This is point of inquiry, welcome to Point of Inquiry, a production of the Center for Inquiry.
I’m your host, Lindsay Beyerstein, and my guest today is iconoclastic science journalist and researcher Gary Townes. He’s here to talk to us today about his new book, The Case Against Sugar. Gary, welcome to the program.
Thanks for having me.
What inspired you to write the indictment of sugar?
Well, somebody had to hit up, which is about as good an answer as I could give. You know, my research over the years had which I mean, arguably more research on the history and of the science in this field than than anyone had ever done, had come to the conclusion that when we talked about sugar, we were then the arguments about sugar and the health effects about sugar were all misguided or misconceived. And then some one reason for that was because of the influence of the sugar industry and helping sort of shape the arguments. And so I thought somebody had to write a book that kind of correctly laid out what the arguments were. And that’s what I did, assuming I’m correct.
And when you say sugar, are you talking specifically about the white granular stuff or just seem to have a broader purview?
Well, I’m talking about. Yeah, beaten cane sugar, which is the white or brown granular stuff, depending on how refined it is. I’m also talking about high fructose corn. Sirup and other high fructose are up so that we don’t tend to use others to a great extent, the US. So these are these are mixtures, roughly 50/50 mixtures of glucose, simple carbohydrate and fructose, the fructose that makes them sweet and that differentiate them from the carbohydrates you get from starches, starchy vegetables and breads. A point is that these same sugars are the sugars and fruits. And that’s why fruit patients sweet to us. But the dosage is much greater. So the sugar cane, like an apple, for instance, might be 85 percent water.
And then there’s some fiber and then there’s some sugars and but it’s a very small dose. So the amount of sugar in a medium sized apple is might be the amount of sugar, not three ounces of apple juice. Anmol and might take us ten or fifteen minutes to comfortably the apple. We could drink that apple juice and two swallows.
And so toxicologists like to say the dose makes the poison. We not only do we get a much bigger dose, but we get this dose all day long but it hits our bloodstream and it hits a liver that much quicker, which also influences what we how it affects our body.
How do you come down on things like really simple starches, like, let’s say weight, flour, they get broken down really quickly into sugars. Do they have the same liabilities as their refined sugars themselves?
Well, this is a key question. And there are people who disagree with people whom I respect in the field, who disagree with me. But white flowers and again, starchy vegetables like potatoes are digested and absorbed as pretty much glucose alone. So glucose goes into our blood stream and it raises our blood sugar, which another our doctors often refer to blood sugar as blood glucose, and we metabolize it in virtually every cell in our body.
The cane and beet sugar and high fructose corn sirup again, they. Half of those molecules, roughly half are fructose. And that fructose goes to our liver and we metabolize that primarily in the liver. And the argument is our livers didn’t evolve to basically deal with the amount of fructose that we’re dumping on them in modern diets. And they you know, even if populations consumed plenty of honey, they didn’t do it the way we consume sugar from the 1960s onward, which is basically, you know, starting with breakfast and orange juice and sugar sweetened cereals and, you know, sugary snacks and sodas and more fruit juices and lunch with fruit juice or soda and sugary snacks and fruit juices. So we just have a kind of higher dose to more. You know, it’s a fundamentally different thing than what you’re getting from from starches and breads and again, metabolize. A different organ.
If you approach the case against sugar, what is the charge?
Well, let me tell you what the crime is. OK? Because I do I often revert to criminal justice, metaphore. We have obesity and diabetes epidemics worldwide that inevitably manifest themselves after populations transition from a whatever their traditional diet was.
And again, doesn’t matter whether they were diseased, you know, in you with who were living on Cariboo and s.L Meat and then and famine and or whether they were misi in Africa living off the, you know, the meat, milk and blood from the cattle that they heard or they were agrarian populations or wherever they lived, whenever they transition to Western diet and lifestyle.
You see this explosion in obesity and diabetes and the numbers, particularly in diabetes, are stunning. I mean, you have populations, First Nations, people in Canada, where in the 1950s diabetes was almost impossible to find.
