In this podcast, I am speaking with Alex Leaf — a nutrition expert, researcher and teacher of nutrition at the University of Western States — on why myths around proteins, fat gain, and insulin resistance may be hurting your health and your waistline.
In this podcast, Alex will cover
- What fat cell dysfunction is (And how it could be the cause of your chronic condition)
- What your personal fat threshold is and why it’s critical for you to understand
- How nutrition and lifestyle relates to chronic diseases like heart disease, diabetes, neurological diseases, and more
- What is the real cause of insulin resistance (Carbs? Or something more?)
- How science has debunked some nutritional myths about heart disease
- Is protein linked to cancer?
- Should you have high or low protein intake for longevity?
- The effects of collagen and glycine on health and your body
Download or listen on iTunes
Listen outside iTunes
Debunking Nutrition Myths on Protein, Insulin Resistance, Fat Gain and More with Researcher Alex Leaf – Transcript
Ari Whitten: Everyone, welcome back to the Energy Blueprint Podcast. I’m your host Ari Whitten, and today I have with me Alex Leaf who is a certified sports nutritionist and personal trainer. He holds a master’s degree in nutrition from Bastyr University. He’s also a full-time researcher at Examine.com involved in updating the supplement database, editing Examine Research Digest articles, and blogging about nutrition. Alex also teaches young minds about human nutrition and functional medicine at the University of Western States. He enjoys blending the scientific aspects of nutrition with the pragmatic realities of life to help others achieve their goals.
So, welcome to the show, Alex Leaf.
Alex Leaf: Thank you.
Ari Whitten: Yeah, it’s a pleasure to have you, man. So, on a personal note, I have seen a lot of your Facebook posts and I think we’re in a few Facebook groups together that I’m not very active in and you are very active in, but I sometimes read your posts on nutrition and training and you’ve done some very deep dives into the scientific literature on a pretty wide range of topics related to nutrition and human health. And I’ve always been impressed with the level of knowledge and nuance in your posts and the way that you bring research to light to back up all of your assertions and the way that you bring a level of skepticism to claims that you know don’t have good research to support them. So, I’m just very impressed with the way your brain works and the way you approach nutrition and human health from such a strong evidence-based perspective. So just wanted to mention on a personal note that you’re doing great work.
Alex Leaf: Thank you.
Ari Whitten: Yeah, so I have a few different topics that I want to get into this, get into in this discussion with you. But as a sort of entry point, I’m wondering if you can talk a bit about your background and how you got so interested in this. You’re a pretty young guy, what are you in your mid-twenties?
Alex Leaf: Yeah, I’m 26.
Ari Whitten: Okay. And you’ve displayed, from what I can tell, a level of knowledge that is way beyond your years. So, I would imagine you’ve had a pretty strong obsession for digging into the science for a number of years now. I’m just curious how this all started.
Alex Leaf: Well, I was an athlete growing up for most of my life. I started wrestling when I was in elementary school and did that all the way up through college. And part of my experience with wrestling was developing an unhealthy relationship with food and body image. And so, I got really into nutrition secondary to trying to find ways to overcome that.
And being more knowledgeable about what I was putting in my body served as a way for me to feel more in control over my health. And so, it started really with an interest in the Paleo diet through some of the early thought leaders in that, who, I guess not early thought leaders but people who really brought it to the masses like Mark Sisson. And then I started to question why certain things were the way they were, like, “Why couldn’t I have dairy?” Or, you know, in some cases it was like, “Why could you eat sweet potatoes but not white potatoes?” A lot of them didn’t really make sense to me. I didn’t really like the naturalistic fallacy that if our ancestors didn’t have access to them then we shouldn’t eat them because they were interested in survival more so than optimal health.
But, anyway, so I just started looking into more of the research myself in my spare time during college, in my undergrad which was in accounting. And then when I graduated with my degree, I decided I wanted to pursue a career in something that wasn’t related to business because I really enjoyed nutritional science and being able to do something that had direct applicability to everyone’s life.
So, I went and got my master’s degree in that. And around the time I started the master’s program I was also hired by Examine to do some writing and research for them. And now I work for them as one of the main researchers as well as being part of the teaching staff at the University of Western States for their nutrition and functional medicine program. So, I really like what I do because I essentially get paid for doing what I would do if I was procrastinating in a real job anyway.
So, it works out really well and it also forces me to continue learning because I not only have to delve into countless different topics when researching things for Examine, but I get to experience a variety of viewpoints on various topics through interactions with other health professionals as well as students that might bring novel viewpoints to an issue.
Fat Cell Dysfunction – one of the most common nutritional causes of chronic conditions
Ari Whitten: Excellent. I love what you said a minute ago that you’ve kind of made a career out of, you know, getting paid to do something that you just love and would do if you just had free time and you weren’t getting paid to do it. I’m very much in the same boat, you know, this health and nutrition and lifestyle is something I’ve been studying since I was a 13-year-old kid. So, it’s very much something that I literally was doing for 15 years before I ever got paid to do it. So, I agree, it’s pretty cool to make a career out of something that’s just your true passion and your obsession.
Yeah. So, you have a pretty broad landscape of things that you are knowledgeable about with regards to nutrition, human health, exercise, things like that. I would love to kind of do a broad intro into your general paradigm around the connection of, you know, the majority of chronic disease that we’re experiencing, diseases of lifestyle, heart disease, most cancers, diabetes, obesity, insulin resistance, metabolic syndrome, and there’s a number of other things, neurological diseases. There’s a number of other things that you could sort of lump into that, and lifestyle and nutrition specifically.
I’m curious kind of how you conceptualize, in a 30,000-foot view, how you conceptualize the link there. What’s actually going on in terms of, you know, on a physiological level of how nutrition habits are causing some of these conditions?
Alex Leaf: Well, I guess if everything had to be summarized relatively shortly before I expand upon it, I would say that the central issue to most diet related chronic diseases that we see today such as diabetes and dyslipidemia and high blood pressure and all of those would be that there is an excess of energy in the body that is causing fat cell dysfunction. In more understandable terms you could think about it as everyone has their own personal fat threshold that’s determined by their genetics and environment and also possibly their diet and lifestyle. And when you exceed this fat threshold, that’s when you begin to see metabolic abnormalities occur like diabetes.
As long as you stay below that threshold, then you’re not going see those same abnormalities. And because this threshold is unique to every individual it can explain why we see certain diseases like diabetes pop up in people who are seemingly normal weight, others who are obese and why we see people with morbid obesity that don’t necessarily have very many metabolic abnormalities like elevated blood lipids and such.
