McCarbthyism: The woefully misguided war on carbs
It’s spreading like wildfire. The sugar paranoia has now extended to fruit juices in full force. A recent article in the Guardian titled, “How fruit juice went from health food to junk food” painted a picture of fruit juices as the latest culprits in the sweet science of obesity. You see, fruit juice has sugar (from the fruit of origin), and much of that sugar is fructose, and of course, we know for certain that fructose is the reason for the growing epidemic of obesity. Forget the chips and fries and the fact that per capita we consume over 500 kcals more per day of total food than we did in in 1970, before the rapid rise in obesity. Forget that most of those 500 extra kilocalories come from added fats and oils along with flour products. Forget that the increase in sugar consumption has been minor by comparison. According to the USDA food availability adjusted for loss data, our consumption of sugar has increased from 333 kcals per person per day in 1970 to 367 kcals in 2010. It peaked in 1999 at 422 kcals and has been on the decline ever since even as the epidemic of obesity continues to rise. Added fats and oils have been on a steady increase during that same time, going from 335 kcals per person per day to 589 kilocalories, but let’s not divert too much. The article is about fruit juice.
So, how much fruit juice do we drink? In 1970, according to the USDA, we downed about 5.5 gallons of the sweet nectar per person per year (not adjusted for loss). If you figure that the average glass of juice, fresh, frozen, or bottled is about 130 kcals per 8 ounces, that’s about 31 kcals per person per day. As of 2010, that figure was 7.2 gallons, or about 41 kilocalories. That’s a mere 10 kilocalories more of juice more than we were consuming in 1970. The peak year for fruit juice consumption was 1998, similar to that of sugar consumption, when downed 9.2 gallons per year (52 kcals per person per year). And in parallel with consumption of added sugars, fruit juice consumption has continued to decrease since that time, which begs the question; what’s the problem? Fruit juice consumption is a fraction of our total sugar intake, which has been receding for about 15 years and in total makes up a smaller percentage of our kcals than it did in 1970 (14% now vs. 16% percent of kcals then).
So, what do we gain by frightening people away from fruit juice? We could save them a few kcals, but at a price. We reinforce the argument of that sugar is more fattening than other sources of kcals, regardless of the source. In this case, the source could be fresh fruit juice, rich in micronutrients and phytochemicals. Now, granted, there are advantages to eating whole fruit. The obvious advantage is fiber, beneficial to digestion. The side benefit is supposed to be that sugar is absorbed more slowly, which appeals to the argument glycemic index should be considered the prime determinant of the value of carbohydrates. Of course, this argument has so many holes in it that it is the subject of other articles in this blog. It also flies in the face of the war on fructose that casts it as the demon sugar, the real reason for obesity based mostly on studies where rats are fed unrealistically high levels of fructose to the tune of 65% of kcals. Fructose has an extremely low glycemic, which would make the fiber issue mute. Somehow the negative effects of fruit juice seem to magically disappear with the addition of fiber.
The war on sugar sounds so good on the surface that it has become politically correct to support it. But just scratch that surface and you have a tangled knot of reasoning that goes nowhere, that ignores the contribution of fat, which has never decreased in the modern diet despite claims to the contrary. The entire war on sugar and the advice that stems from it is less effective than the old advice to give up dessert for a while if you want to lose weight. And that’s the real problem; In the modern diet we have so mishandled the information on carbohydrates that we can no longer distinguish dinner from dessert
Today the unofficial dogma seems to be that carbohydrates are primarily responsible for obesity and type-2 diabetes. The corollary of this dogma is that carbs, particularly sweet carbs, are items that we simply can’t leave alone regardless of how bad they are for us. Therefore, they must be addictive. Have we gone too far with the carbs-are-to-blame-for-everything strategy? Where will it end? What’s the long-term goal of this approach? Will we effectively say anything more than, “don’t eat too much dessert?” Why are some authors calling for us to treat sugar like cocaine, nicotine, and other known addictive substances? What’s the evidence indicting sugar as an addictive drug?
Because obesity is spreading globally with no end in sight, neuroscientists from the American National Institute on Drug Abuse have suggested that “highly palatable foods,” particularly those rich in added sugar, could be compared to addictive drugs like cocaine. This idea that food addiction explains the uncontrollable spread of obesity is becoming increasingly popular. In fact, some authors suggest that as many up to 20% of the population would present addiction like symptoms to such foods, a proportion similar to heroin users become addicted to the drug. It has been suggested that the widespread introduction of calorically-dense foods in the 20th century parallels the introduction of distilled drinks in the 17th century and injectable synthetic drugs in the 19th century. Proponents of the sugar addiction hypothesis believe that humans were simply not prepared for the rapid introduction of this highly purified substance (though it is in reality no different than stumbling onto a honey-rich hive.
As one can imagine, the sugar addiction hypothesis fosters intense debate. Consider what’s at stake. Sugar producers are not happy with their products being compared to addictive drugs. On the other hand, producers of sugar substitutes have an interest in selling substances that can be advertised as helping to break the modern addiction. And of course this notion places neuroscientists in the center of the discussion regarding obesity and type 2 diabetes. So what is the strength of this argument that hyperpalatable foods, in particular sugar, are so addictive that they can account for the epidemic of obesity and type 2 diabetes in the modern world?