And today one in two adults is diabetic. In the US, you go back to the 19th century, as I do in my book. You’ve got popular. You’ve got to hospital records where, you know, year after year they don’t diagnose a single case of diabetes, despite it being a pretty clear diagnosis and when they were very familiar with. And today, one in eleven Americans had diabetes. Middle Eastern populations were one in five have diabetes. Stunning, stunning numbers. And so the question is, what’s causing it? That’s the crime. And then the argument I make in the book is that sugar why used to be the prime suspect when these epidemics arose. Invariably when these epidemics arose, somebody will say, what if it’s sugar? Because they notice that they tend to follow upon recent increases in sugar and sugary beverage consumption. And yet we got to this point by the 1980s where we saw it as a sort of harmless, benign pause that refreshes. And so that’s that’s what I’m trying to do with this book, is say, you know, let’s get back to this question of why it was and should still be the prime suspect. And then I point out that not only is it at the scene of the crime in every population when these epidemics occur, but it’s also at the scene of the crime in the body where researchers studying diabetes and obesity in particular, there’s a condition called insulin resistance. So we secrete the hormone insulin in response to the carbohydrate content, the carbohydrates we eat. And one of its primary roles is to help us take up the blood sugar as it’s rising and burn it for fuel and type two diabetes, which is the common form of the disease. Ninety five percent of the ninety five percent of all cases are type two and that associate with obesity. And the conventional thinking is it’s caused by obesity. Sensi association is so close, but that’s a disorder of insulin resistance and insulin resistance is thought to start with and buy in from the resistance. I mean, your body’s cells are resistant to the action of this influence. You have to secrete more insulin to do the same job. And that’s thought to start in the liver.
And we all know that correlation isn’t causation. How do we know that the increase in diabetes was a result of an increase in sugar, per say, rather than an increase in calories over rocks? It seems like the two are together.
Yeah, and we don’t, although. We can find populations in the literature. And I point this out, my books, where you have these massive increases in obesity at least, and often diabetes in association with extreme poverty and even malnutrition. So populations where, for instance, the children are malnourished and stunted and mothers or women in the population are obese. And the men have high levels of diabetes.
And so you would I asked myself and I don’t know why the community does. I mean, I discuss it in my books and I can tell you why, but it still mystifies me. If you’ve got starving children, there’s a pretty good chance that the mothers are not eating superfluous calories that they don’t need. Right.
Because in general, mothers will sacrifice anything to make sure that their kids get enough.
Yeah. They didn’t. We wouldn’t be here.
Cancer race would have died out during famines. This would be a and in fact, you know, we know that the biology of a mother, you know, mothers put on fat when they get pregnant so that if they give birth to the child during the famine, they have fuel available on their bodies so that they can still nurse those infants. So you can, in effect, disassociate these obesity and diabetes epidemics in some populations from however you would want to describe, define excess calories if you wanted to design the perfect experiment to prove or falsify this hypothesis.
What would it look like? And why hasn’t it been done yet?
But we do want to design and we have been working on designing the low perfection is virtually effectively impossible to achieve in science outside of mathematics.
So what do you have to do? So the argument of the sugar industry in the argument of the nutritionists and the obesity researchers all along has been that because Type two diabetes associate so closely with obesity and excess fat accumulation, they say it’s caused by access, fat accumulation and then excess fat accumulation is believed to be caused by taking in more calories than we expend. Very simplistic hypothesis that I discuss in depth in my books. So the idea is the way food to influence your body fat, your body weight is through their caloric content or at least the calories that you digest from them. So, you know, carbohydrates, fiber, attach, and then we don’t digest the fiber. It can take more energy to digest protein than fat or carbohydrate. So but ultimately, the idea is that the however many calories make it into your bloodstream are the determining factor. And so it’s the caloric content of the foods that matter. And what I’m arguing is that sugar has effects independent of calories that are all foods have effect independent of calories that are what we should be paying attention to. You could think of it if we were talking about drugs. If we want to know how why anti-depressants did one job and blood pressuring medications that another, we wouldn’t only concentrate on the dose that we give people like milliliters or milligrams. We would talk about the biological effects of the drugs and how they influence enzymes and receptors and the hormones and other factors.