So, this kind of breaks away from a traditional view point of obesity being a disease and being like the cause of many of the comorbidities that occur alongside it because it looks at obesity as a protective mechanism. If we back up and we look at evolutionary history, we’ve never before been in a position where we have access to as much food as we have today. And this is problematic because we’re designed to store excess energy in fat tissue so that we have it available for when there is a scarcity of energy later on since food was not a sure thing when we were evolving. So, our bodies developed a really, really nice system of storing excess energy primarily as fat and then pulling it out of the fat cells when we need to use it.
And this is, this can be captured a lot through what most people would understand as calories in, calories out. That idea is based upon the notion that if you eat more calories than you expend, then those extra will be stored as fat tissue. And if you expend more than you eat, then you’re going to pull on your fat tissue to supply the energy that your body needs and therefore you’ll lose fat mass. Now obviously it’s a lot more complicated than that, but I think that that simplified version sums up things somewhat adequately.
And so, when people chronically overeat as they may be doing today in the modern world, then they’re going to be continually filling up their fat cells. And this is perfectly healthy. In fact, this is what you want to happen when you overeat, you want your fat cells to soak up all of the extra energy so that’s not floating around in the blood because when you think about the causes of a lot of the end stage conditions of diseases like diabetes, they aren’t caused by excess energy intake or by fat mass per se.
They’re caused by things like chronically elevated blood glucose levels, chronically elevated blood insulin, chronically elevated blood lipids. These lead to things called gluco-toxicity and lipo-toxicity. And it damages organ tissues. It’s what causes the damage of nerve tissue, you know, peripheral neuropathy. It’s what causes damage to the pancreas that can lead to insulin dependent type two diabetes. It’s what causes a buildup of fat in the liver to cause nonalcoholic fatty liver disease, which if not dealt with, can lead to cirrhosis and liver failure kind of at the extreme end. The point being, it’s the excess energy in the form of glucose and fat in the blood that damages the body. It’s not anything that has to do with fat cells. And so, if your fat cells are able to scoop up that energy from the bloodstream, then you might be getting fatter or, well I should say you are getting fatter, but you’re also not damaging yourself.
It’s a protective mechanism. Fat cells are very benign, and they’re designed to soak up that energy.
So, as you approach your personal fat threshold, that essentially signifies the amount of energy that can be stored in your fat cells until they start saying, “No, we’re too full.” And so, it’s different between person to person. And as you soak up energy, you only have so many fat cells. And as each fat cell becomes more and more full, it needs to stop taking in energy because if it takes in too much energy, then that cell will become damaged and die and then it’s no good to anyone. You could think of the analogy being a balloon. A balloon will fill up with air, but once it gets to a certain point, you can’t put any more air into it or else the balloon’s going to pop and then you can’t hold any air.
And so that’s what happens with fat cells is they take up more and more energy until they can’t. And that’s your personal fat threshold. And so, they begin to develop insulin resistance so that they have, your body has a harder time getting energy inside the cell. And when that happens, then other fat cells will pick up the slack. But when you start to run out of fat cells, then that’s when you start to see energy accumulating in the blood. And we see that on laboratory tests as being elevated blood glucose levels or elevated fatty acids in the blood because that’s the excess energy that should be going in your fat cells but isn’t anymore because you’re near or past your personal fat threshold.
How physiological dysfunction can lead to heart disease or neurological disease
Ari Whitten: Excellent. So, I want to try and connect some dots here. And, you know, there’s a lot of nuances to this paradigm I want to delve into, but I think it’s clear based on what you’re describing, this connection between this whole process, everything you just went over and let’s say insulin resistance and diabetes. I think that link is very clear. Or even just the process of fat gain and becoming, you know, just carrying lots of excess body fat, being obese and that sort of thing.
What about the connection between what you’re talking about and let’s say neurological diseases like Alzheimer’s disease or the connection with atherosclerosis? Or you could, depending on your preference, you could potentially go into cancers here and the connection between that, you know, for example, insulin, there’s a connection between insulin resistance and excess body fat gain and various kinds of cancers. And numerous other chronic diseases you could mention here, but can you talk a bit about how this physiological dysfunction that you’re talking about connects to, for example, heart disease and neurological diseases?
Alex Leaf: Yeah. So, let’s start with heart disease. So well, first I should say that most diseases are going to be caused by numerous factors, right? You can’t just isolate any one thing, even the personal fat threshold, you can’t just isolate it and say that that’s the cause because there’s always going to be other factors involved. In the case of heart disease and other cardiovascular diseases we can see how having an excess amount of energy in the blood will influence your development of plaque and the risk of that plaque rupturing and causing thrombosis in the sense that when you have a lot of fat in the blood, then you’re going to have greater damage to blood vessel walls because you’re going to have all of this energy essentially hitting up against those walls. And you’re going to have the insulin resistant fat cells be secreting inflammatory molecules that also signal an inappropriate immune response that will damage blood vessel walls. If you have weaker blood vessel walls, then you’re going to have an easier time for lipoproteins, which are the molecules that carry fat and cholesterol through your blood, to penetrate the wall and become oxidized and go into a cascade that ultimately causes the formation and accumulation of plaque. I don’t know if you want to get into that, but…
Ari Whitten: Yeah, I do but let’s maybe come back to that because I first want to get into insulin resistance a little bit more deeply, but I’ll, I’ll let you kind of complete this thought on the other chronic diseases.
Alex Leaf: Okay. So basically, excess energy and the associated factors involved like low grade inflammation from the overfilled fat cells can damage blood vessel walls and make it easier for plaque to form. The excess energy in the blood itself will have some feedback loops with the liver that will cause an increased secretion of low-density lipoproteins in circulation, which means there’s a greater likelihood that they will become oxidized and therefore be involved in the plaque formation process. And this is one of the reasons why we see all of these markers improve, most of the time, when someone who has an excess of fat mass loses weight because the excess energy can now begin to be stored in the fat cells that are having their energy stores drained.
And it’s the same for neurological diseases. Your listeners might perhaps be familiar with the idea that Alzheimer’s disease, for example, has been called type three diabetes and it is, there’s some data suggesting that it’s an insulin resistance of the brain and the brain has a harder time using glucose as an energy source because of that insulin resistance. And also, there is low grade inflammation that contributes to the development and accumulation of amyloid beta plaques within the brain, which is combined with tau proteins is a significant part of how the Alzheimer’s pathology occurs.