Consider the effect of addictive drugs. After inhalation or intravenous injection, they quickly cross the blood-brain barrier to interact or interfere with molecules at the surface of brain cells. The physical/chemical mechanism of addiction can be attributed to four major mechanisms that reinforce self-administration 1) increased dopamine neuron firing 2) enhanced relative dopamine transmission 3) blockage of dopamine reuptake, 4) increased cytosolic dopamine levels.1 In other words, drugs like cocaine interfere with the metabolism of dopamine, an important neurotransmitter necessary for learning. The result is an alteration in mood and behavior that affects judgment and perception such that users may become a danger to themselves and to others. Yet at the same time, the drug can bring on feelings of euphoria. How is this effect matched by sugar?
According to a recent review in Current Opinion in Clinical Nutrition and Metabolic Care,2 foods high in sugar can change brain activity in the following ways: First they stimulate specialized sweet taste cells in the mouth. Then they stimulate the secretion of glucose, “the most drug-like feature.” From there we go to anecdotal evidence that states “people often report seeking out and consuming sweet foods for their drug-like psychoactive and mood-altering effects.” People eat sweet foods to “experience highly rewarding sensations, to cope with stress (e.g., stress or comfort eating), pain or fatigue, to enhance cognition and/or to ameliorate bad mood (e.g., relief of negative affect).” To corroborate this anecdotal evidence, the authors point to studies suggesting that sweet foods in different populations (e.g., adolescents at risk to develop depression; obese women) can elicit “different desirable drug-like psychoactive effects, including affective comfort and alleviation of depressed mood.” However, this is not in itself a convincing indictment of sugar as an addictive substance.
Despite the observations that some people seek out sweet foods for comfort and relief of depression, the magnitude of the “psychoactive effects” is mild and does not seem to match those of drugs2. In other words, sweet foods are clearly not as behaviorally and/or psychologically toxic as drugs of abuse can be, especially at high doses. For an example, unlike drugs, consumption of sweet foods, even when extremely high in sugar, fail to produce any abnormal mental state or change in behavioral disposition. This is why a policeman will not arrest a driver for eating several doughnuts before driving or why “no judge will consider drinking half a gallon of sugar-sweetened soda before committing a crime as a mitigating circumstance.”2 If anything, foods rich in sugar may produce more advantageous effects on decision-making and self-control than disadvantageous ones. Apparently actions of mental self-control require more energy as glucose than actions of normal cognitive thought, and thus sugar may boost self-control under certain circumstances.3 Self-control is more depleting and demands more energy replacement for the affected cells. Since the brain runs on glucose, it’s not surprising that eating sweets yields a reward signal. But that’s not all.
In contrast to behavior associated with addiction to drugs, the desire for sugar and sweetness in foods both may actually promote a helping attitude and encourage cooperation among people.5 It thus seems inappropriate to compare sugar with addictive substances like cocaine from the standpoint of disrupting the metabolism of neurons in creating antisocial and dangerous behavior. Obviously we have to look in another direction to demonstrate that sugar is an addictive substance. The problem of sugar addiction must lie in the excessive reward department. Is sugar just so tempting that it forces us into addiction similar to cocaine? Here the evidence is very circumstantial.
The sugar addiction hypothesis rests on the fact that sugar stimulates reward centers in the brain, the same reward centers stimulated by cocaine, and thus the comparison. In fact sugar and sweetness can be just as rewarding, if not more so, than addictive drugs. In fact, that seems to be the entire case. Sugar sweetened foods are addictive because we like them and because we have a difficult time curbing our craving for them. Therefore they must be addictive. Concludes Ahmeda et al., “Although more research in humans is clearly needed to confirm this conclusion, there is now solid evidence in nonhuman animals showing that sugar and sweet reward can even be more rewarding and attractive than addictive drugs, probably owing to an underlying robust neural substrate. Such biological robustness may be sufficient to explain why people can have difficultly to control the consumption of foods high in sugar when continuously exposed to them.”2
Never mentioned in this entire argument is the fact that glucose supplies energy to the brain, energy that is critical to its function, something you are tempted to overlook when speculating about sugar addiction. By this reasoning, one might conclude that sugar has somehow entered the brain’s exclusive cocaine-rewarding domain, resulting in addiction. The entire sugar addiction proposition is stated backwards. Sugar is rewarding because glucose is a vital energy source, not because it imitates the action of cocaine. Cocaine is the invader of whatever sensing mechanism rewards the detection of brain fuel. Certainly this is a more satisfying and useful conclusion that sugar addiction.
Following the sugar addiction hypothesis to its logical conclusion would lead us to treating sweets as controlled substances rather than merely desserts. In fact, that is the opinion of some authors. Is it just me, or does this seem insane? Certainly there must be a better explanation for the attraction to sweets than sugar addiction, one that leads to a simple and practical strategy. If we persistently crave a source of energy, then maybe it’s because we’re lacking energy. It’s far more useful to ask if the persistent craving for sugar among modern humans is a reflection of both the need for energy and the inability to obtain that energy from sugar alone as a source of carbohydrate. Consider what we already know.
