What ALL effective (dangerous and safe) Weight Loss Diets Have in Common:
All diets that actually work do so because they produce "net calorie deficit". In other words, they cause people to burn more calories than they consume either by reducing consumption, increasing output or both. This isn't a fact that has been determined by experiment, it is an axiom, an inevitable truth based upon the meanings of the terms "input" and "output".
As we have seen elsewhere, there are three macronutrients: fat, protein and carbohydrate. Protein cannot be safely restricted; we require at least 50-75 grams of high quality protein daily or we begin to burn up muscle tissue. Carbohydrate OR fat can however be safely restricted and indeed low carbohydrate and low fat diets are two popular approaches to weight control. Both work and both have the virtue of using calorie SOURCE to their advantage. In every other sense however, low carb and low fat diets are polar opposites. They both deserve some discussion.
Low Carbohydrate Diets
The idea of using carbohydrate restriction to promote fat loss dates to at least the mid 1960's in the US. They were very popular at that time and through the early 1970s but then fell into relative disfavor after receiving a good deal of bad press from the medical establishment of the day. Low carb diets re-emerged on the American scene in the late 1990's with the publication of a book called "Dr. Atkins' New Diet Revolution" which advocated for a very low carbohydrate "induction" diet followed by a more moderately-low carbohydrate 'maintenance' phase.
As in the 1970's the initial reaction of the American medical establishment to the millennial Atkins diet craze was negative. Many doctors, myself included, were convinced, largely by our training, that low carbohydrate diets were dangerously high in fat and protein. I graduated medical school in 1989 fully indoctrinated by the "Framingham Heart Study" that launched our modern understanding of the relationship between cholesterol and heart disease. Diets that advocated consumption of large amounts of red meat and fat seemed crazy; twelve years later, not so much.
Low carbohydrate diets have their place in weight control. They work, they are safe in the short term and, research is starting to show, they are likely safe in the longer term. I am still not sure how livable they are for most people, but certainly some people find low carbohydrate diets satisfying in the long-haul.
The real legacy of the low carbohydrate craze may be that it showed people an easier way than starving or counting calories and that it 'helped' a lot of us physicians to reevaluate our understanding of nutrition.
Low Fat Diets:
Weight loss through fat reduction has a lot of appeals. First, fat is THE calorie dense nutrient (9 calories per gram versus 4 and 4 for carb and protein) so that people can eat more non-fat food, a lot more in fact, and still consume fewer calories. Also, we know that fat has the lowest 'thermic effect' (2-3% versus ~10% for carb and ~ 30% for protein). Finally, much of the human race normally consumes very little fat and seems to stay thin and healthy without many of the chronic diseases that plague affluent western nations like the US.
I began practicing bariatric medicine in 1991 as a staunch advocate of very low fat diets for weight control and while my views today, nearly twenty years later have changed, I still believe that fat reduction is an important component of a sensible long-term weight control plan.
The main drawback to low fat diets is that they don't keep people feeling full for very long so that to be livable, they require people to eat quite often.
Final Thoughts on Macronutrient Restricted Diets for Weight Loss
Macronutrient restriction is a more sophisticated approach to weight loss than simple calorie reduction because it alleviates the burden of having to focus on amount of food consumed (with the inevitable result of having to go hungry) and instead shifts people's attention to the composition of the food. Macronutrient restricted diets are easier than calorie restricted diets, they work and are safe.
If net calories stored as fat, metabolism and hunger each vary by macronutrient, might they also vary by other differences in food?
Glycemic Index is a very popular concept today (2011) and it deserves a great deal of explanation.
Glycemic index is a measure of how foods affect human blood glucose (sugar) concentration over a short time (several hours). Specifically, GI reflects how rapidly and how long human blood glucose levels rise in response to eating a measured amount of a food on an empty stomach. Foods that cause a rapid rise in blood sugar are "HIGH glycemic index" food whereas foods that cause a slow rise in blood sugar are "LOW glycemic index" foods.
Why Glycemic Index Matters:
Recent medical research shows that rapid and significant rises in blood glucose levels caused by "high GI" foods can harm human health and contribute to weight gain.
Let's examine this by using a graph to illustrate the effects of low and high GI foods on human blood sugar levels:
Figure 10: Effect of high and low glycemic index foods upon normal (non-diabetic) fasting human blood glucose concentration over time.
