This is an extended version of the interview with Rick Johnson, author of Nature Wants Us to Be Fat.
RICK JOHNSON [00:00:00] My name is Richard Johnson. I’m a professor of medicine here at the University of Colorado.
SHELLEY [00:00:04] In fact, you direct the Department of Hypertension, or have you changed your position now?
RICK JOHNSON [00:00:09] I was the chief here from 2008 till 2017, but currently I’m simply a professor.
SHELLEY [00:00:17] That gives you more time to research and less that you have to be directing.
RICK JOHNSON [00:00:20] Absolutely correct.
SHELLEY [00:00:22] Are you doing a lot of research?
RICK JOHNSON [00:00:23] I am. I continue to be a researchaholic. I’ve been doing research since the early eighties. It makes up a great part of my life. It’s exciting, exhilarating and hard work.
SHELLEY [00:00:38] It is all those things with a lot of mysteries, a lot of dead ends, a lot of sudden doors that open up.
“This whole story that I’ve written about is like finding treasure.”
RICK JOHNSON [00:00:44] It’s been a series of great surprises and discoveries. The best I can say is that this whole story that I’ve written about is like finding treasure, I found a piece of gold. And we thought that was the best thing in the world. And then we found another one, and then we found another. And then we found a whole treasure chest. It’s sort of like finding King Priam’s treasure. What we’ve realized is that this pathway that we’ve identified seems to be involved, not just in obesity and diabetes, but in many, many current diseases, having a role in cancer and having a role in dementia and other medical problems.
SHELLEY [00:01:22] Backing up just a little bit. You’re in the Division of Hypertension and Nephrology, which means that you deal with things like high blood pressure and kidney disease and gout.
RICK JOHNSON [00:01:36] Yes, that’s right. So I started primarily in the world of kidney disease and high blood pressure. But as my research progressed, I migrated into other fields and ended up studying metabolic syndrome, obesity, diabetes and other conditions.
SHELLEY [00:01:55] Metabolic syndrome is that very strange thing where somebody’s metabolism gets out of balance and they get really hungry for things that they don’t really need. They lose energy. They can’t build muscle as much. They’re more prone to heart disease.
RICK JOHNSON [00:02:10] Yeah, metabolic syndrome refers to a constellation of findings and usually it includes abdominal obesity, high blood pressure, elevated blood sugar, sort of like insulin resistance. So it’s not true diabetes, but it’s sort of pre-diabetes.
SHELLEY [00:02:29] Cells their body can’t take in energy, and the insulin levels are very high.
RICK JOHNSON [00:02:37] You become resistant to the effects of insulin. So the insulin levels go up to help control your blood sugar. But even with that, your blood sugars tend to be a little bit on the high side and then you have elevated triglycerides in your blood, which is fat, and oftentimes you’ll have fatty liver. And this constellation of signs got the name metabolic syndrome many years ago. We now know that about a quarter of all adults have metabolic syndrome in the U.S. and some places in the world. It’s higher. So it seems to be a real common issue.
SHELLEY [00:03:12] In the US it’s common, but in some parts of the world. It’s lower, though.
RICK JOHNSON [00:03:15] Absolutely. So it can be lower. It’s sort of like, in our country, diabetes is present in about 10 to 12% of the population. You go to Samoa, it’s like 40%. You go to Kuwait, it’s like 25%. You study the Pima Indians where it’s 50%. And so diabetes and metabolic syndrome, which kind of run together. they vary quite a bit. We have very high rates here compared to some places like Sweden, but it’s still low compared to countries like Kuwait, Samoa and so forth.
SHELLEY [00:03:52] It isn’t good, but it could be worse.
RICK JOHNSON [00:03:54] It could be worse.
SHELLEY [00:03:55] Rick Johnson, you’ve written some other books. One, you’ve called The Fat Switch. One, you called The Sugar Fix. And now you have a new book called Nature Wants Us to Be Fat.
“We’ve also been able to link this pathway of metabolic syndrome, not just with, you know, classic things like diabetes, obesity, high blood pressure and heart disease, but also, as I mentioned, with things like behavioral disorders, with dementia, with alcoholism and with cancer.”
RICK JOHNSON [00:04:10] Yeah. So this book is the culmination of the work I’ve been doing for the last 20 or 30 years. It’s told like a detective story because that’s sort of the way it was when we tried to figure this out. And it takes us on an adventure story where we try to figure out what causes obesity. We begin by including studies of animals in nature that naturally become obese. We try to figure out why they become obese, and then we relate it to humans. And from that, there were many discoveries. Some of them are very surprising about what causes obesity. And from that comes a whole series of ways to treat obesity, many of which have not been tried before. And we have some data that some of these methods will work. And we’ve also been able to link this pathway of metabolic syndrome, not just with, you know, classic things like diabetes, obesity, high blood pressure and heart disease, but also, as I mentioned, with things like behavioral disorders, with dementia, with alcoholism and with cancer.
SHELLEY [00:05:17] So many paths lead to similar roads sometimes.
RICK JOHNSON [00:05:21] Yeah, it’s sort of like we identified a major, major mechanism that animals use to become fat. And this mechanism is involved in a lot of diseases. And so I think it will turn out to be important in terms of how we approach a lot of our current diseases.
SHELLEY [00:05:43] Let’s start with the punch line. What do you think animals do to get fat?
RICK JOHNSON [00:05:49] They can do a variety of things, but our first big breakthrough was the discovery of the importance of fructose. Fructose is known as fruit sugar; in the wild it’s and fruit and honey. Perhaps many of you are going, ‘Hey, wait a minute, because aren’t fruits supposed to be healthy? I thought honey was healthy.’ It will sound sort of funny to hear that fructose might actually be at the core of what’s driving the whole, you know, metabolic syndrome and related diseases. But it turns out that it really is fructose. And we’ve been able to show how and we’ve also been able to show why natural fruit intake for us is actually healthy. And yet when animals eat a lot of fruit, they become fat.
“ . . .some animals want to gain fat, and that’s to protect them during periods of food shortage.”
SHELLEY [00:06:43] There’s a lot to unpack in all of that. Let’s start with the concept, animals want to be fat. Given how much Americans try not to be fat, why do animals want to be fat?
RICK JOHNSON [00:06:57] The title’s not completely true. Only some animals want to gain fat, and that’s to protect them during periods of food shortage. Most animals will actually try to maintain a small amount of fat, and they’ll regulate it very well. So they’ll have some fat, but they don’t want to get truly obese. And so what most animals do, if they eat too much one day, they’ll eat less the next. If they exercise and run around too much one day and burn too many calories, the next day, they’ll slow down and balance out . . . other than what they expected to do. You know, if they’re actively growing, you can show that by taking an animal and force feeding it so that it gains weight or you can fast an animal so it loses weight against its will. And then if you stop that, they go right back to the weight they should be at that time of the year. So not even goes back to the way they were. They’ll go back to the weight where they feel they should be for that time of the year. But there are animals that want to gain weight, and they do it at specific times. The classic is the animal preparing for hibernation.