We know for example that athletes need a continuous supply of energy in the form of glycogen, a storage form of glucose. We know that unless starch is a prominent part of the diet, glycogen storage is inadequate. We know that in type 2 diabetes, glycogen storage in muscles is compromised. We also know that the brain requires a glycogen store as a starting point of the energy it derives from glucose6. Our craving for glucose isn’t new, but it has always been tempered or complemented by the desire for starch. Here I refer to boiled starch, as baked and fried starches function as sugars. Once we recognize that starch is the necessary complement to sugar, the need for a sugar addiction hypothesis as a motive for overeating vanishes. The simpler explanation is that a deficiency in boiled starch generates the increased need to enhance glycogen stores. The seemingly persistent need for sugar is a reflection of the futility of obtaining glycogen stores for muscle and brain on a reasonable amount of calories when boiled starch consumption is inadequate.
Which seems like an easier course of action? Should we pursue the sugar-is-addictive course of action that places us at war with our own biology and will lead us nowhere? Or should we teach people the difference between dinner and dessert when it comes to carbohydrates? It should be noted that Kenyan distance runners routinely consume 20% of their energy as sugar without becoming addicted.7 At least 50% of their energy comes from boiled starch in the form of corn, beans, rice, and poached potatoes. Our present consumption of sugar is about 14% of kcals, and our boiled starch consumption is about 2 to 3% of kcals. The remainder of our carbohydrates comes from baked and fried starches, which affectively act like sugars. There is nothing mysterious about the craving for sugar once you understand that the two forms of carbohydrate work together to supply energy, which is why they so often naturally occur together in healthy diets. The credibility of the sugar addiction hypothesis rests only on the fact that we’ve chosen to ignore the unique position of boiled starch in our diet. As a result, we’ve allowed it to be virtually eliminated as a staple source of kcals over the last four decades, particularly from the fast food menu. When you turn all of the modern carbohydrates into cake, then cake seems addictive.
- David Sulzer (Neuron, 2011February 24 titled, How Addictive Drugs Disrupt Presynaptic Dopamine Neurotransmission)
- Serge H. Ahmeda et al, Karine Guillema, and Youna Vandaelea, published in Current Opinion in Clinical Nutrition and Metabolic Care 2013, 16:434–439
- Gailliot, Matthew T., Roy F. Baumeister, C. Nathan DeWall, Jon K. Maner, E. Ashby Plant, Dianne M. Tice, and Lauren E. Brewer, Florida State University, Brandon J. Schmeichel, Texas A&M University, Journal of Personality and Social Psychology 2007, Vol. 92, No. 2, 325–336
- Gailliot et. al in an article titled Self-control relies on glucose as a limited energy source: willpower is more than a metaphor, published in Journal of Personality and Social Psychology 2007.
- Meier BP, Moeller SK, Riemer-Peltz M, Robinson MD. Sweet taste preferences and experiences predict prosocial inferences, personalities, and behaviors, Journal of Personality and Social Psychology.
- Suzuki, A., Stern, S.A., Bozdagi, O., Huntley, G.W., Walker, R.H., Magistretti, P.J., and Alberini, C.M. (2011). Cell 144, this issue, 810–823.
- V.O. Onywera, F.K. Kiplamai, P.J. Tuitoek,M.K. Boit, and Y.P. Pitsiladis. Food and Macronutrient Intake of EliteKenyan Distance Runners. International Journal of Sport Nutrition and Exercise Metabolism, 2004, 14, 709-719.
The following link is to an article that a friend sent my way.
I thought it was interesting to note due to the sheer volume of misleading and contradictory information as well as the leaps of logic that characterize the present war on carbohydrates. The bombastic title is designed to grab everyone’s attention. Is everything we’ve been told about how to eat wrong? What is this claim based on? Apparently, central to this supposition is the fact that we have an obesity epidemic that is spreading worldwide and the recommendations for healthy eating put out by the USDA haven’t changed significantly since 1977, which, by the way, is not the origin of government guidelines, only the date of the McGovern committee. There have been food group recommendations since the ‘50s and general guidelines for nearly 100 years.
The claim that nothing has changed since the ‘70s other than the fact that as a nation we got fatter of course is nonsense. Look at the USDA website (when it comes up again due to the government shutdown) and what has changed is obvious; we consume over 500 kcals more per person per day than in 1970, most of which comes from added fats and oils and flour, along with a smaller increase in sugar. We eat less fresh potatoes and much more French fries, and there has been a massive increase in the fast food industry that has a much greater influence on out diet than any guidelines. The author spends a great deal of time criticizing conclusions drawn from The Nurse’s Health study quoting Gary Taubes, a prominent Atkins disciple and self-proclaimed guardian of “good science.” The point the author wants to make is that epidemiological studies due not demonstrate cause and effect, only correlations. It’s not new information. In fact, there are misleading conclusions drawn from the Nurse’s Health Study, particularly regarding the negative effects of potatoes on our health.
