Is Sugar Really Toxic? Sifting through the Evidence

Our very first experience of exceptional sweetness—a dollop of buttercream frosting on a parent’s finger; a spoonful of strawberry ice cream instead of the usual puréed carrots—is a gustatory revelation that generally slips into the lacuna of early childhood. Sometimes, however, the moment of original sweetness is preserved. A YouTube video from February 2011 begins with baby Olivia staring at the camera, her face fixed in rapture and a trickle of vanilla ice cream on her cheek. When her brother Daniel brings the ice cream cone near her once more, she flaps her arms and arches her whole body to reach it.

Considering that our cells depend on sugar for energy, it makes sense that we evolved an innate love for sweetness. How much sugar we consume, however—as well as how it enters the body and where we get it from in the first place—has changed dramatically over time. Before agriculture, our ancestors presumably did not have much control over the sugars in their diet, which must have come from whatever plants and animals were available in a given place and season. Around 6,000 BC, people in New Guinea began to grow sugarcane, chewing and sucking on the stalks to drink the sweet juice within. Sugarcane cultivation spread to India, where by 500 BC people had learned to turn bowls of the tropical grass’s juice into crude crystals. From there sugar traveled with migrants and monks to China, Persia, northern Africa and eventually to Europe in the 11th century.

For more than 400 years, sugar remained a luxury in Europe—an exotic spice—until manufacturing became efficient enough to make “white gold” much more affordable. Christopher Columbus brought sugarcane to the New World in 1493 and in the 16th and 17th centuries European powers established sugarcane plantations in the West Indies and South America. Sugar consumption in England increased by 1,500 percent between the 18th and 19th centuries. By the mid 19th century, Europeans and Americans had come to regard refined sugar as a necessity. Today, we add sugar in one form or another to the majority of processed foods(PDF) we eat—everything from bread, cereals, crunchy snacks and desserts to soft drinks, juices, salad dressings and sauces—and we are not too stingy about using it to sweeten many raw and whole foods as well.

By consuming so much sugar we are not just demonstrating weak willpower and indulging our sweet tooth—we are in fact poisoning ourselves according to a group of doctors, nutritionists and biologists, one of the most prominent members of which is Robert Lustig of the University of California, San Francisco, famous for his viral YouTube video “Sugar: The Bitter Truth.” A few journalists, such as Gary Taubes and Mark Bittman, have reached similar conclusions. Sugar, they argue, poses far greater dangers than cavities and love handles; it is a toxin that harms our organs and disrupts the body’s usual hormonal cycles. Excessive consumption of sugar, they say, is one of the primary causes of the obesity epidemic and metabolic disorders like diabetes, as well as a culprit of cardiovascular disease. More than one-third of American adults and approximately 12.5 million children and adolescents in the U.S. are obese. In 1980, 5.6 million Americans were diagnosed with diabetes; in 2011 more than 20 million Americans had the illness.

The argument that sugar is a toxin depends on some technical details about the different ways the human body gets energy from different types of sugar. Today, Americans eat most of their sugar in two main forms: table sugar and high-fructose corn syrup. A molecule of table sugar, or sucrose, is a bond between one glucose molecule and one fructose molecule—two simple sugars with the same chemical formula, but slightly different atomic structures. In the 1960s, new technology allowed the U.S. corn industry to cheaply convert corn-derived glucose intro fructose and produce high fructose corn syrup, which—despite its name—is almost equal parts free-floating fructose and glucose: 55 percent fructose, 42 percent glucose and three percent other sugars. Because fructose is about twice as sweet as glucose, an inexpensive syrup mixing the two was an appealing alternative to sucrose from sugarcane and beets.

Regardless of where the sugar we eat comes from, our cells are interested in dealing with fructose and glucose, not the bulkier sucrose. Enzymes in the intestine split sucrose into fructose and glucose within seconds, so as far as the human body is concerned sucrose and high-fructose corn syrup are equivalent. The same is not true for their constituent molecules. Glucose travels through the bloodstream to all of our tissues, because every cell readily converts glucose into energy. In contrast, liver cells are one of the few types of cells that can convert fructose to energy, which puts the onus of metabolizing fructose almost entirely on one organ. The liver accomplishes this primarily by turning fructose into glucose and lactate. Eating exceptionally large amounts of fructose taxes the liver: it spends so much energy turning fructose into other molecules that it may not have much energy left for all its other functions. A consequence of this energy depletion is production of uric acid, which research has linked to gout, kidney stones and high blood pressure.