Notice several things.
1. High GI foods cause glucose levels to rise very fast and very high.
2. High GI foods cause glucose levels to FALL very fast and very low. In fact, high GI foods consumed after a fast actually cause blood sugar levels to fall BELOW normal. This causes people to experience great hunger.
3. The "area under the curve" is greater for high GI foods than low GI foods.
Now, to understand how high GI foods can harm human health we need to add one more parameter to our graph and that is insulin level.
Insulin is the hormone, made in an organ called the pancreas that tells the cells in our muscle and other places to absorb blood glucose. Insulin is secreted into the blood by the pancreas (in non-diabetic people) in response to increases in blood sugar. Insulin levels fall when blood sugar returns to normal.
In the graph above, I have added curves representing blood insulin levels associated with the blood sugar curves in the earlier graph. Let's focus upon the purple insulin curve which belongs to the red "high GI" curve. Notice that insulin levels rise in response to the rapid rise in blood sugar but also notice that the response takes time and is not instantaneous. This is because insulin synthesis and secretion takes time. The effect of this delay is that a bit too much insulin in produced in response to a very rapid increase in blood sugar so that blood sugar not only falls rapidly, but it also falls too low before finally recovering to a normal level. During the time that blood sugar has fallen below normal, a person generally experiences intense hunger; more than the normal hunger associated with fasting. This leads us to the first problem with high GI foods:
High GI foods trigger rebound low blood sugar that increases hunger.
The second problem with high GI foods has to do with insulin. High levels of insulin, repeated over and over again, day after day and year after year will eventually lead to insulin resistance. This means that the muscle and other tissues in the body that normally respond to insulin by absorbing blood glucose (and thereby lowering blood sugar)--that these tissues begin responding less and less well to insulin and in turn are less and less effective at lowering blood sugar levels. This sort of insulin resistance has another more familiar name: type 2 (adult-onset) diabetes.
High GI foods cause high insulin levels that MAY contribute to Insulin Resistance, Metabolic Syndrome and Type 2 Diabetes.
To be clear, I am not suggesting that a high-GI diet will CAUSE diabetes. In fact, the biggest risk-factor for type 2 diabetes is obesity, particularly abdominal obesity, but… high GI foods can contribute to obesity and, because of their independent effects upon insulin resistance, can contribute to type 2 diabetes.
THIS is why glycemic index matters so much and why it is far more than just a curiosity.
Understanding Glycemic Index
Glycemic Index is not easy to understand and several points need to be emphasized:
1. GI is non-intuitive: Nobody can predict the exact GI of a food without measuring it.
2. GI can change dramatically by adding other foods
3. Generally, adding low-glycemic or non-glycemic foods to high GI foods will LOWER and not raise the overall GI of a meal.
4. GI is only useful for foods that contain absorbable carbohydrate. This means the GI is not measured for "non-glycemic" foods like pure meat, eggs, fat or pure fiber.
5. GI can only be determined through measurement of blood sugar level in ten human volunteers over many weeks.
6. Because of this, it is very labor-intensive and expensive to measure the GI of foods.
7. Because of the work and high cost involved in measuring the GI of foods, only about 4000 foods have actually had their glycemic indices measured. In other words, we don't know the GIs of many foods.
8. It is easier to predict a low-GI food than a high-GI food. To put it another way, nearly all foods with dilute carbohydrate that is mixed with lots of fiber, protein or fat will have a relatively low GI, BUT, not ALL foods that are nearly pure carbohydrate will necessarily have a high GI. This means that generally, you're safe eating whole grains, whole vegetables and fruits (except watermelon which is high-GI). Also remember that foods with very little carbohydrate like meats have almost no effect on blood sugar.
Eating a Low-GI Diet:
Avoiding foods that rapidly raise blood sugar is not difficult. You will need to memorize perhaps twenty high-GI foods to avoid, but other than that you simply need to know that if a food contains carbohydrate (starch or sugar), it's GI will be low if it also contains abundant fiber, protein or fat. For example, boiled white rice eaten plain is a high-GI food, but boiled brown rice is not and especially not if you eat it with meat, vegetables and a little fat. I will discuss these sorts of GI-lowering strategies later in the book's cooking chapter.
