I just got done reading Gary Taube’s 500-page masterpiece called “Good Calories, Bad Calories: Fat, Carbs, And The Controversial Science Of Diet And Health.” It is a must-read, for entertainment value, at the very least, for Taubes attempts to disprove what feels like the entire body of nutritional research.
The premise of his book is simple: not all calories are created equal. Also, scientific agendas led by money, politics, and ego are not trustworthy. Science is full of bad science, much of which is referenced all the time.
If T. Colin Campbell can be criticized for lumping animal sources of protein and high fat diets (by virtue of animal food consumption) together as the axis of nutritional evil, then can’t any scientist be questioned?
Taubes does an impressive job recounting the last century of nutritional science and its exploration of causes of Western diseases, lumped neatly together as metabolic syndrome. He explains how there’s no evidence to suggest that saturated fat has anything to do with heart disease. That the Atkins diet for weight loss makes perfect sense. That vitamin C deficiency might have more to do with starch consumption.
For a geek like myself, it was the best read I’d had in a long time.
But something was bothering me…
After devoting a week of my time to trying to dig to the bottom of the Denise Minger vs. China Study issue, and shaking my head at her paleocentric fans, and then reading this book I started to feel very insecure about my own diet. The one which extols the Almighty Carb.
I was a vegan for while, before I’d developed more knowledge in the field of nutrition. It was a nice gig. I was fit, healthy, and even astonishingly accused of using steroids by my co-workers. I’d never been into pizza, or pasta, or carb-heavy meals because I knew they were nutrient poor, and I certainly hated eating added sugar of any kind, knowing that it offers nothing good beyond the joy of sweetness.
I was a whole grains enthusiast. I still am, despite all the research and articles written about phytic acid, fermentation, mold, and insulin spikes.
Because I had to be. I was an endurance athlete. And when I wasn’t an endurance athlete, I was a laborer and a hiker, and a fitness trainer off and on and off and on again.
When I first read The Paleo Diet, I was stoked. It was everything I loved about simple living and raw food. But it went against everything I felt as a comfortable almost-vegan. The meat. My god, the meat quantities called for were absurd to me.
But it wasn’t the presence of meat that bothered me. My line of reasoning from The China Study, as I melded information from that book into the pool of other things I’d read, was that animal foods don’t kill people; they simply displace whole plant foods that heal people.
No worries, because the Paleo Diet allowed for all kinds of plant foods… well… except for anything with concentrated carbs like grains, legumes, and even potatoes. Bummer.
I felt like I was being sentenced to death. I couldn’t imagine a worse world than one without more concentrated carb sources.
But I tried it. And I crashed and burned in about… hmmm… three days.
You just can’t bike 20 miles a day and work as a fitness trainer 8 more hours a day without the carbs. It was the same crash and burn I experienced when I dappled in raw during my competitive rowing years; raw is another diet that does allow for many concentrtaed carb sources.
I talked to one of my associates, who would later open his own Crossfit gym. He handed me The Paleo Diet for Athletes.
This was a joke! You can’t claim a diet to be Paleolithic and optimal for human performance and yet have another book for special populations (athletes!). Weren’t paleolithic men super active? I felt like something was wrong with the low-carb aspect.
I went back to my old ways of eating and saved money that would otherwise go to meat. I ate the same amount of vegetables and ate my calorie-dense carbs and felt great again.
So when Gary Taubes, through the first 300 persuasive pages of his book, had me on the verge of thinking I was diabetic due to my carb consumption, I worried. I couldn’t speak with authority about the medical research he referenced. Surely he’d read more than I had!
But when Taubes delved into what causes obesity and fat accumulation, I began to doubt. While nutrition has been a big deal for the last 100 years, exercise physiology has only been on the table for half the time. I was sick of hearing about discussions of diet without exercise.
In fact, most discussion of nutrition completely neglects the exercise/movement aspect of human health. Fuel is a fine thing to study, but let’s not forget that the machine needs incentive to burn it.
Taubes, hypothesis by hypothesis, debunked the set point hypothesis, the lipostat hypothesis, the thrifty gene hypothesis, the energy balance hypothesis, and just about every other hypothesis attributed to body weight.
