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You said you tried the Atkins Diet, the low-carb, high fat diet.

JEFF VOLEK

Yes. That was almost 20 years ago in the early 90s.

Did you feel like a heretic doing that?

JEFF VOLEK

Well of course.  I was actually working in a hospital at the time.  I had just completed my degree as a registered dietitian, and I was  working with patients and counseling them on low fat diets.  Here I was experiencing a dramatic, positive response in my own body to a very low carbohydrate diet.   I always knew I wanted to go back to grad school and study nutrition and exercise.  Shortly after working in hospital for a year I actually did that.   I became obsessed with learning more about low carbohydrate diets.

Was it because you were surprised by your own body’s reaction.  Or were you surprised that something that worked well for you was so widely condemned.

JEFF VOLEK

I think both.  I certainly wasn’t learning about low carbohydrate diets in the classes I was taking.   It wasn’t taught, and so I was doing this on my own in the library late at night, day after day, spending hours just trying to find as much research as I possibly could.  And everything I was learning and reading about  was supportive of low carbohydrate diets, and this was the early 90s, so this was before the resurgence in research of low carbohydrate diets.  But there was actually  quite a bit of work done back in the 60s and 70s.  And of course Steve Phinney had published  work in the 80s, and it all was very favorable, and it was shocking to me that this work was not followed up on and that we were  promoting, carte blanche, low-fat diets with no caveats or recommendations for alternative approaches.  So this became an obsession that really has  continued on to this day to learn more about these diets, and I was fortunate in my graduate work to have the opportunity to study this.  It was actually my dissertation to examine low carb diets.  So for the last 12 years I’ve actively been pursuing research trying to answer the basic questions related to how humans and how people adapt to low carbohydrate diets.

Has it become your religion to study this?

JEFF VOLEK

Well I think as a scientist it would be reckless to say I view this as a religion but the analogy is not a bad in that  people do view nutrition with sort of a religious vigor.  The data should rule the day, and yet, in my experience talking about nutrition with my many colleagues and other researchers, they don’t like to deal with this data.    I think a lot of scientists, when they deal with data that is in conflict with what they have been promoting for years, they deal with that in a way I would describe as cognitive dissonance.   They don’t really criticize the data.  At the same time they don’t embrace it.  They ignore it, they reject my grants or reject my papers.  And at the same time when you deal with these people face to face, and try to debate them, they often back down

When you say they back down, is it because they’re tired of hearing from yet another low carb advocate, or do you mean that when they actually listen,  they start to agree 

JEFF VOLEK

It”s quite common that they ignore us, and it’s probably fair to say that they do get tired of hearing this message, but it’s data.  It’s hard science data, and it’s difficult for them to deal with.   It’s an uncomfortable truth.   I think many of them are coming to realize they built their careers on saying something different and so, I do in some way understand their reluctance to embrace this because their careers, and to some extent the livelihood of their labs, may be dependent on promoting an alternative message.  And the message is, based on the science, we need to recognize that people vary widely in their ability to metabolize carbohydrate.   So we have a carbohydrate tolerances.

A lot of  people say that there is one best diet.  The USDA certainly seems to say that.  School lunch program certainly seem to say that.   Is it your impression that people differ in what kinds of foods they do best with.

JEFF VOLEK

Absolutely.   We have essentially a one-size-fits-all dietary recommendation and the fundamental  problem with that is that we have a heterogeneic population that doesn’t respond uniformly to that diet.  And this is not trivial because the number of people who really respond well to a low-fat diet is probably the minority of people.  Most people have some degree of carbohydrate intolerance and so would actually benefit from restricting carbohydrate not fat.  But that does vary from person to person, and so we should be seeking ways to find the right diet for the right person, and that probably starts with finding the right level of carbohydrate  Some people may need to restrict carbohydrates to less than 40 g a day.  Others may be able to tolerate 100 g per day.  So it depends on the person.  Most dietitians agree we need to embrace personalized nutrition.  But that  viewpoint is oddly juxtaposed with this sentiment that we all need to follow the dietary guidelines

When it comes to kids we have children that we know need glasses.  We have children where we know that they need to sit at the front of a room otherwise they lose their attention.  We have a lot of variation that we know in how children learn and how people learn and we acknowledge and we support.  The one variation I can think of in children and the kinds of food they get, if they have a serious allergy to peanuts, we’ll watch out for that.  Or if a child is overweight then we’re likely to tell the child to count calories more.

JEFF VOLEK

Focusing on counting calories is not the best approach.  But coming back to your analogy of food intolerances, we’re very sensitive to people with lactose intolerance or gluten intolerance, and this is  why introduced the term, carbohydrate intolerance.  People have varying degrees of carbohydrate intolerance, and there’s a very strong physiologic basis for identifying that as a concept and if you view it in that perspective it’s a intuitive what you would do to a person with a carbohydrate intolerance – you would restrict carbohydrates, and that, in fact is what we have studied, and when people with carbohydrate intolerance restrict their carbohydrates below a level at which they metabolize it appropriately, all their clinical markers get better.

Now, we have a very low carbohydrate, very high fat, ketogenic diet for epilepsy – meaning a diet with such low carbs that the body is constantly in fat-burning mode and making a special, easy to use fat called a ketone.   If a child has epilepsy a lot, one way to break the cycle, in many cases, is to restrict carbohydrates almost to nothing and feed a whole bunch of fat.  In many cases after two years of that very extreme diet, a child can have pizza party, and in many cases, that child is now well enough to eat pizza without any more epileptic seizures.  Could carbohydrate intolerance be the same? Could it be  a diet that you don’t have to do it your whole life?  Could it be like having a broken ankle, where if you rest the carbohydrate handling in the body, it gets well enough to handle carbs again?  Is  carbohydrate restriction just something you need for a little while?

JEFF VOLEK

Great question and we don’t have a lot of solid research studies, but observationally and my clinical  experience, some people, when they restrict carbohydrates and lose significant amounts of weight, do improve their carbohydrate intolerance, such that they can, in a maintenance phase, reintroduce some level or carbs.  However that’s not universally true.  There are other people who will remain insulin resistant if they eat carbs, and even after they have lost significant amounts of weight.  In order for them to maintain their weight loss and maintain their metabolic health, they need to continue to restrict carbohydrates indefinitely.  So it really comes down to the person, and in many ways their underlying level of insulin resistance and whether or not that improves with weight loss.  And some people, they’re just genetically programmed to have a level of insulin resistance.  And the only way they can manage that is to restrict carbohydrates.  That’s why we advocate a sustainable, very low carbohydrate diet for people that are on the far end of the continuum of carbohydrate intolerance..  Many people will be able to reintroduce carbohydrates and still see improvements in insulin sensitivity.  But that has to be monitored on an individual basis and that’s where the tailored approach comes in, and each person has to chart their own path on this journey.

Charting your own path can involve measuring your hip to waist ratio and looking at how much you weigh, but it would be pretty neat to look in side our own blood and see if there is something there that is changing — one of those mysterious but important things we call blood markers.  Are you seeing any blood markers you think would be good for people to monitor? 

JEFF VOLEK

Objective markers certainly help people, in terms of having a having a number that they can use to help guide them down this path.  You know at this point, a lot of it is subjective in that you look at the scale and look at how you feel and you look at if you have cravings for carbohydrates.  These are all indicators that perhaps you are consuming too many carbohydrates   But we are looking at biomarkers that would provide an early sign that your body is mismanaging carbohydrates.  That really means that when you’re ingesting carbohydrate, a lot of it is being converted to fat in the body.  And you don’t necessarily  feel that And it does not show up right away in standard clinical markers But we are looking at some some biomarkers that would provide an early indication in converting dietary carbohydrate into fat, and this is causing a lot of collateral damage and sabotaging your weight loss efforts.  So this might, down the road . . .  we’re still validating this and hopefully it will be available sometime in the future.

In your book, the Art and Science of Low Carbohydrate Living,  you mention this marker is called of a POA .  What does that stand for

JEFF VOLEK

POA stand for palmitoleic acid.  It’s a particular fatty acid that we have measured in blood that responds very sensitively to carbohydrate intake.

In some of your research that you’ve published, you’ve found s that sometimes people who do well on low carbohydrate diet and also do great on a high carbohydrate diet, either one – their POA levels stay low no matter what you’re feeding them.   But other people if  their POA level is low on a low carbohydrate diet,  it will be climbing very quickly as you add carbohydrate back in.   That’s what we’re studying, and it varies from person to person.  Can you describe the new study?

JEFF VOLEK

What we’re doing now is are studying people who are essentially going through a dose response test of different levels of carbohydrates and we start them out at a very low level of carbs so that they’ll be adapted to fat-burning – that is, their body is producing ketones.   They’re consuming about 35 g of carbohydrate per day.  This is a heroic effort on the part of my dietetic students – we’re preparing all the food over a five and a half month period.

You know, 35 g of carbohydrate is not very much carb.  It’s maybe two salads, and two bowls of leafy kale and half a cup of sliced onions and a half a cup of broccoli.  That’s about it. 

JEFF VOLEK

Actually, you’d be be surprised at the variety of foods you can incorporate into a 35-grams a day diet.  In fact, our subjects have expressed great satisfaction with this diet.  In fact, after they’ve through all the diets, they come back to wanting to go on the low carbohydrate diet.

What’s a typical lunch for 35 grams of fat?

JEFF VOLEK

They may have a salad with chicken on it and a high fat dressing, olives as garnishes.  It’s rich,  particularly in fat.  It is not overly high in protein, which is a common misconception about low carbohydrate diets.   It has non-starchy vegetables such as lettuce, cucumbers, radishes, broccoli, asparagus, cauliflower, etc.   We’re taking these people through increasing levels of carbohydrate gradually, introducing carbs over time to identify a breakpoint, if you will.  We want to know at what point do they start to divert the incoming dietary carbohydrate into fat, and our hypothesis is it will vary from person to person.  Some people may be able to tolerate higher levels of carbohydrate; others may have a low tolerance.  We’re also measuring POA, palmitoleic acid, in the blood as  well as saturated fat in the blood and other standard clinical markers.  We’re also trying to understand what is the best tissue to measure this particular fatty acid in.  It has different concentrations in different cells and different lipid fractions in the blood so we want to understand the place to measure this in for people.  So, we’re hopeful that, when this  study is completed, we will have enough evidence and validation to launch this commercially, and it soon will be available for people to test and guide them to their own personal level of carbohydrate intolerance.

So you have the idea of using the POA, this marker to indicate at what level of carbs the carbs start to turn more quickly into fat.

JEFF VOLEK

Exactly, and that’s the key.  This marker increases quite rapidly when your body’s converting carbohydrate into fat, more so than any other market we are familiar with it and more so than any other fatty acid.  So it provides an early sign before you’ve started to gain weight and before your other markers, your triglycerides, for example, are elevated.  This will tend to show up quicker, so people can use this as a guide to say, y look I’m dangerous zone.  I’m still consuming too many carbohydrates, and my body’s not processing them in a healthy way.

What about all those people who have already gained weight?  If they want to lose weight, could this marker also be good for them?

JEFF VOLEK

They still need to decide what level of carbohydrate they’re going to consume to lose the weight, and if their body is converting, even when they’re losing weight, still converting carbohydrates into fat, that’s not likely to result in a lot metabolic health, and it’s not likely to be sustainable.  So I think it can be used initially to see where you’re at.  Some people may not need to restrict, carbohydrates to 35 grams, if the POA level is still at an appropriate range, so it would help it would help to guide them to the appropriate level of carbohydrates to lose weight.  But we think it’s in particular valuable as you enter into weight maintenance, because that’s where a lot of people get tripped up on low carbohydrate diets.  They do quite well initially but then they reintroduce carbs into their diets for weight maintenance, and they exceed their carbohydrate tolerance, and that’s when they gain weight back.   And that’s where you see a lot of recidivism in terms of weight gain and people enter into this yo-yo of cyclic rate loss then weight gain.

I wonder whether this approach might help no matter what diet someone choose.  For instance, if somebody chooses a Joel Furhman, higher carbohydrate mostly vegan diet, and they restrict their calories for weight loss.  Dean Ornish, Weight Watchers, any diet where you’re restricting calories, the challenge is always in the weight maintenance phase, to NOT gain the weight back.  So this could be a clue for any of these diets about whether carbs are being converted quickly into fat.

JEFF VOLEK

Exactly and this test could be used really with any diet, but our assumption is that if you’re eating a low-fat diet is high in carbohydrates unless you’re very lucky and fortunate in terms of your metabolism to be able to process those carbohydrates then your POA level might be in that danger zone.

Now Jeff, how about someone who eats a lot of fat and very low carb.  You can eat too much fat, can’t you?

JEFF VOLEK

You can.  Certainly, calories matter, even on a low carbohydrate diet.  But it’s my experience is that it’s very rare for people to overeat fat when you’re consuming carbohydrates at a level below your POA tolerance, because you are  primarily burning fat for fuel, and you have a better fuel flow to all the cells in your body, including your brain, and you just don’t have those cravings and you don’t have the hunger and appetite issues that you have when you’re over consuming carbohydrates.

So you still think that even on a high fat diet, the good carbs could be the kindle that gets appetite started again, and this POA marker might be a way to figure that out.

JEFF VOLEK

I think so because when you’re keto-adapted, you at this remarkable ability to skip meals and not feel hungry, because your body’s relying on fat for fuel.  Most people — even people who are very lean — have 40,000 kcal worth of energy in their fat stores.  That can last them for several days, even if you exercise.  So you can skip a meal, and you don’t have this fuel crisis for your brain because it can burn ketones or for your muscle cells because there’s plenty of fuel around.   However if you’re depending on carbohydrates for fuel, and you miss a meal, that can turn into a crisis and that can trigger appetite of hormones and so forth which can lead to excessive consumption of calories.

Now you’re a weightlifter, and you could say what matters the most is burning excess calories through exercise.  But you haven’t been talking that way.  You’ve been focussing on food.

JEFF VOLEK

I’m a huge advocate for exercise.  But the whole field of exercise science is much more complex than we make it out to be.  If you’re using exercise as a weight-loss tool, that’s different than using exercise to excel at sports.  So we have to be careful in how we prescribe exercise for people.  It’s  very contextual.  For example, in many people exercise is a very poor weight loss tool.

They just get hungrier.  

JEFF VOLEK

They get hungrier, and their metabolic rate goes down.  So simply telling people to exercise more to lose weight doesn’t work very well. That’s been born out in many studies now.  But if you’re an athlete and you want to improve your performance, obviously training the right way, which is a whole other issue, is important.  I’ve always been a huge supporter of nutrition being critical to experience the optimal benefits in a training program.   So you may have the best training program in the world, but if you don’t eat the right fuel to perform the exercise and to recover from exercise – there is a whole new area of recovery nutrition now,  But if you don’t have the right nutrition, you won’t experience the benefits of the training programs.  So that’s why it’s so important to be integrating the fields of nutrition and exercise to optimally affect performance and health.   And there are so many misconceptions and mythologies about nutrition and exercise that it can be a minefield to navigate through.