Now consider the authors theme: Since USDA guidelines haven’t changed much since 1977, the scientists who promoted the guidelines should be blamed for the obesity epidemic. Is there any demonstration that Americans have assiduously followed USDA guidelines? Have Americans even come close to following any government-suggested guidelines? Are the USDA dietary recommendations perfect? No, they are not perfect, but that’s not the claim of the article. The claim is that “bad science” in the form of dietary recommendations has given us faulty information, not some faulty information, but all faulty information. Yet the entire theme of the article is based on a faulty premise that the guidelines themselves are responsible for obesity, not the application or lack thereof.
All of the opinions quoted and the limited data presented are from one or two authors already committed to promoting extreme low-carb diets, authors who scour the literature in search of anything that suggests their extreme opinions may have some validity. The leap in logic is that since dietary recommendations regarding fat and cholesterol are based on studies that are incapable of demonstrating the specific link to heart disease, that we know nothing about healthy eating and should pay attention to Gary Taubes who promotes a very high fat diet, nearly double the present fat intake, a position that has no scientific support other than the distortions integral to books mentioned in the article. Note that the author’s conclusion on diet suggests that starches should play no role in the modern diet. This of course ignores that fact that grains, beans, and potatoes constitute a food group that has fed virtually all civilizations for thousands of years and has never been associated with obesity until the modern diet became “Westernized.”
This type of writing unfortunately shapes a lot of public opinion with regard to carbohydrates. Understanding carbohydrates is the key to planning a healthy diet and yet there is no other topic in nutrition in which there is more misinformation. If you are looking for someone to blame for the obesity epidemic, look no further than the media that publishes ridiculous articles like the one above. It’s not scientists fault that people continue to follow celebrity gurus that offer quick fixes. Personalities sell diets, not science.
On a side note, it is amusing that this article appears in a media outlet that considers itself left-leaning while at the same time advocating a diet that would bring starvation to billions of people. Placing the world’s staple foods off limits for the sake of meat and fat not would be a disaster for the environment and for billions of people who would be displaced to grow food for animals instead of people. Science journalism has reached a new low.
How many times have you heard the following statement? “Science has proven that we don’t need carbohydrates at all.” This is always stated as if it was some kind of revelation and of course justification for a very low carb diet. If you don’t need to eat carbs, that must prove that they are useless, and therefore we shouldn’t eat them, right?
Considering the popularity of the current low-carb diet fads
in America, why is quinoa suddenly all the rage? Quinoa is, after all, a grain and grains are
full of carbohydrates and carbohydrates are the cause of the obesity epidemic,
right? The reason for the spike in
quinoa consumption in America is simple.
Quinoa is marketed as a high-protein
grain (sorry) food as if the
fact that it’s a grain (shhhh) grain-like substance doesn’t even
register in peoples’ minds. It’s amusing
to read article after article touting quinoa as “super food,” “gluten-free,”
and “high in protein.” (It is of note
that there is no scientific definition of super food. The term exists as an
advertising slogan only. A super food is
anything you want it to be.) starch
(sorry) complex carbohydrates. Starch is
off-limits for low-carb dieters who mistakenly believe that it leads to
obesity. We have to hear about quinoa
being high in protein and fiber, never mind the fact that you can get about the
same amount of protein in a large potato as you can form one cup of
quinoa. And of course since the only
good carbohydrates are the ones you can’t digest, quinoa is touted for its
fiber content, even though that same potato carries more fiber a cup of quinoa.
Potatoes have been branded as “bad” carbohydrates while quinoa, isn’t branded
as a carbohydrate at all.
grain (damn!) food are playing to the modern of carbohydrate phobia
and participating in the general miseducation when it comes to nutrition. If
Americans were educated in nutrition they’d know that starch (when boiled or
steamed) is itself an important nutrient that structurally resembles glycogen,
the critical store of glucose held in muscles, liver, and brain. Boiled potatoes rank far higher on the
satiety index than any protein, and the idea that fiber provides satiety is
absurd considering fiber provides little to no energy. The truth is that starch, is satisfying,
nourishing, and helps to fill the body’s glycogen stores. Starch provides a lasting form of energy and
yet advertisers must avoid mentioning this key component in quinoa for fear
that the public will see it as fattening.
Lucky us, another celebrity, Gwynneth Paltrow, has come up with a diet book, this one pushing all the right low-carb buttons, no doubt arrived at by Paltrow’s extensive nutrition research and understanding of biochemistry. Let’s see what low-carb buttons do we have to push in order to make a lot of money on a diet book? You have to prattle on in the usual manner about refined and unrefined carbohydrates and give some kind of incoherent explanation about how the unrefined ones raise insulin levels and make you fat, because of course everyone knows that the only job insulin can do is to make you fat. It can’t possibly drive glucose into muscle cells so that they can store glycogen, which gives you energy to move. We don’t really need glycogen anyway; it’s a carb, and all carbs suck. We don’t need energy either. We’re better off living in a state of ketosis. Never mind that your brain uses 20% of your resting energy and that your brain runs on glucose, using ketones only in an emergency, since it won’t run on fat.