Is this an argument about the nature of causation? So are you saying that, you know, if you look at people who gain weight. Yes. They will have consumed more calories than they expanded. But it was not the consumption of the excess calories that caused them to become overweight. It was something else that caused the overfeeding.
It was well, was something else that caused the excess fat accumulation, which in response cause what we are calling overfeeding nonresponse is cause. So, you know, in metaphor I often use when I lecture. If if if you if a room fills up with people, a restaurant fills up with people, it’s meaningless to say that that more people entered that left because that’s obvious.
The question is, why did people go into that restaurant and not the restaurant next door? And there are a lot of variables that might you might discuss, like maybe the food’s better or they’re having a party or the restaurant next door is closed or it’s 95 degrees and outside and one restaurant has air conditioning in.
The other restaurant doesn’t you know, maybe one restaurant has big bouncers at the door who yank people off the streets and from inside, don’t let them leave. So there are these conditions having to do with the conditions inside the restaurant, the conditions outside the restaurant. The conditions at membrane of the restaurant, which is the door and the big bouncers, but you don’t care that more people into them leave because that’s obvious. But we have this hypothesis of obesity that says that all we care about is how many people enter and leave. So anyway, let me get back to the experiment, which was your question, which is somehow you have to separate out the effect of the calories consumed from the effect of the type of foods that supply those calories. And you could do that by carefully thinking about how to basically use your randomizing your subjects to diets have dramatically different macro to turn composition. So one diet might have a lot of sugar. The other diet has no sugar or one diet might have a lot of all carbohydrates. The other diet replaces all those carbohydrates with fat that will have dramatically different effects on this hormone insulin, which tends to determine whether or not our fat cells want to accumulate fat. And then you have to fix the calories people consume. Scientists say you control for the calories. So you’re only looking at the effect of the macronutrients, independent of the calories, and you’ve been you tried to design the experimental situation such a way that if there is an effect, you maximize the possibility that you’ll see it. Because what we’re looking in, what people often forget is that the kinds of effects that would explain human obesity, common human obesity and so diabetes are exceedingly subtle. So if you store, say, 20 calories a day and you’re fat tissue that you don’t bar, that might be one one hundredth of the calories you consume every day. Or in my case, because I’m a big guy, one one hundred and fiftieth. So I need one hundred and fourteen fifty bites of food, each bite is 20 calories and I burn off a hundred and forty nine and one hundred and fifty. It ends up in my fat tissue every day. I’m going to gain 20 calories a day. I mean, that’s equivalent to two pounds of fatty ear, which is 20 pounds in a decade and 40 pounds in two decades. I’m going to go from being lean in my 20s to obese in my 40s merely by this sort of infinitesimal trapping of calories in my fat cell. So we’re looking for a very subtle effect. And I would argue that it’s too Satoh actually to be detected in any experiment done today, which is again, we’re getting back to this question why these experiments haven’t been done. They have, but they’re usually looking for effects of around 150 calories a day, which is 15 pounds of fat in a year. Independent of how many calories you can. So that’s one hundred and fifty pounds of fat in a decade. So you have to set up the experiment to maximize the possibility that you’re going to see this tiny effect. And that’s an expensive thing to do. And it takes in an excess. You have to really think deeply and critically with, you know, to come up with those experiments. And because of the community has thought, oh, it’s just about eating too much. They never went to that trouble.
What are some of the factors that you would want to see in an experiment to maximize your chances of seeing this very subtle arrangement that you’re looking for?
