Introduction
Dr. Eric Westman: From time to time, I interview very interesting people, clinical users of low-carb diets, and researchers of low-carb diets. Tell us a little about where you’re from, how you got into low-carb and keto, and where you are today. Then, I have lots of great questions for you.
Dr. Lucia Aronica: I am Lucia Aronica. I am a lecturer at Stanford University, teaching everything about epigenetics and diet. Epigenetics is the science that explains how the environment can influence our gene expression and health. I focus on nutrition and specifically different types of diets, from keto to low-carb and recently even vegan diets.
I am Italian. I was born in Naples, where I studied medical biotechnology, and then I moved to Vienna, Austria, to pursue a PhD study in epigenetics. Then I was in Oxford for a couple of years, and then I joined Stanford for my second post-doc to realize my dream of combining epigenetics with nutrition.
At the time I joined Stanford, the Stanford DIETFITS study had just begun. This was the largest randomized clinical trial ever undertaken to compare a low-carbohydrate, low-carb, and low-fat diet with 609 overweight and obese participants, men and women. The trial collected numerous data about genetics, epigenetics, and the microbiome. This is also the largest randomized clinical trial in what we call precision nutrition, so nutrition is personalized based on molecular markers that are unique to people like genetics, epigenetics, and the microbiome. For me, that was a unique opportunity, and since then, I’ve been working at Stanford, teaching at Stanford, and enjoying my journey there.
Eating to optimize health
Dr. Eric Westman: The idea of matching nutrition to somebody’s metabolism, isn’t that one of the goals of personalized nutrition? Maybe we shouldn’t all eat the same thing for some reason. It’s not based on geography, ethnic group, or religion. It would be more based on what genetics you have. Someone should eat this way and another person should eat another way to optimize health?
Dr. Lucia Aronica: It’s not only about genetics. While nutrigenetics is probably now the most discussed science in personalized nutrition or precision nutrition, there are other emerging sciences, including the microbiome and epigenetics. I see these molecular markers as an opportunity to personalize, I think, 20% of your diet to improve your health.
What I mean by that is, for everyone, there is an 80% that is universal. Unprocessed food, and that’s going to improve the nutrition for everyone. It’s universal, and I think what is universal is more important. Then there is, I think, 20% or 15%, depending on the person, that can be personalized. We are talking about food intolerances. They have a genetic component, but sometimes also a microbiome component.
We are also talking, for example, in epigenetics. We can see from your blood whether you are starting to develop diabetes or not. Some epigenetic biomarkers of diabetes show up even before your glucose or insulin levels get altered. This is a way to say your genes are starting to see a change. Maybe you should start using your carbs. Using your carbs even without knowing this information is probably ideal. There’s still value in this additional personalization, without forgetting that what is universal still remains the most relevant thing we can all do.
Macronutrients
Dr. Eric Westman: There’s more in common with healthy diets, even though they may be extreme carnivore or herbivore. There’s more in common with these diets, and studies show it can be healthy because of the lack of processed food. Even though people make it seem like there’s a big difference.
Interesting, 80%. I didn’t think it was that high. You come at it from a physiological standpoint. Protein is what the human body is made of, and protein is what we need to replenish our cells. That’s such a commonality; you’re not going to see much difference in protein for people.
Why don’t we take one macronutrient at a time? What have you learned about epigenetic expression, and what take-home points might you be able to tell our audience about a range of proteins, fats, and carbohydrates? Is protein one of those things that is more common for everyone or different?
Dr. Lucia Aronica: Before diving into the macronutrients, which I think is the most relevant question for your audience, I want to point out that probably at least until now, personalized nutrition is more useful for micronutrients. There are genetic variants that may be able to tell you whether you can’t absorb certain vitamins and micronutrients efficiently, such as vitamin D, vitamin B9, or folate. You need to pay extra attention to get that from food. This is where science is stronger now.
Epigenetics
Regarding your question regarding my work with epigenetics and different diets, especially for the diet study, we didn’t really look at protein. I agree with you, protein from proteios (Greek) is the nutrient that comes first. We should try to incorporate protein in each of our meals, and then different people may want to have fewer or more carbs. I know that your audience likes to have fewer carbs. I forgot to mention I am a low-carber myself, so I started a keto diet more than 15 years ago and have been alternating between a keto and a low-carb diet. My carbohydrates come only from vegetables. I’m Italian, but I don’t eat pasta, bread, or pizza.