SHELLEY [00:08:09] Oh, yes. Those bears that get so big before they go to sleep.
RICK JOHNSON [00:08:13] Yes. So a bear, for example, will maintain its weight during the summer, but in the fall, suddenly it will become hungry. Really hungry. It can gain as much as eight or ten pounds a day. They can be eating 20,000 calories a day and they will increase their weight as much as 50%. And the way they tend to do it is by eating a lot of fruit. We think of fruit as healthy, but we are eating. You know, how many berries or grapes do you eat, Shelley?
SHELLEY [00:08:48] I don’t eat very many grapes, actually.
RICK JOHNSON [00:08:50] Let’s say you eat a bowl of grapes. You know, bears getting ready to hibernate will eat 10,000 grapes in 24 hours. So we’re talking a different level of fruit. Orangutans, when they want to gain weight, they’ll eat fruit and they’ll gorge. And I mean, they’ll get into a tree and they’ll eat fruit after fruit after fruit and eat it fast and consume and get a lot of sugar. Normally, a fruit will have like five grams of fructose, maybe ten. When we’re eating fruit, we tend to eat only, you know, one or two fruit at a time. But a bear or a orangutan or an animal that wants to eat fruit to gain weight, they’ll eat a lot more relative to their weight. They’re getting a lot more sugar. I’m calling that sugar, but it’s fruit sugar, also known as fructose. That’s what makes fruit sweet. And animals that want to gain weight will pick ripe fruit, and ripe fruit has more sugar. When a fruit ripens, the sugar content goes up. And when that happens, the fructose will increase. Also good vitamins tend to go down as the fruit ripens. So things like vitamin C tend to decrease as a fruit ripens. Vitamin C actually can block some of the effects of fructose. In the early part of when the fruit is just beginning to grow, it’s very tart. It has a lot of fiber, potassium, all these things that slow the absorption of fructose. so it discourages animals to eat it because they’re not going to get that much sugar. But as the fruit ripens, the sugar content goes up, the vitamin C content goes down, the all the other good things go down. And now the fruit is more suited to stimulate this metabolic switch where they start gaining weight and become hungry and so forth. That’s sort of how it works. So the animals that eat a lot of this fructose trigger a biologic switch. And this was what we been trying to uncover, an actual biologic mechanism that triggers weight gain, obesity, insulin resistance, a rise in blood pressure, all the features of metabolic syndrome, and they’re all all there to help us survive. When I was taught about metabolic syndrome, when I was a medical resident, it was told to me as something that’s pathologic. You know, insulin resistance is not a normal thing. We shouldn’t be insulin resistant. Metabolic syndrome is a disease. Actually, it’s not a disease. It is a normal biologic process that animals trigger when they need to gain weight.
SHELLEY [00:11:54] That was so interesting to read in your book. Nature Wants Us To Be Fat, about the animals that migrate, such as geese. When they prepare for migration, they get fatty livers. If people get stuck with these conditions, they’re really sick. But the geese only have the fatty liver when they’re traveling lots of miles and they need the extra energy. Humming birds! Every day, they end up at the end of the day with a fatty liver, but then they burn it up overnight and go back to needing more food. And so they’re very robust in being able to handle things that would cause metabolic syndrome, in us. Meanwhile, hummingbirds, their blood sugar goes up above 400.
RICK JOHNSON [00:12:36] They basically become diabetic and fat during the day when they’re drinking sugar water and then they burn it off at night despite the fact that they are so metabolically fit. If they drink pure sugar water all day long, their livers turn pearly white, ‘the fattest of all livers of birds’, one researcher wrote, and they develop frank diabetes and then they burn it off. It’s an amazing story about the power of sugar, that it can take an animal that is so metabolically fit and cause them to become diabetic–hummingbird feeders. So you put sugar water to get the sugar. Water and nectar are pretty much the same.
SHELLEY [00:13:16] A hummingbird can basically become a diabetic by the end of the day, but by the next morning they’re so healthy and burned it all off. The fats and all of the metabolic symptoms of what we call diabetes, that they just start fresh the next day.
“If you switch a fruit fly to pure sugar, it will become obese.”
RICK JOHNSON [00:13:33] Exactly. And here’s a really interesting story, Shelley. Fruit flies are flies that love fruit and they eat fruit and that’s pretty much fruit juice. But there’s other things in the fruit. If you switch a fruit fly to pure sugar, it will become obese. They’ve actually shown that flies will become diabetic and obese.
SHELLEY [00:13:58] A fly can become obese and diabetic?
RICK JOHNSON [00:14:01] Yeah. And then they die.
SHELLEY [00:14:04] As you think about it, a fly is trapped inside of an exoskeleton. So it would cause all kinds of extra pressure and problems for it to become obese.
RICK JOHNSON [00:14:14] Yes, it’s true. Ants will become fat if they eat sugar. You can’t tell because they’ve got this exoskeleton. So the fat’s inside. But ants can become quite fat from sugar. And there are some ants that will search out sugar. They love sugar more so than other types of foods.
SHELLEY [00:14:35] Rick Johnson I hear you saying that natural sugars found in the wild as fruit and berries generally are okay for animals, but our human style of sugars, even some of the animals that are used to sugars, it’s too much for them.
RICK JOHNSON [00:14:48] So refined sugar probably can overwhelm animals and nature.
SHELLEY [00:14:53] Does it overwhelm us as humans?
RICK JOHNSON [00:14:55] Absolutely. For sure it does.
“Animals with the sweet sensation knocked out still will seek out sugar water even though they can’t taste it.”
SHELLEY [00:14:57] But Rick Johnson, refined sugar is in most of our foods.
RICK JOHNSON [00:15:01] Yes, it is. And most of our foods In fact, 70% or more of processed foods have sugars put in them. And you want to know something really interesting/ If you take an animal and you knock out its sweet taste so it can’t taste sweet, it will no longer care for artificial sugars like Splenda. Sugars wont give it any kind of dopamine surge. There’s no pleasure with that. But those animals with the sweet sensation knocked out still will seek out sugar water even though they can’t taste it. We found that it’s because when you drink fructose, for example, the metabolism of fructose is what’s involved in the craving response for fructose.
SHELLEY [00:15:44] It’s not our taste buds? Rick Johnson,so many people say that we have been doomed as a human population because we have enough food, and the food just tastes so delicious. So of course, people eat too much. You’re saying something different?