Is that why you’re written this new book on the Art and Science of . . . .

JEFF VOLEK

The Art and Science of Low Carbohydrate Performance, which is more or less an addendum to our previous book I wrote with Dr. Steve Phinney – The Art and Science of Low Carbohydrate Living.   Really the first book was geared more toward healthcare professionals, and trying to empower them with the knowledge to teach low carbohydrate diets and their clinical application.  But Steve and I are both athletes and have actually studied low carbohydrate diets in the context of endurance and strength performance, and we have  a lot of athlete friends who said, hey what about us?  Can we benefit from a low carbohydrate diet?  So we wrote this book down to specifically address the low carbohydrate athlete who wants to go against the grain, so to speak, and is not interested in carbohydrate loading and all the sugary carbohydrate drinks and can they actually perform exercise with very little carbohydrate.  The answer is with a couple of weeks of adaptation to a low carbohydrate diet, yes, they can perform this way, and sometimes even better.

Does this low carb diet for athletes work best for athletes in endurance sports and should sprinters stay away from it?

JEFF VOLEK

That’s a great question.   Clearly from a metabolic standpoint,  being able to burn fat more efficiently is incredibly valuable to an endurance athlete.   Especially the ultra endurance athletes who are exercising for two hours or longer.  You’re going to run out of carbohydrate and glycogen in your body.  You’re going to run out of fuel very quickly.  So being able to utilize fat efficiently is incredibly valuable.  So  strength athletes and high-intensity athletes they are performing at an exercise intensity that may rely on glycogen, so it’s not as clear cut how they would benefit.  But many of these athletes, on a low-carb diet, lose body fat.  They maintain their muscle mass while losing body fat, so this improves their power to mass ratio.  So they’re more powerful and they have more energy to do their training but they don’t lose their muscle endurance and their strength, so this is a valuable adaptation for even strength athletes.

So would you suggest to a sprinter, perhaps, train on a low carbohydrate diet, and then on race day or two days before, go ahead an eat that big plate of pasta?

JEFF VOLEK

It’s possible and this is one approach.  We haven’t formally studied this idea of reintroducing carbs strategically, or around workouts or before a race,  But anecdotally, I know athletes in Europe who follow this concept of, train on a low carbohydrate diet to induce a lot of the positive metabolic adaptations, and then, before an event, carb load.  I think it does make some sense, but this hasn’t been really studied intensely and it would be a little concerned about that approach if people were just exercising for metabolic health, and they had carbohydrate intolerance, because that might set them up to potentially exacerbate some of their metabolic problems by reintroducing carbs — even a single carbohydrate meal can allow them to lose some of their metabolic adaptations that they have achieved with a low carbohydrate diet.  So switching back and forth is not something they can do efficiently, compared to an athlete who is insulin sensitive.   So there are some caveats with that approach.  But for myself, I was a a power lifter, and I was using low-carb diets to help maintain my body weight.   I was competing in a weight class where I tried to be as lean as I could without exceeding a specific weight, and I found it was very effective to maintain my weight near my competition weight, whereas my colleagues would try to lose 20 to 40 pounds before a meet and sometimes lost a lot of strength too.   So it does have implications for power lifting.

How much do you weigh and how much weight did you used to lift?

JEFF VOLEK

When I was competing, I was a little heavier than I am now.  I was competing in the 181 pound weight class.

And how tall are you?

JEFF VOLEK

I’m 5′ 10″,  and my best squat at that weight was 600 pounds at that weight.  And I also dead-lifted 600 pounds.  My bench press was not as good.  It was 330 pounds.   Those were respectable but not good enough to compete in national or international competitions, but it allowed me to have fun, and I enjoyed it.

Jeff Volek is the coauthor of the best-selling book, The New Atkins for a New You.  He’s also the co-author of two more recent books, with Steve Phinney, The Art and Science of Low Carbohydrate Living, and The Art and Science of Low Carbohydrate Performance.  In addition, Jeff’s a professor at the University of Connecticutt.  He’s focused his career on studying low carb diets, not just for weight loss, but as a lifestyle choice that may improve the health of people who suffer from diabetes and heart disease. And he’s a weight-lifter.  For more, here’s part 1 of a 2-part interview with Jeff Volek.

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Jeff Volek, who are  you?

JEFF VOLEK

I’m a professor at the University of Connecticut where I study nutrition and exercise research.

If I were to do an arm wrestling match with you right now, who do you think would win?

JEFF VOLEK

Well I have bad elbows from arm wrestling my brother when I was young, so I think it would be a close battle.

I’m surprised to hear you say that, because, how many pounds can you lift?

JEFF VOLEK

I used to be stronger, but I still try to be strong.  I’m a power lifter at heart.  I used to compete over a decade ago and I have several meets under my belt.  Now I’m 43 years old and I’m suffering from a lot of the collateral damage from lifting too heavy of weights.   I still enjoy going to the gym and trying to out-lift the young guys there.

What does that mean?  How much weight can you lift?

JEFF VOLEK

I’m not not so into lifting heavyweights anymore, but I still can squat probably 500 pounds and dead-lift close to 500 pounds, if I’m warmed up enough to have all the kinks worked out.

Well, Jeff Volek, there’s so much talk  about whether exercise or how we eat or how many calories we eat or what kind of food we eat is what makes the biggest difference in health.  In a way, you’ve been in all these worlds, by looking at exercise and whether calories in, calories out makes a difference, and you’ve done research into what kind of calories –  fat, protein and carbohydrate.

JEFF VOLEK

I have been interested in diet for a long time, and I came upon low carbohydrate diets fairly early on in my research career, and my initial interest was more in the clinical application of diet in terms of weight loss and risk for diabetes and heart disease.   However I’ve also had had a passion for sports performance, so I kind of live in these two worlds of the clinical application of diet and also of the sport performance of diet and the health aspects, and well-being aspects of diet.  Now more than ever, over the last decade I’ve sensed these two worlds colliding, because in both of those worlds we’ve advocated high carbohydrate diets and low-fat diets as being ideal.

Who is we?

JEFF VOLEK

I guess we is the the mainstream consensus, the dietary guidelines.  It’s the dietary recommendations.  But you have to realize, in the sports world, we have the high carbohydrate paradigm, high carbohydrate loading has been around for just as long as the dietary guidelines have been around.  So I guess in many ways they reinforce each other.  What our researcher is  showing is, maybe that’s not quite as straightforward as we thought it was.

Did you start out thinking that a high carb diet is the best way to go?

JEFF VOLEK

I’m a trained dietitian.  My undergraduate degree was in dietetics, so I recognize myself as a dietitian first, and of course I’ve gone on and studied nutrition at a higher level than most dietitians.  But as a dietician, I was indoctrinated with this low-fat paradigm.

That’s a harsh term — indoctrination means that it was pushed into your brain as opposed to being a scientific exploration.  That’s a loaded term.   Did you choose that on purpose or not?

JEFF VOLEK

The curriculum in dietetics is very much focused on low-fat diets.

I think that most dietitians would say that the curriculum focuses on low-fat diets because it’s the better way to eat and it’s obviously more scientifically correct and it’s not indoctrination.  It’s just the best way to go.

JEFF VOLEK

That’s what’s presented, and  until you challenge the dogma really — it’s at the point I would characterize it as a dogma, that humans have evolved to adapt to low-fat diets and that’s the best diet for weight loss, and it’s the best diet for disease prevention and overall health.  Until you challenge that at a higher level, which I think requires at least graduate level education  . . .

Now Jeff Volek, some of the best minds in the country will respond that really when it comes to weight loss and maintenance what matters is how many calories you take in versus how many calories you burn.  So, for instance, what if you have some skim milk that you’ve flavored with chocolate and sugar, to make it more palatable for kids.  And what if you have the same amount of whole fat milk that has no sugar in it, and it’s made more palatable because it has high-fat.   The higher calorie of those two choices will be the whole milk, and if you follow calories-in, calories out as your guide, then definitely you should avoid having kids drink the unsweetened, higher fat whole milk, and instead have kids drink the sweetened, chocolate flavored skim milk.  After all, sugar-flavored skim milk has fewer calories than whole milk.  There are great scientist who will say it’s calories in calories – calories out that matter.  

JEFF VOLEK

I’m not so sure I would argue with calories in calories out as far as weight loss.  But clearly the type of calories you consume affects your metabolism in very complex ways.  So just focusing on low-fat foods is certainly a way to consume fewer calories at that meal.  But does it affect your appetite?   Does it affect your satiety and your satisfaction?   Yes of course!

So when you say metabolism, you mean things such as appetite, and whether you’re hungry or not.  Whether or not you have energy after you eat a meal and during the day.

JEFF VOLEK

Absolutely.  And consuming that low-fat milk may allow for fewer calories to be consumed at that meal.  But what happens one hour later when children get hungry and those kids are seeking out snacks and other high carbohydrate meals to satisfy that craving they have.  It’s a fuel crisis they’re having because their blood sugar is low.  If they would’ve chosen the whole fat milk, it has a few more calories, but more fat calories and fewer carbs, so they would’ve been more satiated and had less fluctuation in their blood sugar and insulin levels and likely would consume less calories over the entire day.

I gather that you’re explaining the journey you took from advocating high carbohydrate diets to low carbohydrate diets.

JEFF VOLEK

Well, I followed what I believed, during my training in dietetics and I think it was in 1991, I  had graduated from dietetics and obtained my registered dietitian status.  That’s when I  decided to read the Atkins book.  Dr. Atkins’ book, and at that time I was following a very low-fat diet.

Did that work for you, a low fat diet?

JEFF VOLEK

I never really felt that great on a low-fat, high-carb diet.   I’ve never had a weight problem, but I never felt like I had a lot of energy and I always felt all the fiber I was eating was not agreeing with my gastrointestinal system.   I had a lot of GI symptoms at the time.  So I said what the heck!  I’ll try the Atkins diet.  And it was nothing short of an epiphany.

(This is part 1 of a 2-part interview)

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Ron Krauss, there’s so much debate about saturated fat.  Some studies say it’s perfectly fine to have it, and yet as a standard policy in most health clinics and with institutional recommendations, it’s, “keep the saturated fats low.”  Meanwhile, your research has been a little frustrating.  You don’t come out clearly saying one way or the other.  Instead you say, it depends.  It depends on what the saturated fat is eaten with. 

RON KRAUSS
I don’t know if I have to apologize for the way things really are, but that’s the way they are.  And it’s not my fault.  (laughs)  My job is to help people understand how saturated fats work in the body, and explain it in the simplest possible way.  We’re trying to work towards giving people that understanding, but simply the idea that saturated fat itself has an effect on health, outside the context of what one’s eating, is already a naive concept.  Our studies are showing that how saturated fats interact with other foods is really more important than even we had realized when we started this work.  And what we’ve learned about saturated fat, over the years, has shifted what we think.  My first studies were driven by the hypothesis that lowering fat its good for you.  This was in the old days, and I came out of that background of expecting lower fat diets to be healthier, and we wanted to study lower fats diets.

When was that?

RON KRAUSS
We did our first studies in 1989, so it’s been over 20 years ago.  I’m somewhat shocked to realize how long I’ve been doing this kind of work, but along the way we’ve learned things we didn’t expect to see.  In fact for me the most important advances and the most interesting ones certainly are the ones that come out with opposite results from what you started with, where you expected one result and the results came out differently.  And that happened when we first studied lower fat diets, thinking they would benefit the individuals who had higher heart disease risk, such as people who had the more dangerous, small particle LDL cholesterol, the pattern B profile, for example.  What we found, to our surprise, initially, was that when we fed these low fat diets and reduced the fats by substituting carbohydrates, which was at that time and still remains the current paradigm, we really didn’t achieve what we had wanted to achieve.  There was some improvement in the overall amount of cholesterol in the very small percentage of individuals who had very high amounts of small LDL particles in their blood already, but what was really astonishing to me at the time was that the majority of people we studied, the high percentage of people who had the normal metabolic profile, with more of the safer, Pattern A, larger particle LDL, a very large percentage of those people we studied actually shifted into the riskier, pattern B mode when we reduced their saturated fat intake.  We did the equivalent of changing their hair color from red to blonde, or maybe blonde to red, by putting them on a lower fat, higher carbohydrate diet, so we elicited what we think now is an underlying genetic susceptibility which is very common in the population.

And we’re not just talking hair color here.  We’re talking about something that actually changed their health, because the increase in the smaller particle patten B LDL lipoproteins were an indication of greater health risk.  So it was bad news.  It seemed that giving most people the supposedly healthier, lower fat, higher-carb diet made them more at risk for heart disease.

RON KRAUSS
Yeah, and we were certainly concerned about increasing heart disease risk, so we turned our attention ultimately away from feeding higher carbohydrate, lower fat diets, to doing the reverse, to lowering carbohydrate and raising fats, and that’s where we intersected with the world of people very interested in very low carbohydrate diets.  We sort of worked our way into studies along those lines and ultimately published a study five years ago, in which we systematically compared different dietary approaches,  keeping in one case, saturated fat constant and in another loading the diet up with saturated fat, and what we found is that in our study groups, the reduction of carbohydrate alone improved metabolic profile in the majority of individuals, independently of saturated fat intake.

Was that the 2006 American Journal of Clinical Nutrition Study?  In that study, you had a range of carbohydrates that people ate from 54% of calories as carbohydrates to 26% of their calories as carbohydrates.

RON KRAUSS
We had three levels.  The low was 26% carbohydrates, the high was 54%, and then we had 39% in between.

And you also varied the amount of saturated fat.  In some of those people you fed them 8% of their calories as saturated fat and in some you fed them 15%.

RON KRAUSS
That’s right.  When we lowered carbohydrates in their diets, we raised the fats.  So, on the lowest carbohydrate diet, the 26% carbohydrate diet, we jacked up the fat content with either monounsaturated or saturated fat.  That is, either an olive oil type of monounsaturated fat versus, in this 2006 study, a saturated fat, mostly dairy fat.

And you didn’t see much difference when your study subjects switched from eating more monounsaturated fats to eating more saturated fats.  But when their carbohydrate intake went up or down, you saw significant changes in their blood cholesterol.

RON KRAUSS
Yes.  The improvement was clearly due to the carbohydrates.

Meaning lowering the carbohydrates generally lowered the risk factors that showed up in their blood.

RON KRAUSS
That’s right.  The improvement was clearly due to reducing the carbohydrates.