And speaking of ketosis, if you really want to sound like a deep and thoughtful reviewer of Paltrow’s book, you’ll say something like this: “no one, not even a child, actually "needs" to eat carbs.” Yes we can make carbohydrates from non-carbohydrate sources, like protein. We do it when we’re starving or when we give up carbohydrates because we read a celebrity diet book. Can we make enough glucose to keep us out of ketosis? Of course not, not even close, but that doesn’t matter. Why let facts get in the way of a deep philosophical point. Here’s a philosophical point to ponder: Your body will sacrifice protein from vital organs just to make glucose in order to keep your blood sugar stable when you’re starving. Maybe eating carbs isn’t such a bad idea after all.
Another good button to push is one that sounds the alarm about starches, starchy carbs, and especially refined starchy carbs. The word starchy sounds really nasty and fattening. Why would anybody eat starchy carbs? I don’t know, why don’t you ask billions of Asians who have used rice as a staple food for thousands of years without becoming obese until they switched to a westernized diet? Better yet, why not ask all the best marathon runners in the world, or any athlete who needs endurance? Maybe they would say that without starchy foods they get that “special hunger,” the one Paltrow likes her family to experience, and lose the race. There’s actually a very good reason why all civilizations have built their diets or around starchy staples. The fact that we don’t understand how to use them in the modern diet doesn’t negate their importance.
And of course there’s always the gluten-free button to push. It should be noted that gluten isn’t a carbohydrate but rather a protein that occurs in a very few grains, like wheat and its relatives and to a lesser degree rye and barley. Gluten is only a problem for people with celiac disease, a very tiny portion of the population. And even if you do have to stay away from gluten, you don’t have to live on a low-carb diet, and certainly not a no-carb diet. The vast majority of starchy foods contain no gluten. By the way even though the headlines in the Guardian say “no-carb diet,” it’s really nothing of the sort. The title is there just to grab attention. The language surrounding low-carb diets is generally very sloppy, which allows authors an escape clause. And you need an escape clause because no one stays on a low-carb diet without cheating. Cheating is part of a low-carb diet. It’s a necessity. It’s a protective instinct that helps you survive the reading celebrity diet books.
Dr. Oz is at it again peddling a new promise in a bottle. It’s hard to keep up with his product endorsements. It seems like every episode of Dr. Oz show ushers in a new group of gullible Americans willing to fork over their hard-earned cash for the promise of an easy weight loss solution in the form of a pill. The latest product is Raspberry Ultra Drops that is the supposedly the “hottest” new supplement to hit the market, never mind the thousands of other supplements that have promised the same results and have failed to deliver anything other than profits to a CEO. Raspberry Ultra Drops contain a “powerful African mango extract” that “has been shown in medical studies to be beneficial.” The fact that the mango extract is African always seems to impress consumers who continue to believe the secret of lasting weight loss lies hidden in some exotic location. Among the other typical phrases used by the diet industry to hawk their products are the claims that these drops have “top fat-burning ingredients” that “can help detox your body.” Of course there is no mention of how these fat-burning ingredients work, nor is there any mention of how this product detoxes the body (whatever that means).
Billed as Mediterranean Diet vs. a low-fat diet, the latest dietary study published in the New England Journal of Medicine blasted across the headlines as if it was going to finally blow low-fat diets out of the water and demonstrate their ineffectiveness compared to a higher-fat the Mediterranean-style diet, rich in nuts, fish, and olive oil. “Low-fat diets have not been shown in any rigorous way to be helpful, and they are also very hard for patients to maintain, a reality born out of the new study,” said Dr. Stephen E Nissen, Chairman of The Department of Cardiovascular Medicine at the Cleveland Clinic Foundation. “Now along comes this group and does a gigantic study in Spain that says you can eat a nicely balanced diet with fruits and vegetables and olive oil and lower heart disease by 30 percent. And you can actually enjoy life.” Okay, just to be clear, the American Heart Association and the American dietetic Association have always recommended a diet rich in fruits and vegetables with healthy fats like olive oil. But let’s get back to the study and see how hard it was for subjects in the” low-fat” group to maintain their diet.
Let’s look at the protocol of subject support as presented in the supplemental information presented in the New England Journal of Medicine along with the study. There were three groups, one given supplemental olive oil, (4 tablespoons per day), one given supplemental nuts (1 oz per day), and a control group, given instructions to lower their fat intake. Under the section titled peculiarities of the intervention by group assignment, you could read the details of instructions given to the groups. They are summarized as follows:
Mediterranean diet groups
Dietitians gave the subjects the following list of recommendations: a) use olive oil abundantly in cooking and dressings b) consume at least two servings of vegetables per day (one of them fresh) c) consume at least 2 to 3 servings per day of fresh fruits including natural juices d) eat legumes at least three times a week e) eat fish at least three times per week, including fatty fish f) eat nuts more than once a week g) eat white meats rather than red meats h) cook at least twice a week using tomato garlic and onion with or without herbs to dress vegetables, pasta, rice, and other dishes. The dressing is called sofrito. Those are the dos.
Eliminate or limit cream, butter, margarine, cold meat, pate, duck, sugar- sweetened beverages, pastries, industrial bakery products (cakes, donuts, or cookies), industrial desserts (puddings, custard), French fries, or potato chips, precooked cakes and suites.