The interesting thing is that these are, to me, foreign foods. What I mean by that is that we humans are very simple creatures of habit, and we crave what we often eat. As a teenager in Italy, when I was hungry, I craved pasta. Now that I’ve not been eating pasta and bread for years, when I’m hungry, I crave salmon, meat, and vegetables. I don’t even think about pasta.
Dr. Eric Westman: You crave what you eat. Some of my patients say, “No fruit? I can’t believe it.” I’ll ask them, “Ask me if I eat fruit,” and they’ll say, “Do you eat fruit?” and I say, “No, I don’t eat fruit.”
Dr. Lucia Aronica: Exactly. This behavior modification is fascinating. Why is it for some people and some not? I was able to do it with no health issues. I didn’t have diabetes and I didn’t have a compelling reason. I did it to experiment with my diet when I left Italy. I didn’t have my mom around cooking pasta every day for me.
I do this diet, which is perhaps also a bias. I know the benefits of it for me, and that’s why I also joined the Stanford diet study because I wanted to specifically look at the role of fats and carbohydrates in epigenetics. We didn’t really focus on protein because the diets we compared for DIETFITS were both healthy diets based on unprocessed foods. We compared a low-carb versus a low-fat diet.
You may know, and maybe your audience doesn’t, these diets were designed to be very low-carb or very low-fat at the beginning during the first two months, with a target of fewer than 20 grams of carbohydrates a day for the low-carb group – actually, that’s a keto diet – and then less than 20 grams of fat a day for the low-fat group. Then people were encouraged to increase their carbohydrate or fat intake during the following 10 months to find a diet that was sustainable for life.
This is almost a recipe for disaster, so people started to eat more and more carbs. At the end, there was a significant overlap between the diets. Both diets consumed the same amount of protein, around 20% (of total daily calories). So, I was not able to look at differences of protein on epigenetics.
What we did was, we carried out two analyses and epigenetic analysis, which I still haven’t published, but it’s my next paper. One, we looked at the biggest losers from the study, those who lost the most weight on low-carb and low-fat, and we looked at the whole gene expression and epigenetics across the genome, so the entire DNA. What we saw confirmed what we expected, upregulation, so turning on genes that are required for fat metabolism on the low-carb diet. We know that a low-carb diet makes you a fat burner, while epigenetics can confirm that there is, at the gene expression level, this upregulation.
We also saw some interesting things on the low-fat diet, with the upregulation of genes involved in cancer protection, especially colon cancer. There are many other pathways that we looked at. I think one interesting thing that I remember was an activation of the immune cells, natural killer cells, that are very important, especially for the defenses against viruses on the low-carb diet. This is in line with some studies that say the low-carb diet overall supports lower inflammation and immune function.
This was the first thing that we observed: turning on different genes on different diets. The second thing was looking at the biomarker of diabetes I mentioned to you and your audience before. We have some epigenetic biomarkers, which are really signatures written on your genes that can tell something about your life exposures: exposure to smoke, too many carbohydrates, and even toxicants. These are all epigenetic biomarkers. I can look at your DNA and tell you what you did in the past.
We looked at one biomarker of diabetes called ABCG1. This is a gene that is implied in diabetes, and according to the model, the hypothesis is that when people gain weight, this gene gets turned off epigenetically, and this turning off of the gene contributes at the molecular level to the pathology of diabetes because this gene is required to protect you from diabetes. So there is the excess carbohydrate and overweight, then at the molecular level, this makes it worse.
The good news is that when people lose weight, the gene gets expressed again and gets modified epigenetically. That’s exactly what we saw. We saw these effects on both diets, and this is the caveat with many studies. Because both groups lost significant amounts of weight. Weight loss is always a confounder in this case, so we don’t know whether the difference between the low-carb and low-fat was masked by both groups losing weight. That’s good news for people.