And so if you’re having insulin resistance of the fat cells, you’re going to have excess energy in the blood, which means that your brain cells are going to be exposed to more of this energy, and in order to preserve themselves from that too much energy they have to make themselves insulin resistant so that less energy gets to them. And so, then you have a contributing factor towards neurological diseases. It’s the same for peripheral neurological diseases like I mentioned earlier with diabetic neuropathy. It’s because the excess energy damages the nerve tissue in the myelin sheaths, and it contributes to those issues.
Ari Whitten: And the capillaries like delivering blood flow to the various…
Alex Leaf: Yeah. The vascular damage, and that’s the same for the capillaries in the brain as well. That excess energy, it damages the vascular tissue and so you have less oxygen delivery and that can damage brain tissue.
How insulin resistance actually functions in the body
Ari Whitten: Excellent. So, there’s probably a sizable portion of listeners who are a little bit confused by one thing you’re talking about, which is conceptualizing insulin resistance as a function of sort of fat cell overload, chronic calorie over consumption. A lot of people out there are under the impression that insulin resistance and diabetes is high blood sugar as a result of eating sugar and carbohydrates and sort of… They’re operating under this idea that, “If I eat lots of sugar and lots of carbs, that’s what makes me insulin resistant, and that’s what, you know, gives me high blood sugar chronically. And that’s what gives me diabetes and that’s what also maybe causes Alzheimer’s.”
If you’re conceptualizing Alzheimer’s as type three diabetes. You’re presenting a different paradigm here which is conceptualizing the causes of insulin resistance in a very different way. And I want to just emphasize that distinction. I want you to go into that. And you’re also talking about insulin resistance as not just being a sort of pathology, as being a bad thing. Yes, it’s part of a pathology, but it’s also a protective mechanism. It’s sort of a body’s, the body is doing something intelligently to protect itself. So please just kind of emphasize that more so. I guess I’ll ask very directly, is the cause of insulin resistance people eating sugar and carbohydrates?
Alex Leaf: No. No, not at all. And I think that that idea is easily dismissed by some early research done by Dean Ornish and Walter Kempner, who used like 90 percent carbohydrate diets that were essentially vegan as well where they fed people literally pure cane sugar and like white rice…
Ari Whitten: The white rice diet.
Alex Leaf: And that was all they ate, and they lost a bunch of weight and resolved their diabetes. Certainly not a healthy diet, but it definitely disproves the myth that sugar and carbohydrates cause health problems. Now they can contribute, certainly, especially added sugars from things like soda pop. But I, you know, any diet can be followed in a healthy or unhealthy way and all the foods and macro nutrients can contribute to disease in one way or another depending on the individual. Perhaps not directly, but certainly indirectly by their effects on things like energy expenditure, appetite, you know, how they just make you feel, your overall wellbeing, which can have downstream impacts on eating behavior and your stress response which would then influence eating behavior potentially. So, you know, there’s many roads to Rome, but they certainly do not cause insulin resistance in and of themselves. They can contribute, yes.
Ari Whitten: So, let’s delve into that a bit more because there’s probably people who are now skeptical of you by saying that there is no connection. So, I want to be clear that you’re not saying there is zero connection, but there is maybe an indirect connection that we can draw through some of the factors that you just mentioned. But what essentially, let me sort of rephrase this, you’re saying that sugar and carbs, by eating sugar and carbs, that is not directly causing insulin resistance.
Alex Leaf: Yeah, correct.
Ari Whitten: But over time things like consumption of added refined sugars or refined carbohydrates can play into the food reward and palatability of the diet as well as modifying some of the other factors you just mentioned like appetite and hunger hormones that ultimately influence chronic calorie balance. And those things predispose to chronic calorie overconsumption, and that is a key driver of insulin resistance.
Alex Leaf: Yes, exactly. So very simplified example is that we know that when people drink soda pop, they don’t compensate for those calories as fully as they would if they ate a real meal, even when the macronutrients in the meal are matched. And so, people can drink soda and still, and that will ultimately increase energy intake which can slowly result in some fat gain over time.
Similarly, if we want to break it down on an individual level, you will find people who could drink a soda pop and maybe it gives them so much energy that they go and they burn, through being more active, they burn more energy than that soda provided, so it benefits them. Whereas other people, perhaps that actually reduces their desire to go out and be active. And so then even if they were to eat less to compensate for that soda, the amount of energy it provided, then they wouldn’t be as active. So, their energy expenditure would go down. So, they could still be in a surplus of energy that would cause fat gain. And so, a lot of it does depend on the individual. We can’t deny how certain things might impact one person differently from the other, that’s just a reality. But especially, to isolate out a macro nutrient or a nutrient in general as the cause of something is, in my opinion, very myopic and usually not supported by evidence.
The role of dietary fat in insulin resistance
Ari Whitten: With that in mind, I’ll also ask sort of the flip side of this. So, on one hand we have a lot of people in the low carb keto/Paleo worlds who are promoting an idea of sugar and refined carbohydrates, or carbohydrates in general in some cases, being sort of the direct cause of insulin resistance. Sometimes even people trying to promote it as the direct cause of fat gain and obesity, carbohydrate theory of obesity. That’s another sort of discussion but that also is a myth. On the flip side, there’s a lot of vegan diet gurus out there who are uniquely trying to put the blame on insulin resistance and fat gain on, oftentimes, animal saturated fats or saturated fats more broadly.
What is in your opinion, you know, we just addressed sugar and refined carbohydrates, but what is your take on the role of dietary fat and maybe animal fat in particular in the context of insulin resistance?
Alex Leaf: I think it’s equally flawed. You can’t just focus on a single nutrient. And I think a great example of this is if we look at the different effects of fat that comes from dairy products. So, there is a molecule that in dairy products will naturally surround the fat in dairy. It’s called the milk fat globule membrane and it basically turns all of the milk fat into little balls, little balls of fat. And this is present in raw dairy and it’s present in yogurt and cheese and heavy cream. But it is destroyed when milk is homogenized or when the milk is churned to form butter. And we see that when you consume pure fat, for example, when you consume otherwise identical macronutrients from butter as compared with cream or as compared with cheese, we see that they have different health effects. For example, saturated fat is probably best known for raising the level of LDL particles in your blood, and that effect does not appear to occur when the saturated fat comes from cheese or heavy cream, but it does occur when it comes from butter.
And mechanistic studies in animals have shown that an explanation for this discordance is potentially owed to the milk fat globule membrane, which will reduce fat and cholesterol absorption in the intestines and have increased excretion come out in your poop. And also, the milk fat globule membrane itself appears to be absorbed into circulation and bind certain receptors on various cells and tissues in the body to alter how they synthesize cholesterol.