And yet, my own experience with myself and my clients was screaming “Bullshit! Every fat person who voluntarily lost weight will be first in line to tell you how counting calories works! This whole industry speaks about nothing but the efficacy of calorie-logging. I’m starving at the end of my active day, and to tell me that energy balance isn’t significant is a joke. Damn you Taubes, stop blaming carbs! And that goes for the rest of you Paleo-Meat-centric-Atkins-Price enthusiasts-otherwise-known-as-’low-carbers.”
Before I proceed, let me make this clear: I’ve always prescribed the whole foods diet. Don’t adulterate your food!
A few more things you should know, to help identify my biases:
- I’m an endomorph. Scandinavian: broad and tall with a propensity toward easy muscle and fat.
- I was a very serious endurance athlete.
- My BMI is 27, with a body fat range of 20-23%, depending on my lifestyle.
- I am loyal to the high carb, low fat, low protein camp of nutritional protocols.
- I eat a whole foods, high whole carb (aka-slow carb) diet with liberal plant fats and with limited amounts of unprocessed (or minimally processed) animal products.
- I occasionally drink alcohol and usually regret it the next day. I also eat other forbidden foods, either frequently and in great moderation–or infrequently and immoderately.
What follows will not be my rant against the Paleo movement, because frankly, I agree with it. It won’t be a blind defense of The China Study.
No, this will be my response to the persecution of carbs.
Much of the information I’m about to share is merely a summary of a very impressive seminar led by Dr. Robert H. Lustig called Sugar: The Bitter Truth. Note that this seminar was released after the publication of Taube’s book, and I therefore cannot fault Taubes for the omission of this information. I encourage everyone to check out this seminar, and watch it at least twice. Also, it should be known that Robert H. Lustig isn’t exactly a friend of carbs.
But before I enter the scene of glucose metabolism, I’d like to breeze over a few of Taubes’ conclusions, so you’ll get a feel for my incredulity:
- Dietary fat of any type is not a cause of obesity or metabolic syndrome. I argue it is half-responsible.
- The problem is the carbohydrates in the diet due to their effect on insulin secretion. The more easily digested the carb, the worse this effect is. Not all carbs are created equal. This is an unfair blanket statement; and he leads his readers.
- Sugars–sucrose and HFCS–are particularly harmful because the combo of fructose and glucose raises insulin and floods the liver with carbs. This is more to the point, but a slight mis-statement.
- Through their direct effect on insulin and blood sugar, refined “fast carbs” are the dietary cause of metabolic syndrome–and the most likely cause of cancer, Alzheimer’s, and other chronic diseases of civilization. Again, not all carbs are created equal. Also, I doubt carbs cause cancer, but cellular fuel might reasonably help grow cancer, which is a cluster of cells.
- Obesity is a disorder of excess fat accumulation, not overeating or sedentary behavior (energy balance). Ask any post-collegiate 20-something how much weight they gained after getting their first desk job. But sure, there’s a tipping point for obesity somewhere, which makes it metabolically different from overweight.
- Consuming excess calories does not cause us to grow fatter. Caloric deficits do not lead to long-term weight loss; it leads to hunger. I can prove to you that consuming excess calories causes me to grow fatter. Am I some kind of exception? The body is smart and can accommodation fluctuations in inputs; but bombard it long enough, and it will lose the battle.
- Fattening and obesity are caused by an imbalance in the hormonal regulation of adipose tissue and fat metabolism. I agree with this idea, but it is not a comprehensive cause of fattening.
- Insulin is the primary regulator of fat storage. When insulin is high, we store fat. When it falls, we release fat. Agreed, mostly. But this is contingent on energy balance and replete glycogen stores. Fat storage is also contingent on other hormones.
- By stimulating insulin secretion, carbs make us fat and ultimately cause obesity. The fewer carbs we consume, the leaner we will be. How do you account for whole foods vegans who follow diets of 10% fat? They eat starch all day long and don’t get fat.