The idea behind glycemic load is that the amount of carbohydrate containing food consumed can alter its effect upon blood sugar. For example, a teaspoon of a very high-glycemic food like pure glucose will hardly change blood sugar at all while a large amount of a medium-GI food might. In other words, amount matters. NOT a big surprise.
For the record, the formal definition of glycemic load is:
Glycemic Load = Glycemic Index X Grams of Absorbable Carbohydrate
Do NOT bother to remember this. The point is simply, once again and as with all foods, AMOUNT MATTERS.
People generally like and seek sweet tasting food. Undoubtedly humans were first exposed to sugar from fruits and from honey.
Until about ten thousand years ago, humans were all hunter gatherers who made a living off the raw land. Groups of people could not stay long in one location because they would quickly use-up all the nearby foods.
This all changed with the invention of agriculture in a place now called Iraq sometime between 8,000 and 10,000 years ago. Although the beginnings of agriculture remain obscured by time, it is reasonable to assume that it started when humans understood that seeds from high-quality food plants often grew back into more high-quality food plants. At any rate, the first farmers left their mark about that time and in that place. From there, farming spread across the middle east and gradually throughout the "old world". Coincidentally, farming was invented in the New World at about the same time.
The archeological record shows that almost as soon as farming began, selective breeding of plants began also. This brings us back to the subject of sugar by way of sweet fruits.
Many wild fruit plants including the apple, apricot and grape "began" as very sour and pulpy wild vegetation. Early farmers began experimenting with cross-breeding fruits from different regions and found that some of the progeny produced sweeter fruits than any of the parents. The seeds from these "better" plants were then grown, ulimately crossed and grown again in cycle after cycle. To this day, the tradition continues and explains why consumers still find new varieties of sweeter and sweeter fruits almost every year. Selective breeding, far, far more than modern gene-splicing has created super-fruits from ancient sour apples.
The principle effect of this has been a dramatic increase in sugar content of fruits. I mention this to refute a common argument: namely, the claim that all fruit must be healthy because our hunter gatherer ancestors ate them.
The truth is that our hunter-gatherer ancestors ate nothing even remotely like modern fruit. If you want to experience an ancient fruit, eat a wild crabapple or gooseberry. No, modern fruits are veritable candy compared to their original ancestor fruits. The claim that "fruits must be good because humans have been eating them for a hundred thousand years" is based upon a false premise.
So having disposed of THAT argument, let's resume our examination of the history of sugar.
No matter how sweet fruits might be, they aren't crystalline sugar. No matter how sweet honey may be, it requires effort and risk to obtain. This means that human sugar consumption remained very low for a very long time down the ages.
It was sugar cane that changed all this. Sugar cane appears to have originated in southeast Asia. There is evidence that as early as 350 AD, humans in that region and in India were cultivating sugar cane for its sweet juice. Sugar cane spread over the next thousand years to nearly every tropical location in the "old world". People quickly learned that sugar cane could be mechanically pressed to extract more juice and that the juice could be dried into beige crystals of "sweet salt" (what we call today "raw sugar).Crystalized sugar became a very sought-after commodity in Europe and fetched an extremely high price. The expense of sugar meant that it was a "spice" available only the very wealthy and to royalty. Interestingly, about the time that sugar became available to Kings and Queens, those same royals began to experience a dramatic increase in the incidence of two diseases: dental caries (tooth decay) and obesity. In fact, obesity became so strongly associated with wealth and social status that is was considered extremely beautiful as many of the paintings of the Dutch artist Reubens attest. We can thus see early evidence for an association between sugar consumption and obesity.
Sugar production increased dramatically when the cane was introduced into the New World. By the late eighteenth and early nineteenth century, the Caribbean became the "sugar basket" of the entire world. Demand for sugar combined with the back-breaking labor required to grow sugar cane was a leading cause of, if not the single most important cause of the expansion of slavery in the America's and indeed, sugar became so strongly associated with slavery that to this day, many Quakers avoid sugar having been told as children that sugar is "made from the blood of slaves". Despite it's shameful heritage, the popularity of sugar grew exponentially during the nineteenth century, especially in the United States which was geographically near to the cane plantations of Jamaica and Cuba.