So, in the liver’s case, they reduce cholesterol, they reduce the expression of genes involved in cholesterol synthesis within the liver, which means that you’re going to have less very low density lipoproteins and therefore low density lipoproteins secreted, which means that you’re going to not have that same blood lipid response that you get from butter. And that’s when macronutrients are otherwise identical. We also, now that isn’t to say that, you know, saturated fat is amazing and you should, you know, gorge on it. But it’s kind of, it’s just to prove the point that we shouldn’t focus on macro nutrients because the food supplying them as well as the dietary pattern in which those foods are consumed as well as the health status and preferences of the individual eating that diet are all going to influence how something affects their health.
Nutrition myths on heart disease
Ari Whitten: Yeah. Got you. I want to come back to heart disease now. There is another myth around heart disease, which is, you know, kind of… Well, I mean, I don’t want to say myth, but let’s say, you know, on the one hand we have sort of the conventional medical model of heart disease which largely revolves around, this is a much oversimplified version of it, but it’s certain blood lipid profiles, certain LDL numbers and LDL sub-fractions and lipoprotein sub-fractions and things like that, are directly influencing our cardiovascular risk of heart disease development, atherosclerosis.
And so, we need to modify the numbers of those particular molecules floating around in the blood. On the other hand, we have a lot of people in the low carb movement, the Paleo movements, the keto movement, things like that, basically trying to debunk that whole paradigm and say, none of that’s true. Your blood cholesterol numbers don’t matter. Cholesterol is actually a good thing. You should be eating lots and lots of saturated fat and good fats and things like that. And butter is not bad for you. And dietary cholesterol is not bad for you and all that sort of stuff. And basically, all those people have it wrong, and, you know, within conventional medicine. So, I’m curious what your take is on all of that landscape that exists there.
Alex Leaf: Oh, man. Okay, so heart disease…
Ari Whitten: And you can give like maybe a summarized version because I know this could be a two-hour discussion.
Alex Leaf: Yeah, definitely. So, the quick hit summary would be that heart disease isn’t owed to any one thing, right? There’re several factors involved when you look at the pathophysiology of how plaque forms. And the one thing we can say with absolute certainty that no one can disagree with is that the formation of plaque in the arterial walls requires inflammation and some level of damage to the artery walls. It also requires apoB carrying lipoproteins, which include VLDL, VLDL remnants, LDL particles, this includes both small and large. A lot of people will say that the size of LDL matters, and it doesn’t once you correct for the number of particles, LDL particles in the blood, size is not predictive of heart disease. And chylomicron remnants. So, to give a visual of this, chylomicron remnants are found in plaque beneath the arterial walls and it is 70 nanometers in diameter.
The large fluffy LDL that a lot of people say is protective is 30 nanometers, 30 to 40. And the small dense LDL that they, that does become oxidized and incorporated into the plaque more easily is 20 to 30. So, the size…
Ari Whitten: Just let me jump in because there’ll be some listeners, probably a large portion of listeners, who are not familiar with the jargon of those different terms. So, can you kind of summarize what, the point that you’re trying to make as far as why the size of those different components matters?
Alex Leaf: Yeah. So even the large LDL particles are still small enough to enter into the artery walls and form plaque. That’s the point. So, and when you look at studies evaluating the size of the particles, the size does not matter when the researchers take into account the number of LDL particles in their blood. Because that is the ultimate risk factor, is the number of particles in the blood. Why? When there are multiple causes of heart disease, why is that particle number so important? It’s because if you imagine a bunch of boats that are holding cargo in a lake, let’s say the cargo is the cholesterol content. If you have one boat with a ton of cargo, that’s like having a big puffy LDL particle, right? That’s one of those big fluffy LDLs that’s supposed to be protective. The chance of that boat, hitting the shoreline is very low regardless of its size. Now, if you have more and more boats in the water in the lake, more and more LDL particles, then the probability that one of them will hit the shore increases. It’s a pure numbers game. The more particles in your blood, the greater the likelihood that some of them will enter into the artery wall and will begin to be oxidized and become part of the plaque forming process.
Now, some people might say, “Well, that doesn’t matter because you have to have inflammation and the artery wall has to be damaged for them to be able to enter through.” And for the most part they are right. What they are overlooking is that everyone has inflammation and damage going on all the time, right? It’s, inflammation is a natural part of living, right? It’s an essential part of our immune function. And so that damage is occurring all the time and our body is just repairing it as normal as it can be. And so, there’s always going to be a chance for those LDL particles to enter in and cause the plaque forming process. You don’t need to have super high levels of inflammation for that to be a risk factor, although having higher levels certainly increases the risk because it’s like you would reduce the size of the lake, right? There is going to be more opportunities to hit the shore for that boat. Also, another overlooked factor is that having a ton of LDL particles in the blood themselves can damage the artery walls and can cause that inflammatory response in and of itself.
So, you know, to say that cholesterol is the only thing that matters is completely inaccurate. But to say that it doesn’t matter at all is equally inaccurate. And when you’re dealing with heart disease, you really need to look at the big picture of who this person is. You know, you need to see what their cholesterol levels are. What’s their HDL functionality? HDL being the “good cholesterol.” What is their level of insulin resistance, what is their level of inflammation? What does their diet look like? You know, if you have a super healthy athlete with higher levels of LDL particles in their blood, but they have, you know, very low biomarkers for systemic inflammation, they have very low biomarkers for insulin resistance, they’re athletic, they eat a healthy diet, however you want to classify that. Then is the high LDL a concern? Yeah. But is it something that actively needs to be intervened upon? I don’t know, you know, that’s something that person would have to work with their doctor for. But I don’t think we have enough data to suggest that that population would be at risk, certainly not at the risk we would see in the general population who had elevated LDL levels.
Ari Whitten: Excellent. So, I want to get into another topic of nutrition, which is protein. And this is, I think, it’s interesting in 2018, I think protein is still a pretty controversial topic, remarkably. And there’s so many different opinions out there on this. From the vegan diet gurus who are generally trying to sort of use arguments like, you know, we only need this much to reach protein sufficiency and, you know, maybe it’s 40 grams a day or 70 grams a day or something like that and, you know, anything beyond that is excessive and anything beyond that’s going to increase IGF-1 and going to increase, you know, cancer growth and mTOR activation and decrease longevity and these kinds of arguments.
On the other hand, I would say on the, maybe if we looked to a group of people that’s in that sort of very polar opposite camp, it would be this sort of fitness crowd and bodybuilding crowd that’s generally emphasizing very large amounts of protein for its emphasis on helping muscle growth, helping fat loss and generally optimizing body composition, which is the main concern there. And even there’s some interesting data around like older people eating more protein and sort of avoiding frailty and things like that. What is your general take on protein consumption in the context of longevity and disease prevention and what level of protein consumption do you feel is safe or unsafe?
