Archive for 'carbgrrl'

Baseline health and Paleo 2.0

With Gary Taubes blogging and the extended low-carb/paleo community hopping, I feel less of that ol’ carbgrrl blogging pull, but I follow all the goings-on with keen interest.

One recent post over on Hyperlipid analyzes fasting insulin and — get this — accidental weight loss among the obese. Here are some excerpts that may be mind-blowing to the nutritionally uninitiated:

[O]ut of only five subjects, one obese person became a food refusenick. Various studies have had similar compliance problems, with obese participants refusing food. … What is more interesting is the trend in accidental weight loss.

My take home message is that the lower the carbohydrate intake (and it is reasonable to assume the lower the fasting insulin) the harder it is to consume enough calories to maintain the obese state. It’s possible, but not easy.

I think this decrease in hunger probably only occurs in obesity. For those of us who have adopted a LC [low-carb] eating pattern without the need for weight loss (and still have little excess fat) there are clearly other factors coming in to play, as there will be when a previously overweight person approaches target/ideal weight, what ever that might be.

The experience is actually quite familiar to those of us who have managed to lose serious weight by controlling our carb intake and thus our insulin production. Once you’re able to burn your own body fat for fuel, the uncomfortable hunger pangs of a lifetime of diets fade into memory. It’s remarkable.

What’s being suggested above is that this is a normalization process, back to some baseline of health and body weight. You know how the diet industry insists that you shouldn’t think of them as diets but rather lifestyle changes? It’s the right idea, but — if you’re doing low-fat and “chronic cardio” — the wrong lifestyle.

Gary Taubes relays Bob Kaplan‘s downright poetic way of thinking about this in a recent post:

A restricted-carbohydrate diet doesn’t make you lose weight; it corrects your weight.

A restricted-carbohydrate diet doesn’t make you lose water weight; it corrects your water weight.

A restricted-carbohydrate diet doesn’t improve serum lipids; it corrects serum lipids.

A restricted-carbohydrate diet doesn’t improve health; it corrects unhealthiness.

I think we’re entering into a kind of Paleo 2.0 phase, where many of us are discovering that our “target/ideal” limits are something short of our personal wishlist due to accumulated damage over time. I’ve been trying for several years now to “get the last 20 pounds off” without success, and I’m not alone. (I do feel that I’m asymptotically approaching better health, and I’m strongly motivated by the idea of delaying the effects of aging by avoiding AGEs!) The good news is that the evidence is also starting to accumulate, and people are cottoning on to it earlier in life. Oh, to be able to do things all over again…

Seeking escape velocity from nutritional Bizarro World

The new book from (The Great) Gary Taubes is finally out: Why We Get Fat: And What to Do About It.

Taubes is obviously a man on a mission, nearly bursting with frustration at the anti-scientific and near-religious wishful thinking that has been passing for diet, nutrition, and public health advice for the last few decades. Near-religious? Yes — really. Why else would we be told this by “experts” for so long, even though their theories can readily be falsified?

If we’re fat and we can prove that we eat in moderation — we don’t eat any more, say, than do our lean friends or siblings — the experts will confidently assume that we must be physically inactive. If we’re carrying excess fat but obviously get plenty of exercise, then the experts will assume with equal confidence that we eat too much. If we’re not gluttons, then we must be guilty of sloth. If we’re not slothful, then gluttony is our sin. [WWGF, p. 29]

But Taubes keeps his vexation in check, using his energy instead to boil down the evidence in his magnum opus Good Calories, Bad Calories to its essence for easier reading. (You may recall that I once called GCBC “a 50/50 split between ‘gripping’ and ‘a hard slog'”.)

Most of all, he uses plain logic and helpful metaphors, along with tinctures of hard science and hard data, to show how diet experts’ arguments and advice — like “Just eat less and exercise more” and “Low-carb is dangerous because our brains need glucose to function” — amount to little more than “Who are you gonna believe, me or your lying eyes?” The logic and the data are useful for applying appropriate skepticism when you face the latest scientific paper that goes awry in its very first sentence by asserting that access to “unlimited calories” and an “increasing sedentary lifestyle” are the problem. Here’s something useful to know (and not all that surprising to learn): we’re exercising harder than ever.

