat Head Kids GoFundMe campaign.