Alex Leaf: So, my current position is that more is better based on the available evidence and inferences drawn from that evidence. So, starting on the disease front, we have a ton of solid data that suggests that eating higher protein diets can help people reduce their appetite, increase their energy expenditure, and ultimately aid in fat loss and more importantly, adhering to whatever diet they choose to follow. And this, when we come full circle back to the personal fat threshold, if they’re creating and sustaining that energy deficit by eating more protein, then they’re going to already resolve a lot of health issues as they return below their personal fat threshold and begin to restore metabolic normality in the body. And whatever level of protein intake that it takes to accomplish that is going to be what someone should aim for. Because when you are in a position where losing fat mass is going to improve your health that much, such as when you have obesity, then losing fat mass should be your number one priority because, I mean, obesity itself reduces lifespan.
So, if you restrict protein intake thinking you are going to extend your life, that extension is more than likely going to be offset by the fact that you are fat, you know, to kind of put it bluntly. So, returning your body to a healthy body composition with a normal amount of fat mass and a healthy amount of muscle mass, which protein is absolutely essential for gaining, is the number one priority of anyone who wants to optimize their longevity, quality of life and their overall health. So right on that I just said protein is essential for gaining muscle. Where the debate lies is how much. Where no debate lies is that the amount is greater than the current recommended daily intake of 0.8 grams of protein per kilogram of body weight. In fact, so more recent data suggests that everyone from a healthy 20-year-old adult up to a 65-year-old senior requires a minimum intake simply to satisfy their body requirements for protein of about 1.2 grams of protein per kilogram of body weight. And that’s a minimum and that’s when they are sedentary.
So those amounts obviously increase if you are more active, especially if you’re an athlete or someone engaging in weight lifting or resistance training because you’re going to be breaking down more of your muscle tissue and it requires that protein to be repaired. Those individuals, it’s generally recommended that they eat upwards of 2.2 grams of protein per kilogram of body weight. And for simplicity it’s one gram of protein per pound that you weigh. Now, there is much, much, much less data looking at intakes greater than that. It is suggestive of certain benefits with regard to regulating fat mass, but no benefits with regard to regulating muscle mass. For the most part, I think if people were to eat upwards of one gram of protein per pound of body weight, they would probably be better off. And that’s, of course, combining it with regular exercise, especially resistance training.
Ari Whitten: Got you. What does your general take on the…? There are some diet gurus out there who try to draw a link between either protein more broadly or specifically animal protein consumption, meat or red meat specifically, and cancer or sort of earlier death, you know, decreased longevity. What’s your general… Having explored the research on protein consumption and, you know, from many, many facets, very in depth, what’s your general take on that?
Alex Leaf: So, the only data that they draw upon to make those conclusions is either observational or studies conducted in animals. So observational data cannot be used to draw cause and effect relationships. But to entertain the observational data idea anyway…
Ari Whitten: And just real quick, for people not familiar with that term, just explain what observational data is and why it doesn’t imply causation.
Alex Leaf: Yeah. So, it would be like, let’s say I collected data on the entire US population about how long they lived. And then I collected data from little forms they had to fill out about their dietary habits. And then I tried to see if there was a connection between the two. I could do that, and I could see what’s called “an association” where possibly, “Oh look, people who eat more protein from animal products tend to die at a lower age than people who eat less protein from animal products.” Well, that’s great, but it doesn’t tell us if eating less protein was the actual cause of that earlier death. It just tells us that the two are linked. There could be countless other variables that are also linked to both of those outcomes that explain the relationship with no direct link between those two variables.
But we can’t account for everything because all we are doing is looking at a bunch of data and seeing if we can draw lines between it. Nonetheless, to entertain that idea of what I just said, when you look at observational data, you’ll also notice that only protein from animal products in the elderly is associated or linked to better quality of life, muscle function, physical function, and overall health status, even if it’s linked to a shorter lifespan. And so, you have to ask yourself, “Well, let’s assume there is a cause and effect relationship, would you rather live to be 70 but spend ages 50 to 70 not able to live on your own, being confined to a nursing home, you know, or a walker? Or would you rather live to be 65 and spend ages 50 to 65 being able to walk on your own, continue to drive a car, live in your own house and do whatever you want?” Right? We have to differentiate quality of life and what’s called health span from simply lifespan. Of course, you know, it’s up to everyone to determine what matters for them. Certainly, some people living as long as they possibly can might be the ultimate goal. And for them then by all means, do whatever you can to extend your lifespan. However, for most people I would venture to bet that they care more about the quality of their life more so than how long they live necessarily.
Ari Whitten: And you’re under the impression that there is a clear link between increased health span and functionality and animal protein consumption specifically?
Alex Leaf: No, no. I think that observational data shows a link and certainly animal protein is going to be the easiest way to obtain adequate overall protein intake that does lead to better physical function.
Ari Whitten: So, you’re saying like basically just if we’re leveling the playing field and we’re only arguing using observational data only, there is still an issue of, you know, kind of you’re seeing this trend in the elderly of increased health span or functionality associated with increased protein consumption in animal protein.
Alex Leaf: Yeah, exactly. Exactly. When we get down to it, what matters for the aging population is maintaining physical activity and specifically resistance training and then eating enough total protein to support that. And that protein can come from plants. Like you could eat an entirely plant diet and get as much protein as you need. It’s just you need to be a lot, you would need to put a lot more thought into it because plant proteins not only have a worse amino acid profile, but the protein within them is also less available to the body to be used. You’re going to end up pooping more of it out and so your actual protein intake would need to be a lot higher. And this could be circumvented by using vegan based protein powders which demonstrate the same digestibility as animal-based protein powders because they are so heavily processed. But, you know, a lot of people, especially in the general population aren’t going to be using those. And a lot of the people who form arguments against animal protein, like the vegans also tend to want to eat like a very pure diet and they might see protein powders as being un-pure or dirty. And so, they would avoid them.
Ari Whitten: Yeah, I’ve seen people kind of lump it into the same processed food umbrella…
Alex Leaf: Yeah, exactly.
Ari Whitten: Of donuts and soda and ice cream and pizza and things like that. I think that is a definite mistake of semantics because, you know, there’s actually really good data for a lot of protein powders showing that it is perfectly compatible with good health and even supportive of good health in many cases.