Well, the first thing you want to see is you want to use subjects who you know. So the idea is something in the diet is causing obesity. Remember, the conventional thinking is that people just do too much and they exercise too little. But something is causing obesity and it clearly doesn’t trigger obesity and everything because the world is full of people who stay lean their whole lives. Right. So how if I mean, maybe they’re just the ones who eat moderation and run marathons because they they have more willpower than the rest of us. But assuming that’s not the case, that they they’re not susceptible to whatever this phrase, that terminology is, obesogenic factor is. So you got to start with people are obese, right? Because that’s the only way, you know, they’re susceptible. Otherwise, if you start with lean people, you’re doing your experiment on the one group. The one part of the population that has proven that they can tolerate whatever this factor is and not accumulate fat because of it. C.A.R. with obese people. And then ideally, the way I think about it, you want to remove what you think that factor is. And if you’re right, those people will lose weight pretty quickly because they won’t be consuming that trigger anymore. So I think the problem is sugar and refined grains, and I think it’s their influence on insulin. So if you put your obese subjects on a diet that’s free of carbohydrates entirely and replaces those carbohydrates with fat, which doesn’t trigger insulin secretion. And if I’m right, though, most to all of those people should lose a significant amount of weight. So now you’ve got people where you remove the triggering factor and you found out indeed before he even did the experiment, that they’re susceptible to it. Because remember, it’s a tiny effect we’re looking for. So we do want to find people who we’re confident are susceptible. And now you could once you’ve got them, having lost a significant amount of weight, you can fix their calories at whatever calories they’re consuming. And now you just add back the factor that you think is the cause, that you add back to carbohydrates. And he had back the sugar. So it’s sort of this is what you would do to see if somebody has an allergy to foods. It’s called an elimination diet. Remove the food and if they do, the symptoms go away. Rash, gas, cramps, whatever it is, then you add the food back and the symptoms come back. And that’s a pretty good sign that they’re that whatever food you took away and added back is the cause of the symptoms. Well, we’re saying what I’m saying is a symptom of consuming these foods is obesity. So if you take it away, they should lose weight. And if you add it back. They should gain the weight back, and because we have to demonstrate that this isn’t a calorie effect, you know, that it’s a it really is, the foods and the calories are just a measure of the dose. Then we have to fix the calories of the that these people are eating. And, you know, add the carb, take the swap the carbohydrates in and out. To me, that’s the simplest experiment. It’s still well, it’s debatable how many subjects it would need. I like simple experiments with a few subjects, but the researchers with which we work prefer and they may be right to do this in many, many subjects. So, you know, that tends to over 100. And then you can randomize you could swap in and out different macronutrients to see if the effect you see is really caused by, you know, what you’re adding back at. At the point at which the randomized or maybe it would have happened anyway, even if you didn’t add it back. So again, that’s what I mean. No experiment is perfect, but there are experiments that can be done that that would do a much better job than any experiment to date, including some of my own nonprofit has funded. And we hope to get these new experiments funded that that could settle this by any account.
The food industry has an outsized impact on nutritional recommendations in the United States at every major food commodity, has its share of lobbyists, said persuaders. Why did fat lose? I mean, irrespective of the science in the Titanic struggle between sugar and fat as played out by corporations in the 20th century?
Well, that’s a good question. I mean, part of it is there is no industry that well, I guess the dairy industry had the most to lose. So if you go after sugar, you’re going there is a sugar industry that only sells sugar and has an enormous amount to lose. And this is the sugar industry had back in the 1930s, Franklin Roosevelt was complaining that this was far and away the most powerful lobby had ever dealt with the sugary beverage.