…[I]n the United States … the obesity epidemic has coincided with what we might call an epidemic of leisure-time physical activity, of health clubs and innovative means of expending energy (in-line skating, mountain biking, step and elliptical machines, spinning and aerobics, Brazilian martial-arts classes — the list goes on), virtually all of which we were invented or radically redesigned since the obesity epidemic began.

There are many ways to quantify this epidemic of physical activity. Health-club industry revenues, for example, increased from an estimated $200 million in 1972 to $16 billion in 2005 — a seventeen-fold increase when adjusted for inflation. The first year that the Boston Marathon had more than 300 entrants was 1964; in 2009, more than 26,000 men and women ran. [WWGF, p. 42]

I suppose I’m no longer truly in the target audience for this book, since I can already recite many of the arguments in my sleep. And logic may have very little power over those with a vested interest in believing the opposite. But if you’ve struggled with weight (or — neologism alert — “diabesity”) and have been following along here but haven’t yet read GCBC, I recommend WWGF to you, either as a standalone work or as a gateway drug to the hard stuff.

Paleo-empiricism, or: carbgrrl alunda ool

A chance encounter in a blog comment thread a few months back led to my discovering an incredibly rich vein of metabolism/nutrition research, commentary, and community known as “Paleo”. Since then, I’ve spent a lot more time reading, and pondering, and trying-out, than writing (sorry it’s been so quiet around here).

What is paleo (or the paleo diet, or the primal diet, or the evolutionary metabolic milieu, or…)? Below I’ll provide links to what have become favorite sources, but here’s my description: It’s a way of eating and living that takes advantage of our best knowledge of how humans evolved to eat and live in order to optimize our health and longevity today. It tries to provide the “why” to the “what” of metabolism science that I’ve been exploring here for a little over a year. And to a first approximation, it’s not all that different from my take-aways from the Atkins book I read in 2004.

It’s all been very exciting, for a variety of reasons.

First, it seems that many folks writing on this subject came to it the same way I did, through reading (The Great) Gary Taubes’s Good Calories, Bad Calories. There’s what you could call a “paleo movement history” that stretches back decades in some cases, but there’s a modern movement that’s suddenly become extremely active and prolific, in large part due to the publication of GCBC and the controversy it stirred. Thanks, TGGT!

Second, there is an admirable tone of rationalism and empiricism that pervades the discussions — on the intertubes, no less. What really works, and why? How can we test outcomes, not just make guesses? There are even real cardiologists and other medical professionals blogging on this stuff, bucking the conventional-wisdom trends of their profession and making a real difference in people’s lives. The blogospheric disagreements can get pretty “hot”, but facts and research are still king. Offering scientific backing to smart skeptical readers has been an essential part of why I write about this stuff, and it’s wild (and not a little intimidating) to find so many more sources.

Third, I had gotten stuck in my efforts to control my weight with a classic Atkins-style low-carb approach, and so I knew I didn’t have the whole picture but wasn’t sure what else to try. I found several answers (and a metric ton of finger-lickin’ recipes) among the paleo sources, with relief, and they confirmed some sneaking suspicions I was beginning to form.

I’ll expand on the above themes over time. But for now, here’s a quick tour through the top paleo-and-related sources that have come to rest in my feed reader (not meaning any disrespect to the many other great sites!):

  • Free the Animal by Richard Nikoley: This site is how it all started to snowball for me. Richard is relentlessly honest with himself and his readers, has a wicked tongue at times, and produces “food porn” like you’ve never seen.

  • Fat Head by Tom Naughton: At Mark Wilcox‘s urging, I finally saw the movie, and then found the blog. Great stuff, served with great humor (Tom’s a professional, people — don’t try this at home).

  • PaleoHacks by Patrik: Crowdsourced paleo knowledge and ideas!

  • PāNu by Kurt G. Harris MD: He’s the guy who calls it the “evolutionary metabolic milieu”, or EM2 for short. (Handy paleo acronym finder here.) Hey, and he does Venn diagrams too; what’s not to like?

  • The Healthy Skeptic by Chris Kresser: Thanks to this guy, I actually kicked my 18-month Prilosec OTC habit. Awesome.

  • Primal Wisdom by nutritionist Don Matesz: I got my first exposure to serious hunter-gatherer society research here.