Alex Leaf: Oh, yeah. Especially with aging. One of the biggest issues you encounter with people as they get older is, they lose their appetite. It’s actually been termed in the literature as being called anorexia of aging. And I mean anyone who’s had to take care of their grandpa will know that, you know, they just start to eat less and less food. And that’s one of the reasons that you see muscle wasting in the elderly. And that’s an area where protein powders have significant benefits because, you know, when you combine a reduced appetite with trying to get someone to eat more protein, which is the most appetite suppressing macro nutrient, then you run into trouble. And it’s going to be a lot easier to get grandma to drink a protein shake than it is to get her to eat the equivalent amount of protein from steak or some other form of meat. It’s certainly going to be a lot easier than trying to get her to eat that amount of protein from something like legumes or grains which have even more volume that would need to be consumed to get that amount of protein.
Does protein cause cancer?
Ari Whitten: Yeah. I want to come back real quick to this animal protein link with longevity, disease, cancer. You mentioned kind of the, if you’re leveling the playing field and only using observational evidence, the sort of pros and cons versus lifespan versus health span and functionality. But irrespective of that, or maybe inclusive of that I should say, looking at that plus the other layers of evidence that we have from randomized controlled studies, animal studies, kind of the whole body of evidence, given whatever limitations still exist in that literature, what is your take on the link if there is any link between animal protein consumption or protein more broadly and cancer and longevity?
Alex Leaf: Yeah. So, the biggest limitation is that we don’t have any randomized controlled trials. We don’t have any human interventions for longevity. All the data that we do have comes primarily from worms and fruit flies and rodents, mice in particular. And there’s like literally only three studies, maybe four actually on monkeys. And that’s the data that’s being used to suggest that protein restriction extends lifespan. And that’s problematic for a number of reasons. For example, with mice, mice demonstrate a metabolic rate that is seven times greater than humans when we normalize it to how much the mice weighs relative to us. So, another way to think about it would be to say you burn 2000 calories per day. If you were a mice or a mouse, if you were a mouse then you would be burning 14,000 calories per day. And so, things that impact the generation of energy and the metabolism of muscle tissue are going to have a far more pronounced impact in mice than in humans.
And so, when you restrict protein in a mouse it’s just by nature going to impact their lifespan a lot more than it would a human because the body will begin to down regulate nonessential but health promoting functions like immune function and protein synthesis in order to conserve what protein is already on the animal itself. And so, by down regulating these processes you extend lifespan. You essentially conserve energy in the organism. But you’re going to, again, reduce certain things that, although they aren’t essential for survival, they might be essential for living the best life you can, like immune function and muscle protein synthesis and reproductive hormone secretions, sex drive. Because all those require that the body thinks there is a surplus of energy available. When you restrict protein, the body thinks you’re starving. And so, it’s going to say, “Nope, you cannot reproduce, you cannot build new tissue. We need to conserve what we have because we don’t know how long we’re going to need to hold out before food becomes available.” And even in mice, the data is contradictory. There was a wonderful study that took 14 different strains of mice and put them all on the same life extending diet, and it showed that there was a genetic component where over half of those strains of mice actually had a reduced lifespan on that diet. Whereas only a handful of the strains extended their lifespan. And so, a lot of the life extension research is conducted in the species of mouse that, where it has a known benefit, but there are some genetic species where it reduces lifespan. And so, you know, how would this play into humans? Certainly, I mean, you know, how would those interventions affect humans based on our genetics?
Ari Whitten: So, there’s a lot of limitations based on the current state of the literature and …[crosstalk]
Alex Leaf: To sum it up I would say that the available evidence does not make it appropriate to draw conclusions about how protein restriction would affect the lifespan of a human.
Ari Whitten: Got you. And you’re generally not super, you’re not overwhelmingly impressed with the observational evidence linking protein consumption or animal protein consumption.
Alex Leaf: No. So, if we, if I take a step back and summarize the big picture it’s this: It’s that… So, the currently available evidence for lifespan extension in humans from protein restriction is not convincing and it cannot be adequately applied to humans because it’s been done in other species that have notable limitations towards applying that information to humans. On the flip side, we do have an overwhelming amount of consistent data in humans that shows that eating more protein as we age benefits quality of life, and also theoretically benefits lifespan by reducing the risk of things like sarcopenia and frailty, which are currently the leading causes of death and hospitalizations in the elderly population. And so, I see no reason… I mean that isn’t to say someone needs to go and, you know, gorge on protein every day. That’s ridiculous. It’s just to say that they need to, they’re better off eating more protein than eating less. For the average elderly person, 1.2 grams of protein per kilogram of body weight as a minimum.
And I would say that, you know, they should be, depending on their activity level, they can eat upwards of 2.2 grams of protein per kilogram of body weight and they would be fine. There is not convincing data that those levels of protein intake have adverse events on longevity, health or other aspects of health, including the cancer stuff you mentioned. There is not any convincing data that protein itself causes cancer. Certainly, eating a bunch of protein can facilitate the growth of cancer once it’s been established in the body, but it won’t cause that cancer to be there to begin with. And there’s a lot of…
Ari Whitten: Probably what you were talking about before as far as chronic calorie over consumption and the state of insulin resistance and chronically high blood lipids and blood sugar probably could also accelerate the growth of cancer.
Alex Leaf: Yeah, and chronic inflammation. Oh, definitely. Yeah, definitely. Because you’re going to promote a very adverse environment for your cells. And it’s going to damage the DNA of the cells and potentially lead to their inappropriate growth and replication. And that’s what cancer is.
How the blood reacts to carbs and fats
Ari Whitten: Yeah. Got you. I have two more topics that I want to discuss. One very briefly, I just want to bring it up because you did a very nice article on the subject. And then I want to get into collagen and glycine because you’ve done some great work there as well. So, the first one is the topic of blood glycemic responses to mixes of carbs and fats. And, you know, there’s some interesting findings that you’ve written about there because, you know, there’s been an idea floating around for a while that, I think for maybe decades, that if you consume fat with carbohydrates that it sort of blunts the glycemic response and you don’t get as big of a surge in blood sugar or blood insulin and things like that. What did you find in the research that you looked at on this subject?
Alex Leaf: So, eating them together. So, when you eat meals that are high in both fat and carbohydrate, this includes if you’re an otherwise healthy person and the affects appear to be more pronounced in people with diabetes. But what occurs is, yes, the fat reduces the spike of the blood glucose. But it just prolongs the amount of time that your blood glucose will be elevated above fasting levels. If we think back to the chronic energy overload issue, what this means is that, or I should say what we know is that it’s having excess energy in the blood floating around, that’s what damages tissues and causes health problems. When you eat meals high in carbs and fats, ultimately, you’re going to have elevated blood glucose and insulin levels in the blood for a longer period of time compared to if you were to eat them separately. And this is problematic for the reasons we just discussed in theory. There is no data available that has actually tested how separating carbohydrates and fats within the meals you eat in a day impacts health. So, it’s pure speculation on my part
Ari Whitten: Right. And it’s not necessarily black or white. Like you’re not, it’s not saying you have to have a meal that is 100 percent let’s say protein and carbs or protein and fat with no carbs. It’s just a matter of like you would… Basically the speculation is sort of if you minimize fat in a meal that has lots of carbs or vice versa, you minimize carbs in a meal that has lots of fat, that could be better off.
