There is absolutely no evidence to suggest that you can kind of choose the way you get fat. Like that's quite frankly ridiculous. This is the problem with people who pick out mechanistic data and use this to drive a narrative. You can literally find a mechanism for anything to prove whatever you want, because mechanisms are only small parts of the story. The summation of all the mechanisms is shows up as human outcome data.
Welcome to The Proof Podcast, a space for science-based conversation exploring the health and longevity benefits that come with mastering nutrition, physical exercise, mindfulness, recovery, sleep and alignment. Facts, nuance and trustworthy recommendations minus the hyperbole. Hi friends, great to be here with you. I'm your host Simon Hill, I'm a qualified physiotherapist and nutritionist with an undergraduate science degree and a master's in the science of human nutrition.
Welcome to the very first, quickie episode, a shorter bite-sized version of the proof where we tackle one single topic in around 20 minutes or less. Today I sit down with Lane Norton PhD to talk about some recent claims made online by Ben Bigman PhD about insulin and seed oils. Bigmen, a low carbohydrate diet advocate, took to social media to tell people that both insulin and seed oils cause our fat cells to increase in size.
As you're hearing this conversation, the more technical term for referring to a fat cell that increases in size is our dipesite hypertrophy, a dipesite being a fat cell and hypertrophy meaning to grow in size. The specific claim Bigmen made was keep insulin low and control seed oils and fat cells can stay smaller and healthier. This sounds amazing, adopt a low carb diet, keep insulin low and avoid seed oils and we could cure metabolic disease and obesity.
But is this really an accurate reflection of where the evidence lies? Following several people in the community sending me this post, I reached out to Lane Norton, friend of the pod, to help us go through the claims and clear any confusion. Please enjoy, this is me and Lane Norton. Hey Lane, welcome to the quick version of this show. Thank you so much for joining me. Thanks Simon, appreciate you having me.
So let's dive straight into things here. I recently saw a little bit of a back and forth on Twitter between you and Dr. Ben Bigmen, who is a professor and biomedical scientist I believe. And he seems to be interested in metabolic health and is a big proponent from what I can see of low carb diets. He has quite a large following online and I did a little bit of research and it seems that the two of you have had some dialogue previously where you have kind of disagreed on a few things.
And I couldn't find anything where or anywhere where the two of you had had a verbal conversation about this. So I invited both of you on. You said yes, he didn't reply. So here we are. Let's start with the most recent claims that Bigmen made and here's a direct quote lane. Keep insulin low and control seed oils and fat cells can stay smaller and healthier. Keep the insulin low and control the seed oils and fat cells can stay smaller and healthier.
Give me a very quick soundbite. What's your initial reaction to that? This is like two truths in a lie or sorry a truth in two lies basically. So he said you know small antipocytes are still metabolic healthy. So you're better off at the same fat mass and I don't want to I'm probably going to get the quote exactly right. But at the same fat mass you're better off having more smaller fat cells and you are smaller number of large fat cells and two things control that.
Literally a gas which is from seed oils and insulin. There are two variables chronically elevated insulin and linoleic acid the primary polyensaturated fat from seed oils. Both of these molecules through two totally different mechanisms will push fat cells to go from hyperplasia which is small but more abundant to few and large. Now I couldn't really find much evidence other than some really weak mechanistic evidence on linoleic acid.
And as far as insulin goes. Yeah it's well known that insulin can drive free fatty acids into antipocytes. However we're all I'll discuss why that doesn't really matter outside the context of energy balance. What I found really disingenuous about what he was saying is he's speaking as if if you're going to gain fat you're better off having hyperplasia than hypertrophy. Right. Okay. There is absolutely no first off we don't even know if hyperplasia happens in adult humans.
We suspect that it may in very obese people and possibly even people who go through periods of yo-yo dieting but there's like the idea that you can control whether or not you have hypertrophy versus hyperplasia. There is absolutely no evidence to suggest that you can kind of choose the way you get fat like that's quite frankly ridiculous. And as far as the whole you know insulin goes it this is the problem with people who pick out mechanistic data and use this to drive a narrative.
You can literally find a mechanism for anything to prove whatever you want because mechanisms are only small parts of the story. The summation of all the mechanisms is shows up as human outcome data so let's just look at the human outcome data because we have trials where they equate calories and protein and very the amount of carbohydrate and fat.
And very conclusively show that there's no difference in fat loss or fat gain from over feeding or under feeding carbohydrate versus fat so who cares about like one mechanism out of thousands. Right. So just to kind of clarify this for listeners who may not have seen the different claims that he was making in that tweet. So there's two parts. The first part as you summarized is that he's essentially saying that we can select between hyperplasia and hypertrophy.
You're saying that that's not true. The second claim he's saying is that in order to sort of avoid this hypertrophy and to promote hyperplasia instead we would want to reduce our exposure to insulin or to two compounds. One is insulin and the second is linoleic acid which is often said in the same sentence as seed oils even though it is found in other foods as well. So with regards, I understand what you're saying there about hyperplasia and hypertrophy.
With regards to that second claim to do with those two compounds, he says both of these molecules push fat cells to go from hyperplasia to hypertrophy. So what evidence have you seen that he's using to make that claim because that's a particularly strong claim to be making. Basically, the evidence he's using is in vitro cell line data and maybe some rodent data but no human data whatsoever.