Read, cook, move, and enjoy…

Oh yeah. What’s with the babbling in the post title (again)? Having seen the movie Caveman way back when, some friends and I picked up on its made-up vocabulary and use it to this day. “Alunda” means love, “haraka” means fire, “ool” means food…)

Low-hanging fructose

Simon Phipps often feeds me tidbits — intellectual rather than gustatory — having to do with nutrition. Recently he recommended I watch a lecture by Dr. Robert Lustig of UCSF in August of last year, called Sugar: The Bitter Truth.

This lecture is really better described as a call to action with biochemistry diagrams. Lustig argues that fructose is an evil that’s been behind the rise in obesity and metabolic syndrome of the last few decades; that soda, juice, and sports drinks loaded with sucrose or HFCS are the single biggest factor in childhood obesity (his specialty); and that we had better start treating fructose as the chronic hepatotoxin it is and stay the heck away from it. I agree.

The lecture series is called Current Controversies in Nutrition: Letting Science Be the Guide. Well, yeah — what other guide have they been using all this time, for goodness’ sake? You know, I started my series admitting a worry about looking like a loon…no more. Richard Nikoley, primal blogger extraordinaire, often talks about Modern Ignorance and the ways in which supposed experts tie themselves in knots because of broken preconceptions about stuff we used to understand instinctively. (Richard blogged this lecture, and also another I’ll touch on here sometime soon…) It sure looks like Lustig is emerging from a cave of institutional ignorance, blinking — and pissed off. Good.

Lustig’s obsession with fructose probably doesn’t give an accurate picture of all the factors in play. He seems to think glucose is just fine to consume in whatever quantity — it’s the “energy of life”, he says (around 1:26:00) — and so I suspect he’s misguided about the evils of spiking one’s insulin over and over, in addition to spiking one’s triglycerides. Remember that the glucose that feeds our brains and bodies can be made from practically any old thing lying around, as I’ve discussed before. And in GCBC, (The Great) Gary Taubes discusses the pernicious effects of eating fructose and glucose in combination:

Because sucrose and high-fructose corn syrup (HFCS-55) are both effectively half glucose and half fructose, they offer the worst of both sugars. The fructose will stimulate the liver to produce triglycerides, while the glucose will stimulate insulin secretion. And the glucose-induced insulin response in turn will prompt the liver to secrete even more triglycerides than it would from the fructose alone, while the insulin will also elevate blood pressure apart from the effect of fructose. [GCBC, Ch. 12, p. 201]

I have a couple of other quibbles (I’m not sure Lustig’s lust for fiber is entirely warranted), but it’s absolutely worth watching if you care about this stuff.

Occam’s lunchbox

(This is part 2 of “The science of feeling peckish”, promised way back in April. Thanks for the encouragement/prodding in the original comments thread about finishing the series.)

I hope you’ll stick with me for this rather technically dense post. As always, I will gladly accept all error corrections and pointers to research that disputes or usefully refines the information below.

Regurgitating (sorry) Part 1

As we join our story already in progress, we recall that the 1976 article “The Physiological Psychology of Hunger: A Physiological Perspective” made the following points in reviewing energy metabolism:

  • The various parts of the body are largely source-agnostic when it comes to getting energy from the diet: carbs, fat, and protein are broken down into their constituent parts and used all over the place. (A couple of small exceptions become important later on.)

  • The brain is always fed first and steadily; you’d pretty much have to be on a desert island surrounded by a fishless sea for many days before making a dent in your brain’s energy supply. And in fact, all your tissues get an adequate supply pretty much all the time, despite the fact that you don’t graze constantly.

A few cautions before we proceed: First, we’re talking physiological hunger here, not emotional bingeing, or missing lunch because you’ve got a deadline. Second, the research used to support the discussion in the article is mostly about laboratory rats. There are precise parallels when it comes to energy metabolism among the higher mammals, however, so don’t be offended if I use the word “you” below…

Hunger Hypotheses on the (Dinner) Table

The Friedman-Stricker article addresses two popular hypotheses for explaining what triggers hunger. They both posit a special role for the central nervous system:

  • The glucostatic hypothesis: The brain responds to blood-borne signals about your level of blood sugar, making you eat when it dips (mmm, dip) and lay off the food when it’s sufficiently high.

  • The lipostatic hypothesis: The brain responds, instead, to signals about your level of body fat. You could think of this as a “fat set point”.