Mechanization replaced slavery on the sugar cane plantations during the latter part of the nineteenth century and further reduced cost so that by the early twentieth century sugar was a commodity that nearly everyone could afford to purchase and consume. The introduction of the sugar beet (which doesn't need tropical climates to thrive) even further lowered the price of sugar. The twentieth century was really the first era in human history when millions of human beings became able to aquire and consume sugar in substantial amounts. Not coincidentally, the twentieth century's latter half marked the start of what is now called "the obesity epidemic"; the dramatic increase in weight and weight-related illnesses seen in "first-world" societies and above all, right here at home in the United States. Sugar is not to blame for all of this epidemic, perhaps not even most of it, but it is, beyond any reasonable doubt, a very large contributor.
The story grows even more interesting during the 1970's and 1980's.
During the 1970's sugar prices fluctuated wildly on the world market and after a spike in the early part of the decade, world sugar prices fell very low and threatened to bankrupt US sugar growers. This led the United States Department of Agriculture (USDA) to enact a series of import tariffs on foreign sugar that allowed US sugar producers to dramatically increase their prices. This meant that by the early 1980s, American sugar prices were double the world average. The expense of sugar in this country created a real hardship for American food and beverage companies that used sugar in their products, especially for soft-drink makers like Coca Cola and Pepsi.
In order to reduce costs, soft-drink makers in the US embraced a new kind of sweetener in the early 1980's. This new sweetener was as sweet as sugar (ounce per ounce) and it's price was dramatically lower than sugar's. It was made in an industrial process, invented in the late 1950s and perfected in Japan in the late 1970s that converted corn starch into a mixture of two sugars: glucose and fructose. Of course you have probably already guessed that this new sweetener was non-other than high fructose corn syrup. Again, and not coincidentally, the American obesity epidemic exploded at almost exactly the same time. Let's turn now to the subject of this new and increasingly controversial sweetener.
High Fructose Corn Syrup
Most of the dry weight of kernels of corn is starch. Starch is a generic name applied to very large "polymers" of the simple sugar called glucose that are all "chained" to one another through a chemical bond called a "glycosidic" bond. When we eat starch, be in corn or potato or wheat, an enzyme produced by the pancreas called "amylase" begins to break-up the long chains of starch molecules into smaller and smaller chains and eventually into individual molecules of glucose which we can then absorb from the gut into the blood. Thus all eaten starch is converted into glucose and then absorbed. The reason that starch doesn't taste sweet is because, of course, pancreatic amylase only digests it into glucose after the starch has entered the small intestine. (Footnote: Actually humans do produce another starch-digesting enzyme called "salivary amylase" that is found, as the name implies, in saliva. If you retain a small amount of starch in your mouth for a few minutes you may indeed notice a sweet taste as the salivary amylase in your own saliva begins to digest it. END FOOTNOTE)
Obviously, if starch could be "pre-digested", say in a factory, into glucose, then starch could be converted into sweet-tasting sugar which generally fetches a higher price than starch. This is how old-fashioned Karo corn syrup was born.
Old fashioned corn syrup is nothing more than chemically-digested corn-starch. Originally the digestion was accomplished by mixing the starch with a strong acid and heating it. The acid would break the chains up into glucose. Today, "old-fashioned" corn syrup is made by adding an amylase enzyme purified from bacteria to corn starch. In any case the result is the same: old-fashioned corn syrup is a mixture of glucose and maltose (two-glucose chains) and maltotriose (three-glucose chains) and higher-numbered glucose chains. The main point is that "Old -Fashioned" Karo corn syrup contains only glucose and its chains. It does NOT contain any fructose.
This makes Karo corn syrup a weakly sweet material (about one-half as sweet as sucrose (table sugar)) that is great for pecan pies and fake maple syrup, but not very economical as a sweetener for mass-use.