The human body strictly regulates the amount of glucose in the blood. Glucose stimulates the pancreas to secrete the hormone insulin, which helps remove excess glucose from blood, and bolsters production of the hormone leptin, which suppresses hunger. Fructose does not trigger insulin production and appears to raise levels of the hormone grehlin, which keeps us hungry. Some researchers have suggested that large amounts of fructose encourage people to eat more than they need. In studies with animals and people by Kimber Stanhope of the University of California Davis and other researchers, excess fructose consumption has increased fat production, especially in the liver, and raised levels of circulating triglycerides, which are a risk factor for clogged arteries and cardiovascular disease. Some research has linked a fatty liver to insulin resistance—a condition in which cells become far less responsive to insulin than usual, exhausting the pancreas until it loses the ability to properly regulate blood glucose levels. Richard Johnson of the University of Colorado Denver has proposed that uric acid produced by fructose metabolism also promotes insulin resistance. In turn insulin resistance is thought to be a major contributor to obesity and Type 2 diabetes; the three disorders often occur together.

Because fructose metabolism seems to kick off a chain reaction of potentially harmful chemical changes inside the body, Lustig, Taubes and others have singled out fructose as the rotten apple of the sugar family. When they talk about sugar as a toxin, they mean fructose specifically. In the last few years, however, prominent biochemists and nutrition experts have challenged the idea that fructose is a threat to our health and have argued that replacing fructose with glucose or other sugars would solve nothing. First, as fructose expert John White points out, fructose consumption has been declining for more than a decade, but rates of obesity continued to rise during the same period. Of course, coinciding trends alone do not definitively demonstrate anything. A more compelling criticism is that concern about fructose is based primarily on studies in which rodents and people consumed huge amounts of the molecule—up to 300 grams of fructose each day, which is nearly equivalent to the total sugar in eight cans of Coke—or a diet in which the vast majority of sugars were pure fructose. The reality is that most people consume far less fructose than used in such studies and rarely eat fructose without glucose.

On average, people in America and Europe eat between 100 and 150 grams of sugar each day, about half of which is fructose. It’s difficult to find a regional diet or individual food that contains only glucose or only fructose. Virtually all plants have glucose, fructose and sucrose—not just one or another of these sugars. Although some fruits, such as apples and pears, have three times as much fructose as glucose, most of the fruits and veggies we eat are more balanced. Pineapples, blueberries, peaches, carrots, corn and cabbage, for example, all have about a 1:1 ratio of the two sugars. In his New York Times Magazine article, Taubes claims that “fructose…is what distinguishes sugar from other carbohydrate-rich foods like bread or potatoes that break down upon digestion to glucose alone.” This is not really true. Although potatoes and white bread are full of starch—long chains of glucose molecules—they also have fructose and sucrose. Similarly, Lustig has claimed that the Japanese diet promotes weight loss because it is fructose-free, but the Japanese consume plenty of sugar—about 83 grams a day on average—including fructose in fruit, sweetened beverages and the country’s many meticulously crafted confectioneries. High-fructose corn syrup was developed and patented in part by Japanese researcher Yoshiyuki Takasaki in the 1960s and ’70s.

Not only do many worrying fructose studies use unrealistic doses of the sugar unaccompanied by glucose, it also turns out that the rodents researchers have studied metabolize fructose in a very different way than people do—far more different than originally anticipated. Studies that have traced fructose’s fantastic voyage through the human body suggest that the liver converts as much as 50 percent of fructose into glucose, around 30 percent of fructose into lactate and less than one percent into fats. In contrast, mice and rats turn more than 50 percent of fructose into fats, so experiments with these animals would exaggerate the significance of fructose’s proposed detriments for humans, especially clogged arteries, fatty livers and insulin resistance.