Then there were the dietitian’s demands: the two meals a day seated at a table for at least 20 minutes. If you drink use wine, 1 to 3 glasses per day. Eat the following items whenever you choose: nuts, eggs, fish, seafood, low-fat cheese, chocolate, and whole grain cereals. Limit cured ham, red meat (all fat removed), fatty cheeses. Supplemental nuts and olive oil were supplied to the appropriate groups.
Reinforcing these guidelines was a 14-item questionnaire that scored participants according to their compliance so that adjustments could be made individually to assure that recommendations were met. This was supplemented by quarterly meetings. Subjects were monitored with urine tests for markers of olive oil and nut consumption.
The control group
Instead of a questionnaire, the control group was given a leaflet that contained recommendations for following a low-fat diet. It included a list of low-fat foods to purchase, including bread, cereals and pasta, rice, potatoes, fruits and vegetables, beans, lentils, and chickpeas, low-fat milk, cheese and other dairy products, lean fish and seafood, chicken and duck with skin removed, and low-fat meats. There was also a list of foods to avoid and instructions to cook with less fat and how to remove fat from foods. The following is part of the cooking instructions. “Employ simple cooking methods, such as boiling, baking or broiling. Avoid stewing, frying, breading, and the use of sofrito (a kind of salsa that is used to dress vegetables pasta and rice).
After the initial meeting, when the control group was given cooking instructions, they were presented with the leaflet and told that the next meeting would be in one year. In other words, the control group was not given the intense monitoring and encouragement to follow protocol as was the experimental groups. The quarterly meetings for them did not begin until after three years into the study. “In October 2006, three years into the trial, we realized that such a low grade intervention might potentially represent a weakness of the trial and amended protocol to include quarterly individual and group sessions with delivery of food descriptions shopping lists, meal plans and recipes (adapted to the low-fat diet) in such a way that the intensity of the intervention was similar to that of the Mediterranean diet groups, except for the provision of supplemental foods for free.”
Is it any wonder that there was low compliance in the control group? Was it really that a low-fat diet is that difficult to stay on? They were given almost no support for the first three years compared to the experimental groups that were tightly monitored. And just how low-fat was the “low-fat” group? The fat intake reported as percent of calories, beginning of study to end for the three groups was as follows: olive oil group 39.2 ± 6.9 to 41.2 ±5.4, nut group 39.4 ± 6.5 to 41.5 ±6.1, and the "low-fat" group 39.0 ± 7.0 37.0 ± 7.0. Three years into the study, they decided that maybe the lack of intervention and failure to follow instructions on the part of the low-fat group was influencing the study, and they should intervene more. So, there was no low-fat group and compliance was based on vastly different treatment of experimental vs. control groups. It should be noted that low-fat, according to the American Dietetic Association and the American Heart Association is about 20 per cent of calories, Ornish and Pritikin organizations who demonstrate reduction in CVD with diets that use 10 per cent of calories from fat.
Dr. Ornish gave his critique of the study in an article published in the Huffington Post. “The low-fat diet group patients were discouraged from eating fatty fish that are rich in omega-3 fatty acids that are highly protective from cardiovascular disease.” Dr. Ornish pointed out that there was no significant reduction in heart attacks, deaths from cardiovascular causes, or death from any cause. The most important conclusion, according to Dr. Ornish, the most responsible conclusion should be, “We found a significant reduction in stroke in those consuming a Mediterranean diet high in omega-3 fatty acids when compared to those who were not making significant changes in their diet.”
Then Dr. Ornish seemed to repeat the same old low-carb mantra that has become so common in today’s carb paranoid world. “Also, the researchers appear to have done everything they could to bias the outcome in favor of the Mediterranean diet by encouraging the low-fat diet [group]to increase consumption of foods that are known to increase the risk of cardiovascular disease including bread, potatoes, pasta, rice, and not to limit their intake of sodas, which also increase cardiovascular disease risk.” Unless he’s talking about French fries, none of these starches, that are staples for most of the world, are associated with increased cardiovascular disease. In fact, if you look at the Mediterranean pyramid, you’ll find at the bottom, as staple foods, potatoes, rice, and pasta. This is in contrast to the dietary guidelines represented in the Harvard healthy eating pyramid the new Harvard version of the myplate that treats these foods as mere candy.
While the control group was encouraged to increase their use of potatoes, rice, and pasta, the experimental groups were virtually required to do so as part of their use of sofrito and were given specific instructions to avoid potato chips and French fries, but not potatoes. In the end the experimental groups increased their intake of legumes, refined cereal potatoes, and decrease their intake of pastries and cakes, a beneficial change in carbohydrates that favored the use of boiled over baked starches. Of course that is something no one ever reports on even though it would be difficult to show increased health benefit without this change.
There was no low-fat group in the study, so it was not a high-fat versus low-fat diet experiment. And it said nothing about compliance or ability to stick with a low-fat diet regimen. It was however a reminder that experimental and control groups should be treated exactly the same way if results are to be meaningful. In general, it showed what we already knew, that shunning the processed foods, rich in sugar, saturated fat, and baked starch in favor of more fruits, vegetables, and legumes, and changing to healthier fat sources is a good thing. What's disturbing is the lack of journalism in reporting what actually happened.