Summary
Dr. Eric Westman: Let me see if I have this right. Let me unpack that just a little bit. When I think of diabetes and I teach someone that food raises the blood glucose and diabetes is defined by an elevated blood glucose, it makes sense to lessen the food that has glucose in it, so a lower-carb diet will help with diabetes. Because of that, just eating the carbohydrate raises the glucose; you don’t have as much that comes down. But what you’re saying is that there’s more to it than that. Let’s say you’re gaining weight, the blood glucose is going up, you’re gaining weight. This process hits the genes and stops the production of an enzyme or system that prevents diabetes.
Gaining weight facilitates diabetes because you don’t have that gene. It’s the inhibition of an inhibitor, right? So inhibiting an inhibitor means you’re more likely to have diabetes. But if you’re a fat burner, if you’re not eating foods that raise blood glucose and take you toward diabetes, you’re actually influencing your genetic expression of other sorts of processes. So, it’s not just the blood glucose and the A1C or the glucose in the cells that cause all the diabetic problems. There are other things going on as well. Does that summarize that?
Dr. Lucia Aronica: That’s an excellent summary. There’s more to the story. Diabetes has also a molecular backstage.
Possible predisposition to diabetes
Dr. Eric Westman: I’ve often suspected, I don’t know how to disprove or what data set to use, that the blood glucose itself is not really the entire problem with diabetes. Because we’re seeing people who don’t eat carbohydrates in a keto or a carnivore type of diet, and their blood glucose doesn’t come down to where the range is of those who eat carbohydrates. A lot of my patients will be surprised and shocked if their blood glucose goes over 100 mg/dL (5.6 mmol/L). I reassure them because they are not eating all those carbohydrates or gaining weight. I reassure them that that is a healthy process; it’s not just the blood glucose.
I wonder, in your data set, if you looked, or could you look, to separate that so that, let’s say, even if someone had a mildly elevated blood glucose in the pre-diabetes range, did they not have the predisposition toward diabetes because of these other factors? Does that make sense?
Dr. Lucia Aronica: Yes it does, and we didn’t look at that. We still haven’t published the data. That’s a nice suggestion.
Dr. Eric Westman: You might just look at the variable total carbohydrate intake. The kind of thing that I imagine in the patients, but I can’t study it, is that the most benefit for someone on a keto diet to prevent diabetes – most of it is from the blood glucose lowering. That’s not all, like a mountain stream coming down the mountain and you have a dam. The water level is kept pretty constant, but there’s all this water coming down here, and the water being the carbohydrate oxidation, all of the damage from the metabolism of the carbohydrates.
I wonder if these are other sorts of processes – it could be neurologic, could be other vascular sorts of consequences that are not directly related to that blood glucose. I don’t think you can get diabetes in a world without carbohydrates. I know that’s a strong statement, but what would your response be to a world without carbohydrates? In a carnivore world, an animal like a lion, and a growing number of humans, it’s really difficult to have diabetes.
Dr. Lucia Aronica: That’s also my assumption. You are the expert here. Type 2 diabetes is eventually an excess of lifelong excess of carbohydrates and sugar. It’s a recipe to give yourself diabetes. That’s my assumption and understanding in a nutshell.
Matching fat levels and carb levels for different people
Dr. Eric Westman: When we’re talking about optimal fat and carbohydrate levels for people, if the protein is great, we don’t have to change that too much, but how do you look at matching fat levels and carb levels for different people? Or is that still kind of a toss-up? Can science tell us that you have this genetic type, so you should eat this way, and you have this one, you should eat that way? How far along are you with that?
Dr. Lucia Aronica: That’s a very beautiful question. The answer is, from a nutrigenetics standpoint, I think we are not there, and we will probably never be there. As I mentioned before, nutrigenetics is mostly useful for micronutrients. The reason is that, yes, some genes may predispose people to break down carbohydrates or fats more efficiently when they are born, but as we all know, it is the exposure to carbohydrates and sugar during a lifetime that has the strongest influence on whether you should restrict carbohydrates and go for a keto diet or a low-carb diet or not.