In a series of meta-analyses examining dozens of human studies, John Sievenpiper of St. Michael’s Hospital in Toronto and his colleagues found no harmful effects of typical fructose consumption on body weight, blood pressure or uric acid production. In a 2011 study, Sam Sun—a nutrition scientist at Archer Daniels Midland, a major food processing corporation—and his colleagues analyzed data about sugar consumption collected from more than 25,000 Americans between 1999 and 2006. Their analysis confirmed that people almost never eat fructose by itself and that for more than 97 percent of people fructose contributes less daily energy than other sugars. They did not find any positive associations between fructose consumption and levels of trigylcerides, cholesterol or uric acid, nor any significant link to waist circumference or body mass index (BMI). And in a recent BMC Biology Q&A, renowned sugar expert Luc Tappy of the University of Lausanne writes: “Given the substantial consumption of fructose in our diet, mainly from sweetened beverages, sweet snacks, and cereal products with added sugar, and the fact that fructose is an entirely dispensable nutrient, it appears sound to limit consumption of sugar as part of any weight loss program and in individuals at high risk of developing metabolic diseases. There is no evidence, however, that fructose is the sole, or even the main factor in the development of these diseases, nor that it is deleterious to everybody.”

To properly understand fructose metabolism, we must also consider in what form we consume the sugar, as explained in a recent paper by David Ludwig, Director of the New Balance Foundation Obesity Prevention Center of Boston Children’s Hospital and a professor at Harvard. Drinking a soda or binging on ice cream floods our intestines and liver with large amounts of loose fructose. In contrast, the fructose in an apple does not reach the liver all at once. All the fiber in the fruit—such as cellulose that only our gut bacteria can break down—considerably slows digestion. Our enzymes must first tear apart the apple’s cells to reach the sugars sequestered within. “It’s not just about the fiber in food, but also its very structure,” Ludwig says. “You could add Metamucil to Coca Cola and not get any benefit.” In a small but intriguing study(PDF), 17 adults in South Africa ate primarily fruit—about 20 servings with approximately 200 grams of total fructose each day—for 24 weeks and did not gain weight, develop high blood pressure or imbalance their insulin and lipid levels.

To strengthen his argument, Ludwig turns to the glycemic index, a measure of how quickly food raises levels of glucose in the blood. Pure glucose and starchy foods such as Taubes’s example of the potato have a high glycemix index; fructose has a very low one. If fructose is uniquely responsible for obesity and diabetes and glucose is benign, then high glycemic index diets should not be associated with metabolic disorders—yet they are. A small percentage of the world population may in fact consume so much fructose that they endanger their health because of the difficulties the body encounters in converting the molecule to energy. But the available evidence to date suggests that, for most people, typical amounts of dietary fructose are not toxic.

Even if Lustig is wrong to call fructose poisonous and saddle it with all the blame for obesity and diabetes, his most fundamental directive is sound: eat less sugar. Why? Because super sugary, energy-dense foods with little nutritional value are one of the main ways we consume more calories than we need, albeit not the only way. It might be hard to swallow, but the fact is that many of our favorite desserts, snacks, cereals and especially our beloved sweet beverages inundate the body with far more sugar than it can efficiently metabolize. Milkshakes, smoothies, sodas, energy drinks and even unsweetened fruit juices all contain large amounts of free-floating sugars instantly absorbed by our digestive system.

Avoiding sugar is not a panacea, though. A healthy diet is about so much more than refusing that second sugar cube and keeping the cookies out of reach or hidden in the cupboard. What about all the excess fat in our diet, so much of which is paired with sugar and contributes to heart disease? What about bad cholesterol and salt? “If someone is gaining weight, they should look to sugars as a place to cut back,” says Sievenpiper, “but there’s a misguided belief that if we just go after sugars we will fix obesity—obesity is more complex than that. Clinically, there are some people who come in drinking way too much soda and sweet beverages, but most people are just overconsuming in general.” Then there’s all the stuff we really should eat more of: whole grains; fruits and veggies; fish; lean protein. But wait, we can’t stop there: a balanced diet is only one component of a healthy lifestyle. We need to exercise too—to get our hearts pumping, strengthen our muscles and bones and maintain flexibility. Exercising, favoring whole foods over processed ones and eating less overall sounds too obvious, too simplistic, but it is actually a far more nuanced approach to good health than vilifying a single molecule in our diet—an approach that fits the data. Americans have continued to consume more and more total calories each year—average daily intake increased(PDF) by 530 calories between 1970 and 2000—while simultaneously becoming less and less physically active. Here’s the true bitter truth: Yes, most of us should make an effort to eat less sugar—but if we are really committed to staying healthy, we’ll have to do a lot more than that.