Alex Leaf: Correct. Yeah. So, there’s only a few thresholds that have been investigated in the research. One of them is the type of carb. So, these effects are seen regardless of whether you eat processed grains, cooked potatoes, cooked beans or fruit. But the effects aren’t seen when you eat a ton of fibrous vegetables. So, things like lettuce or broccoli, cauliflower, asparagus, Brussel sprouts, cabbage, etc. So, if you’re going to eat a bunch of fat, you can still eat a ton of vegetables with it. Just don’t like put butter on your potato. The other threshold is the amount of fat. So, I did say, you know, don’t put butter on your potato. But the reality is that if you’re eating a bunch of carbs, like a big pasta dinner, the goal would be to keep your fat intake beneath about 15 to 20 grams. And that’s actually quite a bit, or at least you know, it is in theory because you don’t need to cook a lot of those starchy meals with any fat added. But if you’re eating out a lot, places will. Why? Because fat makes food taste better and so you enjoy it more. And that’s kind of another issue about combining them is, especially if you’re dieting, combining fat and carbohydrates is going to make the food more palatable and there’s a greater likelihood that you’ll eat more and therefore, especially if you’re not diligently tracking your food intake, then there’s a likelihood that you might non-consciously be eating more food than you anticipated and more energy and therefore could sabotage your dieting efforts.
The effects of collagen and glycine on your body
Ari Whitten: Excellent. So, the last topic that I want to cover is glycine and collagen. You’ve post, I’ve seen you do a number of posts on this subject and post some interesting research on this. Can you give… And this is actually I would say unique in the sense that it’s not typical to find somebody who is more in the sort of fitness, you know, evidence-based fitness and nutrition circles, sort of bodybuilding circles, which I know you are. Also, you know, you’re in some more broad health circles as well. But I’d say your kind of more solidly towards the evidence-based fitness and nutrition folks. It’s not common for those folks to be talking about collagen and glycine. It’s more common for the sort of Paleo ancestral crowds to be talking about it. So, you’re kind of unique in that you’re talking about this subject. What is your general take on why you think consuming collagen and consuming glycine is so important?
Alex Leaf: Okay, so collagen. Collagen I would say is the most important because collagen is the main dietary source of glycine. So, I’ll mention that again when I talk about glycine, because you can just consume collagen to obtain that glycine. But collagen itself is something important to consume for, I would argue, overall health because we know that collagen molecules are absorbed intact in the body and they stimulate the synthesis of collagen within the body. Certain collagen molecules are even directly incorporated into joint tissue to facilitate the development of new cartilage in those joint cavities. And so, we do have data in humans showing that things like hydrolyzed collagen and even just plain old gelatin, those are the same things by the way. It’s just hydrolyzed collagen is gelatin that’s been broken down a little more so that it dissolves in cold liquids as well as hot.
Anyway, so we do have human data showing that it can benefit osteoarthritis, which is basic wear and tear of the joints and it can benefit collagen synthesis in athletes. One particular study showing that taking 15 grams of collagen before doing some jump rope exercises increased collagen synthesis in the body. And when we consider that collagen is the most abundant protein in your body that plays an essential role in bone health, joint health, skin health, fingernail health, you know, it’s really easy to see why supporting optimal collagen synthesis is going to be important. It’ll make you feel better, perform better in theory and look younger, right? I think that the esthetics department is probably the most researched area with collagen where we have a lot of data that taking collagen supplements will improve hydration levels in the skin. It will reduce skin damage from sun exposure, and it will contribute to skin turnover and a younger appearance. And that’s been shown many times across several randomized controlled trials.
And the other reason that taking collagen is important is because it supplies glycine and glycine is a traditionally non-essential amino acid that your body should be able to make enough of. But, in theory, when you look at the pathways that the body can use to make glycine, it comes up a little short running a glycine deficit of about 10 grams per day depending on how much protein you eat. For the average adult it’s about 10 grams per day. And without glycine you can’t make adequate collagen. And, you also can’t perform other important functions like methylation reactions in the body that are involved in liver health. The synthesis of glutathione, which is one of your body’s most important antioxidant molecules, relies on having adequate glycine. And in fact, glutathione synthesis is one of the biomarkers used to test for glycine insufficiency because if you’re not consuming enough glycine and then you’ll start to pee out a marker, a biomarker that forms when the intermediates of glutathione synthesis accumulate. And when you supplement glycine, then that marker goes down because those intermediates are able to attach to the glycine molecule, which is the final step for creating glutathione.
Ari Whitten: Excellent. Very good stuff. One thing that you mentioned there that, the last I checked the literature I had not seen this, was that collagen molecules can get absorbed intact. I remember seeing arguments from people saying, “Hey, there’s no reason to think that collagen should support collagen synthesis directly in our bodies, or that collagen, you know, by consuming collagen it would build up collagen in the tissues, cartilage and things like that because it’s getting enzymatically digested into its sort of amino acids and so there is no real reason to think by consuming collagen it supports collagen directly.” But you’re saying that’s not accurate.
Alex Leaf: Yeah, that’s completely false. We have data that definitely shows that collagen peptides are absorbed intact. And that when we even attach radioactive isotopes to them so we can follow their location through the body, it shows that once they’re absorbed a lot of them will enter circulation and go straight to joint tissue where they get incorporated into the joint tissue and stimulate the synthesis of collagen within the joints and cartilage.
Ari Whitten: And now you have radioactive cartilage.
Alex Leaf: Yeah, exactly.
Ari Whitten: Nice. That’s very cool. I was unaware of that.
Alex Leaf: I don’t know if you put show notes beneath your thing, but I can send you over the studies for that.
Ari Whitten: I do. Yeah, I would love that actually. It’s great to see that. I think even just as recently as maybe two years ago, I remember seeing someone sort of post something, maybe it was Adel Moussa at SuppVersity talking about like somebody putting forth an argument of why taking collagen shouldn’t directly sort of support cartilage production or collagen synthesis in the body. But that’s, but then you blend that with the studies that had already existed, for example, Rodin’s showing that it does support collagen production, does support cartilage synthesis and things like that. So, it was hard to make sense of that sort of literature that seemed conflicting and this absolutely makes sense of it now.