Ultimately the authors present an alternative view, which I’ll get to in due time.

“Brain and Brain. What is Brain?”*

Much of the research examined in the article involves making lesions in the brains of rats, specifically damaging either the ventromedial hypothalamus (VMH) or the lateral hypothalamus (LH), and seeing what happens to weight, hunger, and feeding in various conditions (like shaving their fur off to make them cold, or even administering the dreaded “tail pinch”). A moment of silence, please, for these poor rats.

ernestfigueras / CC BY-SA 2.0

In general, it’s known that VMH lesions stimulate hunger and lead to weight gain, and LH lesions do the reverse. This is called the “dual hypothalamic model” (and initially led to speculations that the VMH is the “satiety center” and the LH the “hunger center” of the brain, but things got a little more sophisticated in the next iteration). Here’s how the two hypotheses predict these effects.

  • Glucostatic: There are “glucoreceptors” located in the VMH, and they detect when blood sugar is low or when available blood sugar isn’t getting properly used.

  • Lipostatic: Damaging the VMH either messes with a brain “hunger center”, taking off its controls and making you way hungrier than normal, or it turns up the dial on your “fat set point” so that you feel compelled to meet the higher requirement.

A Taste of the Arguments Against

The gross effects of messing with rat brains do seem generally supportive of one of these choices. But dig a little deeper (no, not murine-cerebrally) and the evidence doesn’t look as great. The article goes into a lot of technical depth; here is my best attempt at a summary of the “con” positions.


The idea that there are glucoreceptors in the VMH was already weakening at the time the article was written. For starters, originally it was noticed that small dips in blood sugar are indeed associated with hunger, so this formed the core of the hypothesis. But since diabetes involves both higher blood sugar and greater hunger, the hypothesis had to be refined to say that the brain is suffering from less-efficient use of the blood sugar you’ve got. However, it turns out this refinement doesn’t help; more on this below.

In addition, feeding behavior in the presence of lesions, lab conditions such as excess cold, and treatment with substances like insulin tends to float in surprising directions.

Finally, as Taubes adds in GCBC, this hypothesis doesn’t explain things like weight gain back to normal levels after an illness.


It’s a funny thing: Rats with VMH lesions add body fat even before they begin eating, even if they’re prevented from eating for many hours. So if the rats’ brains are telling them to eat, the eating doesn’t seem to be the first effect in line. And it’s known that the lesion immediately causes higher levels of circulating insulin (geez, why didn’t they say so before?), with effects similar to seasonal obesity in animals who migrate or hibernate (and, hmm, similar to other effects I’ve discussed in the past).

And in any case, positing a lipostat in the brain simply doesn’t get you very far. In particular, Taubes notes, it doesn’t explain why the very obese have an elevated set point. It’s all a bit circular:

Saying that we’re all endowed with a lipostat that monitors our adiposity and then regulates hunger appropriately is just another way of saying that our weight remains remarkably stable, whether we’re lean or obese, and then assigning the cause to a mysterious mechanism in the brain whose function is to achieve this stability. [GCBC p. 428]

Sugar Sugar, Ah, Honey Honey

It’s worth looking more closely at the diabetes problem for the glucostatic hypothesis. It reveals a metabolic story that goes way beyond a simple blood sugar level.

Diabetes kind of looks like starvation. The body madly breaks down fat into ketone bodies (ketogenesis) for use in the periphery of the body, since those parts need insulin to make use of the glucose and there isn’t any to be had. But the body also madly makes new glucose (gluconeogenesis). The brain must think it’s in heaven since it actually gets plenty of that fine, fine stuff, but the rest of the body is out of luck — unless it can get more of the stuff it can actually use:

[T]he fat content of the usual laboratory diet can be viewed as “diluted” with carbohydrate, material of little metabolic significance during diabetes. The hyperphagia [extra feeding] of diabetic animals thus resembles the increased feeding that occurs in intact rats when food is diluted with nonnutritive bulk and may result because the decrease in utilizable metabolic fuels in the diet reduces the diet’s capacity to satiate the animal. …. [D]iabetic animals maintained on a high-fat diet do not display hyperphagia despite continued impairments in glucose utilization. [TPPH:APP p. 418; citations elided; bold added]

So even the more modern version of the glucostatic hypothesis of hunger seems off.