It might seem silly to emphasize that, but we really need to say it more than once — that the improvement was due to increasing fats and reducing carbs, because that’s backwards from how most people think it works.

RON KRAUSS
Yeah.  I like to think the world has come around but obviously that’s not true.  We looked carefully at the saturated fat effects.  With more saturated fat in the diet, we did see a signal for an increase in the overall amount of cholesterol in their blood.  But when we looked more carefully, that slightly increased amount of total cholesterol was not being carried by more of the dangerous, small particle LDLs.  It seemed to be carried more by larger particles.  Actually, in the people eating more fat, and fewer carbs, the total particle concentration, which most people in our field think is a stronger signal of risk that total cholesterol, the total number of particles did not go up.

Let’s go into a little more detail here, because this idea about “total cholesterol” versus “total particles” is worth understanding. You’re saying that in people who ate more fat and less carbohydrate, and in fact, who ate more saturated fat, they had a little more total cholesterol fat in their blood, but it was mainly being transported in big, fluffy LDL particles, which are the kind that scientists who study heart disease consider pretty safe.  In this study, the people eating more saturated fat, did not have an increase in the kinds of LDL particles you consider more dangerous, which as the small, BB-sized, pattern B LDL particles.

RON KRAUSS
Yes.  When people ate more fat and less carbohydrate, the number of small particle LDLs remained low, and switching from monounsaturated to saturated fat didn’t increase their number at all.  In fact, when people switched from mono- to saturated fat in this study, the large particle LDLs might have gone up a little bit, and the small particles went down.  So by anybody’s current criteria about whats’s important for heart disease risk, saturated fat caused no increase in risk.  That was clear to people who understand the role to the lipoprotein particles, as opposed to the overall cholesterol level, which I’m sure for some people is a subtle distinction.

And it all starts with how the cholesterol fats are carried through the blood.  They’re carried in particles, which each include one protein called . . . .

RON KRAUSS
It’s Apolipoprotein B  (ah-PILL-oh-PROE-teen Bee) Also known as Apo B

Apo B.  Just one protein per particle.  And that protein is like a mesh bag that is holding a whole bunch of fat inside of it – a lot of cholesterol fat.  So one Apo-B protein per bag.  Some Apo-B proteins enclose small amounts of fat — those are small-particle LDLs.  Some enclose large amounts of fat–those are large particle LDLs.  So . . . if you poured out all those bags at once, and measured the total amount of cholesterol that was in all of those bags, that would be the “total cholesterol” number you can see on a typical heart disease risk test.  Just the cholesterol poured out of all those bags.  But you seem to be saying that it’s equally important to simply count the number of bags — that is, the number of Apo-B particles that had been carrying the cholesterol.  And also looking at the size of each bag.  How about it?  When it comes to heart disease risk, is the total amount of cholesterol a key piece of data?  Or is it more important to count how many LDL particles, that is, how many “bags” are holding the cholesterol?

RON KRAUSS
Both numbers can be helpful.  But most people certainly in the field of cholesterol and heart disease understand that the number of particles matter more than just how much cholesterol they carry overall.  In terms of health, the first order of business is to make sure the total number of particles in a person’s blood is maintained in the healthy range, because that’s what dictates heart disease risk.  Beyond that, when the total amount of cholesterol is unusually high, you’ll almost always find that the total number of LDL particles is high.  And looking even deeper, when the total number of LDL particles is higher than normal, I and many of my colleagues would argue that the biggest concern is warranted when the number of smaller particles is high, not the larger ones.

So, if you have a lot of cholesterol fat in your blood, and it’s mainly being carried in a “normal” amount of LDL particles which are large, fluffy ones, that’s less of a concern than when the same amount of cholesterol is being carried by an unusually high number of little tiny particles.

RON KRAUSS
It’s definitely associated with lower heart disease risk if the cholesterol is carried in larger particles, and that’s because there are fewer of them.  Some people who study heart disease report that total cholesterol levels are not very different between patients with and without heart attacks.  If you look deeper, you may find that those patients who have heart attacks, generally have more LDL particles in their blood, compared to people who don’t have heart attacks, even when their cholesterol levels are similar.

So you’re saying that if a person just counted the number of Apo-B protein particles in their blood, that would be a better indicator of heart disease risk than measuring the total cholesterol in their blood.  If you have a whole bunch of those, you probably have a lot of small particles.

RON KRAUSS
Apo-B is a a sort of first approximation of the particle concentration.  It’s not measuring it exactly, but it’s a whole lot more accurate at predicting risk for heart disease, than just measuring the total amount of cholesterol itself.  This is being acknowledged more widely in the first of heart disease assessment.

Has anybody told the American Heart Association this?

RON KRAUSS
The AHA, the American Heart Association, and I’ve served on their advisory board, the AHA, does two things  It promotes scientific research and it makes statements from time to time.

But their policy statements don’t reflect the importance of counting LDL particles yet.

RON KRAUSS
No  There’s still a lot of debate about whether we should be advancing beyond the old LDL “total” cholesterol risk assessment, to understanding it based on particle concentrations, but I think we’re moving in the right direction.  Getting back to how all this applies to what kinds of fat to eat, and how much fat to eat, in our 2006 Study in the American Journal of Clinical Nutrition, we included one branch of the study that involved eating a really high saturated fat diet, with lots of dairy fat, which is the main dietary source of saturated fat for most people.  Beef also contains some saturated fat, but in dairy, it’s much higher.  That higher amount of saturated fat seemed to cause no adverse increases in LDL particle numbers, compared to feeding people higher monounsaturated fats, such as olive oil.  And in our 2006 study, the blood work was better when feeding people higher fat diets, than when feeding them lower fat and more carbohydrates.  But keep in mind, this was in the setting of lower carb and a mixed protein diet, proteins from various sources from white meat and dark meat and chicken and fish and beef.

Tofu

RON KRAUSS
Tofu.  It was just a mixed diet all together.  In that setting, with carbohydrate intake kept moderately low, saturated  fat did not raise Apo-B.  It didn’t raise the number of LDL particles.  It didn’t increase inflammatory markers either.  It didn’t raise any of the really meaningful basis of heart disease risk.

So that was an interesting study which showed that eating more saturated fat does not increase heart disease risk.  But then, there’s that newer study you’ve done that involves saturated fat and red meat.  And it’s a fascinating study because of some clues it gives about how health may be affected by both saturated fat and red meat.  Right now there’s a great deal of concern that eating red meat may be dangerous for people’s health.  But the question is why.  In your recent study,  you hint at a reason why. 

RON KRAUSS
We published a paper this past fall in the Journal of Nutrition, in which we reported the results of the study that we carried out as a followup to the one we just discussed.  Now, in the interest of full disclosure, I have to say that the first study was funded the National Dairy Council, and we used fairy fat and dairy products liberally in that study, since they’re high in saturated fats.  The second, more recent study was funded by the National Cattleman’s Beef Association because they felt, and frankly we felt at the time, based on the evidence we had, that feeding a high saturated fat and low carbohydrate intake would have the same benefit on a high beef diet as as on a mixed protein diet, and bottom line is that when we did the study, we found out that was not the case.

So using what you learned from your 2006 study of a mixed-protein diet and high saturated fats, in this new study, you kept carbohydrates somewhat low, and fats somewhat higher, just as you did in 2006.  Really, the main difference was that this time, you didn’t feed a variety of protein sources.  Your test subjects just ate lots and lots of beef.  And this time, you found that “healthy” blood work depended not only on what kind of protein people ate, but what kind of fat the people WITH the protein.  So if you get out your Sherlock Holmes hat and pipe, what were the clues and what did they mean?

RON KRAUSS
To begin with, keep in mind, this was a very high beef diet.  People were eating beef breakfast lunch and dinner.  So this is really way outside of what we would ever consider to be a usual health practice.  Maybe some people do it.  But not many.  We were really interested in the metabolic impact of this diet.  To get as many clues as possible, we fed people in either the context of lean beef alone, or with extra saturated fat, mostly from diary products.  Again, that’s because most of the saturated fat we get in our diet comes from dairy products.  There’s some saturated fat in beef, but more in dairy fat.  To make things as clear-cut as possible, in this study, we fed the same beef product to two groups.  Lean beef, low in fat, without any added saturated fat.  For one group, we added lots of dairy fat, to increase saturated fat.  For the other group, we kept saturated fat low, but kept total fat basically the same by using an unsaturated fat–basically olive oil.  So between the two groups, let’s say the difference was the equivalent of a cheeseburger versus a lean hamburger dressed with olive oil.  That sort of describes, in a nutshell the kind of differences we were looking for.  When we did blood work on the groups, the group who ate lots of beef with low saturated fat, meaning the olive oil, didn’t seem to have any adverse effects.

Meaning the blood work you did on that group didn’t reveal an increase in the LDL particles and other biomarkers that indicated heart disease risk. 

RON KRAUSS
We didn’t see any adverse effect if we just fed a high beef diet in the absence of saturated fat.

So, in your study, a lean burger without cheese looked on the surface as the one to do.

RON KRAUSS
That’s true from our study.  However, keep in mind, there may be other effects from eating red meat that still might mean it’s something to limit in the diet.  After all, there are studies from the epidemiology world that are very convincing pointing to red meat itself as associated with many disease outcomes ranging form cancer to heart disease to diabetes.  In our study, our measurements were strictly focussed on the metabolic risk factors for heart disease and diabetes.  In that setting we couldn’t detect a real significant signal.  That doesn’t mean there aren’t other adverse effects being revealed by other techniques.  But in our case, we analyzed total cholesterol and the number of LDL particles and blood sugar measurements and inflammation measurements, and we didn’t see anything particularly dangerous occurring when people ate lots of red meat but kept the saturated fat very low.

What’s interesting is what the punchline is going be be.  So keep going!

RON KRAUSS
The punchline is that we expected that because these diets have low carbohydrate, when we fed the high saturated fat level along with the red meat, we would see a pretty benign metabolic risk profile.  Just as we did with low saturated fat and red meat.

But that’s not what happened!

RON KRAUSS
This is one of the surprises that keep life interesting for us for us as researchers and also for the world out there who happens to be looking over our shoulder.  In this case, the surprise was that the combination of the high beef diet and the high saturated fat diet caused very serious increases in all of the cholesterol related risk factors we had been measuring, including total particle numbers, small LDL, total LDL cholesterol, inflammation, whatever we looked at, we saw an adverse effect.

Everything went wrong.

RON KRAUSS
This was in contrast with our earlier studies where the same amount of saturated fat and very similar carbohydrate intake but a diet not loaded up with red meat, had no adverse effect even if it had lots of saturated fat in it.

So if you put on your Sherlock Holmes hat and get our your magnifying glass, what is it you found was the likely smoking gun here?

RON KRAUSS
I wish I could give you a definite answer to the question.  But fortunately, the fact that we had these two very different results with two different kinds of protein led us to propose to the National Institutes of Health, one of the nation’s leading funders of health research, which hopefully will stay that way, a new study.  We are glad that it’s being funded by the National Institutes of Health, as a neutral ground if you will, between the world of sponsors from the food industry.  NIH is allowing us now to investigate in a detective-like matter what is going on, and also test directly in a head to head manner, three different diets.  All the diets will have the same amounts of saturated fat.  But one is high in red meat, one is a non-meat, vegetarian diet where the protein comes from vegetable sources, and one is an intermediate diet, with meat from chicken, primarily.  We’re doing this study to determine whether the source of protein influences the response to saturated fat in the way we suspect it will from these earlier results, and we’ll do some blood work that will allow us to investigate possible underlying mechanisms.

You think there are clues in the beef.

RON KRAUSS
Perhaps some other component of beef, not necessarily the protein, but something that comes along with it, such as iron would be one example, that may have an adverse effect in conjunction with saturated fat.

In a detective novel, the writer often throws in a red herring, and a red herring is designed to take someone off the track.  But in your case, the color red, which is caused by the iron in meat may actually be the smoking gun.

RON KRAUSS
That’s one possibility.

Why would the iron in red meat, when coupled with saturated fat, increase risk factors for inflammation, for small particle LDL, for higher blood sugars, and all the rest?

RON KRAUSS
This is just an idea.  This is in our whole discussion the one area where we do’t have data . . . yet.  But it’s an intriguing hypothesis.  Because it’s known from genetic, metabolic and population studies that the iron content of the liver, which stores most of our iron for our needs for red blood cell production and many other metabolic processes . . . if that amount of iron within the liver is excessive, it can lead to impaired sugar metabolism and predispose even to diabetes in the extreme case.  High levels of iron in the liver also can be associated with abnormal lipid profiles, with higher amounts of small particle LDL.  So we already have evidence that high iron levels in the liver are a potential determinant of things that can influence risk for diabetes and heart disease.  And since iron comes from what we eat, it could be related to the dietary response that we studied.  Why beef should have a particularly high effect on hepatic iron is a possibility we’re interested in, along with the question of why beef would create this risk for us, in particular, when we consume saturated fat.  So while we don’t have data yet, we do have an intriguing collection of clues that maybe would lead to definitive conclusions from Sherlock Holmes.

You’re still awaiting the results from your study, though you have some suspicions.

RON KRAUSS
It turns out that heme iron, the form of iron in red meat, is absorbed pretty efficiently into the body.  That’s why red meat is considered a good, or maybe in this case, we should just say, an abundant, source of dietary iron.  But even though it’s more bioavailable, heme iron still requires certain factors for absorption.  In checking to see why saturated fat could potentially increase the amount of iron coming in from beef, what I discovered buried in the literature is that certain kinds of saturated fat, beef tallow being one of them, and the saturated fat called stearic acid being another, both promote the absorption of heme iron.  And both saturated fat and stearic acid are found in dairy products and in the fat that comes with red meat.   So it’s our hunch that the combination of eating both an abundant source of iron and the fat that helps the body absorb that iron, might be what converts this style of eating into a dangerous risk profile that raises small particle LDL, blood sugars, inflammatory markers, and so on.

And that risk might also be a consequence of modern day living.  Looking back in time, people used to be in wars and accidents more often, and during those times, they had more parasites in their blood that would be going after the iron in the body.  They might have been bleeding out more of their iron stores, and more vulnerable for iron deficiencies.  So we may have evolved to conserve iron, and way back then, it may be that eating foods that promoted iron uptake was actually protective.  But these days we don’t have the parasites to sip on our iron stores, and we don’t have the blood bleeding out of us as much.  So Ron Krauss, to make up for our cleaner, more peaceable times, if someone likes cheeseburgers and they like them nice and juicy and covered with high saturated fat cheese, should they reduce their iron stores by giving blood more often?