RICK JOHNSON [00:16:06] It’s a little bit more complicated than that. So we have five tastes. One is sweet, one is salty, one is savory–umami, and there’s bitter and sour. So there’s actually three tastes that we really like sweet, salty and savory. And the other two are sort of meant to help us avoid foods that are bitter or sour because many times they’re not good for us. Now the sweet is your sugar, right? What we know is that if you knock out the sweet receptor, animals will still like sweet food. And that’s because of the metabolism. They will reduce how much sugar they eat, they’ll eat less sugar. But if you give them a choice between sugar water and regular water, they will be able identify the sugar water even though they can’t taste that it’s sweet.
SHELLEY [00:16:59] Rick Johnson, other scientists who’ve studied sensing molecules inside of our bodies report that sensing receptors on cells in our digestive tract, are very similar in their makeup to the taste bud receptors on our tongue. So when you knocked out that taste of sugar in lab animals, is that just referring to taste receptors for sweet on tongue or is that referring to all of these receptors for that kind of substance?
RICK JOHNSON [00:17:29] So it turns out that the study that was done where they knocked out the sweet receptors included the taste bud sweet receptors, but there are sweet receptors in the gut. However, we here at CU Denver knocked out just the taste, only the taste, leaving the sweet receptors intact in the gut. And we knocked out all taste. And when we did that, the animals still like sugar.
SHELLEY [00:17:57] You did this with mice?
RICK JOHNSON [00:18:00] Yes. And what we found is that if you knock out the taste receptor, you reduce the amount of sugar you eat, but you still become obese from sugar. And sadly, you become more sensitive to the effects of sugar. So you eat less sugar, but you’ll still become more obese.
SHELLEY [00:18:16] That’s another part of your story that we’ll get to in just a moment. I want to keep giving people the punch line, though, which is that your research has shown that if people reduce their consumption of sugary drinks, plus foods that have added sugar, it can do a huge benefit for their health. But if someon’e health is already broken somewhat by these kinds of foods, there may be other things they need to pull out of their diet as well. That’s a quick summary. Is that fair to say?
“Fructose sugar is the PRIMARY driver of obesity.”
RICK JOHNSON [00:18:47] Not fully. Fructose sugar is the PRIMARY driver of obesity. You’re totally right in that part. Sugar or high fructose corn sirup make up about 15% of our diet. Some children are eating 25% of their food is sugar. Children, adolescence and also disadvantaged populations are often eating a higher percentage of sugar. And so fructose-based sugar is your number one driver. You’re right. But there are other drivers of obesity, and they’re very important. So I don’t want to say that they’re distant second or third. They are involved. Originally, when we were studying this, we were thinking, hey, it’s all sugar, you know? And so my first book (The Sugar Fix), hey, let’s just cut out sugar and fructose. But it wasn’t enough. It’s not enough.
Bread, Rice and “The Polyol Pathway” lets the body make its own fructose . .
And that is because of the sad discovery by our group that there are other foods that trigger this switch, the survival switch. And this switch can be triggered by foods such as high glycemic carbs, bread. Rice, potatoes and chips. These foods do not contain fructose, but they actually can trigger the switch. And what we found is that the way they work is they stimulate the production of fructose in the body. So it isn’t just about the fructose we eat. It’s about the fructose we make. And no one was really thinking of foods as working by causing us to make fructose. Everyone was thinking it was the foods we were eating.They were thinking it’s the carbs and the protein and the fat. But it turns out that these carbs, which we call high glycemic carbs, when you eat them, they release glucose and the glucose gets into the blood and your normal glucose (in your blood) is like 80 to 100. But when you eat a high glycemic carb, the glucose in the blood can go up transiently, maybe to 120, 140 or 150, but it’s transient. So everyone just says, well, don’t worry about it. Or if you do worry about it, they say, Well, the problem is that it stimulates insulin and insulin puts fat on you. And so the thought is that high glycemic carbs could be a cause of obesity, primarily through this mechanism (of raising insulin). But what we found is that when the when the glucose levels go up, that triggers the body to make fructose from the glucose. And the glucose can be converted to fructose through a chemical reaction. And we call that reaction the polyol pathway.
SHELLEY [00:21:49] Polypll sounds like everything thrown in, including the kitchen sink, poly all that.
RICK JOHNSON [00:21:54] So it sounds like that; it was a name given to it a long time ago, but it’s been known that the body can make fructose, but no one thought it was important. What we found is that that a number of foods trigger the production of fructose in the body and animals use this so not all animals eat fruit to become fat. There are animals that don’t eat fruit that become fat other ways. One way is high glycemic carbs. They will cause obesity.
SHELLEY [00:22:22] Now, when you say high glycemic, you mean any food that you eat that turns quickly into sugar.
RICK JOHNSON [00:22:28] By turns quickly into glucose, and then your glucose levels go up in the blood. And when that happens, it triggers the production of an enzyme that converts some of the glucose to fructose. So the glucose isn’t actually what causes the obesity. It does a little bit through stimulating insulin. The real way high glycemic foods cause obesity and diabetes is because they get converted to fructose in the body.
SHELLEY [00:22:56] You know, Rick Johnson, for a long time there has been debate about whether the body can make fat on its own or it’s only food that you eat that turns into fat. That was the idea 20 years ago. But your thought about this metabolic switch where the body shifts and turns, other energy that’s taken in other food into fat through these pathways is part of this unraveling of a deeper secret to how we get fat.
RICK JOHNSON [00:23:24] Yeah, so let’s just talk about how the fructose works. So fructose is unique among nutrients. Think of energy as two forms of energy. You’ve got the energy that we are burning all the time that we’re using up, and we call that energy ATP. And that energy is in our cells. And it’s allowing me to talk to you right now. It’s allowing you to talk to me. It’s allowing you to stand up and do all the things that you are doing. And it allows me to eat, walk, talk, pre everything. So ATP is our main fuel and we can store fuel. And when we store our energy, it’s in the form of fat or sometimes glycogen. Glycogen is sort of the storage form of carbohydrates, but it’s fat. That’s our main storage fuel.
SHELLEY [00:24:16] Well, that makes sense because it would take a lot of sugar cubes stored on the body to be able to store enough energy. And fat is much more efficient at storing energy.
RICK JOHNSON [00:24:26] Yes, it’s like nine calories per gram. So when you store fat, it’s a great way to store energy. So it turns out that the place where ATP is made are in energy factories that we call mitochondria. And these mitochondria are pouring out the ATP that allows us to do what we want. The mitochondria actually use oxygen to help make this ATP. So much of the oxygen we breathe is used to help make energy that we use. So what fructose does is. Really clever. What it does is it generates a substance called uric acid. And our data suggests that what the uric acid does is it sort of quiets down the mitochondria. It does so by causing oxidative stress to the mitochondria. And when that happens, the mitochondria produce less ATP. And so where does the energy go? If you make less ATP, the energy goes to fat. And so it sort of shuts the calories we’re eating to fat instead of immediate energy.