The Mind-Body Connection

But wait, there’s more to the “con” position. The very assumption that the hunger trigger originates in the brain is suspect. All this nasty work to produce weight gain etc. in lab animals is highly unusual; as already noted, the brain lives in an energy bubble and never wants for anything whether you’re feeling peckish or not.

There’s another candidate — an organ on the periphery of the body that (a) already orchestrates fat-burning and other energy processes in our bodies and (b) is unique among its surrounding organs in that it can’t process ketone bodies but can handle fructose:

[I]t is not likely that pronounced decreases in cerebral glycolysis [energy usage in the brain] ever occur except under nonphysiological experimental conditions [rat abuse], because the brain is normally protected from such emergencies. …. Our recent findings that insulin-induced feeding is abolished by infusions of fructose, but not ketone bodies, strongly implicate the liver as the origin of the hunger signal. [TPPH:APP p. 422; citations elided]

Yep, if you inject ketone bodies directly into an insulin-treated rat’s bloodstream, the rat still wants to raid the fridge — and it appears to be because its little liver is still starving.

The Friedman-Stricker article discusses a particular event in the liver that could trigger the hunger signal: a shift away from “oxidative metabolism” (the Krebs cycle for making energy out of anything) to direct production of glucose and ketone bodies (gluconeogenesis and ketogenesis — remember these from “diabetes is like starvation” above?). This seems to be the initial sign that your body is starting to “run on fumes” and needs to fill the tank again.

(The authors have continued to push the ball forward; here’s one sample of recent research to determine how the liver signals the brain that eating would be a good idea right about now.)

Occam’s Razor

So after trying really really hard, scientists couldn’t quite put their finger on an actual brain center that controls levels of fat or blood sugar. And brains don’t ever want for anything, but sometimes livers do. And the totality of the energy metabolism story, not just one substance or another, is on display when each hypothesis is examined.

The simplest explanation for hunger and weight-balancing would be a homeostatic system, like so many others in the body. Taubes notes, “Life is dependent on homeostatic systems that exhibit the same relative constancy as body weight, and none of them require a set point, like the temperature setting on a thermostat, to do so.” [GCBC pp. 428]

And indeed, Friedman and Stricker show that the caloric homeostasis hypothesis fits the facts much more closely than do the others: Hunger returns when the total utilizable fuel level in your body, rather than a store of a particular kind of energy, drops below some critical level. After all, brains and bodies generally don’t distinguish between energy sources. And more insulin stimulates more frequent meals, while less insulin allows body fat to be mobilized, which appears to stave off hunger.

(If you’re a regular reader, you might think this is a blinding flash of the obvious. Please tell the diet industry.)

Taking pity if you’ve gotten this far, I’ll spare you the dry conclusion from the Friedman-Stricker article and let Taubes bring it home:

This hypothesis of eating behavior did away with set points and lipostats and relied instead on the physiological notion of hunger as a response to the availability of internal fuels and to the hormonal mechanisms of fuel partitioning. Hunger and satiety are manifestations of metabolic needs and physiological conditions at the cellular level, and so they’re driven by the body, no matter how much we like to think it’s our brains that are in control. [GCBC pp. 432-3]

Luckily, we can use our brains to understand this mechanism better — and turn it to our advantage.

A real horrorshow

It’s frustrating to see “news” stories about diet and metabolism that get something right, sort of, but for really harmful reasons.

Yes, popcorn is deliciously seductive. Yes, it’s bad for you to eat a medium-sized popcorn/soda combo (“Movie Popcorn Has Shocking Calories, Fat”). But there’s no actual evidence to suggest that the “12 pats of butter” in it is the reason.

From (The Great) Gary Taubes’s GCBC:

In the mid-1970s …, [Ethan] Sims and [Elliot] Danforth [of the University of Vermont] believed that obesity was most likely caused by chronically elevated levels of insulin, and that the elevated levels of insulin were likely the product of carbohydrate-rich diets. In the 1980s, their opinions changed and fell into step with the prevailing consensus on the evils of dietary fat. ….