For example, let’s say that you get a nutrigenetic test, and it tells you that you are predisposed to burn carbohydrates very efficiently and that a high-carb diet is good for you. But if you have been eating carbohydrates and sugar all your life, and by now, you have pre-diabetes or type 2 diabetes, should you follow what the genetic test tells you? Of course not. This is where I tell people not to rely on these recommendations. Many companies are making these recommendations on micronutrients, and I think these recommendations are misleading. Not because they’re not really based on science; there is some scientific evidence there, but it doesn’t make a significant clinical impact on people’s lives. Considering their overall lifestyle, the diet they have had until now is more important.
In general, I think, independently of diabetes, a low-carb diet and keto diet are great options for those with diabetes and overweight. I honestly think that a low-carb diet, in general, is a nutrient-dense diet because, basically, if you eliminate all refined grains and sugar, which we all agree is a good thing, whether across all diets, we agree that that’s a good thing. If we do that, we are eating a low-carb diet. Then the question is, should you also eliminate fruit or not? I think that’s where personalization is useful, but not so much based on genetics, but based on markers like insulin and glucose, in general, glucose response or insulin, HOMA-IR, and lipids. Also things like activity level.
I know people who are extremely fit and engage in lots of physical activity, and their muscles are really glucose sinks. They may be in ketosis with 100 grams of carbohydrates a day. This is where these factors play in personalizing the recommendation to say, maybe you are an athlete, and you have lots of muscle, you are still in ketosis with 80 grams of carbohydrates. That’s great. I think these factors are more important for personalization than genetics. With epigenetics, we are still not there. I’m more interested in the mechanisms to look at what happens backstage of diabetes and these other diseases, also from an educational standpoint, to tell people it’s not only about your weight or your blood sugar. You are actually modifying your genes. You may want it or not, and I believe, maybe because I’m a teacher, that these things can contribute to behavior change.
Even thinking that there is a possibility, we don’t know, there is a possibility that these epigenetic modifications may be transmitted to future generations. For example, we know that obese men have different epigenetic modifications in their sperm cells, and these modifications regulate genes that control appetite in the brain. There is a potential. We didn’t demonstrate it because we don’t follow the children of these men, but there is a potential for epigenetic transgenerational transmission of food cravings. If we think that we don’t have only a responsibility for our blood glucose, but we’re really modifying our genes and perhaps affecting generational outcomes.
Studies
Dr. Eric Westman: That’s in all of the in utero, so the baby is exposed to what the mother is eating, and all of it is very fascinating, although it can be erased with environmental change, right?
Have you ever watched the show Naked and Afraid, where people go out into the middle of nowhere, and they try to survive for 21 days? They lose a pound or two per day. An extreme environmental change can overcome genetics. Total starvation is what it is, but it’s not healthy. I don’t recommend that people do that.
Let me switch gears a bit. If you can’t tell me what my perfect diet is yet, there’s some wiggle room there. Within the studies that you’ve been able to do, I was so happy to see that you landed at Stanford and worked with a group that I have to say is probably the best randomized trial data sets we have on nutrition because Professor Gardner and the group there ranged the macronutrients across the entire spectrum.
Most people will do a study, and the range of carbs is very small, and it really doesn’t tell us about the genetic expression change that can happen in ketosis, for example. It was surprising, and I was thrilled to see that you were able to take a study. Could you explain the study? You looked at the ultra-low-fat, ultra-low-carb within the data set, and I need to know just a little politics about how this happened because Professor Gardner describes himself as a vegan, and it seems like he’s reluctantly studying these animal-based diets. I don’t know him all that well personally, so I don’t know if that’s true. There’s a study that had a wide range of macros, and then the study you did looked at the extremes.
Dr. Lucia Aronica: The study you mentioned compared the people who stick to a keto diet or an ultra-low-fat diet.
For the keto diet, we used the threshold of 30 grams of net carbs per day. I know that you prefer total carbs, but we did net carbs.
Dr. Eric Westman: Net carbs just mean more carbs to me.
Dr. Lucia Aronica: We did it to also acknowledge that we prescribed a whole food diet, so we wanted to reward those people who actually ate most of their carbs from vegetables.
I think a 30-gram net carb threshold can work for some people to be in ketosis. We didn’t measure ketosis, I want to point that out, we used a 30-gram net carb for the keto group and a 15% maximum of calories from fat for the ultra-low-fat group. We did that because of the critique we received from people who were disappointed that we didn’t look at the extreme diets.