Alex Leaf: Yeah. So, I mean, just as a general rule of thumb, a lot of people will make that argument in general about how, you know, your digestive tract just breaks everything down anyway. And so, it doesn’t matter what is the source of the protein that you’re eating. But that’s not completely true. There’s always going to be some little like protein peptides, like little protein fragments that are not fully broken down into the amino acids and those are absorbed intact. And it’s these molecules that have bioactive activity in the body and cause a lot of the health benefits that we associate with eating certain things. Like whey protein, for example, supports glutathione synthesis in the body because it’s rich in glutamil cysteine residues that are absorbed intact.
Ari Whitten: Yeah. Interesting. On this note, I have one sort of last side note of question, which is there are some people who make an argument that taking single amino acids has unique metabolic effects. For example, we could mention glycine in this context, like taking a glycine only supplement as opposed to collagen. Based on the research that you’ve seen, do you think there’s any reason to suspect that taking glycine by itself would have superior affects in any way to taking collagen?
Alex Leaf: I wouldn’t say superior. I mean, you’re going to miss out on a lot of the benefits from those collagen peptides, like increased collagen synthesis. Certainly, consuming glycine would support glycine requirements. But, you know, I think that it would be better to get it from collagen because of the added benefits.
Ari Whitten: Sort of the same argument around like branched chain amino acids. Should you take branched chain amino acids or essential amino acid supplements with these free form amino acids versus, you know, let’s say whey protein or other whole food protein sources.
Alex Leaf: Yeah. So, the benefits of like BCAAs and EAAs compared to whey protein for example, they don’t pan out. Whey protein is a more powerful stimulator of muscle protein synthesis and it also supplies an array of amino acids that help kind of balance things out. As one example, taking a bunch of branched chain amino acids can mess with neurotransmitter synthesis, specifically serotonin in the brain because they will compete with tryptophan uptake through the blood brain barrier. You don’t see this with whey protein because it supplies tryptophan and so there is no excessive competition there. But if you just take pure amino acid supplements, you disrupt that natural balance and you can contribute to, if you’re susceptible to it, you can contribute to certain things like depression and such.
Ari Whitten: Excellent. I want to wrap up maybe with a couple quick, very practical tips if you have, and you can keep this very short and to the point because I appreciate you’ve kind of spent an extra bit of chunk of time with me. But we’ve spent a lot of time debunking myths here and kind of going into nuances of how certain nutrients affect us. On a very just sort of practical level based on all the research you’ve done, if you could give let’s say two, maybe three things if you want, but two very quick practical tips of where you would recommend people focus their energy and attention if they’re interested in eating better to improve their health, their energy, their longevity, and avoid disease. What would be those top two or three things that you would suggest they focus on?
Alex Leaf: Okay, I’m going to make it three things and they’re all related. So, the number one thing for people who want to optimize their health, longevity and quality of life would be to eat a diet that allows them to obtain a healthy body composition where they remain below their personal fat threshold and maintain ample amounts of muscle mass. This doesn’t mean you need to be lean like enough to have a six pack or whatever. It just means that, you know, you don’t want to be walking around with a gut. The second thing which can facilitate that goal would be to eat adequate protein because protein will help with appetite regulation and, therefore fat loss, as well as it’s the only nutrient that can support the growth of muscle tissue. The growth and maintenance of skeletal muscle tissue. So, to say it for a last time, that amount, depending on activity levels and preference should be between 1.2 and 2.2 grams of protein per kilogram of body weight. That is roughly translated to about one half to one grams of protein per pound of body weight. And the third thing would be to supplement with some collagen in the form of hydrolyzed collagen or gelatin in the amounts of 10 to 30 grams per day to supply glycine and also facilitate the turnover of collagen tissue in the body.
Ari Whitten: Excellent. Well, Alex, this was awesome. I really appreciate having you on the show and appreciate the extra time you spent with me. We covered a huge range of myths and cutting through a lot of the myths of different dietary camps out there and bringing some nuance to this discussion. I really appreciate your time. Where can people find more about your work and follow you?
Alex Leaf: So, people can follow me and find out about my work at my website, which is going to be my name dot com. So alexleaf.com. They can also follow me and my colleagues at Examine.com for staying up to date on the latest nutrition supplementation research. And they can find me on Facebook.
Ari Whitten: Awesome. Well thanks so much Alex. Appreciate it and have a wonderful rest of your day.
Alex Leaf: Thanks Ari. This was a lot of fun.
Debunking Nutrition Myths on Protein, Insulin Resistance, Fat Gain and More with Researcher Alex Leaf – Show Notes
Fat Cell Dysfunction – one of the most common nutritional causes of chronic conditions (6:19)
How physiological dysfunction can lead to heart disease or neurological disease (15:45)
How insulin resistance actually functions in the body (22:09)
The role of dietary fat in insulin resistance (28:00)
Nutrition myths on heart disease (33:00)
Does protein cause cancer? (55:27)
How the blood reacts to carbs and fats (1:03:22)
The effects of collagen and glycine on your body (1:08:05)
If you want to learn more about the work Alex does, go visit his website.
Studies mentioned in the podcast
You can learn more about the studies on collagen here:
Consuming hydrolyzed collagen leads to the appearance of food-derived collagen peptides in the blood, meaning that our digestive system does not simply break down the collagen we eat into its constituent amino acids.
Moreover, animal research shows that these dietary peptides are incorporated into bodily cartilage, which is further supported by a controlled trial showing that consuming gelatin increases rates of collagen synthesis in healthy adults.
Collagen proteins are an essential component of joint cartilage. Joint pain can occur for a variety of reasons, but the most common are simple wear-and-tear (e.g., osteoarthritis) and the more complicated immune-mediated breakdown (e.g., rheumatoid arthritis). Several small controlled trials have shown that supplementation with undenatured type-II collagen is able to significantly improve joint pain among people with osteoarthritis and rheumatoid arthritis. Similarly, hydrolyzed collagen has some evidence supporting its use among people with joint pain from osteoarthritis.
The biological mechanisms explaining the benefits of collagen supplementation on joint pain are not fully understood. Animal research suggests that benefits may be mediated by reductions in several pro-inflammatory molecules and a reduction in cartilage breakdown. This in turn may be owed to the ability of type-II collagen to attract beneficial immune cells to the site of the afflicted joint. Another possibility is that dietary collagen supplies the necessary precursors for the synthesis and repair of connective tissue throughout the body.