Indeed, it has long been known that the sweetest simple sugar (single "link") is fructose (nearly twice as sweet as table sugar), the predominant source of sweetness in many fruits. Unfortunately (for the sugar industry), pure fructose was very expensive to manufacture. But in the mid 1970s, a chemical-industrial process was engineered that allowed companies to convert weakly sweet glucose corn syrup into a much sweeter syrup containing 42% fructose 50-52% glucose and a small percentage of other sugars. The up-shot of this process was (and is) that it allows for the economical conversion of ordinary corn syrup into a syrup that is roughly as sweet as table sugar. This process, combined with the high price of sugar (sucrose) in the US (caused by import tariffs as discussed earlier) meant that high fructose corn syrup suddenly became a cheaper sweetener than table sugar. From the mid 1970s until the mid 2000s, the production and consumption of hfcs increased dramatically.
Figure 7: Consumption of Various Sugars in the United States
Sugars are carbohydrates that taste sweet. Simple sugars are the smallest sugars and the best way to imagine them is as individual links that have been separated from a chain. We are primarily exposed to three simple sugars: glucose, fructose and galactose. Slightly larger than simple sugars are "di-sacharides" and these are formed from two simple sugars that are chemically bonded together (imagine a "chain" that is two links long). We commonly eat several disacharides: lactose (glucose chained to galactose), maltose (glucose chained to glucose) and sucrose (glucose chained to fructose). Lactose is found in milk, maltose in malt and sucrose is table sugar, the stuff that is sold in stores in big bags and in cubes. More rarely, we eat "trisacharides" and these include maltotriose. As sugars get "bigger" than three "links", they lose their sweet taste rapidly and at some point around ten links-long, we stop calling them sugars and begin referring to them as starches.
Whether "starch", or sugar, we cannot absorb carbohydrate into our blood from our gut until those carbohydrates have been chemically "broken down" into simple sugars (until all the "chains" and been cut-up into individual links). This means that all carbohydrate is ultimately absorbed in the form of glucose, fructose or galactose. While glucose is highly relevant to glycemic index, galactose, being a much more rare simple sugar, is less so. Fructose, which is often called "fruit sugar" (because many fruits derive much of their sweetness from fructose) is a simple sugar that deserves a chapter all its own because research is now showing that unlike glucose or galactose, fructose, when eaten in large amounts, can harm our health and contribute to obesity and it can do so in a manner that is totally different than any other sugar, especially glucose.
When we eat fructose, it cannot be chemically processed or used in any way by our body until it has been chemically changed into glucose or other molecules by the liver. Thus, fructose itself can be absorbed into the blood from the gut, but it must and will be processed by the liver before energy can be extracted from it and before it can be utilized in any useful manner. Unfortunately, the liver can only "process" fructose slowly. So when we eat something like an apple which has a little fructose and a lot of fiber, the fructose is absorbed slowly and the liver is "happy". On the other hand, when we drink a 64-ounce soda sweetened with high fructose corn syrup, the fructose contained therein is very rapidly absorbed leading to a very rapid increase in blood fructose concentration. At this point the liver's ability to convert fructose into glucose become "saturated"; essentially the liver can't work fast enough. The consequence of this saturation is that the liver begins to convert fructose into fat, specifically into "triglyceride". This can damage the liver and raise blood levels of triglyceride thereby increasing a person's risk for heart disease. Excessive fructose intake may be the second leading cause of fatty liver change (second to alcohol abuse).
Worse still, fructose appears to cause people to become insulin resistant. We have already seen how high-glycemic index foods can lead to insulin resistance, but fructose, even though it is technically a "low-glycemic index" food, may be even worse.
Finally, when normal-weight rodents (mice or rats) are fed a high-fructose diet for several months and then allowed to eat freely after that, they become morbidly obese because they have become resistant to a hormone called leptin. Similar rodents who were fed high-glucose diets do not become obese: they revert to a normal weight. Thus it appears that high fructose diets in rodents cause leptin resistance and obesity.
Is the same thing true in humans?
It may be.
Humans, like mice, produce the hormone called leptin, and leptin's primary role in all of us is to suppress appetite and eating. Does fructose trigger leptin resistance in people like it does in rodents? The jury is still out on that question; but obviously, it might. Further research should clarify the answer.
Summary of Data on Fructose:
Although there is legitimate controversy surrounding the matter, abundant scientific evidence suggests that fructose can act as a metabolic poison in the human body and thereby lead to obesity and fatty damage to the liver. These effects are proportional to the amount of fructose consumed and to the amount of time (years) that it is consumed. Small amounts of fructose found in whole fruits are not harmful.