The diets, with time, as I mentioned before, became more similar to each other. This was a 12-month intervention, so at 12 months, we told people you can increase carbohydrates and you should increase carbohydrates and fat. Also, for this reason, we didn’t use the 20-gram threshold because we literally told people to increase their carbs. We used 20 grams as a recommendation for the first two months, and then we told them, please go and increase your carbs and fat. What we did is we looked at the people who, at three months, so one month after we told them to increase carbohydrates or fat, were still consuming less than 30 grams of carbohydrate a day for the keto group or less than 15% of calories a day for the ultra-low-fat group. We found something surprising.
First of all, only 18 people were in the keto group and 21 in the ultra-low-fat group, and these numbers may sound unimpressive at first, but if you consider that these dieting diehards really decided, a little masochistically, to maintain such lower intakes of carbohydrate and fat after being given the green light to increase their consumption, I think that’s quite remarkable. What we found is that both groups experienced significant benefits. When it comes to dieting, masochism works. Both groups lost about 20 pounds, so twice as much as the overall population at 12 months. In only three months, they lost twice as much as the overall population in 2 months. They had a reduction in insulin resistance, as measured by HOMA-IR, of 30%, and they experienced improvements in lipids.
That’s the difference; that’s where things become interesting. The keto group experienced a transient and mild increase in LDL cholesterol at 3 months. We know LDL cholesterol is the elephant in the room when we talk about low-carb and keto diets for health because there is the concern that these diets increase LDL cholesterol and that this is going to cause heart disease. But the story doesn’t end there. When we followed people over the following 9 months, we saw that the LDL increase was only transient, so it disappeared over the following nine months. The people in the keto group experienced significantly greater improvements in triglycerides and HDL. The triglycerides went down, I think it was more than 60%, and the HDL went up. The ratio of triglycerides to HDL is an important cardiovascular risk factor, sometimes more important than LDL alone. The people in the keto group switched. Usually, this ratio should be ideally less than 2 or 1.5, or even better, 1. It depends. My ratio has been 0.3 for the last 15 years. That’s the magic of a low-carb diet. It’s possible. Let’s say shoot for less than 2 at least, or 1.51.
The keto group, at the baseline, and the beginning, had a ratio of 4.7, very concerning. They ended up with a ratio of 1.8, which is still in the healthier range. The low-carb group only decreased a few points, I think it was 2.9 to 2.7, so the keto group experienced significantly greater cardiovascular benefits.
Then there was a final surprise, and for me, this was the most surprising factor of the study. The people following an ultra-low-fat diet ended up consuming, over the following nine months, at 12 months, they were consuming 50% more refined grains than when they started the trial, whereas the opposite happened to the keto group. At 12 months, they were eating 50% less than when they started. Despite this, at 12 months, they were not anymore (inaudible). I think both groups increased their carb and fat intake. The keto group, at 12 months, was eating around 80 grams of carbohydrates a day, so not a keto diet anymore, but a low-carb diet. The low-fat group ended up eating around 26 grams of fat a day.
Both groups increased their consumption, but there was something behavioral. The keto diet had long-lasting behavioral effects on people, which I think illustrates something contrary to what many people say on social media, that you need to stick to a diet forever to reap the benefits. Yes, you can’t go back to a processed diet, but what if some people may want to stick to a keto diet forever because they need it or because they like it?
What if you try a keto diet for three months? Maybe that’s the fix for your carbohydrates because you learn a lot of things when you go on a keto diet. You need to start to read the food labels, which is very good. Realize the hidden source of carbohydrates. There is more sugar in a tablespoon of barbecue sauce than in a donut. You learn a lot. It’s like going to school again, and that experience can teach you. Maybe you’re not going to stick to this diet, but it’s an eye-opening experience that can have long-lasting effects. In the end, these people ended up just doing what everyone thinks is the most important thing for health, reducing refined carbs and sugar.
Dr. Eric Westman: Very interesting, and despite the difference in macronutrients of the ultra-low-fat and ultra-low-carb, they both had improvements in insulin resistance.