One potentially relevant observation that Sims and his colleagues neglected to publish, for example, was that it seemed impossible to fatten up their subjects on high-fat, high-protein diets, in which the food to be eaten in excess was meat. …. [T]he volunteers would sit staring at “plates of pork chops a mile high,” and they would refuse to eat enough of this meat to constitute the excess thousand calories a day that the Vermont investigators were asking of them. ….

Those fattening upon both carbohydrates and fat, on the other hand, easily added two thousand calories a day to their typical diet. Indeed, subjects in some of his studies … [took] as much as ten thousand calories a day. [GCBC pp. 310-1; bold added]

Well. Doesn’t that put a different spin on things?

We could practically make popcorn-eating a medical test. If it makes you hungrier rather than full, you’re courting trouble. And if you promise you won’t touch the stuff but you end up eating three-quarters of the bag your husband bought for himself (ahem), you’re in serious scrawny-pancreas territory.

Exercise: it’s torture, I tell you


Sometimes you have wonder about “conventional wisdom” (and what makes it different from “actual wisdom”). Until about 40 or so years ago, it was conventional wisdom that you shouldn’t exercise to lose fat because exercise tended to make you more hungry. Then the CW changed to “you must become a hamster on a wheel” — without any evidence to back it up. Now it appears that we may be undergoing a much-needed correction.

I only recently discovered (h/t Pat) a great New York Magazine article from 2007 recounting the state of science in this area, called The Scientist and the Stairmaster. Naturally, it’s by Gary Taubes. (I think I’m going to start calling him The Great Gary Taubes, or TGGT for short, much as I’ve shortened GCBC.) Here’s a snippet, but as always, it’s worth reading the whole thing:

Just last month, the American Heart Association and the American College of Sports Medicine … suggested that 30 minutes of moderate physical activity five days a week is necessary to “promote and maintain health.” What they didn’t say, though, was that more physical activity will lead us to lose weight. Indeed, the best they could say about the relationship between fat and exercise was this: “It is reasonable to assume that persons with relatively high daily energy expenditures would be less likely to gain weight over time, compared with those who have low energy expenditures. So far, data to support this hypothesis are not particularly compelling.” In other words, despite half a century of efforts to prove otherwise, scientists still can’t say that exercise will help keep off the pounds.

And now I notice that Time jumped on the new-CW bandwagon last month with Why Exercise Won’t Make You Thin.

Do I exercise? Well, yeah, but I have to fight the hunger it brings on. I lift weights and such to increase muscle mass, stave off loss of bone density (two decades ago I would have said “build bone density”, sigh), increase my VO2 max, and just generally feel more vital. But I’ve given up on endless medium-intensity cardio to lose weight — because insanity is doing the same thing over and over again and expecting different results.

Speaking of doing the same thing over and over again, what do you suppose that grainy photo at the top represents? In 2006, as part of the XML Summer School events (this year’s School is coming up fast! sign up now!), I had the privilege of going on a special tour of the Oxford Castle, which had recently opened to visitors. It was put to use as a prison for many centuries, and it was nasty in there. The “terrible prison conditions” they talk about on the website included this primitive Stairmaster, with which they’d punish prisoners by making them climb for eight hours a day.

I can take a hint.

Chocolate Frosted Sugar Bombs

“But what do you eat for breakfast?”

That’s the first question everyone asks when we get to talking about low-carb eating. Admittedly, it took me a while to figure out what to do. The obvious answer, eggs, can take time if you don’t plan ahead. So here’s what I really do eat for breakfast, in case you want to try the low-carb way and you’re looking for ideas.

Breakfasts That Only Seem Carby

(Hey, if Tim can toast-blog, why can’t I?)

Almost every morning I have Oroweat Whole Wheat Light bread, toasted, with plenty of good-quality butter and sometimes a bit of low-carb jam (any flavor of Hero Sugar Free Preserves is my favorite). When traveling to destinations with toasters I usually bring some Oroweat along.

The Pacific Northwest bakery Franz also has a Net 4 line that’s low-carb. Good, if a bit sour-tasting, and tends to go off faster for some reason.

Favorite bread: Carb Krunchers Rye, bought online and kept in the freezer. It actually says “rye” with quotes on the package; it’s not real, but its caraway seeds have a magical ability to transport me into rye-land.

Next bread I’m going to try: Julian Bakery’s Smart Carb #1.