RON KRAUSS
(LAUGHS) You’ve asked a question that has come up in other contexts as well.  Does keeping people’s iron level low reduce risk of heart disease?  For instance, there are people who claim that women who have a natural protection from heart disease when they’re menstruating lose that protection after they go through menopause, because without that monthly release of blood, their iron levels can build up.

So, does giving blood and reducing your iron stores that way reduce heart disease risk?

RON KRAUSS
We don’t know.  The real way to check this would be to not focus on the iron in someone’s diet, but instead, do blood work to reveal how much of the potentially dangerous iron you have in your system.  That would be an interesting study to do sometime.  As for now, there’s absolutely no basis yet for therapeutically reducing iron stores, for instance, by giving blood, as a means of reducing heart disease risk.  The best way to reduce your risk, right now, is to stay away from the cheeseburger diet.

But to get the answer through blood work might be challenging.  It’s very hard to measure with any accuracy what the heme level of iron is in the liver.  It’s a different measurement than the standard “annual checkup” measure of iron in the blood.  Getting a good measurement of the liver’s iron . . . . It’s a very  very hard bit of data to get.

RON KRAUSS
There are markers . . . and we haven’t measured all of them yet.  Part of the funding we’re getting from the new NIH grant will allow us to measure some of these more accurate markers.  So it may be possible for us to tease out more information.  The standard iron tests in the blood are not sufficient.  That’s where we need more information, and why we’re doing this new study.

Stanford Genetist Mike Snyder hopes to study 250 Prediabetics

Here’s part 2 of an interview with Stanford Geneticist Mike Snyder about the new study he’d like to do, checking the “omics” of 250 prediabetics, to give an enormously comprehensive profile of their genes, their genetic expression, and more, as they live their lives, with some becoming diabetics, and we hope, some finding better ways to never become a full-fledged diabetic.  - Shelley 

LISTEN (7 Minutes)

MIKE SNYDER

We’d like to take on analyzing diabetes further because it really is a huge problem.  It’s mushrooming.  Some people estimate that up to 50% of the population will be diabetic within 20 or 30 years.  That’s a huge, huge problem.  Given how little we know about how it’s such a complicated disease, I don’t see how we can’t go in and by analyzing it in this molecular detail learn a lot more about what’s going on.  Hopefully some of that information will be valuable for treating people and helping to ameliorate this condition.  That’s really the goal .

How many people will be in your next study?

MIKE SNYDER

We’re trying to get funding to study about 250 people so that’s a pretty large study.  I think that’s a large enough cohort to give us a snapshot of what might happen

I wonder if researchers similar to you, using somewhat different platforms, were to pool their information with other people doing similar studies around the United States looking at similar markers in the blood, would that help, just to get the numbers up higher for how many people are being looked at?

MIKE SNYDER

I certainly am a big fan of collaborating with anyone doing related things.  And I’d be happy to do that.  I like to think we’re studying nearly everything you can but you can always study more.   For example, you could study the micro biome.  You could study all the things that are going on in people.  But we are doing all the standard medical tests.

The micro biome would be an interesting addition.

MIKE SNYDER

We’re loaded with microorganisms.  You may know we have several pounds of microorganisms inside ourselves.  In fact more cells in our body are microbes than they are our own cells, and so they certainly are thought to have a huge impact on our metabolic states and such and so we do want to analyze those.  At some level, we’re going to collaborate with others to help do that and that will be a terrific thing to add as one example, and as you point out there are many other things we can add as well.  In an ideal world we’d like to add them with people collaborating with us  using the same samples as we do, to learn more about the samples.

Are you saving your samples right now.  And I hate to be this graphic, but if you’re planning to analyze your micro biome, are you getting samples of your poop?

MIKE SNYDER

We’re about to do that.  We have not done that yet, but yes that would be certainly one of the things to do.  One reason we chose me in the first, in fact the way this all started was we chose me because we would then have somebody who we could get lots of material from, so to speak.

Well that’s right.  The researchers just came here to your office and started taking blood!

MIKE SNYDER

Right!  It’s a real convenience factor which is quite nice from a scientific standpoint and so this is really a very nice thing to have.   We thought we were taking plenty of material to do everything we wanted with, but suddenly you discover more things to do.  And more people get involved.  We started out this study with just a few people but by the time we published this paper we actually had 40 different collaborators because there were lots of different people who wanted to join in because it was a was a pretty unique study, and in the end a lot of the material is close to gone for the first part but on the other hand we are collecting new material as we go forward and we’re getting better at using less material so we are trying to save some as we go forward so that other groups can analyze it, and several people have now approached me about getting access to some of it.  We hope to be able work with some of them to  better analyze all the different constituents of the blood and what that means for health states.

Do you ever think about the Einstein quote about knowledge?  The one where he said that knowledge is like this cup of coffee on your table.   All things that we know are like the coffee – that is, what’s inside the cup.  What we know that we don’t know is like the upper lip of the cup – that is, its circumference.  And what we don’t know that we don’t know is everything else.   what we know that we don’t know is the circumference or knowledge.  We all want more knowledge, but as that happens, the circumference becomes larger, and we become more aware of what we don’t know, which makes it a little bit frustrating 

MIKE SNYDER

That’s certainly true of the study.  I think many more questions came up than got answered as we went along and to me that’s exciting because it’s more problems to solve and I think that’ll happen for a while.   You’re right, you’re  absolutely right there’s a lot more to learn.

But that would be a unique disease to solve.

Oh, absolutely.  And hopefully would affect the lives of many people.

Stanford Geneticist Mike Snyder

In March 2012, Stanford scientist Mike Snyder published a groundbreaking study in Cell that showed the most detailed biological profile of a person ever done.  It includes two years of monthly data, meaning Snyder’s DNA, plus measurements of the constantly changing rise and fall among proteins created by his genes, many of his metabolic byproducts, special immune system cells that point to infection or autoimmune disease, and more.   And in the middle of all this monitoring, Snyder developed Type 2 diabetes, allowing researchers to track the molecular changes connected to it.  The good news, he caught the condition early, and changed his lifestyle so that not only did the researchers get to track his “markers” as his blood sugars shot up and he became a diabetic.  They also got to track his markers as his blood sugars gradually went down over time and he “un” became a diabetic.

Here’s part 1 of a 2-part conversation with Stanford geneticist Michael Snyder. .  It begins with Mike getting yet another blood draw in the name of science . . .  Shelley – Meandmydiabetes

LISTEN (about 45 Minutes)

MIKE SNYDER
It turns out . . . so they want to, um.  They want me to give some blood.     Is that going to gross you out?

Oh, this is great.  Do you want your blood taken in audio?

SCIENTISTS
Unless he starts screaming.

So you’re rolling up your sleeve . . . this is only audio, so you’re going to have to narrate.

MIKE SNYDER
Okay.  Very good.  I’m rolling up my sleeve.  We’re doing another blood draw this morning so that we can do another sample of one of my Omics profiles.

And what’s you’re name?

MIKE SNYDER
My name is Michael Snyder.  I’m Chair of the Department of Genetics and I’m also the Director of the Center for Genomics and Personalized medicine.

It looks like you’ve done this so many times, you don’t even mind doing it anymore.

MIKE SNYDER
Well, that’s right.  Not a problem.

My goodness it looks like you have out about 2000 tubes to put the blood in.  How many are there?

SCIENTIST
Tennish.  About ten tubes.

And who are you?

SHIN LIN
I’m Shin Lin.  I’m a cardiology fellow at Stanford.

RUI CHEN
My name’s Rui Chen.  I’m a postdoc in Dr. Snyder’s lab.  We co-authored the Cell Paper.

How many times have you poked this guy?

CHEN
I’ve never poked this guy because I’m not a medical doctor but he’s been poked many many many times.  This is the 41st time now.

In the last two years?

CHEN
This is the  41st time now

MIKE SNYDER
I had lost track!  So what we’re looking for is a very detailed molecular profile of what’s in my blood and the idea is that we’ll be able to follow health states much much better this way than if we simply measure a few things as is currently done.  So right now when you get a blood test about 15 things are measured.  What we would like to see happen in the future is that you’re measuring thousands of things.   We are measuring in fact 40,000 things, different components every time.

And when you measure, what are you measuring.  Standard stuff?  Proteins.  DNA?  What are you measuring?

MIKE SNYDER
We are measuring RNA, which is what gets made from the genes.  We measure proteins and we measure metabolites.  We also measure antibodies to see if I’m making antibodies against anything that might suggest something’s wrong.

Meaning antibodies against something you want your body to fight, or antibodies against things you really don’t want your body to fight, because it’s fighting you!

MIKE SNYDER
Mostly, we’re looking for the latter, antibodies that are recognizing things we don’t want to see.

LIN
Allright. ready?   One, two, three.

You even look at the needle as you’re getting poked.

MIKE SNYDER
Yeah, I follow what’s going on.

So it looks like 8 tubes.

MIKE SNYDER
I think it’s 10 total.  The different tubes are for different things.  There’s one tube used for the antibodies and then another that’s used for standard medical tests and then a series of eight other tubes for the measure of all the components I mentioned to you before.

And you’re using your own technology for measuring the RNA?

MIKE SNYDER
That’s right, RNA sequencing… it lets us measure literally the expression of every single gene in the body

That’s what?    20,000 proteins?

MIKE SNYDER
It’s 20,000 genes but interestingly each gene makes more than one protein on average so you can get different RNAs made from the same gene.

To measure these, are you using the high-tech device called a mass spec machine?

MIKE SNYDER
We use mass spec to follow about 4,000 proteins at each time point, and then we use very special tests for some very interesting proteins called cytokines which are quite biologically interesting.  They don’t get detected by mass spec, and they’re not very common in the blood so you have to use special methods for that.

Are you using aptamer technology?

MIKE SNYDER
No.  We’re using pretty much standard antibody assays but set up in a high throughput fashion

Standard assays.  So could Quest Lab do this for anybody, or are you special?

MIKE SNYDER
Right now they can’t.  But we think in the future this can be optimized so anyone can do it.

But right now, even the fact that you, personally, got to see what’s in your own blood and your own DNA plus your own proteins is very special.   Nobody gets to do that.

MIKE SNYDER
That’s right.   Nobody certainly has looked at things at this level before, so that’s what makes this study unique.

Did you have to get special permissions to look at your own blood this closely?

MIKE SNYDER
You do.  You have to  enroll in the study, so I had to consent myself, essentially, to become part of this study, although I actually enrolled with a close collaborator Kari Nadeau, and so she’s in fact the one who consented me, but we do hope to enlarge the study.  We’re now are applying for approval to be able to look at lots of different people.

Did I read the study correctly that you also looked at your mom’s blood?

MIKE SNYDER
Yes, well, we certainly sequestered her DNA and we’ve done a limited analysis on her blood.  She was a very willing participant in the study.  She’s a very curious person by nature and so she wanted to take part in this.

So you had a somewhat normal person and I’m assuming she’s not a scientist?

MIKE SNYDER
She’s retired schoolteacher.

And she was okay finding out all kind of things about what’s in her blood?

MIKE SNYDER
We haven’t found anything so problematical for her yet -  she’s 83 years old and going strong so we’re not expecting . . . anything we find out her case is likely to be good news.

Just so our listeners know, we’re doing this conversation as tube after tube of blood is being drawn from your arm.

MIKE SNYDER
That’s right.

No big deal

MIKE SNYDER
No big deal.

Now as part of this you found out that you are not only prone to diabetes but that you are indeed, a diabetic.  What was that like to find out?

MIKE SNYDER
So we discovered that early in the study, when we sequenced my DNA and it suggested I was at high risk for diabetes.  That was a bit of a surprise because I was not aware of that running in my family

Now, you’re a slim person and you look athletic.  Were you his way when you found out that you are prone to diabetes?

MIKE SNYDER
I might’ve been slightly heavier — 15 pounds heavier, but generally I do not fit the profiles of someone who has diabetes.

How old are you now?

MIKE SNYDER
I’m now 56, and we started the study when I was 54 so I guess I got the first news that I was prone at 54.

How did you decide that you weren’t just at risk for diabetes but you might have it?

MIKE SNYDER
I had been tracking all the things as you see now.  We are currently tracking by blood components.

So right now, you’re holding the little piece of gauze in the crook of your arm to keep the blood from continuing to flow because you’re done now?

LIN
Well, actually, we’re going to have to poke you again because the flow got too slow.  Is that okay with you?

MIKE SNYDER
That’s fine.

LIN
Okay

So this is all part of it

MIKE SNYDER
That’s right.   You’re seeing real life.  And . . . I lost my train of thought.

At some point you wondered if you actually were a diabetic instead of just a potential one.

MIKE SNYDER
Yeah, so what we’ve been doing is following my blood complements all along, and in fact, they had been running normal.  But because of my genome sequence . . .

You mean your blood sugars?  What were you monitoring that was your clue?

MIKE SNYDER
Well we were following everything, but blood sugar, in particular, because of the diabetes concern.

That’s a test that anyone can do.

MIKE SNYDER
It is, and in fact, it had been done routinely as well as by the methods we were using.  But the key was when we went to a specialist who looks at glucose metabolism and went for very fancy tests.  This was in Gerry Reaven’s group, here at Stanford.  And she looked at me and certainly didn’t think I was at risk for diabetes nor did I at the time.  But when we did that first measurement it turns out my glucose level was high even before we started the test.

How high was high.

MIKE SNYDER
It was 127

And that was fasting — that was going in without eating anything

MIKE SNYDER
It was fasting and we repeated the test and it was still high.   And it went up even higher after that first one during the test — up to 150 and probably more important is that there’s another test, called hemoglobin A1C, that was also high. The  first measurement was 6.4 and then later 6.7

LIN
1-2-3

Look at this, you’re smiling as you get poked again.

MIKE SNYDER
I’ve had this done before.

Now, the first hemoglobin A1 you had before you even started this test, would have defined you as a diabetic.

MIKE SNYDER
Well,  we did not do an early hemoglobin A1C because there was no reason to think I was diabetic and also because my glucose levels were quite low early on in the test.

And what were they?

MIKE SNYDER
They were in the 90 to 100 range, depending on whether I was fasting or not.

So they started out in the 90s and 100s which was sort of normal and then at some point they went up further, and then you said, hmm, maybe we should go check with Gerry Reaven’s group?

MIKE SNYDER
No, actually, they went up the first time I went to see Gerry Reaven’s group.  So I just happened to go there for the fancy, this glucose metabolism test, and at that first measurement my blood sugar and A1C were high, and the reason they was high, we think, is because I went to do it after this viral infection.

Well, that’s right, you’ve written that you were doing fine in terms of blood sugars, and then you caught the flu, or something like that.