I'll say it again - there is no requirement for dietary carbohydrates in humans.
Incorrect.

Given that there have been a number of native cultures that subsisted on zero-carb diets for thousands of years, you should provide more than a bare assertion, if you want to convince...

). The Effects on Human Beings of a Twelve Months' Exclusive Meat Diet

The brain is one big glucose sucking machine.

Your Brain on Ketons

And now let's really get down to the mitochondrial level. Mitochondria are the power plants of our cells, where all the energy is produced (as ATP). Now, when I was taught about biochemical fuel-burning, I was taught that glucose was "clean" and ketones were "smokey." That glucose was clearly the preferred fuel for our muscles for exercise and definitely the key fuel for the brain. Except here's the dirty little secret about glucose - when you look at the amount of garbage leftover in the mitochondria, it is actually less efficient to make ATP from glucose than it is to make ATP from ketone bodies! A more efficient energy supply makes it easier to restore membranes in the brain to their normal states after a depolarizing electrical energy spike occurs, and means that energy is produced with fewer destructive free radicals leftover.
What does it all mean? Well, in the brain, energy is everything. The brain needs a great deal of energy to keep all those membrane potentials maintained - to keep pushing sodium out of the cells and pulling potassium into the cells. In fact, the brain, which is only 2% of our body weight, uses 20% of our oxygen and 10% of our glucose stores just to keep running. (Some cells in our brain are actually too small (or have tendrils that are too small) to accommodate mitochondria (the power plants). In those places, we must use glucose itself (via glycolysis) to create ATP.) When we change the main fuel of the brain from glucose to ketones, we change amino acid handling. And that means we change the ratios of glutamate and GABA. The best responders to a ketogenic diet for epilepsy end up with the highest amount of GABA in the central nervous system.
One of the things the brain has to keep a tight rein on is the amount of glutamate hanging out in the synapse. Lots of glutamate in the synapse means brain injury, or seizures, or low level ongoing damaging excitotoxicity as you might see in depression. The brain is humming along, using energy like a madman. Even a little bit more efficient use of the energy makes it easier for the brain to pull the glutamate back into the cells. And that, my friends, is a good thing.
Let me put it this way. Breast milk is very high in fat. Newborns spend time in ketosis, and are therefore to some extent ketoadapted. Breast milk is also high in sugar, but babies' brains are so big they can handle a lot more sugar than us full-grown folks. Being ketoadapted means that babies can more easily turn ketone bodies into acetyl-coA and into myelin. Ketosis helps babies construct and grow their brains. (For those interested in nitty gritty details - babies are in mild ketosis, but very young babies seem to utilize lactate as a fuel in lieu of glucose also - and the utilization of lactate also promotes the same use of acetyl-CoA and gives the neonates some of the advantages of ketoadaptation without being in heavy ketosis.)
We know (more or less) what all this means for epilepsy (and babies!). We don't precisely know what it means for everyone else, at least brain-wise. Ketosis occurs with carbohydrate and protein restriction, MCT oil use, or fasting. Some people believe that being ketoadapted is the ideal - others will suggest that we can be more relaxed, and eat a mostly low sugar diet with a bit of intermittent fasting thrown in to give us periods of ketosis. (A caveat - I don't recommend intermittent fasting for anyone with an eating disorder without some extra support and consideration). Ketosis for the body means fat-burning (hip hip hooray!). For the brain, it means a lower seizure risk and a better environment for neuronal recovery and repair.

>>Burning fat is aerobic, burning sugar is anaerobic.

“Fat burns in a carbohydrate flame.”

http://books.google.com/books?id=L4aZIDbmV3oC&pg=PA194&lpg=PA194&dq=Fat+burns+in+a+carbohydrate+flame&source=bl&ots=WltVrdGl5R&sig=EQpbJBD6Lj7IJYBFO1xMwOfNnDQ&hl=en&sa=X&ei=bXrrUf-NH6SVygHP8ICQCg&ved=0CDIQ6AEwBQ

Been 30 years since I took exercise physiology, but looks like that’s still the case.