SHELLEY [00:25:37] You said that it’s not just sugar. It’s not just fructose that can cause this to happen. Unfortunately, this polyol pathway indicates there’s some other foods people eat, especially if this pathway is already running. That will lead to somebody still having problems with their metabolism, with gout, high blood pressure, heart disease, obesity. What are some of the other foods that do this?
RICK JOHNSON [00:26:05] So we’ve already mentioned high glycemic carbs. That’s why a low carb diet is so effective or a keto diet, because it’s removing not only sugar from the diet, but these high glycemic carbs. And when you do that, the fat doesn’t cause obesity because you have to be hungry. You have to lose your ability to regulate your weight. The fructose makes you lose your ability to regulate your weight so that you’re hungry and you’ll keep eating.
SHELLEY [00:26:31] The fructose leads your body to have trouble recognizing where its balance is for health.
RICK JOHNSON [00:26:38] That’s correct. And so the way it does that is it induces a thing called leptin resistance. Leptin is a hormone that’s released by the fat cells that tells us when to stop eating. And normally, animals are very sensitive to leptin and they won’t eat more than they need, and they will just maintain their weight. But in order to gain weight, you have to lose your ability to regulate the way the way fructose does. That is, it causes the body to become resistant to leptin so that when leptin goes up after a meal, it doesn’t tell you that you’re full. And so you end up eating more. And most people who are overweight or obese are resistant to leptin. You know, this was a big discovery years ago that people with obesity don’t respond well to leptin. And you can show that by injecting leptin in people or in animals, and normally you appear censored, selected, and you get an injection of leptin, you’re going to quit eating or reduce your food intake. But if you’re leptin resistant and you get a shot of leptin, you’ll just keep eating. And fructose makes you keep eating once you get left.
SHELLEY [00:27:44] So there’s one camp that would say that the reason that Americans, for instance, have these metabolic challenges and so much obesity, something that they didn’t have 50 years ago as a population, is because food just tastes so darn good. But you describe something where it becomes an addictive, desperate craving. If somebody’s hormonal balance, their metabolism, their fructose signaling is out of whack.
RICK JOHNSON [00:28:13] Yeah, the fructose drops the ATP in the cells, so your immediate energy is less and your stored energy is more. What happens when the ATP levels go down? You sense that low energy and you get hungry, and so you eat more and you become resistant to leptin. And so you’re eating more. Over the last century, the plates of food that people get gets bigger and bigger in the restaurants. And it isn’t because that’s a good thing to attract you. They’re doing it because they know that if they don’t, you’re going to leave hungry. And if you leave hungry, you’re not going to come back. So it turns out that there’s a biology that’s going on and we’re eating more and exercising less because of a switch that’s been activated. And in fact, that switch will drop your metabolic rate, but only while you’re resting. This is important for survival because if you’re trying to survive, you want to be able to forage for food. And so while you’re foraging, you maintain normal energy. But as soon as you quit, your resting energy, metabolism drops.
SHELLEY [00:29:16] Hibernating bear wants to not move very much because it’s hibernating.
RICK JOHNSON [00:29:20] But that’s after I’m talking about when they’re searching for food. So when they’re searching for food, they’re going all over looking for food. They’ll be spending energy then. But to help conserve and to put more fat on for the time when they hibernate, they’ll actually become less active. When they’re resting, when they sleep, they actually sleep more deep. And then the next day they get up and so forth and forage for food. You raise the question of what other foods can do this. This is a discovery that came out of this whole work.
“The fattest animal in the world’s the whale. And it’s not eating fruit.” How fat stores energy AND water, for whales, camels and the fat-tailed lemur.
What happened was when we realized that the body can make fructose, we began. And to think about animals in the desert and animals in the oceans, you know, the fattest animal in the world’s the whale. And it’s not eating fruit. It’s not eating bread. So how does it get fat? And so one of the questions was what other mechanisms could drive fat? And the way we tried to figure it out was kind of a pretty cool way. You know, what is the benefit of fat for an animal in this ocean? And here’s the trick. When a whale burns fat or when any animal burns fat, you’re making energy, right? But you’re also making water. So what’s really interesting is fat doesn’t contain water. But when you burn fat, you produce water. You produce water and carbon dioxide. And this has been known since, you know, like the 1900s. Fat is a source of water, not just energy.
SHELLEY [00:30:58] Rick Johnson, you’re implying that one reason that some animals store fat isn’t just for energy, it’s so that they can get fresh water.
RICK JOHNSON [00:31:06] Right. One third of the water that a whale gets comes from its fat.
SHELLEY [00:31:11] And your book was fascinating to read, talking about a desert lizard that makes its tail extremely fat when there’s enough water and food so that during the drought season it can survive and have enough water.
RICK JOHNSON [00:31:27] In hot climates and dry climates. Animals don’t really want to have fat on their body because that can increase their body temperature. So they tend to put the fat in their tails or like on a hump on their back, like the camel. And this way, the fat and the hump can be used to produce water, but it’s not going to overheat them when they’re wandering in the desert. Once we knew that these animals were using fat as a source of water and actually there’s a primate, the fat tailed dwarf lemur.
SHELLEY [00:31:58] That fat tailed part of its name is the clue.
RICK JOHNSON [00:32:00]. Yes, that’s the clue. And what it does is during the dry season, when there’s very little water around, it will effectively hibernate. They call it estimate. It’s like hibernation, but they go into a hollow in the tree and they live off the fat and their tail. And they use it not just for energy, but a key part of it is to get the water from it. So once we knew that fat was a source of water, then we knew that animals would want to put on fat as a means to provide water.
SHELLEY [00:32:31] Rick Johnson You seem to be saying that animals evolved to take advantage of the fact that fat is a stable way to store energy and also to store water.
“Mild dehydration could be a stimulus for fat”
RICK JOHNSON [00:32:42] Yes, exactly. And this opened up the idea that maybe mild dehydration could be a stimulus for fat, because if you were mildly dehydrated, it would be like an alarm signal to you to say, hey, I might need to find water. And so you would look for water. You could turn on a hormone called vasopressin, which helps concentrate the urine. But couldn’t fat production be also part of this? And so we started studying this and we found that this possible pathway gets turned on in dehydrated state. So if you become dehydrated, your body starts to make fructose to help store fat as a source of water. And then we went on and realized that actually dehydration is not a good condition to be in. The classic dehydration is a situation where you’re losing water like diarrhea, vomiting, like an animal that has bled or something and it’s gotten dehydrated in those circumstances. It’s not really great for the animals. So it would be wiser for the animal to not lose water, but figure out how to gain water. And one way to do that is to eat salt, because if you eat salt, you’re not actually losing any water, but you’re increasing the salt concentration in your blood, which is the same thing that happens when you lose water. But now, when the salt concentration goes up in your blood, that stimulates the paleo pathway. And now when you eat even calves that don’t raise your glucose up, now you’re going to convert those to fructose.