The beverage industry has a very powerful lobby, but even a company like Coca-Cola, PepsiCo, if they and they’re doing this and they did this in the 1950s, they don’t really care that much if they sell sugary Coca-Cola or Diet Cokes because they get they they make money. Either way, the only one who loses when they sell Diet Coke is the sugar industry. When the government started, I think incorrectly going after fat in the 60s and 70s, they were going after saturated fat, which is found in animal products and found in dairy products. But the meat industry, for instance. So having the meat have relatively is a major source of saturated fat, even though the primary fat in Bee, for instance, and is the same model on saturated fat that defined an olive oil patch. They could make low fat version. They could sell lean proteins. They weren’t. It wasn’t like the sugar industry where you just don’t sell sugar anymore. They could adjust their product to meet the dietary recommendations. Yeah. The milk industry went from selling only whole milk to selling home milk and skim milk, the whole milk and two percent fat, one percent fat. So the dairy industry can adjust. You could even sell low fat cheeses. Low fat yogurt exploded in popularity and they’re all labeled as hard healthy because they’re lower in fat. So all these industries could adjust. The only one that kind of had a problem was eggs. And even the egg industry started producing eggs that were supplemented with like omega three fatty acids where the chicken you basically the research you do is to create your products so that it matches the nutritional wisdom. The. It was for the sugar industry was the only one that really if we go after sugar, they can they can try to diversify to use sugar and other products other than things we eat. But other than that, they just lose business. They can’t make low sugar versions of sugar.
The way the dairy industry can make low fat versions of milk in cheese bottom is your argument about sugar in the diet kind of unsafe at any speed argument. Whenever you’re eating in sugar, you should be eating less. Or is it more? A kind of dose makes the poison kind of argument that you should be watching your sugar intake and come back if you have metabolic symptoms?
Well, I and I discuss both of those, and I don’t actually provide a definitive choice. The argument I make when we know that cigarets cause lung cancer, but we and we know there’s a point at which you’re going to smoke one cigaret too much and you’re on the road to lung cancer that you might have been might not have been on had you smoked less. Right. It’s not like he’s smoking a cigaret and you’ve got lung cancer.
There’s at some point sort of the problem of the heap. Yeah. At some point someone’s got to keep them. But you don’t know when that green goes across. Yeah.
You don’t know when you get there. So what we we don’t tell people to smoke in moderation. We don’t say smoking too much causes lung cancer. We say smoking causes lung cancer. And we tell people to stop, don’t smoke. That’s the advice.
You know, but we share your article argument with sugar. I mean, when you’re encountering things that are important to eat like fruit. I mean, is it fair to say eat the sugar that’s in fruit and not their sugars or something?
Well, for instance, I’m not so confident that it’s important to eat fruit. So I realize that’s a radical statement to make that fight all the caveats that I threw in there. But in fact, we have two different. Well, let me just put it this way. I’m sure it’s fruits perfectly fine and might be even beneficial for people who are mean and healthy today. But think about food for somebody who has diabetes, who’s got all these wonderful vitamins, micronutrients. And yet they have to take insulin to cover the fruit. So do you want somebody with diabetes taking more insulin so that they can eat an apple? I don’t know. I mean, I think if you posed a question like that to a diabetes specialist, they might hesitate for a second if it was phrased that way, even though they might otherwise say that fruits as part of a healthy diet. And we know that diabetes lies on a spectrum of disease that includes all of metabolic syndrome and is associated with obesity and insulin resistance. So what point on that spectrum? You decide. Is it okay for our bodies to if we could secrete Leisinger? I don’t know the answer to that. I don’t want to. I mean, I the title of my book, The Case Against Sugar, at one point was Stealing Christmas. The Case Against Sugar because I ran it on stealing.
Yeah. So it sort of, you know, if sugar if sugar causes diabetes, OK, which is to me a viable argument, maybe it’s wrong, but I think it is, as I say in the book. This were a criminal case. I could get an indictment. I’m not Trichy get a conviction. And the evidence certainly doesn’t exist to examine, you know, to exonerate sugar if it causes diabetes. And I think it’s important we say sugar causes diabetes. Not eating too much sugar causes diabetes because we don’t know what that means. And if sugar is addictive and people certainly act like it is. What is moderation mean to someone who. Has a partner who can stop their sugar consumption or who maybe would find it easier to eat. None at all. Then tea, some sugar. This is a cigaret argument again. I mean, clearly, moderation, cigaret consumption is better than smoking a pack a day. But I for one who used to be a smoker and I’m incapable of doing moderation if I smoke one cigaret. I’m back to being a smoker and I’m going to think about it all the time, even if I can keep it to, say, four or five cigarets a day, which I am confident will not cause lung cancer or heart disease or emphysema. My life is gonna be dominated basically by my thinking about when I can have my next cigaret, and I know this because it’s been like that in the past.