MIKE SNYDER
It was respiratory syncytial virus infection which is a fairly common cold but not as common as some others.  Anyway, it pretty nasty version.  I was out of work for several days and shortly afterward, I happened to go for this test, and that’s when my blood sugars skyrocketed and they were up for several months before I changed my diet and I changed my exercise habits and such,  It took a while but my levels of glucose gradually did come down to normal.  So it was temporary in the sense that it lasted several months before we started and then took some time to come down.

LIN
Thanks.

MIKE SNYDER
We’re done.

LIN
Good bye now.

MIKE SNYDER
They need to run off to process the samples.

The action is always good.   Getting back to your story, you got diabetes and then you “un” got diabetes without taking medication.   So what did you change in how you ate and exercised?

MIKE SNYDER
Yes.  I changed both my eating and exercise habits and I also took baby aspirin every day although I don’t think the latter was what made the difference.

So you don’t think the baby aspirin was making a big difference, but what did you change about the way you ate?  What did you change about what you ate for breakfast?

MIKE SNYDER
Before this was diagnosed, I was probably the world’s worst eater.  I ate lots of sweets and desserts, cakes, whatever, candy bars etc. And so April 13 last year I completely cut all that out, and I haven’t had desserts since except in the form of fruits and things like that.

Alright then, what did you have for breakfast today?

MIKE SNYDER
Well today I didn’t eat breakfast because I was going to give blood this morning!  That was a fasting sample.

What did you have for breakfast yesterday when you did not give blood.

MIKE SNYDER
I guess I had Cheerios with blueberries..

And  for lunch?

MIKE SNYDER
I usually have either a salad with chicken, or sometimes they have some sushi here, or sometimes I have some chicken on rice sort of thing.  I don’t eat much pasta anymore.  I used to eat a lot of pasta before all this was diagnosed and as a consequence I would say, with my eating habits changing as well as my increase exercise . . .  I pretty much always ride my bike to work. though today I didn’t because I have to take someone somewhere, but as a rule I ride my bike to work.  When I increased my exercise I would probably ride even more places and things like that so I doubled the amount of biking.  I started running again which I used to do but haven’t been doing up to the point I was diagnosed.

You are exercising more, you cut back on the total amount of carbohydrates, especially sugars.  Do you have a sense of what your ratio is of fat to protein to carbohydrate?

MIKE SNYDER
It is known in detail, but I don’t know off the top of my head

Do you eat more fat.  Do you eat fewer carbohydrates?

MIKE SNYDER
I definitely eat fewer carbohydrates overall, I eat more probably more protein and more salads and things like that.

You’re still keeping your fats pretty low,  you’re not a fat eating person?

MIKE SNYDER
Well I guess I eat some.  I have high cholesterol and high triglycerides and I do take simvastatin which is a statin.  That has been very effective at lowering my cholesterol and triglycerides, but you know I also do watch a little bit on that end, so I guess I eat some fat

Here we are getting to talk about the intimate details of what is inside your blood that are supposed to be private for most people, unless they want to share it, and you’re sharing it all with the world.  What are you finding out about your triglycerides and cholesterol, now that you’ve changed to a diet with less carbs for the sake of your diabetes?

MIKE SNYDER
Well, the cholesterol and triglycerides have probably mostly come down because of the statins, so I’m a good responder.  We know that because they came down even before I change my diet.

Have they come down further now?

MIKE SNYDER
I think they’re running around the same, to be honest, so what’s come down the most with my change of diet and exercise has been the sugar levels.

So to bring your sugars down, you didn’t need to make a huge radical change of what you ate.  You cut out the deserts and you exercised more.  Some diabetics have to cut out almost all the carbs and  you didn’t have to do that.

MIKE SNYDER
Well I would say I’ve changed my diet pretty dramatically.  I used to eat lots of pasta and lots of sweets.  And all that has pretty much gone.  So it really has changed quite a bit.

Now, tell me this, since we’ve talked about how you eat now and how you exercise, let’s go back to Gerry Reaven’s lab.  What kind of test did they do?  Did they did check not only your blood sugars but your insulin levels and some other hormones.  Did they do the test, over time, as you were eating food to see how your bloodwork responded to the food?

MIKE SNYDER
Mostly they monitored glucose metabolism using various agents that block uptake and things like that, so they’re following the details of how you metabolize glucose.

So they injected glucose into your blood and they injected insulin to see how those two interact?

MIKE SNYDER
Yes, they’re following exactly how you metabolize glucose.

Did they find out that your body was needing to use a lot more insulin to make things happen, or was your pancreas putzing out and not having enough insulin

MIKE SNYDER
Well the nice thing is I was still classified as insulin sensitive, that is, I wasn’t insulin resistant, which is often associated with diabetes.  In my case I was still, at least I appeared to be, insulin sensitive, and we think that’s because I caught this early because I’ve been following myself all along, so I could see when this first increase occurred.  Now we did do more testing before I changed my diet and probably more than a month went by, but ultimately, once I was diagnosed, and it was very clear after repeated tests that I did have high glucose, we did change my diet and  because I caught it early I think that’s why I was so insulin sensitive and I could do something about it.  That’s a  general issue with disease.  If you catch it early, you can usually control it by simple means, But if you catch it too late, there is usually damage done and it’s really problematic:.  Had I waited a longer time before changing my diet and exercise, it’s possible I would have needed drugs.

You were lucky!   Most people catch diabetes  years after they started having the problem.

MIKE SNYDER
Under normal circumstances as a healthy person I would normally go to the doctor maybe once every three years. That means I would not have caught this high glucose right away, and so probably a year or two after it happened, or something like that and by then there could have been significant damage.  So the nice thing is it was caught early, and I was able to manage it and I’ve changed my lifestyle and to be honest, I feel better because of it.

Well, if you were insulin sensitive and your blood sugars were still going up, does that mean your pancreas was stressed and not able to produce as much insulin as you needed?

MIKE SNYDER
We don’t know for certain why this occurred.  My insulin production seems okay.  We’ve measured that over various time points.  But it may be more the way my body’s utilizing and responding to the insulin that’s the change.

There’s some  talk about how insulin is important for allocating and managing what is happening with your immune system, and if you’re sick your insulin needs to say, ‘I need to go work with the white blood cells and make them work better.’

MIKE SNYDER
The relationship between insulin and getting sick through infection and various things is still an area where things are not very well understood.  Certainly what people can say is that stress responses are very much associated with type II diabetes.  Viral responses have not been shown, with the exception of some of the chronic cases, but I think what’s particularly surprising about our study is that it’s very clear that this appeared after that nasty viral infection, so we did make a connection though it may just be that the viral infection caused general stress, which in turn led to the increase in sugar and this type II diabetes onset.  These are some of the things we hope to understand better as we do more experiments and follow up with more people.

It sounds like you would be a believer of people saying that “It was after I had surgery,” or “It was after my father died and I had a divorce, that all of a sudden I had diabetes.

MIKE SNYDER
We do think that’s a likely scenario.  That after these situations people are at risk for a having this happen, and I think it would make a lot of sense for people to go and get checked out on a more frequent basis after life stresses shall we say.

Thank you for explaining the details of your story and how you got better, and congratulations on feeling better. It was also interesting in your published article for The Cell, in reading the discussions about the potential for this research, and thinking about  just how you caught this problem, it sounds as though it didn’t take anything fancy to catch your early diabetes.

MIKE SNYDER
We have the tools right now to discover whether somebody has early diabetes, just by following glucose.  I think what was special my case is that l I don’t have any of the obvious features that people expect with diabetics and I also didn’t have obvious family history.

Did you have symptoms that made you go, hmmm.  Was your vision getting a little blurry, or were you thirsty more often or using the bathroom more often.

MIKE SNYDER
None of that so much and certainly not before all this kicked in and we did measure my vision and stuff after my glucose level shot up, and after that, we were checking for glaucoma and checking my retina, and everything looked fine. So again we think we caught this right after it happened

So you weren’t showing any symptoms, and you didn’t notice a change in how you felt.  It was just the blood sugar on a glucometer and also your hemoglobin A1C.  Just your average blood sugars over three months plus finger pricks to see what your blood sugar is in the moment.

MIKE SNYDER
That’s right.

But you did all this fancy DNA stuff and protein stuff.  You didn’t need those to diagnose it, but as a scientist you’re looking at all the data and saying, there are some other markers here that are fascinating?

MIKE SNYDER
Yes, if I knew I was going to get diabetes I could’ve just measured glucose.  But we didn’t know that going into the studies.  So we are trying to follow everything that’s going on for any potential disease that comes up so that we might be able see what early markers are there in general and the other thing I would say is that diabetes is probably clearly not one disease,  It’s  probably hundreds of diseases and if you look at it everybody is a little different.   I don’t fit the classic case of someone getting diabetes.  Diabetics generally have much a higher body mass index is, so what we think, and others think as well, is that diabetes is 100 diseases so we think by following all these different markers we hope to be able to see how many different kinds there are.

Well before we go on, just so people know, how tall are you and how much do you weigh?

MIKE SNYDER
I’m always five foot nine, but at the start of the study I was 162 pounds and now 147 pounds.

Probably your body mass index is putting you  below average, for body, and in the fit category

MIKE SNYDER
I like to think so.

Right now as we talk about diabetes as a disease, I wonder whether you’re thinking of diabetes as several diseases or if there’s a new way to think about disease.  For instance, did you find out during this time period that your inflammatory markers went up?

MIKE SNYDER
We did, because I went through these viral infections — I  have been through four viral infections now, two initially since we published this study and it’s  pretty clear that during each of these infections you see a lot of inflammation going on and inflammatory markers going up.  Interestingly, after this RSV infection that I mentioned earlier, there was a big inflammatory response at the time of infection, and there was also a spike one or two weeks later which may or may not have something to do with the onset of my blood sugars shooting up.

Many researchers say that what’s happening with chronic inflammatory markers is a clue to all kinds of disease states.  Are these the markers that you were most intrigued with in terms of how they changed or was there something else?

MIKE SNYDER
We’re following everything.  We don’t know what it all means yet to be honest.  We’re still analyzing the data.  We do see some very interesting pathways and things changing, markers that are showing up in these complex pathways and we’re still trying to understand what all means.

Can you tell me about it, or does it need to stay a secret now — all of these millions and millions of markers that you’ve been collecting?

MIKE SNYDER
There’s nothing secret about the data, and anyone can download the data and re-analyze it for themselves.   All I can say right now is that we are following these 40,000 components and we see things are going up and down.  The inflammation responses are a no-brainer.  We see that happening during these infectious times and just before the onset of diabetes.  Going back to your earlier question, the inflammation has been associated with lots of different diseases.  That might be a downstream effect of the disease, like inflammation has been associated with cancer and other sorts of diseases as well and so some of this may be downstream events.  And that’s fine.  We do want to see them, but we also want to see the earliest events because those are the things that are probably triggering the disease.  If we can catch those markers early and find markers for those and catch those early enough and then also try and understand exactly what’s going on that might give us a better handle on how to treat the disease in its earliest possible state- catch and treat -  I should say.

And also you’re indicating that in your case you didn’t have to have to add any  diabetes medications and you  didn’t have to start injecting insulin.  Instead, you changed your lifestyle.  Was it  motivating to see in your bloodwork what was happening to you?  Did seeing the information help you realize you had a health issue ahead and maybe you don’t want to eat all that ice cream?

MIKE SNYDER
It was clear I had a health issue, and so I dealt with it.  But to be honest with you the only  thing I really do miss out of changing my diet as is the ice cream.  But that’s a small price to pay for maintaining your health.

There’s a potential that this kind of information might motivate more people to take care of their health, as you mention in The Cell article, in your discussion section.  But right now the FDA does not allow people to know all of this cool stuff about what’s happening in their blood.  Right now we don’t have affordable ways that people can regularly check their hemoglobin A1C’s and their insulin levels, let alone these more complex tests,  That’s out of the  price range of most people.  So we have both the fact that we don’t have the information available — it’s barred from most people to find out all that you found out.  Plus, it’s expensive.

MIKE SNYDER
Well,  I don’t know how much it is truly barred, in the sense that you can’t access it, so much as it’s not affordable.  For these latest technologies we’re using a million-dollar mass spectrometer — that’s for measuring the proteins, and we’re using an $600,000 mass spectrometer for measuring metabolites.  And the whole sequence, so that the setup cost for this was enormous.   But now we can analyze the samples for around $2500 apiece although we’re analyzing them in exquisite detail

$2500 a piece, give or take a little bit of research and development costs up front!

MIKE SNYDER
A lot of research and development up front.   The point is, I think what will happen is like everything in science — it’s very expensive to do it now, and it’s not accessible because this is a research project.  It truly is.  It has to be, because we’re still trying to understand the data and what it means for all the issues associated with this.  But I’d like to see in the future this become quite inexpensive, so it could be done as a home test.  Quite frankly, so instead of pricking your finger and measuring one simple thing which is glucose, you can measure 5000 things and actually get a much clearer picture what’s going on.

A much clearer picture about what’s going on is important to you and I’m thinking about what’s going to happen with the people that are in your next test. you mentioned that you’re going to try to do this with a broader range of people — not scientists?

MIKE SNYDER
That’s right.  We’d certainly like to make sure everyone we talk to who we enroll in the study understands what it’s all about and what to do and so they need some level of sophistication to be able to comprehend what we want to do.

Most studies are done in a double-blinded placebo style, meaning that you don’t get to know each person individually  as much as you have them be a data point.   And the test subjects don’t get to know what the data says about them.   They just get to know the fact that they were part of a general study.   In your personal case, it was motivating for you to hear what your information was.   Are you planning to do this study in the double blinded way, or are you planning to do it in a way where you can inform people about what their blood says about them as you go along?

MIKE SNYDER
Well, I personally would like to inform them about what their blood says as we go along simply because I think it can help them, rather than hurt them, if their glucose shoots up or something.   But to back up a little bit, the study will be focused primarily on pre-diabetics, meaning people at risk for diabetes who are starting to show some high levels of glucose and we also  know already just from statistics that about a third of them will become diabetics, so we are going to be following an at-risk population, and we will follow them in time, and presumably, like me, some of them, we will see their glucose shoot up and we will see what’s happening in those earliest events.  What kind of life stresses that’s associated with, if any, and that sort of thing.

So you want to see what’s happening in their lives individually so you can tie that back with what you see.  Now are you just going to tell them about the markers that they could get by going to a doctor to hear about their blood sugars and maybe their insulin levels and A1Cs or will you also tell them about this wide world of inflammatory markers and say here’s what we’ve seen here with your inflammatory markers too?

MIKE SNYDER
Well, we’ll tell them  what we understand.  I’m not sure there’s a point in telling them what we don’t understand.  If there is a strong inflammation response and we see that it’s associated with a health risk I guess we probably would tell them.  I assume that if  there’s a strong inflammation response it is associated with something and so we’d want to figure out what that something is.