SHELLEY [00:34:24] Oh, because this is a way to get the body to store more fat, which means store more water. That implies you’ve found that if somebody’s eating a lot of salt in their diet can also be increasing their fat storage, increasing a lot of these. Yeah. Parts of the fructose pathway that can be damaging if it’s on too long. Yeah.
“Salt will help us store fat. . . . salt could cause obesity”
RICK JOHNSON [00:34:45] So just like we have a taste receptor to encourage us to eat sugary foods, we have a taste receptor to ask us to eat salty foods. And it’s for the same reason because salt will help us store fat. So it was an evolutionary. Principal to try to get us to store fat. And it turns out that almost everyone who’s overweight or obese tends to be dehydrated. They have slightly higher salt concentrations in their blood. And if you do fancy testing bio impedance, where you measure dehydration through that mechanism, they have a 12 fold increased risk for being dehydrated compared to a lean person. Basically, it’s because of all the salt and also sugar dehydrates as well. And so these two things activate the production of fructose in your body.
SHELLEY [00:35:35] Rick Johnson I’m making the checklist of ideas from your book. Nature wants us to be fat for helping a body be in better balance in this modern world with all of these extra foods that we can eat or substances we can take in. And in the book, you’re suggesting that people might be better off eating less salt, eating less sugar, eating less concentrated fructose, not fruit juice. Correct. Or the table sugars that have a combination of fructose and glucose in them. Also, you mention that if people, when they’re hungry, drink water, they might actually reduce the craving for food at that point.
RICK JOHNSON [00:36:13] Yeah. When we realized that salt could cause obesity and we showed it in animals and we then did clinical studies in people and showed that salt intake correlates with an increased risk for diabetes and things like that. Others have found it to be realized that there was more than one mechanism to drive obesity. Not only sugar, but high salt is playing a role. Interestingly, the way high salt works and actually even the way sugar works partly is by making you appear dehydrated. So when you drink a soft drink, your blood tests will show you get dehydrated, not hydrated. That stimulates the production of fructose to the development of obesity.
SHELLEY [00:36:55] There were some studies some time ago, maybe they weren’t even studies where soda companies tried to get long distance runners to drink sodas, to advertise their product. And the poor runners were so thirsty that they threw the soda cans away just to get regular water.
“Hydrating with water might actually be a mechanism to block obesity.”
RICK JOHNSON [00:37:10] Yeah, it’s been shown in experimental studies. Anyway, so we decided that hydrating with water might actually be a mechanism to block obesity. Right. And people have been talking about water intake and drinking 6 to 8 glasses a day. And, you know, all these people run around with their bottles of water and they swear that it makes them healthier. And yet there’s all these physicians that. Right, hey, you don’t need to drink extra water. The kidneys are going to do the work for you. If you don’t drink enough water, the kidneys are going to concentrate the urine. They’re going to take care of you that way.
SHELLEY [00:37:42] It all depends, doesn’t it? Because somebody who is eating in a way that means they’re not triggering this fat switch, survival to switch. They may not need as much water to drink, but somebody whose metabolism is out of balance in this place where their cravings are high, it may be a different story.
RICK JOHNSON [00:37:59] Actually, if you get dehydrated, you’re going to activate the switch. Dehydration activates the switch. So it may be that the kidneys can control the urine output so that your blood volume ends up being normal. But if it’s been activated to try to hold on to water, it’s also been activated to make you fat. That’s the problem. We tested this by taking people and giving them salty soup. What’s great about soup is you can hide the salt in it. And when we gave them salty soup, we could show immediately their blood pressure went up right away and they activated the switch. We could show it, but if you gave it with water, you could block that. And if we took animals on sugar and we gave them extra water, we could reduce their risk for obesity, even if they ate the same amount of sugar. So it turns out a lot of the way this is working is through dehydration.
Vasopressin, Dehydration and the Polyol Pathway
You know, about ten years ago, it was discovered that people with obesity tend to have a circulating hormone called vasopressin that’s high. And no one understood why people with obesity have this elevation in their hormone called vasopressin. Invasive pressing is the hormone that holds on to water, and it does so by reducing the amount of urine you make or concentrates the urine. It’s what makes the urine dark yellow. And so everyone was thinking, oh, this is what vasopressin does. This is what I learned in medical school. Vasopressin is the hormone that blocks us from losing too much water through the urine. But in some animals, vasopressin has other mechanisms. For example, in the frog, vasopressin prevents water loss through the skin of the frog. And there’s some evidence that vasopressin may actually reduce the loss of water vapor from the lungs. So we thought, well, maybe vasopressin is involved in obesity. Maybe it tries to store fat. And when we studied it, we found that Faisel pressing was in fact. A hormone that drives fat. And that it’s working not to the classical receptor it does for urinary concentration, but it works through a special receptor called the V1 B receptor. And when that happens, pays a press and actually drives fat production. It’s actually part of how sugar causes fat.
SHELLEY [00:40:19] And so all of these are examples where you’re eating food, maybe your body even needs the energy, and instead your cells are shunting the energy, not into something you can use to breathe or move or something like that. But instead your body is shunting more of it into storage as fat. Yes. So you’re saying dehydration all by itself can trigger this so that you’re not using the energy in your body to repair yourselves? You’re using it to turn this energy into fat.
RICK JOHNSON [00:40:50] Yeah. So we talk about hydration. Hydration is good because it will reduce your risk for being fat to be well hydrated. If you’re dehydrated, it’s going to turn on the switch. But there’s a new phrase that’s called under hydrated and under hydrated refers to the fact that you start by being a little thirsty, but you’re able to correct it. So you’re able to hold on to water and kind of turn off this mechanism so you’re no longer thirsty. But what’s happened is your urine still concentrated because everything’s working to keep you in balance. You’re still turning on vasopressin, you’re still turning on the polyol pathway, and you are now hydrated normally, but at the expense that these systems are turned on. So you’re under hydrated. And when that happens, you’re actually triggering the fat production. You think you’re hydrated, but you’re only hydrated so that you’re no longer thirsty. But all the systems to hold on to water are still turned off.
SHELLEY [00:41:54] Well, we have talked about so many different ideas that tie in with what we choose to do, starting with having high concentrated forms of fructose in sodas, in fruit juices, plus foods that are very starchy can end up triggering the same pathway that starts to store fat. How dehydration and salt can both trigger this pathway as well.