Dr. Lucia Aronica: Yes, and that’s a puzzling question. Maybe I can also ask why. There’s the weight loss component there, so these were overweight people.
Clinical trials
Dr. Eric Westman: That’s the easy answer. I forget the average BMI, but I think the study did not really reflect an obesity medicine practice. My average BMI is about 35, and I explained that there’s a weight loss phase and a weight maintenance phase. I love that you came to that, and you’re not in an obesity medicine clinic. You’re doing clinical trials with obese or overweight people, but not too much.
I need to switch gears to the treatment of diabetes. The study was a bit surprising that the world’s best group on randomized trials, your group, didn’t reach out and ask anyone who was using keto diets how to do it. When I read Professor Gardner’s paper on the Mediterranean versus keto, we had to write a letter to the editor, and Dr. Kalayjian and I did write a letter because it wasn’t really what we do in clinical practice. It was very strange. It was hard to do, and of course, then the comment in the paper is, “This keto diet was hard to do.” You were teaching it in a way that none of us clinicians choose. Also, one of the medicines was dropped for the treatment of diabetes. Comparing two different diets, the medicines were only dropped for the keto group, and I was like, “Wait a minute, this isn’t a fair fight.”
When your team gets together to design studies, can you perhaps suggest reaching out to clinical doctors who have been using this for 25 years?
Dr. Lucia Aronica: That’s a great idea. I was not involved in planning that study. I think that would be a win-win for everybody because, as you mentioned, the clinical implementation of the keto diet is that your group, and other people like Jeff Volek, have been doing this for years and know how to teach people. Also, there’s this idea that a keto diet may not be sustainable, so these ideas sometimes get in the way because then the design and the recommendations are based on doing it only for a little while. Yes, I’m with you. And in that case, I think it was a study comparing a Mediterranean diet, and it was defined as Med Plus. The Med Plus is basically a Mediterranean diet without pasta, pizza, bread, and refined carbohydrates, which is a low-carb diet, and this is a Mediterranean diet that doesn’t exist on earth because I am Italian, and I tell you that’s not the Mediterranean diet I was eating. The point is a message for the readers. I think in general there is a lot of polarization in nutrition, and the reason is that if you look for it, there is a study supporting any nutritional religion you want to follow.
The point that people need to understand is that there are studies, but there are different studies. Epidemiological studies don’t allow us to conclude anything in terms of (inaudible). Not only hypothesis-generating and even the randomized trial. They need to look at the design, at the outcomes, and there are limitations. The bottom line is, don’t get frustrated to hear one day that one thing is true and the next day that the opposite is true. It will always be like that unless we change. As consumers of health, we have a responsibility. We cannot change the system; we have the responsibility to understand that it’s all about our interpretation.
Even these clinical trials, the clinical trials at our nutrition group, which are very good quality, have their limitations and they need to be interpreted in the right way before making any conclusion.
Funding
Dr. Eric Westman: In my clinical practice, I’ve gone beyond the surrogate markers of the blood, the triglyceride and HDL. The metabolic syndrome is what low carb treats and we say that that reduces cardiometabolic risk, and that’s our model that we use. Total and LDL cholesterol goes down with a low-fat diet and was the only outcome in the Twin study, which I was quite critical about after the fact. If you’re watching this, please don’t worry about the LDL. We have research going on now that is fascinating, that in the context of a low-carb diet, it may not mean the same thing.
Where do we get the funding, and the interest to do the outcome study? The outcome study meaning death and dying and heart attacks and diabetes comparing different types of diets because we can do intermediate outcome studies for a year or forever. Lucia, you’ll be funded forever in your career, but you won’t know the answer, which is, do the outcomes really differ? In my randomized trial training, we only needed 50 people to show a difference in low glycemic versus low carb for type 2 diabetes using an A1C as the marker with a typical American diet. In fact, someone with type 2 diabetes and the existing heart disease.
You take the sickest of the sick, and now I realize this is probably not the population that you could do a study of, and you’d have to collaborate with cardiologists or at least internists who are studying this. Maybe the VA (Veteran’s Affairs) might be a possible place where you take people with type 2 diabetes and heart disease and you randomize them to three diets. The model of ultra-low fat, ultra-low-carb, and then the American diet, and then in five years probably there would be separation in life and death sorts of things, the MACE (major adverse cardiac events), the cardiovascular outcomes. Is this on anyone’s radar screen to take the sickest of the sick and to randomize them to different diets? I think that that’s a really important step.