In the February issue of The European Journal of Clinical Nutrition, one of the cofounders of the glycemic index defended this controversial measure as the standard by which carbohydrates should be evaluated. TMS Wolever attempted to quell the criticism of glycemic index by demonstrating first that common methods of calculation are faulty and partly responsible for the variance we see in many of the tables representing the glycemic index of various foods. A common error is to view glycemic index as simply the area under the curve (AUC) of blood glucose levels over two hours in response to eating the carbohydrate in question compared AUC of the standard, which is generally glucose. That’s an expression of the general glycemic index concept, not of the actual calculation, which is more complex. The real equation takes the average AUC in subject x elicited by the consumption of 50 g of the test food divided by the mean AUC in subject x elicited by the consumption of 50 g of glucose on two or three separate occasions. The final GI is the mean of these calculatrions in n subjects. The current internationally accepted GI method stipulates that n, or the number of subjects tested, must be greater than or equal to 10. A calculation that fails to meet these criteria is not a valid glycemic index.
The implication in pointing out the exact calculation for glycemic index is that the variance we see in glycemic index tables, different values for the same food, is a function of imprecise methodology and that if everybody used the same sanctioned method, there would be no inconsistencies or at least they would be minimal. In other words, white rice would not be 49 and 89 in the same table. Boiled potatoes would not vary from one table to another. This may or may not be true. However, even if you could guarantee precision in all tables everywhere, that wouldn’t explain the most glaring flaw in using glycemic index as an indicator carbohydrate value—false equivalency.
Inherent in glycemic index is the assumption that if two foods have the same number, they are effectively equivalent. They produce the same metabolic results. In other words jellybeans are equivalent to boiled potatoes because they have the same glycemic index, and I’m perfectly justified in treating them as equivalent foods with respect to carbohydrates. Pizza and many candy bars are equivalent to beans, though these seem like ridiculous comparisons. Yet no one tests glycemic index to see if these comparisons are valid. In other words, we never try to make glycemic index fail. Researchers set up experiments that are designed to demonstrate its validity by only testing certain foods. This protects glycemic index from serious scrutiny.
The following is a quote from Walter Willett of the Harvard school of Public Health in regard to the use of glycemic index in planning a diet. “You can’t use the glycemic index to rule your dietary choices. For example, a Snickers bar has a glycemic index of 41, marking it as a low glycemic index food. But it is far from a health food. Instead, use it as a general guide. Whenever possible, replace highly processed grains, cereals, and sugars with minimally processed whole grain products. And only eat potatoes—once on the list of preferred complex carbohydrates—occasionally because of their high glycemic index and glycemic load.” Glycemic index has enough credibility to condemn potatoes but not to endorse Snickers bars. Now according to Wolever, it is unfair of me to criticize glycemic index in this manner because I’m confusing glycemic index with glycemic response. “GI is one determinant of glycemic response; others include the amounts of carbohydrate, fat and protein consumed.” So, what we’re calling the glycemic index of the Snickers bar is in reality the aggregate of values for the Snickers bar components. Does that really matter when it comes to practical application? Okay let’s bend over backward to be fair and only compare carbohydrates that are low in fat.
According to glycemic index tables presented by the University of Sydney website, boiled potatoes have a glycemic index of 89 or 49, depending on which value you choose. Let’s assume 89 is the correct number because we know that boiled potatoes have a high glycemic index. The figure 49 may have been a problem with methodology. Boiled rice also has a high glycemic index, 75 to 89. For comparison will use jellybeans, which have a glycemic index of 80 and are low in fat. Boiled potatoes and steamed rice have sustained populations for thousands of years without generating obesity or diabetes as an inevitable consequence. Could they be replaced by jellybeans? If glycemic index is to be considered the primary determinant of good carbohydrate, the answer should be yes. Here’s how Wolever handles a similar criticism:
“In a debate about the clinical utility of GI at the 2010 Experimental Biology meeting, it was suggested that GI had limitations as an indicator of carbohydrate quality because many high GI foods such as whole grains and starchy vegetables are linked to positive health outcomes, while many low-GI foods, such as sugar-sweetened beverages (SSB) and fructose, are linked to negative health outcomes. Are these statements accurate?” Wolever’s answer is to deny the question. “Do whole-grain foods and starchy vegetables have a high GI? In the 2002 GI tables, there are 102 values for wheat and rye breads of which 35 are whole grain or whole meal. The mean GI for the 35 whole-grain breads, 63.3, is equivalent to that of the 67 other breads, 63.1, and the distribution of low- (<55), medium (56-69) and high-GI (?70) values for the whole-grain breads, 23, 46 and 31%, respectively, is similar to that for the other breads, 21, 34 and 45% (P=0.40). Similarly, for the 46 GI values for mashed, sweet or whole potatoes, 20% are low-GI, 28% medium-GI and 52% high-GI. Finally, of the 20 GI values for soft drinks, sports drinks and sucrose, 10% are low-GI, 60% medium-GI and 30% high-GI. Thus, it is incorrect to assert that whole grains and root vegetables have a high GI and SSB have a low-GI. In reality, the GI of all of these foods may vary widely depending upon their variety, composition and processing.” In other words, there is too much variation in glycemic index tables to pay attention to any so-called anomalies. So rather than test the hypothesis that glycemic index is the primary determinant of carbohydrate value, we must simply accept it as fact. But that’s not the only thing we should accept as fact.