I owe Joe Andrieu big-time for introducing me to a granola product called Flax-Z-Snax. Follow this link to get it straight from the source and save money. This stuff tastes so good you’ll be tempted to overdo it. It’s good plain or with a splash of half-and-half or Calorie Countdown milk, but amazing with Dannon Light ‘n’ Fit low-carb vanilla yogurt. I’m always worried these latter two products will be discontinued; you have to hunt for the supermarkets that carry them. I’ve also tried and liked Dixie Carb Counters granola (and appreciate that it’s a lot harder to overconsume).

Breakfasts That Don’t Look Carby in the Least

Favorite: There’s an Original Pancake House within walking distance of my house. Why make eggs when you can get someone else to cook them? Their huge fluffy five-egg omelettes are awesome, especially stuffed with cheese, onion, and bacon. (Great for lunch too.) I can only ever eat about half, and take the rest home.

Weekends: Eli makes a mean cheesy scramble (scrambled eggs with cheese, onion powder, and half-and-half). By the way, real cream is much yummier in morning coffee than milk is. I prefer a scant tablespoon, or what my sister refers to as “a molecule”.

Making ahead: Speaking of my sis, she worked up this recipe for no-crust mini-quiche muffins


Preheat oven to 350°F.
Quantities only seem important with the eggs and cream; otherwise load it up and have fun!

  • Red onions chopped
  • Red peppers chopped
  • Scallions chopped
  • Diced ham
  • 2 cups shredded cheddar cheese
  • 6 eggs
  • 3/4 cup half-and-half or heavy cream [the latter is less watery]
  • Salt
  • Pepper
  • Pinch of garlic powder
  • 7 or 8 shakes of hot sauce

Sauté onions and peppers till soft.
Mix all ingredients.
Spray muffin tin with cooking spray.
[I load the lumpy ingredients before pouring the egg mixture on top.]
Bake for 40 minutes or until golden brown.
Eat and enjoy!

Hybrid Breakfasts

Eli may specialize in cheesy scrambles, but I specialize in the Sunday morning egg sandwich. Two eggs fried over medium, some good cheddar, pre-toasted and buttered low-carb bread, the whole thing assembled and grilled — and served with low-carb strawberry jam. It’s got to be strawberry; this is tradition. (Forgive its tar-like appearance in the picture.)


Breakfast in the Before-Time

The one supermarket aisle I still swoon over is the one with all the breakfast cereal. I had a bowl of cereal (or two, once the insulin resistance kicked in) nearly every day of my life until 2004. I had Kellogg’s Sugar Frosted Flakes — yes, they still proudly had “Sugar” in the name back then — right through high school. In college it was Grape-Nuts with honey, sometimes microwaved. Later, I got sophisticated (what with the Bread & Circus stores all around) and went the granola-with-yogurt route.

The most counterintuitive part about starting a low-carb routine is staring at a plate of eggs and bacon and wondering: Can this be right? Review the facts, and you’ll conclude it’s the rare cereal that’s “part of a balanced breakfast”.

Fat Head

My low-carb pal Mark Wilcox pointed me to this movie. I haven’t seen it yet, but it somehow (ahem) reminds me of the politico-nutritional mess we’re in. Two headlines I saw today, right next to each other:

  • USA Today: Obesity is a key link to soaring health tab
  • San Diego Union-Tribune: Senators inch toward deal on health care

Sorry, but I just don’t trust senators to get it right on health and nutrition. What if senators had something to do with the problem in the first place?

In GCBC, Gary Taubes relates the controversy around Dietary Goals for the United States, produced by the staff of George McGovern’s U.S. Senate Select Committee on Nutrition and Human Needs in 1977. This document is pretty much the well from which all U.S. public-health “fat bad, carbs good” nonsense springs.

Taubes quotes the Senate testimony of Philip Handler, president of the National Academy of Sciences and a metabolism expert in his own right, representing the NAS Food and Nutrition Board:

However tenuous that linkage [of dietary fat and cholesterol, blood cholesterol, and heart disease], however disappointing the various intervention trials, it still seems prudent to propose to the American public that we not only maintain reasonable weights for our height, body structure and age, but also reduce our dietary fat intakes significantly, and keep cholesterol intake to a minimum. And, conceivably, you might conclude that it is proper for the federal government to so recommend.