- By driving fat accumulation, carbs also increase hunger and decrease the amount of energy we expend in metabolism and physical activity. There’s some back story to this. But carbs also contribute to satiety by raising blood sugar and elevating serotonin.
Wow. That’s some list. And my comments followed in bold. So now let’s dig a little deeper by understanding different carbs.
Here is a list of terms:
- STARCH is a carbohydrate consisting of a chain of a large number of glucose units joined by glycosidic bonds. This polysaccharide is produced by all green plants as an energy store. The most energy-dense starches are grains, potatoes, and legumes. These are “high carb” foods, because they confer the most energy from carbohydrates.
- SUGAR is a short-chain (either a mono or a disaccharide) carbohydrate at its most basic level: glucose, fructose, maltose, lactose, and anything else ending in -ose. All starches eventually break down into glucose, which is a monosaccharide sugar. Half of virtually every disaccharide is glucose.
- CARBS can refer to either starch or sugar, but it usually more liberally substituted for the term “starch,” and also encompasses the group of foods known as “refined carbohydrates,” which includes processed starches like wheat, rice, corn, and potato flour-products, as well as white table sugar and high fructose corn syrup. These are not only “high carb” foods, the are “fast carb” foods, meaning they raise blood sugar both rapidly, and by a lot–unless eaten in small amounts.
- BLOOD SUGAR is glucose circulating in the blood.
- TABLE SUGAR is also called “sugar,” but is really a type of sugar called sucrose. Sucrose is a disaccharide, half of which is glucose, the other half fructose.
- HFCS – HIGH FRUCTOSE CORN SYRUP is infamously added to sodas and prepackaged goods in the United States. It is almost identical to table sugar/sucrose, except instead of being 50% glucose and 50% fructose, it is around 45% glucose and 55% fructose.
Now that we have our list of carbs, let’s take a look at glucose, because glucose is what drives insulin, which is widely regarded now as a bad thing.
As summarized by Lustig…
When you eat glucose, your blood sugar rises, signaling to your brain that you have eaten, and then your pancreas responds by producing insulin, which is needed to push sugar into cells for energy metabolism.
According to Lustig, from a glucose load of 120 calories (2 small slices of bread): 80% will be used up by organs and muscle tissue. Why? Because every cell in the body can use glucose. Glucose metabolism is the oldest form of energy metabolism we know of. Every living thing can use glucose.
Here’s some boring biochemistry: About 20% of a glucose load will go toward the liver. When it reaches the hepatocyte (liver cell) it passes into the cell with the help of insulin and a transporter called Glu2. Insulin binds to its receptor IRS1 (insulin receptor substrate) and tyrosine phosphorolates it, creating pTryIRS1 (active IRS1). This stimulates another messenger called Akt (also known as protein kinase B), which stimulates sterol receptor binding protein 1 (SREBP1). SREBP1 takes an enzyme called glucokinase and turns it into glucose-6-phosphate (G6Pase).
Once you have glucose-6-phosphate, it stays in the liver, and can only get out with the help of hormones like glucagon (created by the pancreas to raise very low blood sugar) and epinephrine (commonly known as adrenaline, key in releasing sugar into the blood when you need it in a jiff.)
This glucose-6-phosphate ends up further processed into glycogen (storage form of sugar in the cells), which is easier for glucagon and epinephrine to source. Glycogen in non-toxic and can be stored in excess in the liver without resulting in liver damage. Glycogen is the body’s preferred source of fuel during exercise and rapid muscular movement. It also gets depleted rapidly during periods of fasting. Why? Because glucose is the preferred energy source.
While most of the glucose-6-phosphate ends up as glycogen, a little bit will end up metabolized into a substrate known as pyruvate. Pyruvate enters the cell’s mitochondria (think “furnace” or “energy factory”) and gets converted into Acetyl-Coa (an important co-enzyme for metabolism). In normal circumstances, Acetyl-CoA from fatty acid metabolism feeds into the citric acid (citrate) cycle contributing to the cell’s energy supply. Other terms for the citric acid cycle is the Krebs cycle, and the TCA cycle.