Dr. Lucia Aronica: I think it is, and as usual, the limitation is funding because there is not a commercial interest in that. There are a few groups that may be interested. I think I know a few groups that may be interested in funding this research. If they are listening, these are philanthropic organizations.
Advice for staying on a low-carb diet
Dr. Eric Westman: I think Dr. Phinney and Dr. Volek have a Department of Defense study funded. It’s not done yet, but looking at heart failure, and now we’re starting to get into diseases that have outcomes of death and dying, which can happen if you take people who have lots of diseases.
If you’re watching and don’t know clinical trial methodology, if something has a high event rate, you don’t need so many people in the study. But if you have a bunch of healthy people who aren’t going to die for 50 years, it’s going to be very difficult to see death as an outcome in a study. You’ll have to go 50 years to see that difference.
I’m not getting interested clinically in triglycerides, and I don’t measure small LDLs anymore. I try to discourage them. I’ve asked my patients to measure their vascular system with ultrasound or CT scan coronary calcium score, although that’s fraught with difficulty in interpreting it. If the coronary score is zero, you have a great likelihood of the next 10 years of not having a heart attack, even if you’re a carb eater. Remember, most of those studies are on people who eat carbs.
With what you know so far and I’m being personal to our group that has already decided to follow a low-carb diet. They’ve probably benefited, maybe their diabetes weight going down, and they like staying on a low-carb diet. What advice would you have for that?
Dr. Lucia Aronica: I hope that this discussion inspired you to keep this lifestyle because beyond the benefits for diabetes and blood glucose control. We know that these diets are more nutrient-dense. By eliminating the refined carbohydrates, you are getting more nutrients. I want to bring you a new perspective on nutrients: some of these nutrients are also epi nutrients. These nutrients are essential for the proper functioning of your epigenetics and your gene expression. By eating a low-carbohydrate diet, you are eating a more epi-nutrient-rich diet. It’s rich in the things you need for your epigenetics and is free from the things you don’t want. It is unprocessed food, so it’s their additive excess sugar that also causes other molecular damage to your cells, from glycation to inflammation.
This is how I got into a low-carb diet. It was not for type 2 diabetes; it was long-term health insurance for me. It means keeping in shape without effort. I don’t need to count calories. I love food, I love eating, and to me, it’s not a disease-treating approach. It can be for many people. We are discovering more and more diseases that can be treated with a keto diet, including some mental health disorders.
There are people like me who embrace a low-carb lifestyle just because it makes things so easy to keep healthy and keep your gene expression healthy with little effort. So keep it up.
What is next
Dr. Eric Westman: What’s next for you in the research domain?
Dr. Lucia Aronica: I’ve been involved recently in some studies with the epigenetic clocks. These are tests that can measure your biological aging, the rate at which your cells are aging that can be different from your chronological age, the one you celebrate at your birthdays. There are some pros and cons of this test. Again, they mostly reflect weight loss, so it’s difficult to study them in the context of clinical studies because most of the effect is attributed to weight loss, not diet. It’s an interesting new avenue for me. Then finally, I’m going to publish the study I discussed today about epigenetic biomarkers. So going back now after having been focused, my latest publication on keto and low carb, and then finally I’m all about education about epigenetics. I’ve created a little course on epigenetics. You can check it out at draronica.com. It’s my university lectures condensed into five modules for non-experts and everyone who wants to get a deep dive into epigenetics, for professional reasons, scientific curiosity, or any other reason.
I think I’m going to write a book on epigenetics and diet, starting with Italian, and then if people are interested, I will translate it into English. I’m very excited. I love educating people about the backstage of their health, just as an additional motivation to keep it up and improve your health.
Dr. Eric Westman: That sounds great, and I become more and more optimistic when I talk to you and the young researchers who are more open-minded. I think the truth will be out. Science will find the truth as long as there are people like you. Thank you so much.
You can watch the full video here.