Savory Flavors, Uric Acid, Airplane Flights and Bloody Marys
RICK JOHNSON [00:42:19] And there’s a third way, too, Shelley.
SHELLEY [00:42:21] These two are big enough, but go on.
RICK JOHNSON [00:42:23] They’re they’re a very big way. So the other thing is we remember we have a third taste. That third taste is called savory. It’s you know why tomato sauce and spaghetti sauce tastes so good? It’s kind of like that cured dried tomatoes taste. That’s why gravies are good. And curing meat makes it delicious. That’s why beer is so good because of the yeast extract. It’s why Caesar salads taste good, you know, because of the parmesan. And it’s why blue cheese dressing tastes good. To some people. The umami flavor is really loved and the umani flavor is due to a substance called glutamate, also to two nucleotides called I am P and amp and sadly I am an amp are directly in the mechanism to generate uric acid. You know, when fructose is metabolized that makes uric acid and it uses these substances that trigger this taste of savory. I amp and amp are part of that pathway. And not only that, glutamate turns out to be converted to uric acid in the body. These three substances can activate the switch as well, and they do so through the same pathway. But just a little bit after the fructose, especially processed red meats tend to be rich in this and things like organ meats and shellfish, beer, they contain some of these substances and they can also make you fat by activating the switch. And the your mommy flavor is basically there to try to attract you to eat these kinds of foods. So it’s a little bit depressing. The good news is the mommy pathway is less powerful because we don’t eat much of it. We only a few grams of glutamate a day, but we eat 70 grams of sugar today. So there’s a big difference in the amount that we’re eating. And sugar is the big boy that’s driving this high. Glycemic carbs are the second big one. But it is true, you can activate this pathway. And, you know, have you ever noticed, Shelly, how people love to drink tomato juice on airplanes? Bloody Marys? Maybe you never knew that, but it’s even in the Internet, they say, you know, why is it that when I fly I like Bloody Marys and things like that? Well, the Bloody Mary has slacks, made a juice that’s rich in glutamate and a little bit of alcohol and stuff like this, which also helps you generate uric acid. And when you do that, it reduces the ATP production and shifts you more to fat storage and. That actually decreases your oxygen needs. So when you go out in a plane and you go to 7000 feet, the oxygen content in the air is just a little bit less. And it’s my belief that that is why the Bloody Mary case so good when you get in an airplane because you’re activating the switch, which has a tendency to reduce your oxygen needs just a little bit.
SHELLEY [00:45:20] Rick Johnson The next time I’m in an airplane, I’m going to order a Bloody Mary.
RICK JOHNSON [00:45:24] Yes. Or 2 minutes or she’ll just see, you know, a lot of people go, I never drink tomato juice or Bloody Marys unless I’m in an airplane.
SHELLEY [00:45:32] But also, from what you’re saying, just don’t do it too often because it can trigger some pathways that now and then to stimulate them and tweak them is fine. But to be stuck in these pathways is really detrimental to health. And people can read your book, Nature wants us to be fat to find out not only all of the details of these mysteries, but also some of the dietary recommendations you have, foods you can eat, ways you can live that will benefit you so that you’re more likely to live a life that has a long health span and be symptom free of some of these terribly painful or die young or be debilitated young diseases.
“Dietary Suggestions from the book, Nature Wants Us to Be Fat”
RICK JOHNSON [00:46:10] And in my book, I actually lay out a plan. And I also believe that you should still be able to eat a little sugar, you should still be able to eat a little bit of high glycemic carbs. And a lot of it is supported by research and experimental studies, including studies where we supplemented patients with with fruits, for example, and showed that natural fruits, when given modestly, actually makes things better, not worse. So please don’t hear this talk and go, Oh my God, I can’t eat anything that’s good, because it’s not true. It’s the problem of eating some foods that are really bad. Like liquid sugar is really bad. Once you understand the mechanism, you can actually figure out the best way to avoid activating this switch and giving you back your help.
“Before creatures evolved to store fat on purpose and for beneficial purposes . . . What was the survival advantage of converting fructose to fat?”
SHELLEY [00:47:00] Now, I was promised 15 minutes, actually, half an hour, but 15 minutes to my own questions.
RICK JOHNSON [00:47:05] Yes, sure.
SHELLEY [00:47:07] So the first one that I have is, before creatures evolved to store fat on purpose and for beneficial purposes . . . What was the survival advantage of converting fructose to fat?
RICK JOHNSON [00:47:18] The advantage of converting fructose to fat has always been helping survive, to provide another source of energy when you don’t have food around.
SHELLEY [00:47:27] Was that the earliest reason for that? For single celled creatures, are there single celled creatures that don’t store fat or that evolved to store fat? And what was the first reason they did it?
RICK JOHNSON [00:47:38] I’m not aware of single celled creatures storing fat that does not involve, from my studies . . . anything that’s storing fat. It tends to be using an aspect of this pathway.
SHELLEY [00:47:51] How about algae? Does algae have this pathway? Algae makes fat and it’s a single celled creature or thing.
RICK JOHNSON [00:47:58] I do not know. I can’t answer that question. But I do think that this pathway has a basis that goes way back in biology.
SHELLEY [00:48:06] It’s a pathway that some animals have taken more advantage of than others. It is intriguingly consistent. But if we step back from that and see what was happening before, what was the reason that these creatures did this?
RICK JOHNSON [00:48:20] So if you go back to the very, very beginning of life. Okay. We’re going to go way, way, way back. The earliest life was thought to just be RNA. They called the RNA world and there was no DNA. There was no proteins. If you were an organism with RNA and the RNA starts to degrade, what you generate is uric acid. So it’s like a degradation product. And so one might consider the possibility that it could become a signaling mechanism because you don’t want to have your RNA degraded. So if you’re an RNA form, uric acid was probably an alarm signal for degradation of the RNA. Today we are in a world has carried over to current life and some of the most important components of RNA are involved in the biology of life. So ATP, for example, the essence of energy, is ab RNA carryover, uric acid is an RNA carryover. When it’s cell alarm signal, things like Nad H and these very important mediators and the biologic reactions in the body are all carryovers from the RNA world.
SHELLEY [00:49:31] So your guess is that it has something to do with RNA which connects with uric acid?
RICK JOHNSON [00:49:36] Uric acid turns out to be a survival mechanism for many, many animals, and has a very basic role in both survival and reproduction. If you’re, for example, a crayfish, you use uric acid to help you survive in brackish waters because it helps decrease your oxygen needs. If you’re a flatworm and you are mating, you use uric acid as your pheromone to tell the other worm that you’re ready to copulate. So uric acid was developed as an alarm signal to help animals and even in bacteria. Uric acid is used as a survival mechanism in the setting of radiation or high heat. So I think that very early on, uric acid took on a role of being a survival or alarm signal.