The citric acid cycle takes Acetyl-Coa and produces ATP (adenosine tri-phosphate) which is the currency of energy. Sometimes you don’t burn off all of the Acetyl-Coa, and so the result is citrate (from the citric acid cycle).
Citrate can be broken down by a three enzymes which are subservient to SREBP1 (mentioned above). These three enzymes (ATP citrate lyase, acetyl-CoA carboxylase, and fatty acid synthase) along with SREBP1 turn sugar into fat through de novo lipogenesis (fat making).
The type of fat created is actually a lipoprotein, a form of cholesterol known as VLDL (very low density lipoprotein). This is the worst kind of cholesterol and is what causes heart disease.
Even so, from a 120-calorie glucose load, Lustig claims less that 1 calorie ends up as VLDL. In the grand scheme of things, this isn’t a big deal.
Repeat: according to Lustig, less than 1 calorie of a 120-calorie glucose load will be implicated in de novo lipogensis, which raises levels of fat in your blood. This is important, because high blood triglycerides are an aspect of metabolic syndrome.
Take home points: Glucose metabolism is the oldest form of energy metabolism. It does not seem legitimate to me that this ancient form of energy metabolism will kill us if we get a lot of it.
See, glucose has an order of operations. When you eat glucose (from starch or table sugar), 20 percent or so will go to the liver for glycogen storage, but most of it gets used up for immediate energy as insulin delivers it for muscle and lean tissue and for the demands of the parasympathetic nervous system. The body will burn glucose as fuel (though not exclusively) as long as blood sugar is elevated sufficiently and glycogen reserves are not depleted. Hence, this is why sugar goes first during a fast–which is a period of negative energy balance. As blood glucose and liver glycogen run low, fat stores release fatty acids into circulation to pick up the slack.
In opposition to glucose, we have fatty acids. Fatty acids represent as much as 50-70% of the energy we expend over the course of a day–even a normal weight person has more calories worth of fat fuel in his body than he has of glucose and glycogen fuel. This energy is very slow-burning and only suitable of low intensity activity, sitting, and sleeping. In conditioned endurance athletes, movement is so practiced and efficient that sugar energy demand is not as great as it would be for the non-conditioned athlete.
Dietary fat is relatively scarce in nature, so it makes sense that the body has developed an efficient way to turn glucose derived from starch into adipose tissue when we consume too much of it, and also if the body’s “fat gauge” decides it prudent to put some aside (i.e., natural fattening during winter months). A mechanism for fat storage is critical, as fat can provide a steady stream of fatty acids as fuel for lower energy endeavors, as well as insulation.
Yes, Taubes, glucose can and will be stored as fat. But this doesn’t cause metabolic syndrome.
If you consume glucose beyond your energy requirements, it will have no choice than to be stored as fat. Muscle tissue can store a small amount of glucose as glycogen (the primary fuel tank is the liver, which does “top off”). If there’s no place for the glucose, it must find its way into the fat tissue. For this reason, if your blood sugar is too high–too high to be used in reasonable amounts by the body’s systems–then much of that sugar has to be crammed somewhere.
This is where energy balance, something Taubes dismisses, comes into play.
If I sit around and eat pasta all day long, day in and day out, in excess, and don’t go and exercise…
- My glycogen stores fill up to the max.
- I get bloated because each gram of glycogen will also support up to 3 grams of water.
- I will accumulate fat because the glucose has no where else to go, especially because it’s easy to take down more energy than you need with a plate of pasta.
- I am hungry much of the time because carbs leave the stomach rapidly and are digested in the intestines. This leaves my stomach open and yawning and pumping more hunger hormone: ghrelin.
- Some de novo lipogenesis will occur in the liver, but really, not that much at all.
Glucose isn’t the bad guy, even if it can make us store fat. We need it if we want to perform–or at least resemble the active, wandering, athletic paleo people we once were. A people who did not subsist solely on meat and fat, but ate many thousands of different plant species, many of them starchy root vegetables and grasses.
Now… what is fat? Fat is a triglyceride. It’s three fatty acids on a glycerol backbone. The glycerol backbone ultimately comes from glycerol phosphate, which a product of glycolysis (glycolysis is the process of metabolizing glucose. Glycolysis yields pyruvate, which is the building block for de novo lipogenesis).