Glycemic index obliterates the distinction between simple and complex carbohydrates. Previous to glycemic index jellybeans, would have been considered simple carbohydrates (sugars) while potatoes and rice would have been considered complex (starches made of chains of sugars). But now we are to simply accept that this distinction does not matter. Structure and function are not linked. Again quoting Willett, “Dividing carbohydrates into simple and complex makes sense on a chemical level. But it doesn’t do much to explain what happens to different kinds of carbohydrates inside the body. For example, the starch in white bread and French-fried potatoes clearly qualifies as a complex carbohydrate. Yet the body converts this starch to blood sugar nearly as fast as it processes pure glucose. Fructose (fruit sugar) is a simple carbohydrate, but it has a minimal effect on blood sugar.”
So what evidence supports the bold declaration that we should now alter the definition of complex carbohydrate to fit glycemic index? Glycemic index itself! If we start with the assumption that the only functional difference between simple and complex carbohydrates is rate of sugar absorption, we are free to simply redefine simple and complex as fast and slow sugars. And since fast and slow sugar is the same as bad and good sugar, the circle is complete. Slow carbohydrates are by definition complex carbohydrates, and fast carbohydrates are by definition simple carbohydrates. And if a carbohydrate is associated with a good outcome, it has to be low glycemic, and if a carbohydrate is associated with a bad outcome, it has to be high glycemic. There are no anomalies because we don’t accept them.
Does the precision of the methodology really matter?
Glycemic index simply declares itself valid because it has a precise methodology for measurement, even though it’s not universally applied. Supporters of glycemic index don’t bother to test the anomalies because the story is so plausible it must be true. Fast absorbing sugars are bad slow absorbing carbohydrates are good. However, precisely because of these anomalies, the best we can glean from glycemic index after thirty years of research is that we should eat less processed food, more fruits and vegetables, and more whole grains. At worst, it misleads us and limits our perspective, suggesting that healthy staples like rice and potatoes are associated with obesity and type II diabetes based on a measurement that declares itself valid. Am I being unkind with that statement? Following is a quote from that same paper:
“This paper addresses the question of whether the GI is a valid marker of carbohydrate quality. The Oxford dictionary defines ‘valid’ as ‘sound, defensible; well-founded’. This subjective definition suggests that validity, like beauty, is in the eye of the beholder. I believe that the GI is valid because it fulfills the following conditions: (1) GI methodology is standard, accurate and precise; (2) GI is a property of foods (that is, it has the same value in nearly everyone); and (3) GI is biologically meaningful and influences outcomes in health and disease in ways that are relevant to almost everyone. Furthermore, there is good evidence that GI beneficially influences more and different health outcomes than other commonly used markers of carbohydrate quality such as whole grains and fiber and, therefore, ought to be part of nutrition recommendations.”
Notice there is no suggestion of a mechanism by which glycemic index can influence so many outcomes given the vastly different composition of foods with the same GI value. Let me suggest a real test of that validity and an explanation of its anomalies that makes sense. Glycemic index depends for its credibility on boiled starch. Remove boiled starch from the glycemic toolbox and you have nothing of value. Make glycemic index succeed on its numbers alone, on its precise measurement of foods that contain no boiled starch, and the healthy outcomes will disappear. The validity of glycemic index is indeed in the eye of the beholder. If the selection of low glycemic foods leads you to boiled starches like beans and brown rice for example, then you’ll see a healthy outcome, but not because of the glycemic index. That’s just boiled starch doing what it generally does, making muscle cells more responsive to insulin and thus reducing insulin resistance. You will not get the same outcome by selecting pizza or ice cream or candy bars that have the same glycemic index as these healthful foods. We know the results of using boiled starches as a staple source of calories within the context of an otherwise balanced diet because it’s been done over and over for thousands of years in countless civilizations. And the healthy outcomes aren’t dependent on glycemic index, boiled potatoes and steamed white rice that have a high GI value will do just fine.
Wolever. “Is Glycaemic Index (GI) a Valid Measure of Carbohydrate Quality?” European Journal of Clinical Nutrition (2013), 1–10.
In an effort to resolve the supposed controversy surrounding the calories in calories out “hypothesis” that states that overeating leads to weight gain, science journalist and anti-carb advocate has co-founded the non-profit Nutrition Science Initiative to answer questions about what drives obesity once and for all. Taubes has made the argument for years that carbohydrates drive obesity and that people can’t get fat from eating fat in what he terms the alternative hypothesis. According to Taubes, insulin is the “fattening” hormone that is largely responsible for the current obesity epidemic. By ignoring the main function of insulin, to drive glucose into muscle cells so that they can use the glucose to make glycogen, Taubes makes the case that obesity is a matter of conspiring hormones and that that endocrinologists have known for 50 years that “insulin regulates fat accumulation.”