SHELLEY [00:50:28] A signal because it was something that was excreted by an organism.
RICK JOHNSON [00:50:32] It was something that was broken down. So when you’re RNA or DNA or ATP is broken down, this is generated. So it sort of says, hey, what’s going on? Are we losing our genes? Are we losing our RNA? Are we losing our energy? So it becomes like an alarm signal.
SHELLEY [00:50:50] ((EXPANDED EXPLANATION)) It seems to me that sometimes when someone finds a reason that’s partway through the evolutionary channel, there may be another reason further back in time that still is there sometimes, and it’s still remains a reason that things happen. I’m not an expert on evolution, and what I say next will probably make an evolutionary scientist scream. Forgive me. Here it goes: The simple example that I think of is shellfish. Shellfish did not evolve to have a shell that opens and closes because long ago, a mollusk without a shell said, “Someday I’d like to have a shell.” Instead, before a shellfish was even a blob without a shell, way earlier in its evolution, it was a single cell, and it was excreting calcium because calcium signaling requires that you have to be spitting out calcium to keep calcium signaling clear inside the cell. That works fine for a single celled creature, and it maybe works for a creature that can move away from where it’s been spitting out calcium. But in mollusks, when the cells got together as a multicellular creature, they evolved to specialize in hanging out in one place where they slurped nutrients out of the ocean. This meant a lot of calcium flowing in and out of them, and perhaps the calcium often built up around them. Eons ago, a lot of those evolving mollusk like creatures probably died by being smothered in their own calcium excretions. Then at some point, by accident or intent or whatever, some mollusks evolved to organize the mounds of calcium into a protective shell. So the calcium that might have smothered them because the calcium that was their fortress. So it wasn’t that the mollusks thought that they would need a shell some time in the far future. And the original purpose of calcium excretion wasn’t to ultimately evolve to make a shell. Originally, those mollusky-things were spitting out calcium to keep signaling in their cells clear. And then later on, they programmed in an evolutionary drive to make shells out of the calcium they excrete. So it was a good evolutionary “invention.” But the drive to make shells out of the calcium . . . that’s not the main reason they excrete calcium. Deeper down in time, those shellfish needed to excrete calcium to keep their signaling pathways clear. And even today, even though making shells is important, it’s probably MORE important for a shellfish to spit out calcium to keep calcium signaling inside each cell clear. That’s still probably more important for these shellfish than the need to make a shell. So . . . how about humans who store a lot of fat — is there something about getting the volatile sugar energy out of a cell that means it’s important to sequester the energy in the more stable form of fat? Is there something about that which is still at play, even in animals like bears who very intentionally store loads of fat because they hibernate? END OF EXPANDED EXPLANATION WHICH WAS NOT PART OF THE ORIGINAL INTERVIEW))
RICK JOHNSON [00:51:55] You know, there are mutations that change things. If this shellfish, this mollusk is spitting out calcium and it takes mutation that allows it to start forming the shell, perhaps that helped it evade a predator. And then it survives. And then it passes that mutated gene to another mollusks.
SHELLEY [00:52:21] And then at that point, it becomes a gene for expressing and creating a shell because the shell has survival advantage. But it didn’t start that way.
RICK JOHNSON [00:52:30] It starts as a random mutation. You know, it’s not like nature wants us to be fat. It’s the fact that in the process of evolution, we develop these protective mechanisms.
SHELLEY [00:52:43] Was it that initially, though? And that’s what I’m curious about, because you’ve done so much to delve into this. I’m curious about this other part. ((FURTHER EXPANDED EXPLANATION — What if the original reason for storing fat in a cell was to take a volatile and unstable form of energy — a sugar, and make it into a more stable form of energy without going to the effort to absolutely spit that energy out yet?)) This may be off base, but one example I could point to is a scientist named, Matthias Heineman, who was looking at the thermodynamics of Why Do Yeast Make ethanol. Why do they spit out this perfectly good sugar energy that they’ve been consuming? ((And they do it halfway through the process of turning that ethanol into usable energy))
RICK JOHNSON [00:53:14] Well, ethanol in the early days, animals couldn’t really eat ethanol. And so it was a way to avoid an animal from eating the yeast. And actually, I’ve done a little work on this.
SHELLEY [00:53:28] That was a benefit of (ethanol excretion), but that was not the original reason that they spit it out.
RICK JOHNSON [00:53:32] The thought is it always begins as a random mutation, and then if there’s a survival advantage, then it stays, it gets passed to the next lineage.
SHELLEY [00:53:41] But Heineman would say that the random mutation was that if a yeast is taking in sugars too fast, then it starts to cause an inefficiency in the middle of the ((metabolic)) pathways, which is toxic. And that toxic inefficiency in the middle ((builds up)) where if it just kept trying to make the sugar that’s being metabolized into ethanol and push onto other things, if it just kept doing that and made the assembly line ((of its metabolism)) do that, it would back up so much ethanol, it would be toxic to the yeast and kill it. And so his hypothesis is that there’s something called the Gibbs equation of thermodynamic whatever. And it’s that at a certain point that little yeast cell figures out that this is too much to handle right now. And if it tries to keep going, it’s going to expend more energy than the effort is worth. And in the meantime, it will have to deal with a buildup of this toxic product and it’ll kill the yeast.
ALCOHOLISM AND THE POLYOL PATHWAY
RICK JOHNSON [00:54:50] Well, I have to say, I’m kind of Darwinian, so the way I view it is that when a mutation occurs, if there’s a natural selection advantage, then that mutation may be accepted and end up then passed into the system. So let me tell you my yeast story. Alcohol story. Our ancestors were not able to drink alcohol, but it could be at about around 10 million years ago, a mutation occurred that allowed our ancestors. They weren’t human then. They were kind of pre-human that allowed them to drink alcohol. It was during a period of famines. Our ancestors were still primarily eating fruit as their favorite food when the fruit trees became more and more sparse. A lot of the fruit they would find might be have already fallen but be fermenting. And so they were not edible. And what we think is that this mutation that occurred allowed the animals to eat the fermenting fruit and to metabolize the alcohol and thereby get some of the sugar that was present in the fruit to help them survive so that it was a survival advantage to have that mutation. But the consequence is that now they can metabolize alcohol. And so not too long after that, alcohol becomes, you know, something that people enjoy and like. And one of the interesting things is alcohol activates the polyol pathway, too. So it’s another way to stimulate sweetness. And in fact, when we were able to show that the craving of alcohol can be blocked by blocking the craving of sugar, that the two are intertwined. And I actually have research funds from the National Institutes of Health to try to develop inhibitors of sugar craving that will also block alcohol craving. So the two are definitely linked.
SHELLEY [00:56:51] From what you said about what people eat. If somebody who has a propensity toward alcoholism drinks enough and avoids sugars and salt and stuff and modifies what they eat, they may not have as much alcohol craving.