On the other hand, you may instead argue: What right has the federal government to propose that the American people conduct a vast nutritional experiment, with themselves as subjects, on the strength of so very little evidence that it will do them any good?

Mr. Chairman, resolution of this dilemma turns on a value judgment. The dilemma so posed is not a scientific question; it is a question of ethics, morals, politics. Those who argue either position strongly are expressing their values; they are not making scientific judgments.

(For your reading convenience, I’ve helpfully emboldened the ethical/moral/political choice I’d make.)

I know I’m always saying this, but: Read the whole thing. And if you’re suspicious about which scientists worked for the Egg Board, just wait till you see where the Frito-Lay funding went.

Like sands through the hourglass

…so are the Carbs of Our Lives. (No? How about As the Pancreas Turns? Maybe not.)

Today’s carbgrrl musings are a little less overtly scientific than at times in the past, and a little more speculative and personal. You see, a friend loaned me a diet book that wasn’t actually 100-percent horrible, and it offered an insight that resonated with me in a big way.

The book was Michel Montignac’s Eat & Lose Weight For Good: The Montignac Weight-Loss Plan, in a UK edition. (This is probably the US equivalent.) My friend and I had discovered a mutual appreciation of GCBC, and she thought I’d like this book too.

Montignac has a wonderfully blunt style, and he seems to enjoy shocking his audience. Very French! He’s written quite a few books, focusing on what I’d call a hybrid low-glycemic/”French girls don’t get fat” approach. This book has a couple of scientific boo-boos, for example extolling the virtues of fructose (?!?). But he has a good handle on the sheer variability of people’s responses to carbs. (Atkins had the same, with his emphasis on finding your personal Critical Carbohydrate Level for Losing.)

This passage reached out and grabbed me:

Some people have been able to remain slim all their life, although they have bad eating habits. This is because they were blessed with a very healthy pancreas that has not lapsed into hyperinsulinism, despite the heavy glycaemia inflicted on it over a long period of time.

Others — and these are the majority — also started off with a healthy pancreas that enabled them to stay slim for many years despite their bad eating habits. And then, when they were about 30 or 35, and certainly by the time were 40, they started to put on weight. In later years, some even became obese and diabetic. Their pancreas held out for several decades, but in the end it succumbed to the abuse it had suffered.

And then there are those, like me, who arrived on earth with a sub-standard pancreas that was inherited. The chances of having a frail pancreas, if your parents were obese and therefore hyperinsulinic, is high. It is almost certain in any case, if the diet from an early age is hyperglycaemic. [p. 47]

I suspect he’s just described my pancreas: feeble, rickety, frail, sub-standard. Some of my friends (probably with brawny he-man pancreata) seem incredulous at the crazy lengths I go to even to avoid gaining weight at this point, having to cut out just about any slightly scary carb and some nominally okay ones (mmm, oatmeal). It’s like I’ve used up my lifetime allotment of normal insulin response.

Notice that Montignac suggests two factors to consider: heredity and environment. (With risk factors on both sides of my family, and with a history of dieting in the idiotic 70’s and 80’s, I bet I’ve got both.) One or both might explain one of the outcomes of an exercise in occupational medicine, done at DuPont in the late 1940’s to help executives lose weight and avoid the new epidemic of heart disease in America. Taubes recounts the tale:

In June 1949, [Alfred] Pennington published an account of the DuPont experience… All of this seemed paradoxical: the DuPont executives lost weight on a diet that did not restrict calories. Carbohydrates were restricted in their diet — no more than eighty calories at each meal. “In a few cases,” Pennington reported, “even this much carbohydrate prevented weight loss, though an ad-libitum [unrestricted] intake of protein and fat, more exclusively, was successful.” …. If [one executive] ate any carbohydrates, “even an apple,” Pennington wrote, his weight would climb upward. [GCBC p. 330, Ch. 20; bold added]

Heredity and environment are the filters through which I now view all women’s magazine articles, studies, and public-health pronouncements about obesity, diabetes, heart disease, and metabolic syndrome. Maybe low-fat does work — for the young, or the pancreatically strong. Maybe it works now but it contributes to later yo-yo effects. If we had an easy way of testing both axes, maybe we’d have a shot at predicting who will lose weight on which diet at which juncture in their lives without lasting damage.

Speaking for myself, I just can’t take the chance anymore.