Here’s how Taubes describes the lifecycle of free fatty acids:
Three free fatty acids must bind to a glycerol if they want to stay inside a fat cell. If glucose was metabolized inside that fat cell, a glycerol is freed for this purpose. If free fatty acids can’t find a glycerol to bind to, then they slip past the fat cell membrane into the blood stream. If these fatty acids are not used as fuel, many of them will head toward the liver, which will repackage them into full-fledged triglycerides loaded on lipoproteins.
In short, when there is plenty of sugar getting shoved into fat cells, there are plenty of glycerol backbones waiting to be occupied by free fatty acids and converted into stored fat.
Some of the triglycerides in our adiopse tissue come from dietary fat; the rest come from carbohydrates. Remember that de novo lipogenesis (creation of new fat) occurs in the liver, and to a lesser extent, inside fat tissue; these are Taube’s words, by the way.
Taubes says the rationale is that the more carbs you consume, the more de novo lipogenesis can occur.
Interestingly, according to Lustig (who provides some great slides in his lecture), only a little bit of de novo lipogenesis occurs in the liver from the consumption of glucose. So how can it be argued that carbs (especially starches) themselves make us fat, regardless of energy balance and exercise?
Taubes states again and again that the scientific literature does not support the theory that energy balance and thermodynamics regulate weight.
I’ve never been completely behind the energy-balance-thermodynamics argument because I know that 2,000 calories of protein and 2,000 calories of carbs, consumed over time, will promote shockingly different body shapes. Yet even though calories aren’t created equal (some lending themselves more to fat production than others), the bottom line is that total calories consumed matters more. This is Exercise Physiology 101, and this principle almost always holds. Even this crappy little study sponsored by Big Corn exploits this sweet little principle in defense of HFCS.
Not all calories are created equal. This is the crux of Taube’s work, and his failure was to distinguish glucose from fructose. By failing to pay proper attention to the fructose, he lumped all the carbs together and over-simplified.
In his delightful breakdown of fructose metabolism, Lustig demonstrates just how differently fructose behaves once inside the body. To quote my previous article on Lustig’s seminar, Sugar: The Bitter Truth, after consuming 120 calories of orange juice…
-60 calories from glucose will break down similarly to the white bread (48 calories to the body, 12 calories to the liver to be stored as glycogen).
-60 calories from fructose will all go to the liver; the liver is the only place fructose can be metabolized.
-In total, 72 calories reaching the liver will need to be phosphoralated (turned into energy–ATP–adenosine tri phosphate). That is a lot–three times the amount, when compared to white bread.
-You lose a lot of phosphate in this process, and so the body provides a rescue molecule, and the end waste product from the metabolism of these calories is uric acid (which causes gout and hypertension, among other things).
-Uric acid blocks the your body’s chemical–endothelial nitric oxide synthase–for maintaining low blood pressure.
-Citrate, again, arises from the metabolism of all these calories and de novo lipogenesis, which promotes fat retention, dyslipidemia, VLDL, and high blood triglycerides.
-In short, from any fructose load, 30% of it will end up as fat.
-An excess of body fat changes the way your body responds to leptin. Leptin is a hormone produced by adipocytes (fat cells). The more fat you have, the more leptin is produced to act on your brain’s hypothalamus. But when there is too much, you develop leptin insensitivity; your brain can no longer recognize it and thinks you’re starving. So you eat more.
Lustig says chronic fructose exposure alone causes metabolic syndrome. Fructose consumption is far more associated with dislipidemia, hypertension, uric acid, heart disease, and other manifestations of metabolic disorder. See more. I think this is an overstatement, but at least much closer to the point.
Taubes himself states that glucose in the blood decreases fatty acid circulation, and the low blood sugar increases fatty acid circulation. Glucose metabolism, the oldest form of energy metabolism, should not logically be responsible for obesity and diabetes. Again and again, Taubes references carbohydrates as though they are all the same; I believe he does this to intentionally mislead his readers.