So I just these are they’re not my argument. They’re far more complex questions than and require far much thought them people put into them when they just say, hey, we should eat figures.
Sugar in moderation or I should give my children sugar in moderation. I think they’re not thinking things through. They might conclude ultimately that they should eat or they can eat sugar in moderation.
But that still doesn’t mean that other people.
It’s also a pretty big leap of faith in the opposite direction that absent definitive proof that I mean, would it really mean in terms of excluding yourself from very important cultural rituals and pleasures and just the convenience of being able to eat normal food on the road to, say, adopted a really radical. No sugar diet? It’s not a radical step to not smoke or two. We never have smoked. But just like you’re asking people to give up a lot on Specter, advocate a no sugar diet as opposed to a minimal sugar diet.
You know, it’s funny. I was I live on. I live in Oakland, California. We had a block. We have a block party every year. And in October, we had our block party. And I was sitting at a table outside the beautiful autumn day in Oakland. And opposite me was seven or eight year old kid. Sorry, boy, wasn’t mine. Although I have two boys that influence how I think about sugar. And also sitting. We have a neighbor who recently passed away. He was 95 years old. But a month before he passed away and he had Alzheimer’s disease, his nurse took him to the block party and he was sitting in a wheelchair in a bathrobe and pajamas, and he was curled over. And both this ninety five year old man and this eight year old child were eating pie with ice cream on it. And I was watching them eat it. And they were both deriving an enormous amount of joy from what they were consuming. And I was thinking I would take this away from them. But the point is and again, this is where the cigaret metaphor is so meaningful to me, because I was a smoker, I once lived in a world in which a meal didn’t end until you had the post cigaret meal.
I could not imagine the joy of a meal without King cigaret. I concluded it. And yet here we have people and now we live in and we live in a world where many people cannot imagine the joy of a block party or the joy of a meal without the dessert, without the pie and the ice cream.
But now that I don’t smoke, can never cross my mind that I need to smoke in order to have to enjoy my life. And so, again, it’s a little more complex. It is indeed. Nobody needs to smoke. We all need to eat. But the question is, if we didn’t have sugar in our diets, would we miss it?
Would it make. And what if we eat like they did in France and at the end of a meal, we had a cheese plate instead of a pastry. Would it matter if we had Kerry instead of unsweetened, you know, bubbly water instead of Coca-Cola, would we be less happy?
Are the French were the French before sugar began to saturate their diet less happy than we are?
Did their celebrations where they lost Joyful if they didn’t include sweets? I even lived in Switzerland for a year. Were the two national Destra cheese on a plate smelted cheese? I couldn’t go to a single party without somebody taking out their rack hatmaker. And you had melted cheese with Corney shawl, the little pickles and onions.
And it was delicious. Festive, festive fondue. Nothing was more festive. True. The chocolate fondue was slightly more festive than the cheese plum do.
But you didn’t have to. The cheese fondue was festive again. It’s just it’s. It’s. And this is my book begins with a thought experiment where what if this is a drug and it just happened to be a drug that has so saturated our lives that we give to our children. At the latest that their first birthday, in fact, it’s clear that in, you know, milk formulas, for instance. So by the time, you know, we just can’t imagine life without it. But are we imagining life without this innocent pleasure or are we managing life without this psychoactive substance?
And I don’t know the answer, but somebody had to write the book and ask the questions, and that’s what I did.
That’s all the time we have for today. Thank you so much for coming on the show.
You know, it’s been great. Thank you. Point of Inquiry is a production at the Center for Inquiry. Become a member and support the advancement of science and reason by going to center for inquiry dot org slash membership.