Now you want to see this happen for two reasons.  1.  For sake of the people to see if it will motivate them to get more information, 2.   You’re going to get research information from it.  But the FDA gets concerned if they think someone’s getting information about something that’s a non-approved medical device, and some of the data that you’re getting is not approved and reference checked by the FDA.  How do you work with that?

MIKE SNYDER
We would only return results through the physician, that is to say . . . let me back up a little bit.  You are absolutely correct that this really is a research project and the primary goal is to study what’s going on in the blood of these individuals and associate it with any other other sorts of changes that are going on in their life — viruses, life stresses, things like that.  So that really is the primary objective.  But we think it’s valuable, and  you are allowed to, if you find things that occur during the course of the study that affect someone’s health, you can relay that to the physician who in turn can relay it to the patient.  That’s how we would handle this data.  In this study, we’re not trying to circumvent any rules about this sort of thing.  The goal would really be to return any research findings that might help the health of an individual during the study.

It’s going to be a fascinating study.  So you’ll give to the patient, through their physician, information to help their health.   Does that mean a Stanford physician who’s in charge of the project or does that mean the patient’s regular, personal physician?

MIKE SNYDER
We have a physician already identified to be part of this and so I think they would be the one to return this information, as needed and as desired.  Some patients may not want to know anything.  That’s fine.  We will just go on as we go on, but if they do want to know some things that are related to their health I think we can certainly tell them.  That that would be the plan.

So that means that the 30,000 or so measures you take take each time for yourself, during this study, you researchers will look at every single one of those markers, for each research subject.  You won’t share all those with the patient. But for the markers that make sense to share, and which have more history behind them, so that the physician can explain to the patient, it depends.  If those “known” markers relate to that person’s health, the physician can tell the patient what’s useful to that person.

MIKE SNYDER
That’s right and in the case of the people we’re talking about since they’re prediabetics, the number one thing we would look out for would be their glucose levels.   And so we can certainly see their glucose levels go up, the physician can then suggest that the patient go to additional tests such as hemoglobin A-1-C. or what have you.  And they can do an official clinical test to see whether anything we discovered in the research project is in fact real and they can use that information.

In The Cell article, you were very eloquent in explaining what you think the potential is for this test and for a future where people find things out early enough, and they get good enough information, so that the health professionals and the person can be motivated to take the right kind of care for that person.

MIKE SNYDER
That’s right.  I think that most complex diseases are, as the name sounds, complex, and diabetes is one of those, schizophrenia, there are many diseases like this and they’re probably not one simple disease and probably again lots of different diseases and so if we can understand  them  better how many different diseases there are, we can treat each appropriately and in the case of diabetes for example some people do respond well to anti-inflammatory drugs and so those do incredibly well with that but then there is another group that’s been unresponsive to this and likewise there’s a group that responds to the drug called metformin and there’s another group that doesn’t respond so it seems like everybody’s a little different, and if we can just figure out how many different diseases there are we would know which ones to treat which way and that could be very valuable then in very rapidly deciding the right treatment for the right person

I can envision a time where instead of telling someone, “You have schizophrenia,” or “You have diabetes,” your health professional could say, “You have a disease that tends to really affect inflammatory pathways and the signaling that goes to your hippocampus, and if we can settle that down and get more normal signaling you’re probably going to feel better.”

MIKE SNYDER
We hope it would turn out as simple as that.   It would be a great outcome of all of this.  Can’t guarantee that this would be the case, but that’s what we hope.

And that’s kind of how you’re thinking, regarding how these markers change and how sometimes they target one organ or one system. You’re looking at the markers as the way to identify health states or disease states, instead of just using our current diagnostic labels for disease . . . and treatment.    Looking at this more comprehensive series of markers would be a different way of looking at a person.

MIKE SNYDER
It’s really to understand what’s going on in an incredible molecular detail.  It’s zooming at a resolution that’s never been done  before.

Thank you for being the first proof of concept person that’s ever done this publicly.  Do you think many people are doing this behind-the-scenes right now?

MIKE SNYDER
Not at this level because it requires a certain level sophistication,  Most people can’t analyze DNA, RNA, proteins and metabolites at the same level our particular group can and our collaborators.  We have some really terrific collaborators with Euan Ashley , Russ Altman, Atul Butte, Mark Gerstein, Kari Nadeau.  It’s really a very unique team that’s been able to come together to do the study.  You really need the right expertise to be able put all this together.   But I hope that someday it will become a lot more standard so that it can be done routinely for everyone.

How soon is someday?

MIKE SNYDER
It’s difficult to predict how long it takes to get from the lab to the clinic.  Usually it takes a lot longer than people think — often 15 or 20 years.   I think some form of the test could come out in in much less time, but not analyzing 40,000 components, and maybe we don’t need to analyze 40,000 components.  Maybe we only need to analyze 2,000 critical ones that can tell everything that’s going on in a so-called health state, so with that kind of information it can be a lot simpler to design a test for the future that specifically looks at those 2,000 things.  And again I don’t know how long.  You’d have to figure out how to do it exactly and then you’d have to have it approved by the FDA and such.  And that would take some time.  But if there’s a demand for these things they tend to move pretty quickly.  Right now a lot of people are getting their genome sequenced which you never would even have thought of 10 years ago

But genome sequencing isn’t as exciting as what you’ve done.  Because once you know what your genes are, they’re not going to be changing very much for the rest of your life.  But our proteins and our metabolites, our hormones, the fatty acids in  our bodies, they change based on what you do and what comes your way and hits you.  Those are changing all the time as opposed to DNA which is holding steady.

MIKE SNYDER

That’s right.  But I think your genome, getting your genome sequenced is an important part of this because it lays the groundwork for what you might look out for But you’re absolutley right.  It’s  only part of the equation, and a bigger part is trying to follow all the other stuff.

How often would you like to see people measure this stuff?

MIKE SNYDER
One possible scenario that would like to see, but not everyone would agree, is that there would be as simple a test as doing  your glucose where, instead of pricking yourself and measuring one thing — glucose — you prick yourself and measure 5,000 things.  You need a very robust test and you need to handle it in an appropriate fashion, so people don’t mislead themselves to think, oh, I’m following myself and that’s good enough.  But it could help you imagine a scenario where you do this once a month or once every two months.  Suddenly you could catch things much much earlier then  if you go every two or three years like most healthy people do, and the convenience would make it quite attractive.   In my mind this would be a great outcome if people can self monitor and catch a lot of stuff early.  It wouldn’t replace them going to the doctor for their annual physical or a biannual physical, what have you.  But it could supplement that and add a lot more information that could greatly help them monitor their health.  If they see something funny they could to go to the doctor much earlier and then get it confirmed.  Catching disease early is really the key.

Someday you’d like to see a test that people can do it themselves, once a month, a test that catches 5,000 different things at once, and if they sign-up for $1000 plan, they can do this once a month and get all that information.

MIKE SNYDER
Something like that would be quite attractive.  I think a lot of people would want to do that.

Jeff Gerber (Left) with Gary Taubes (Right) photo by Barry Erdman

Since low-carb diets are not recommended by the American Diabetes Association or the USDA, it can be challenging to find a doctor who supports a patient making this choice.  Instead, many people who switch to low-carb diets report that when their bloodwork comes back better than ever, their doctor congratulates them on FINALLY doing a low-FAT diet!

Denver Diet Doctor Jeff Gerber prefers to support patients who go low-carb.  On Wednesday, April 4th, Gerber will present a talk at the Boulder Community Hospital on High Fat, Low Carb diets for weight loss and for the treatment of heart disease and diabetes.  Known as the Denver Diet Doctor, Gerber has been using a high fat, low carb diet to promote wellness in his patients for over a decade.  The Wednesday evening talk at Boulder Community Hospital is free and open to the public.  It starts at 7 PM and takes place at Boulder Community Hospital in the Gene Wilson Conference Room, on the basement level of the hospital’s Medical Pavilion Building, at 1155 Alpine Avenue.

If you can’t come , or you want a sneak preview about it, or  you want ideas about how to encourage YOUR doctor to support high fat diets, then listen in:

Listen to Jeff Gerber (30 Minutes)

Click here to view the embedded video.

Ingredients

LISTEN TO INTERVIEW (30 MINUTES)

Editor’s note – “High-fiber, low-net carb” products are often marketed as helpful for keeping blood sugars low.  The idea that a consumer can subtract the “fiber” carbs from the “total carbs,” to figure out “net carbs,” seems logical on first glance.  But like a growing number of  health experts and citizen groups, the Boulder Very Low Carb Diabetes Support Group found that in real life, it doesn’t work that way.  I belong to this group of Type 1 and Type 2 diabetics who are working to stay healthy through diet over drugs.  When we  tested our blood sugars after eating a “low net carb” Quest Peanut Butter Protein Bar, the blood sugars of many members of the group rose roughly 50 points (Here’s the spreadsheet of our results).   Quest responded by asking the group to test the whey protein alone, guessing that this might be the culprit that makes some blood sugars rise.  Overall, in this group of citizen scientists, blood sugars actually went down slightly after drinking water mixed with the whey protein alone.  To discuss this puzzle, and “next steps,” Quest Protein Bar‘s Ron Kane agreed to an interview. And here’s a written transcript, which is paraphased for clarity.  — Shelley

RON KANE – I am one of the guys here at Quest that has been around since the very beginning, one of the founders. I tend to focus on everything from product development to marketing.

Are you a nutrition expert?

RON KANE – Nutrition’s one of those fields that, you have a lot of confidence when you don’t know much, and the more you know, the more you know you don’t know. You have to know a lot to call yourself an expert.

So you’re not a nutritionist or a registered dietician or a clinical nutritionist.

RON KANE  – No. Not at all. I’m fascinated and I read extensively but I don’t have any certification.

Well, Ron Kane, maybe you can help us figure out a mystery that has arisen in our very low carb, diabetes support group in Boulder Colorado. What is it in your net carb, low-carb Quest Peanut Butter Protein Bars, what’s causing the blood sugars in our Diabetes Group to go up?

RON KANE – It’s a weird puzzle alright. To figure it out, here’s some information about us – our main market really is people that are focused on physique competitions, people who are particular about what they eat, and we manufacture our own bar. We don’t use contract manufacturing. One of the reasons we do that is that, then, we know what’s in our bars. I think it’s been a couple of months since I heard how we shipped you guys in your diabetes support group some different products to check out and then you check how it affects your blood sugar. . . Blood sugar . . . we have a lot of people who share information with us. We have physicians who take their blood sugars very regularly or they have patients that do, and they share how our bars affect them with us. From all that, we’ve seen that blood sugar regulation seems like it’s one of those things that’s an art or science that’s very individual. Some people have very strange reactions to all kinds of things. So I can’t say for sure what caused the blood sugar changes in your group that ate our protein bar. I haven’t seen the spreadsheet your group created about your results. But really the protein bar comes down to very few ingredients. You’ve got protein powders, you’ve got nuts, in the form of crushed nuts or nut butters. You’ve got fibers, and there are a couple we’ve used. Inulin and isomalto-oligosaccharide, which is basically a string of non-digestible fibers, either as fructose molecules in inulin and glucos in isomalto-oligosaccharide.

Is that non-digestible fiber like Jerusalem artichokes or something like that?

RON KANE – Exactly. You can get it in leeks, you can get it in onions. It’s a naturally occurring plant fiber. It allows you to take your fiber up and well, different things have been said. I don’t know if you’re familiar with fructooligosaccharides, and a whole bunch of different plant fibers found in nature that are pretty interesting. That could be one of the things . . . I know we’ve definitely had some people, where anything with whey protein . . .

2011 Boulder Diabetes Support Group Quest Bar Tests – Bar and Whey Only

In our diabetes support group . . . when we did a test for everyone, eating the whole Quest Bar, it made about half the people in our group have blood sugars go up roughly 50 points, which is quite a bit, and the rise in blood sugars seemed to peak around the first hour.

RON KANE – Okay.

Some people saw a rise in blood sugar and some people did not. But there were enough who did, you can look on line at meandmydiabetes.com to see the video of people’s responses to their personal results. Many were shocked to see how much their blood sugars went up after eating a low-carb protein bar.

RON KANE  – I remember actually seeing that video.

So you were kind enough to send us the whey protein, wondering whether the whey protein is the ingredient of the protein bar that was raising blood sugars in our group. We mixed it with water and each drank the same amount of whey that you put in your bars. But for us, the whey protein had an effect that was opposite what happened when we ate the whole Quest Bar. We certainly had some outliers where their blood sugars went up somewhat on the whey alone. But overall, our group did not experience the dramatic rise that came from eating the whole Quest bar, and in some people, at the one-hour mark when a Quest bar made so many blood sugars go up, with the whey protein alone, often blood sugars went down. So the net change in blood sugar response was in the opposite direction compared with eating the whole protein bar. Again, this was not a scientific study. For instance, we encouraged people to not eat for 2 hours before the test and so forth. Most people remembered to follow these directions but some people didn’t. We included all their results in our charts, and the net effect was with the whole bar, a number of people’s blood sugars went up pretty significantly. With the whey powder, when we tested it alone, it seemed to be pretty neutral, and an hour after drinking the whey with water, the overall effect on blood sugar seemed to be more down than up. That’s what we’ve seen so far, and the guess in our group is there’s something about the fiber and non-whey ingredients in a Quest Bar that, for us diabetics, makes blood sugars go up.

RON KANE – Has anyone in your group ever tested blood sugar after eating inulin and other plant fibers that are popular.

I don’t know, but some members of our diabetes group were having a discussion about this last night, and the thought is that testing fiber alone would be hard, in terms of flavor. We might have to mix fiber with the peanuts in your bar. That might allow for testing your fiber in a way that people would actually try it.

RON KANE – And we’ve also got a lot of other products coming out that might be interesting to do some studies about, whether they’re scientific or not, just to get some ideas. We have a bunch of products coming out where some will be lacking whey. Others will be lacking the plant fibers. That might also give us some clues, and it’d be interesting to test a bunch of plant fibers. We’ve used chicory root in the past, but that is not as tolerated on a gastrointestinal level. A lot of people have discomfort with chicory root, which is why we don’t use it. As for what raises blood sugars, in the last year, whey protein is the one that is probably the biggest culprits people site, I would would say, I’ve seen responses across the board, there are people who report really high blood sugar readings from it and others who experience the opposite, which is kind of your group’s experience. You’ve had people on both sides. I guess it really depends on the issue. If you notice, our bars are about 42 – 50% protein, depending on the flavor. There’s some people who say look, we experience a blood sugar response, if we simply taste something sweet, even if it doesn’t have calories. When I first read about blood sugar I was fascinated, because I thought this is the answer. Now, having seen all this variability in what people report, I know the picture is more complex.