Insulin is associated with weight gain, for sure, because it crams energy into storage sites. Insulin’s job is to deliver glucose to furnaces and to storage sites. Eating too much, despite Taube’s claims to the contrary evidence, will eventually cause weight gain–especially if it’s carbs, because insulin loves to shove glucose into storage if you’re not going to burn it immediately. It isn’t quite the same story with dietary fat.
The theory that jacked up levels of blood sugar cause a disproportionate insulin responses to the point of insulin resistance makes sense on the surface, and it might be true, but then why don’t we see competitive athletes succumbing to diabetes in hordes due to years of carb-loading?
The fact is that metabolic syndrome and is not caused by carbs (starches) alone. Dislipidemia is a necessary evil in metabolic syndrome.
Taubes made an interesting claim that 30% of a carb load will end up as de novo lipogenesis, and I thought, “Show me the evidence.”
Could it be that Taubes borrowed the same data used by Lustig, who claimed the 30% of every fructose load will end up as fat. (At 1:02.00-1:05.00 in the seminar.)
It isn’t the glucose in the blood that’s the problem. It’s the free fatty acids from de novo lipogenesis and other sources that are implicated in insulin insensitivity.
Therefore in contrast to the originally postulated mechanism in which free fatty acids were thought to inhibit insulin-stimulated glucose uptake in muscle through initial inhibition of pyruvate dehydrogenase these results demonstrate that free fatty acids induce insulin resistance in humans by initial inhibition of glucose transport/phosphorylation which is then followed by an approximately 50% reduction in both the rate of muscle glycogen synthesis and glucose oxidation.
Insulin insensitivity is a product of fat in the blood.
Interestingly, there’s another thing at play: something to which Taubes didn’t give more than an afterthought, and that’s the interplay of fat and starch. On page 307, referencing George Bray, he described how rats fed a high fat diet can become obese. To quote the book, “I could feed them any kind of composition of carbohydrates I want, and in the presence of low fat, they don’t get fat. If I raised the fat content, particularly saturated fat, in susceptible [Taube's italics] strains I would get obesity regularly.” (Maybe this is why T. Colin Campbell’s low fat, near-vegan diet makes for very lean people).
Taubes goes on to say himself, “But some strains of rats, perhaps most of them, will not grow obese on high-fat diets, and even those that do will grow fatter on a high-fat, high-carbohydrate diet than a high-fat, low-carbohydrate diet,” and suggests that fat content would have to be at least 30% of the diet, and thus seems to dismiss the key role of fat.
And yet, the Standard American Diet is 30% fat, or more. Especially with the inclusion of dairy fat. The foundations of metabolic syndrome are laid by excessive fructose consumption, for sure, which can account for every aspect of the syndrome. But it is the supplementation of our diets high in fat and fast carbs that really helps induce obesity, which further exacerbates the feedback loop of metabolic syndrome.
“What do the Atkins diet and the Japanese diet have in common?” It’s an odd question, as the two diets seem diametrically opposed. The Atkins diet is all fat, no carb. And the Japanese diet is all carb, no fat. They both work. So, what do they have in common?
They both eliminate the sugar fructose.
–Robert H. Lustig
If my blood sugar is sufficiently elevated, then I won’t release fatty acids into my blood stream. If my blood sugar is low, then I will. This is a neat, self-regulating negative feedback loop.
But what if I eat lots of glucose and fat!? (i.e. ice cream, cake, doughnuts, potato chips…)
Too much fat and too much glucose in the blood, along with elevated triglycerides from excessive lifetime fructose consumption = obesity and metabolic syndrome.
Now you have a new, nasty, positive feedback loop.
Increased adiposity, after all, will increase leptin and hence leptin insensitivity, which makes you eat more, which gears you toward foods with the biggest macro-nutrient payoff (fat and sugar (namely, glucose) combos like cookies, chips, doughnuts, or a Happy Meal.
There is no food in nature high in both fat and sugar besides breast milk (or maybe durian). And well… breast milk makes us grow bigger.
So it makes perfect sense to me that combining fat (from dietary fat, or from fructose) and glucose is the crux of the issue. Not starch alone.