Carbohydrate management is essential to avoiding “bonking” in endurance events. I can maintain a 75% of Max HR continuous pace for about two hours on just water. Efforts longer than that require carb replenishment.

Also, the primary fuel for the brain is glycogen. (sugar).

Got Gluconeogenesis?
http://en.wikipedia.org/wiki/Gluconeogenesis

[The notion that cells need free glucose to burn is false. Most cells do very well burning fat.] What’s your Marathon PR?

I don't know. I don't run marathons. And doubt that the great majority of humankind ever has or will push their bodies to such unnatural extremes. My aim is good health, not world-class sports performance.

But I will tell you this. Before embarking on a high-fat/low carb diet. I was 10-15 lbs overweight and took blood pressure medication. I also had to avoid salt. My endurance on hot days was nil. I couldn't mow the lawn in summer without wilting.

Now, my weight dropped 15 lbs. My blood pressure dropped back to 115/70. I stopped the medication. My fasting blood sugar dropped into the 80s. No more mid-morning dizzy spells. No more energy highs and lows. And I take extra salt every day in the form of bouillon drinks. Now I can endure the heat without fading.

So the low-carb business is working for me. And, once again, my aim is a good healthy life without the burden of the widespread metabolic diseases that afflict so much of our population. If I were endeavoring to become an extreme athlete of some sort, then I may need to rethink my nutritional requirements. But is extreme performance really healthy?

"A typical food-log entry listed 3,800 total calories. His meals that day included coconut oil, avocados, eggs, almonds, cashews, chicken breasts, beef jerky, string beans, onions, and protein powder."

Sounds a lot like my diet.

When I rode the MS150 a few weeks ago, I was completely bonk-free with just a dixie cup of nuts/m&ms and a dilute cup of gatorade (yellow original of course) at each 10 mile rest stop.

Gotta have enough dietary carbs/proteins in comming in for aerobic metabolism to function - otherwise proteins will be cannibalized from lean tissue to run the citric acid cycle.

"5. Since oxaloacetate is depleted by gluconeogenesis, Dr. Atkins has postulated that fat calories won’t be utilized in
the absence of carbohydrate. Based on what you now know about the citric acid cycl
e, what is the basic falacy of this hypothesis? (Where does oxaloacetate come from when we break down protein?) "
http://www.med.unc.edu/neurology/files/documents/child-teaching-pdf/CITRIC%20ACID%20CYCLE.pdf

Got oxaloacetate?

Aerobic and Anaerobic metabolisms are not mutually exclusive but, rather, synergistic --- with an increased aerobic capacity being a key to being able to process anaerobic waste products.

.Let us NOT forget this Biblical advice: "MODERATION IN ALL THINGS." Just WHERE, in the bible, can this be found?

My mistake. However, regardless of its source, it's still very practical.

Aristotle wisely advised moderation in all things. Gluttons and fanatics self-destruct by refusing to make the tradeoffs necessary to lead a good life. “Don’t tell me that I can’t drink and carouse every night and not succeed in my career!” insists the fool. “I can have it all.”

Well, he can’t. No one can. Aristotle wisely advised moderation in all things. Gluttons and fanatics self-destruct by refusing to make the tradeoffs necessary to lead a good life. “Don’t tell me that I can’t drink and carouse every night and not succeed in my career!” insists the fool. “I can have it all.” Well, he can’t. No one can.

[myth is the idea that fat burning decreases as intensity increases.]

The relationship between anaerobic high intensity and muscle glycogen isn’t a myth. Nor is the difference between the metabolism of fast and slow twitch muscle fibers.

http://www.google.com/search?hl=en&source=hp&biw=&bih=&q=Fast+twitch+vs+slow+twitch&btnG=Google+Search&gbv=1

A 100m sprinter is burning glycogen during the sprint, not fat.

It’s less commonly recognized that “waste” products of high-intensity anaerobic effort (lactic acid for example) are metabolized aerobically.

Thus, the more developed the Aerobic physiology is, the great the Anaerobic effort that can be maintained over a longer period of time.

The associated fitness can be measured by observing recovery HR - as Anaerobic byproducts are metabolized, oxygen debt is reduced, and the HR is reduced to below the Anaerobic Threshold.

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