Blood sugar response is fascinating. But what if it’s more predictable than it seems. For instance, in our case, we’re a group of roughly a dozen people, and we’re seeing some pattern showing up, where, for our group of diabetics, whey did not seem to be a big deal, when it comes to raising blood sugars, but the whole bar was. And so I’m wondering — have you all actually tested your products in clinical trials for anything, to see how people respond, or is it more anecdotal how you get the information.

RON KANE – It really is anecdotal, since we weren’t really targeting a diabetic product or anything. But you raise an interesting point because we’ve always looked at our bars as the whole. Have you guys ever tested like sucralose itself or stevia. Just sweeteners? Have you seen what a sweetener, alone, does to people’s blood sugars?

I think we have anecdotal responses from our group about those, but I have not heard people saying that they steer clear of artificial sweeteners because they raise blood sugars. The reason some people avoid them is because they don’t like the idea of artificial sweeteners. Some people don’t like the taste. When it comes to blood sugars, in general people aren’t talking about sugar substitutes, as much as they’re talking about fiber. I think the issue for our group is that there is a lot of talk and question right now on the internet and in self-help communities about how to choose what to eat based on “Nutrition Facts” standard labels. Specifically, we wonder whether or not it’s wise to subtract all the fiber from the total carbs in a product, on the assumption that only the “net” carbohydrates will affect blood sugar. It’s our inclination and our hunch that you probably can’t subtract out the fiber, when calculating the potential impact on blood sugars of the carbs. What do you think?

RON KANE – What’s interesting about that is I was actually talking to someone about the Expo West last year who was an expert in resistant fibers.

That’s an American Diabetes Association expo?

RON KANE – No, it’s actually the Expos West, natural products expos west, and it’s just kind of a showcase of a bunch of different ingredient manufacturers and people who make products in that industry. One of the things that is interesting is that fibers are digesting in different ways. Some aren’t digested at all in the upper GI tract. Only in the colon, where they turn into short chain fats, which is what feeds some of the probiotic microbes in the colon. That’s how maltooligosaccharides are supposed to be digested, as in inulin. Other fibers are digested much earlier in the process.

Since so many people in our group saw blood sugars go up when eating a low-net carb Quest Bar, it might be that the gut microflora of the people in our group is unusual, and that leads to an unusual way that we are digesting high-fiber products. But there’s another way our group might be special — it’s that this is a group of diabetics. I don’t know enough about the tests that have been done about the ingredients you use, and who has tested them on what and who. I gather from what you’re saying that your products aren’t really tested as a whole item on either healthies or diabetics.

RON KANE
 – That’s really the only kind of testing we’ve done is as a whole product. We’ve never broken it down into its constituent parts.

Who have you tested it on.

RON KANE – It’s really just anecdotal. My mother’s a diabetic. She responded really well to eating our protein bars, although the reports I tend to believe more are, we have quite a few physicians who have shared information with us about patients. Or physicians who are diabetes, and they report their findings to us. I won’t even pretend that we’ve done an analysis of each individual or group reports. The diabetic community, I think , has gravitated to our products, simply because we don’t really use any sugar, maltodextrin, that kind of thing. They look at how the carbs really come from the nuts. Even the proteins we use are completely devoid of lactose. It’s interesting because it would be fun to do a much wider scale study. Although just testing blood sugar . . . It’s a little . . . blood sugar is one of those things, when I first heard about it, I thought this is the answer to everything. The problem is that there’s so much variability. I think one of the people you copied me on is David Mendosa. He’s been writing on the internet about the variability of blood sugar and questions about the variability of blood sugar increases caused by carb forever.

David Mendosa has been writing about fiber and blood sugars a lot allright, and he wrote about the Quest Bar test our group did, and what it seems to show about fiber raising blood sugars about half as much as regular carbs. For me, I’m curious about this in a lot of different ways. Your website shows a lot of body builders and obviously your product is popular with them. Well it’s also the case that your product and other net fiber products are frequently seen in diabetes journals and on websites that cater to diabetics. So certainly, it seems that an emerging market for you, is people with diabetes. And am I right about that?

RON KANE – Yes, I would say there are five or six different markets and I would definitely say that’s one group of people. We have a lot of physicians for example who are telling their patients, eat more protein, and so people kind of find us. So I would say that’s an emerging market. It’s not our main target by any means, since we do’t target that community. But we do have a lot of people from that arena who come to us.

So it’d be helpful for many people to find out what’s happening with diabetics, specifically, when they eat these bars. Our guess that the ideal way to do check it out would be to take it beyond what our citizen’s group has done, where we checked our blood sugars alone. Better, we think, would be to check people’s insulin levels as well as their blood sugars, after they eat this kind of product. In our test, we had everyone come in, and we wanted them not to eat anything after breakfast, so they came in 2 hours after they had eaten breakfast, and we took their blood sugars. Then we took them again one hour later. We took them again 2 hours later. We knew what their fasting sugar was before they had breakfast. We knew their blood sugar two hours later, before they ate the bar. And so on. We can do this because blood sugar readings are inexpensive to do these days.

RON KANE  – Sure.

What would be even better for a diabetic is to find out what is happening to insulin levels because right now, that’s a hidden factor. You could have some diabetics who have a very strong pancreas, but their cells are very insulin resistant. What could be happening when that kind of diabetic eats your bar is that you don’t see much rise in their blood sugars, but their insulin is going through the roof. Or they see both a rise in insulin and a rise in blood sugar.

RON KANE – Right.

Or you could test it on people who have a very weak pancreas. They don’t produces a lot of insulin, and you might see a higher blood sugar rise in them because their insulin never kicks in.

RON KANE – Yes.

It would be very useful for people to better understand the relationship between sugars and insulin, and diabetics are a population where, since they have this deficit in how their body works, their bloodwork reveals some things that you might not seen revealed in a healthy. And we could all learn something from that.

RON KANE – Yes. I remember when I first saw the insulin index, I was surprised and troubled, because fish and things like that were raising people’s insulin levels pretty significantly.

That’s right.

RON KANE – A lot of protein powders did the same thing

Makes sense, since protein consumption triggers insulin release.

RON KANE – Ultimately you’d want to see the insulin-glucagon ratios. That would be the ultimate relationship, I think. My instinct is that a lot of things that we consider low carb cornerstones or the gold standard, such as eating proteins and things like that may not fare well on an insulin index. However, Dr. Eades in his blogs has talked about really, it’s probably the insulin glucagon ratio that’s most important because protein also stimulates glucagon secretion. You have any experience with that?

I don’t. He’s not one of the people who I follow closely. There are some other doctors I’m more intrigued with as researchers. I like Ron Rosedale, Steve Phinney, Jeff Volek, but I think you’re correct that it would be interesting for a number of us to have these experts do a meeting of the minds, and see what they would say would be helpful to know. After all, there are so many net carb products with high amounts of fiber, and it’s a bit of a black box what’s happening when we eat those foods and they’re getting digested inside of us. It doesn’t sound like you’ve done glycemic load studies of your foods.

RON KANE – We really haven’t and it’s interesting, what you’re reminding me of is that we have some products coming out that are higher in fat and lower in fiber. It’d be interesting to also throw those into the mix, these protein fat products . . . and nuts. Ron Rosedale, I’ve read a lot of his stuff, too, and I think what’s . . . it seems to me that the blood sugar readings are sort of grasping at something that’s indirect, and I think your’e right that getting at the hormones themselves, the insulin, the glucagon levels are going to give much better information for how foods affects people. From my understanding, blood tests of these hormones are ordered so rarely, they must be fairly expensive.

I think you or I could get these tests on line, for an insulin blood draw for maybe $90. We could order it, but we’d need, for this kind of test, it’d be most interesting to have it be a 2-hour test, though there’s some thought now that a 5-hour test would be even better as a food challenge. I think it would be so interesting.

RON KANE – That’s fascinating, and it also, it really kind of goes forward in product development because we’ve never sort of taken the front end approach which is interesting which is to say, “Let’s talk some people, and study both healthies, as you call them, and people who are diabetic, because unfortunately, I don’t think anyone knows the answer right now. I’ve looked for it, but you read a lot of conflicting things. Maybe we could do a body of evidence, at least for ourselves Maybe not something that would stand peer review, but something we would learn more about with. I remember whey protein does cause the secretion of quite a bit of insulin.

Whey protein probably triggers responses in the insulin pathway,  because dairy generall contains a lot of IGF, so with that, and the protein, it’s a strong promoter of insulin like responses. And some people have allergic responses or sensitivities to dairy products Who knows what that does to hormones or to inflammatory responses. There are a lot of different possibilities. But I like your idea of, “What if we cooked up a study?”

RON KANE – Yes. What’s interesting is that I remember the branch chain amino acids in particular are insulinogenic. We use milk protein isolate, which is a little bit different than casein. Casein has less branched chains. If you really wanted to do it right, you’d have to start looking at different proteins. Even the word whey protein, as someone who buys this stuff all the time, it’s a really broad classification. You’ve got ionic exchange, you’ve got filtered, and they have different chains of amino acids. I recall six or so that tend to raise insulin. So amino acid by amino acid, even that can affect responses. Plus some people probably do have an inflammatory reaction while the person sitting next to them does not. So it’s a complicated situation, but I think you’re really onto something with the idea of testing insulin and glucagon. Can you test glucagon? I haven’t seen that.

I don’t know. Since insulin and glucagon tend to be counter hormones – when one’s up the other’s often down, then it may be that testing one gives you a lot of information about the other. But you know what we could do, I could and you could contact some of these scientists and some of these clinicians and say, “If you were going to do the perfect, the ideal citizen-based test, of these products, what would you invite the citizens to do, and if there was going to be a clinical trial, of these products, what would be an ideal way to do it?” Then we could approach the American Diabetes Association, after we had done a little more kicking around of these things, and say, “As consumers, since the ADA represents the consumer group of diabetics, could you help figure this out? Could you help us fund a study.”

RON KANE – There’s so much value to the picking apart of it on the way in, so that once you’ve finished a study, or created a product, you don’t get, Oh, wait a minute. You didn’t take this into account and you didn’t take that into account. A year ago, I was looking at the whole glucagon, insulin relationship and I got the feeling at that time that, wow, this whole concept of blood sugar is not enough. I am not a diabetic, but I have been really surprised how much blood sugar an be all over the place. Even cardiovascular exercise, before or after, it can screw things up. Even if I do the exercise the night before, it affects the blood sugar the next morning. I was a little frustrated just checking blood sugars. I think you’ve hit the nail on the head that measuring insulin or insulin/glucagon may be smarter than looking just at blood sugars directly.

Yes, and some of the factors that you’re mentioning would be good to have sorted out too, because exercise in some people lowers blood sugars and in other people it raises them. So it might be good to have some experts guide us in what to be specific about in terms of encouraging people to do or not do before they take this test.

RON KANE – Yes.

 It depends on the kind of exercise, and the person, and when it happens. To have some of these more experienced clinicians and scientists help figure out what to encourage people to do in the 12 hours before the test.

RON KANE – Do you have access to these people or would you be reaching out to them blind.

Let’s go for the really good ones. Let’s go for Steve Phinney. Let’s go for Jeff Volek; We could ask Eric Westman, and we could ask Ron Rosedale, and that would be a pretty good team. Who would you want on this team for kicking around this idea.

RON KANE  – The only other guy I can really think of is . . . Last name is Volek? Jeff Volek?

He’s superb.

RON KANE – He’s great, and Dr. Eades is the only other guy that’s kind of interesting, I think. He’s got a fantastic blog. But clearly, yes. Very interesting.

Then sure, let’s get Dr. Eades involved too. Yes, it’d be fun. What I’ll do is I’ll transcribe this interview, and touch base with some of these folks, and see who else they might recommend, just to say, if we’re going to do this, who should be included. On a related topic, in a citizen’s group, they need to be assured that they’re not hurting themselves with the test they’re trying to do. They’re less inclined to try eating something which they know is going to pump up their blood sugars. But one of my colleagues in this support group, Barry Erdman, pointed out that you there at Quest have some of the best possibilities for truly low-carb diabetes friendly energy bars. And to get this right would be quite a neat thing.

RON KANE – It would, and I have a selfish motivation, as I sit here and think about it, because you can imagine, even if it was an informal board of people that are passionate about it, they could say look, there may already be some answers out there that we can avail ourselves of. And maybe some studies that could be designed to be the tip of the spear to help determine, what’s the new stuff that’s going to come out. Because I don’t think that’s really being done. It whets my appetite just thinking about being able to work with these people to say, hey look. This hasn’t really been done. Being a manufacturer, the biggest problem is that if you contract manufacture, which is how most do it, the way the machinery works, you can’t get stuff to work unless you add sugar or glucose, which is why all the bars on the market are the way they are

 Meaning that to make stuff stir, in the big vats, you have to add some sugar or other bulker stuff to it.

RON KANE – Yes. Our product is so difficult to work with, we originally explored contract manufacturing, but there’s no way you can do it. It took about nine months just to get the stuff to work, and it’s just one of those processes where everybody who looked at it says, oh this isn’t going to come together. We ourselves didn’t want to add certain things, so we just kind of kept pushing through it. I used to wonder, why isn’t more of this stuff out there. I think it’s just the harsh realities of manufacturing on a large scale. We’ve spent a lot of time on that and now, if you had the brain trust of people that really understand what’s going on, and they could say, these are substances we want to add, this is what we want to stay away from and this is the kind of responses people are getting, that is the truly dream come true for us,

Okay, my guess is that these folks would add in in their two cents for some degree of just freedom of sharing of information. But at some point, it might be good for somebody to pay for a real controlled study. Those things are expensive, but somebody needs to do it.

RON KANE – Not only that, but it might be something we’d be interested in, as well as paying these people for them time and putting together an advisory board. To my knowledge, I’ve never seen anything that was done backwards, so to speak. There’s usually a product and then people are trying to figure out if it’s any good. What’s really interesting is building the product from the ground up, saying, let’s have experts put their heads together and we’ll say, “Let’s build products backward.”

And we’d all enjoy seeing what happens with that. And it could answer a larger question because right now fiber is advertised as something to subtract from carbs. And that might not be wise for someone who’s got a weak pancreas or has insulin resistance. And it’d be good to figure out how these products affect people with those increasingly common conditions. Plus, it might give good information to other people as well.

RON KANE – Yes, and the same with the say FDA labels labels sugars. If you look at broccoli, it contains pound per pound more sugar than a quest bar, however, are all fibers treated the same? Probably not. It’s just like amino acids. Most likely different fibers are metabolized differently or not metabolized at all. So that gets us in a lot of trouble is lumping things into three or four categories of macronutrients. The reality is probably much more complicated than that.