RICK JOHNSON [00:57:07] Alcohol craving and sugar craving are linked. And if you stop drinking alcohol, people will tend to want to drink sugar or eat sugar. And if you take people who crave sugar and take away their sugar, they may end up wanting more alcohol.
SHELLEY [00:57:23] That’s right. At AA meetings, the amount of candy is huge.
RICK JOHNSON [00:57:28] Probably. I’ve never been to an AA meeting, but I bet you it is. But I will tell you this as a physician, when I have a patient get admitted for alcoholic liver disease and I go in to see them, there’s usually a soft drink can on the table and both can cause liver disease. In fact, in our animals and we block sugar, fructose metabolism, we can block alcohol induced liver disease. So we actually believe that the liver disease from alcohol is really a sugar disorder. So the two are really linked.
SHELLEY [00:58:04] That was fascinating. I had I had thought that alcoholism had something to do with the P 54 pathway, but my colleague Beth Bennett set me straight. Okay. So it is more it’s a mystery and it’s something where it’s one of these parts of the body that tends to wear out and be out of balance the more that somebody is exposed to this stuff. Yeah, yeah. Lots of things like that.
RICK JOHNSON [00:58:37] This can go really deep
KIDS AND ENERGY AND MITOCHONDRIA
SHELLEY [00:58:41] And, and there’s, there’s some things I disagree with in your book.
RICK JOHNSON [00:58:45] Oh, okay. What do you disagree with?
SHELLEY [00:58:49] Well, you said that one reason that children don’t have these metabolic challenges is because they’re more inefficient at processing the things that lead to fat storage.
RICK JOHNSON [00:59:03] We did a study right here at Children’s. So we took children. You know, fructose is absorbed through a transporter called Glut 5. Glut 5 in a normal animal, Very, very little else in the intestine. So if you give fructose to a person who’s not ever had sugar, they’re going to get cramps and diarrhea because they can’t absorb it. And then over time, as you give them more and more sugar, they turn on these transporters so they can absorb it better. And you can show that in animals easily.
SHELLEY [00:59:35] Oh, this is diarrhea.
RICK JOHNSON [00:59:36] Not diarrhea. I’m talking about absorption of sugar. If I give a load of fructose to a five year old who’s never had sugar.
SHELLEY [00:59:44] That was a rare five year old.
RICK JOHNSON [00:59:45] Yes. In this country. Yeah. So if you give fructose to a five year old in this country who’s had a lot of sugar, it will absorb more than if they had never had sugar because they have the transporter. So we did a study at Children’s where we took kids that were lean, kids that were overweight, and kids that were obese, with fatty liver documented by biopsy. We give them all the same dose of fructose. We measured how much they absorb and all the overweight fat kids with fatty liver. they absorbed all their fructose. People that were overweight had intermediate absorption and the people who were lean had really reduced absorption. So the same amount of sugar it goes in, but not the same amount is absorbed.
SHELLEY [01:00:32] Well, I’ve been around some little kids who after they eat a cookie, it’s like being next to an oven. Their body is burning off the sugar. They’re not getting fat off of the sugar. Instead, their bodies are like an oven that’s just flaming. You can sit next to them, and you’re warm.
RICK JOHNSON [01:00:54] It’s thermogenic. The rapid burning of fructose.
SHELLEY [01:00:58] Is that inefficient or is that effective? Is that child’s body being effective at not being overwhelmed by a substance that is too much for it?
RICK JOHNSON [01:01:08] No. What happens is they’re burning . . .. The ATP levels are falling and they get hyperactive. And then after that, they’ll actually reduce their energy. They’ve activated the switch.
SHELLEY [01:01:24] You know, it’s easier for me to have fat on my body today than it was ten years ago. Is that because my body has finally become efficient at storing fat, or is it because my body is less efficient at being able to cast off excess energy? Would keeping the excess energy within my body be just as hard on my body as it would be for the yeast to use all of the glucose that goes in, instead of sptting out as ethanol.
RICK JOHNSON [01:01:50] There’s multiple reasons for why when a person is young, they tend to be invincible. And then when you get older, your metabolism slows down and you become overweight easier. When you’re young, you tend to have a very healthy mitochondria. Your energy factories are really healthy. Takes a while to dampen them down. Also, the ability to absorb sugar is is reduced in the beginning, but that’s not the main reason. We tend to have a very healthy mitochondria is what kind of keeps you going. And what happens is the way this ((Polyol)) pathway works, it causes oxidative stress to the mitochondria. Each time that happens, the ATP production goes down, the fat storage goes up, but it’s transient and then everything goes back to normal. But when you keep hitting with oxidative stress over time, the mitochondria take a beating and over time they start to decrease in number.
SHELLEY [01:02:49] They get sluggish and they get senescent.
RICK JOHNSON [01:02:51] They get senescent, they fission. The amount of ATP produced stays down.
SHELLEY [01:02:55] They cause more pollution.
RICK JOHNSON [01:02:57] Once the mitochondria are low, then what happens is it’s very hard to lose weight because you’re kind of like reset to that. Higher weight. So you can lose weight, but you’ll want to go right back to that weight. The end of my book, I talk about this and I talk about how you can reverse that. That’s the whole bit about exercising in zone two and stimulating mitochondrial growth and all that.
SHELLEY [01:03:24] With a kid who is obese in your studies, is that kid’s mitochondria more efficient or less efficient than the child who is lean?
RICK JOHNSON [01:03:34] Oh, they’re less efficient. The child who’s obese is less efficient, but oftentimes their mitochondria numbers are still normal. So when you first become overweight or obese, usually the mitochondrial density is still good. Your energy levels, your ATP levels tend to still be pretty good when you’re not eating sugar. Obesity is much more reversible in that very beginning. If you find someone who’s only been overweight or obese for like five years, it’s much easier to cure obesity than if they’ve been obese for 20 years because at that point they’ve lost more of their mitochondrial energy. The longer you’ve been obese, the harder it is to fix it.
SHELLEY [01:04:15] Still thinks it’s fixable?.
RICK JOHNSON [01:04:16] This is the incredible thing. It’s still fixable. My friend Inigo San Millan. he’s the man who’s really done a lot of wonderful work on restoration of the mitochondria. You might want to talk to him because he’s really like the world’s expert and he’s here in the Denver area.
SHELLEY [01:04:37] I have enjoyed talking with you about this and hearing what you’re doing. This one question I have. Well, we’re not quite seeing it the same way as a question, but I do think you’re on to something. And I do think that there may be something driving fat storage beyond storing energy, in evolution earlier, that will be interesting to discover.
RICK JOHNSON [01:05:00] It comes down to uric acid, I think is the key.