You wrote a good article about how some foods that we agree are pretty healthy can be misunderstood if you start looking at broad categories of ingredients.

RON KANE – And a lot of people look at fructose, which doesn’t increase people’s blood sugars, but not many people at this point would say we should be taking fructose in by the truckload. So it’s complicated, but that’s what makes nutrition so interesting.

I hear that you’re curious to learn what would happen if some of these experts weighed in and we just have this dream idea out there of, wouldn’t it be cool if we could devise a way that any citizen group could do this kind of test and figure these things out. Plus we could do it at a higher level, and the citizens could then help double-check the expert’s results.

RON KANE – Yes. Exactly, and maybe a big university would get interested, too. I don’t see why it wouldn’t work. It’s really exciting.

What’s our next step then.

RON KANE – I guess contacting some of these different people, and also I’m going to do a little reading. I guess there are really 2 things. Designing the right protocol, in terms of what the testing requirements would be, and also picking people’s brains to determine what do you think and what are the other things we’re going to test. Broccoli. Are we going to look at that. How do we compare to get a baseline. So picking brains and just kind of thinking ourselves, and I guess after that, actually contacting people and saying, how would we go about doing this

Good idea!

Ski Racer and Low Carb Eater Lindse Vonn

FROM SHELLEY – Readers provide some of the best comments and questions for meandmydiabetes.com.  That’s the case with this series of questions from Fred, regarding high performance athletes and low carb diets, which he posted in an earlier interview with Steve Phinney.  Steve has now responded to Fred’s questions, complimenting Fred’s astute observations and giving further details.  Read on for the exchange between Fred’s  comments and Steve’s replies. 

(PS – For more information on Steve Phinney’s views, check out his books, The New Atkins for a New You, and The Art and Science of Low Carbohydrate Living.  And here on this blog, here all all the interviews that feature Steve Phinney.)

FRED COMMENTED:  I’m familiar with Phinney’s work, mostly through this NIH PubMed article.  Much of what he talks about in your interview is also discussed in his paper but, in his paper, he referred specifically to athletes engaging in sub-maximal activity, around 70% and decidedly aerobic in nature. He also states in the paper that a low-carb diet would probably not be appropriate for competitive athletes.

STEVE PHINNEY REPLIES:

That paper was written 8 years ago, and much has happened since.

1.  We used to have concerns about long term use of low carb where potential risks were not outweighed by obvious benefits (as in diabetics such as yourself).  Since then, we have demonstrated (among other things) that a well-formulated low carb diet reduces serum levels of saturated fats despite copious saturated fats in the diet, that a low carb diet markedly reduces levels of small, dense LDL (the most atherogenic version of ‘bad cholesterol) while raising HDL cholesterol, and that biomarkers of inflammation are reduced by a well-formulated low carbohydrate diet.  Given these demonstrated benefits where we once thought risks might lurk, there are now much lower barriers to looking for more subtle benefits of carb restriction.

Sled Dogs Eat Low Carb

2.  Mike Davis’s work with racing sled dogs adapted to a low carb diet has markedly changed our views about the necessity of glycogen at competition intensities.

3.  A number of professional athletes (eg, Mardy Fish and Lindse Vonn) have gone public about reducing carbs (and there are many others who remain a bit more shy), but it is no longer a secret that both training intensity and volume can be better sustained by some athletes across a prolonged season when carbs are restricted.  See for example the NY Times interview with Lindse Von containing this quote:

Vonn has also sought the advice of a nutritionist, hoping for an energy boost to get her through the nearly 40 races of the World Cup season.

“I always ate healthy, but it wasn’t scientific,” she said. “Now it’s a high-protein diet and no carbohydrates. I have more consistent energy and I don’t get tired after a meal. It does take a very detailed meal plan.”

4.  Jeff Volek performed and published a study of low carb diet plus endurance vs resistance training, showing no restriction in training effects with dramatic improvement in body composition with the combination of low carb plus resistance work.  (Strength & Conditioning Journal:  February 2010 – Volume 32 – Issue 1 – pp 42-47).

FRED COMMENTED:  From your interview, his position appears to have shifted considerably to advocate a low-carb diet for all types of strenuous training, including training for maximal effort activities such as sprinting.

STEVE PHINNEY REPLIES:

For sprinting events, the effects of keto-adaptation are quite variable across athletes and specific events.  One also needs to differentiate between the diet followed in training versus preparation for the event per se.  There are some trainers who advocate ‘train low, perform high’, but I have not seen that supported by objective study.  But given that Lindsey Vonn’s events last about 120 seconds, the neuromuscular intensity of her performance is about as high as it gets.

FRED COMMENTED:  The paper I referenced is from 2004 and could most definitely be out of date if there is more current research from Dr Phinney on athletes engaged in maximal effort. The evidence he presents, on humans, however, seems to be more anecdotal,

STEVE PHINNEY

Certainly the evidence cited above is a combination of both objective research and anecdotes.  In some sports, such as 100-mile ultra-endurance trail runs, individual performance improvement is turning heads.  You can expect to hear more about that in the coming year.

Shelley’s Note – And here’s a lovely video of a very young low-carb athlete.

We lost our dog Brian.  He was 12 years old.  His back legs were rickety and on slippery linoleum, sometimes he would fall.  He was going deaf, and sometimes you had to get right next to him before his ears would prick up and he would hear his name.  Brian was a big yellow lab, and at 85 pounds, he needed a ramp, and my help keeping him in balance, to get into the car.  His dad had died at 9, so we knew he came from a shorter-lived family.  But his eyes were still bright, and once we got on a trail, Brian loved to run.

He still loved to prance up to the other dogs and act like a king.  He was a sweet dog, and a gentle dog.  Years ago, he figured out that cats don’t like a dog’s hello, meaning sniff the nose, sniff the butt and then go play.  He always greeted our cat, Andy, in the catlike way, which meant that Brian would lower his head to the height of Andy, and let Andy rub his face against Brian’s forehead, then he’d let Andy curl back and forth in between his legs.  Brian knew that when our 2-year old neighbor, Rio, came over, it worked the best if Brian would  lie down and wait for Rio to get curious, and get over his bit of fear about dogs.  And then Rio would pet Brian, and Brian’s eyes, clear-eyed until the end, his eyes would shine.

I had planned for some time to do a series about Brian’s health, commencing back in 2010 when the wobbliness in his back legs that was already evident when he was a puppy, started getting much more rickety, and we stepped up our diligence on feeding Brian a low-carb, high fat diet.  I wanted to share how this diet helped him stay in better shape.  I think it did.  Here’s a video of Brian, age 11 1/2, back in June, running to catch the great joy of his elder years, which was a dog-toy – a special soccer ball.

Click here to view the embedded video.

As for what Brian ate, almost every morning, it went like this:

• 1 chopped raw zucchini or other vegetable such as broccoli
• 1 avocado
• about 5 ounces of raw chicken or hamburger (the not lean hamburger, such as 30% fat)
• Something like 30 grams of olive oil or Udo’s choice oil
• Some glucosamine powder for all those rickety joints

That meal came to Brian every morning, in a ritual where Greg required that Brian sit  and wait until Greg grinned and said, “Okay!”  Then Brian would race to his food bowl, and eat in one big inhaled gulp, though really, he always ate his favorite item first, which was almost always the avocado.

Naturally we snuck Brian a few treats all through the day.  A slice of cheese from Greg.  When we’d eat raw, unsalted nuts, Brian would sit and wait quietly, and we’d give him one.  And then there were the special treats of leftover bones from lamb and beef.  In his younger days, Brian never wanted us to see how fiercely he tackled these  He would hurry outside, where he’d dispatch them, showing all his teeth, and keeping at it for hours on end until all that was left was a bone so bare that it looked as if it was fossilized.  Chicken bones?  He ate those like pretzels, in three quick cracks.  In his older years,  he preferred not to take unneeded steps and sometimes chewed bones right in front of us.  Over the years, we learned that if we gave Brian too many bones in a single day, it put too much hard stuff into his digestive tract, and then he’d have a day of constipated poop.  So we gave him bones on a more moderate schedule, and then his digestion settled back into a normal, smooth, regular as a clock, non-smelly poop.  Except when he was spending the night with friends, or with extended family, eating “normal” dog food, in which case his poop got softer and  smelly, and sometimes even runny.  It seemed the way he normally ate really matched with him.

Brian loved to hike . . . any hike.  But as he grew older, he did best on level ground, although a walk on a leash in the neighborhood was terrible for all of us.  Brian would get so bored, he crawled.  He’d realize how much his feet hurt, and  we’d have to drag him home.   As for throwing tennis balls?  He loved that in his younger years.  Out on a trail he’d race those green, fuzzy, zooming balls and catch them in a curling somersault.  He loved to do that, but over time, with his inborn wobbliness already, all those somersaults  messed up his back.  So we threw tennis balls less, and then discovered something better – a dog’s soccer ball.  The ball was soft enough that Brian could grab it in his jaws.  It was tough enough that it never punctured.  It had a handle so that I could carry it without getting all gooped up.  And it was slow enough, he didn’t twist so much.  We all loved that soccer ball, and it made going out on the trails so fun, I learned that Brian had a lot more energy than I had suspected  from taking him for a sidewalk tug-and-pulls around the block.  Out on a trail, with that soccer ball, Brian, age 12, would prance.  He’d run to get it.  We could go three miles and half the time he’d be at a run.

I am grateful for those times with that soccer ball.  I can see in my mind’s eye how Brian would jump into a stream on his gimpy legs to retrieve the ball, over and over until finally, he’d had so much fun, he’d stop and shake in a shower of sparkling water drops, and then he’d gaze up at me ,wag his tail and give me such a happy grin . . . he didn’t notice that he had dropped his beloved soccer ball, and now it was racing away with the creek’s strong current . . . which led me to run into the creek and save it for him.  I loved the way that he was happy when I did that, and his sweetness on those trails, so that even though he had more trouble keeping his balance on the linoleum, and yes, it was clear he was getting older, those times on the trails, those times when he greeted our cats, those times with our 2-year old neighbor, so many times.

The last video I took of Brian with his soccer ball was in the snow, sometime in December.

Click here to view the embedded video.

Brian loved the all that sparkling, fluffy white.  Then just before Christmas, we had an especially heavy snow.  After 2 hours of shoveling and snow still falling,  I didn’t feel like going for a run with him.  So Brian was bored.  I found him chewing on something  – an old leather glove.  He had chewed off three fingers and part of the center.  I took it away, but didn’t worry – he had chewed on socks and shoes and children’s toys from the time he was little.  So what, about a glove?

The next morning, the sky was blue and clear.  We headed to his favorite trail beside the creek.  I threw the soccer ball.  Brian ran, he grinned and had a lot of fun.  But when we got home, getting down from the car ramp, Brian lost his balance and fell off.  I lifted him up, and he wagged his tail and limped inside and seemed to be getting better.  But when we came back from a neighborhood party that night, Brian wasn’t in the house.  We looked all through the yard and finally Greg found him, huddled in a corner, in the coldness of all the brand new snow.  It took Greg and I, together, to carry him to his dog bed.  He threw up, undigested slices of the morning’s  zucchini.  He seemed in the kind of pain that isn’t a wincing, crying out pain, but the kind that calls for serious work, and no noise, and short breaths, and eyes sunken down and far away.  Looking back, I now know what was happening.  At the time, I thought it was all because he had kinked his back when he fell off the ramp.  I slept on the floor, beside him, petting him, waiting for him to get better, as he always had when his back got sore.  By the early morning, he wasn’t better, so we called a 24-hour vet and took him in.

The x-rays indicated the start of pneumonia, but despite Brian’s age, the vet said Brian was healthy, we had caught it in time, and he had an 80% chance of pulling through.  Two hours later, the news grew worse.  There was also an obstruction in Brian’s gut.  Pieces of the glove?  The vet said it would take surgery to get them out.  His chance of survival was now 40%.  But Brian was a fighter, and the vet said that if all went well, in just four weeks, Brian would be back to his old self.  We okayed that surgery, but ten minutes later, the phone rang again.  The pre-surgery blood tests showed that Brian’s blood sugars , which had been in the 70s, had just plummeted to the 20s.  Which meant that  a sepsis infection was gobbling up all the sugar in Brian’s blood.  Which meant a poisonous infection had taken hold.  It was damaging every cell in Brian’s body, and it was getting worse.  It was out of control.  Even this surgeon who loves to save dogs, even he said it was time to let Brian go.

We called our sons in San Francisco.  As we told them the news, all our memories of Brian came flooding back.  All those times when our sons were little, and so was he.  The years of them becoming young men, as Brian grew old and sweet.  We asked our sons if there was a story they’d like us to share with Brian.  Walt said to tell Brian how much he loved how Brian would catch a tennis ball out of the air, without letting it bounce.  Amory said to tell Brian how much he liked that Brian really, clearly, loved all us us, and he also loved that HE was a dog.  We promised that we would tell Brian all of this.  At the pet hospital, they gave us a private room then carried Brian in.  He was clearly sedated.  His eyes were already  far away, and for months he had already been mostly deaf.  We tried to tell him how much he  meant to us.  But each time we began, in a normal, talking voice, it tumbled into sobs.  The only way we could say the words was to whisper them, up close his sweet old head, as though each word was a secret that got told the best where we could smell that nutty outdoor smell of his, and we could touch him, and pet him, and give him one more, final kiss.  We whispered  that there was no way to stop this kind of being sick, so instead of having him linger and get worse and worse, we were going to make it quick.  We shared the stories from our sons.  We told him how grateful we were to know him, and love him.  We thanked him for being such a good dog.  Then we opened the door for the vet to come on in.  Gently, he touched Brian’s paw, then he moved his hand up to where the IV line with the fluids and the sedatives was taped in place.  He stepped back, just for an instant, to adjust a knob on the heart monitoring machine, so its quiet beep went completely silent.  In that silence, as we petted Brian, as we kept on touching him, we watched the vet’s hands deftly moving a needle into the IV, then squeezing the plunger.  Brian’s breathing faded to nothing.  The vet checked his heart and said he was gone.

It was Christmas Eve morning.  Greg and I drove to the trail where Brian loved to chase the soccer ball  The snow was sparkling, the wide blue sky was above us.  The air was still.  It was a beautiful day for a walk like that.  We talked about Brian and how, in his honor, we’re going to keep walking and enjoying life.  Over the weeks since then, we’ve taken many walks.  Many friends have told us how much they, too, loved Brian.  Our sons, in San Francisco, made him a little  shrine.  It has a candle, a photo of them and their sweethearts, from Thanksgiving, all together, all hugging Brian.  And on the shrine they’ve also put an avocado. — Shelley