The idea that linoleic acid is doing this, I mean if that were true, we could just go look and see populations that eat high amounts of linoleic acid and the research says if anything they're actually leaner. So it just doesn't hold up when you actually look at the actual outcome data. Now I'm not saying people should go out and pound down linoleic acid because I know people are going to straw man me.
The other thing I'll say is he seems to understand antiposal or antipocyte biology somewhat well but he completely neglects other portions of it. For example, like this idea that hyperplasia is better, if you create more fat cells, most of the research we have suggests that your kind of body fat settling point is determined by fat cell size.
And if you create, let's say that you could create more fat cells, the research actually suggests that you would continue to gain fat or because small fat cells secrete less leptin. And so your body would actually still sense some sort of quote unquote deficit.
So when we see this in animal models where they increase the number of fat cells, they tend to continue to gain fat until each cell, until the average diameter of each cell is about 100 microns, which is kind of like where things like to sit in these animals. So can you just explain that to me again. So when you have a larger number of fewer fat cells, do you say you get less leptin?
Yeah, so the research suggests that a lot of the secretion of leptin is driven by the fat cell size. So larger fat cells secrete more leptin. And the downside to that is you tend to become less leptin sensitive. It really, I don't want to make too big of a claim about leptin because it tends to be something that's responsive rather than driving these responses.
So, but the research that I've seen even in rodents demonstrates that if you add more fat cells, if you increase the fat cell number, again, there's a study by McLean where they kind of took rats through basically a yo-yo dieting cycle. And actually we're able to show fat cell hyperplasia. What's interesting is those animals did not return to their previous, so they had them diet down, they lost certain amount of their body weight, and then they kind of let them add leptin feed.
And so they gained weight very quickly and actually induced fat cell hyperplasia. Now I'm not saying that this happens in humans because there's no evidence it happens in humans in this condition. But when they, before weight loss, pre-weight loss, their adipocytes were right about 100 microns in diameter. And then when they were finished with weight loss, it was like 85 microns in diameter.
And then they added more fat cells. What's really interesting is they did not stop regaining weight until their average fat cell diameter returned to the pre-diet levels. Only now since they had more fat cells, the overall fat mass was greater. So it really suggests that your body kind of likes this, has a, I don't know, generalized too much, but has kind of a native size of your fat cells that likes to maintain.
And part of that may be driven by fat adipocytes don't just like float around in your body, they're scaffolded onto like an extra set of our matrix. And when you lose weight or gain weight, if it gets too much, or too, sorry, if you lose too much or you gain too much, it actually places a stress on this matrix that tends to drive you back towards what your originally were in terms of like, in effects different hormonal pathways,
left in and so on and so forth. So your appetite goes up or down in response. Now humans, because of the hyperbound will nature of our environment can sometimes eat themselves past that. But it's just again, I'm pointing out a mechanism, but the reason I'm pointing it out is because it just goes to show like I can find a mechanism to support my what I'm claiming too, right?
Only the only difference is I'm not making a strong claim. I'm just saying there's no research to back up the direct claim that he's making. And what would it take? So if there was research to support his claim, looking at human health outcomes, what would that study look like?
So really what you would have to do is you'd probably be looking, I mean, ideally, you'd kind of have a control group and then four different groups. You'd have low seat oil, low low low little egg acid, low insulin, or sorry, low carbohydrate, high little egg acid, high carbohydrate, low little egg acid, high carbohydrate, and then high little egg acid, low carbohydrate.
So you're kind of spanning that bridge. And then based on what he's saying, if you did this, you know, over, I don't know, six months, something like that, and you took a fat cell biopsy of a certain area of fat cells, what are certain, like if you took out a certain, like grandma, like X size, let's say 100 grams of adipose tissue.
What you should see, according to him, is it in the high insulin, high little egg acid group, you would have more fat cells in that, in that 100 grams of fat mass, and they would be smaller in diameter, then say the other group, which should be more hypertrophied. But that study to my knowledge does not exist.
Does that even really matter, Lane, like, I realize like a study like diet fits, for example, like compared to lower carbohydrate diet to a higher carbohydrate diet over the 12 months, the average weight loss was not significantly different between the two groups. Is that enough information for us, or do you feel like we have to go to that extra layer, that extra level deeper to look at fat cells? Is it actually important?
Again, you really pointed out the most pertinent point, which is, who cares? We have the human outcome data. We have over 20 studies looking at comparing low carb versus high carb and everything in between with calories and protein equated. If what these guys are saying is true, you would think you would see big differences in fat loss or fat gain. You just don't. There's no difference. It's pretty darn clear.
Again, if you look at the markers of metabolic health, even in diet fits, that's not really different. It seems to be mostly, and I don't want to say exclusively because that's not true. There may be some unique benefits of low carb on, say, HBA1C, and there may be some unique benefits of low fat on LDL cholesterol.
But they're pretty modest in comparison to the weight loss itself. So really, like what you just said, all this is doing this information, is just confusing people to focus on the wrong things. Which brings me to some of the last questions I have here. Why is this problematic? You spend an enormous amount of time going through this information, addressing it, and you might put up a 60 second or a two minute video, but it takes a lot longer than that.
So a lot of these days, I thought it would shorten it. This is about exercise that we've shown, because nobody helped us to get underway, using food. We're still really getting thinking about what, what is going on here, what is your Şepor and what is going to do with that? Thank you, Dr. look at the overall totality of the evidence and then create that content.
What's the impact that this information could have on someone if they just take it at face value because someone might be thinking in well and someone might be listening and thinking, well, Lane, really, he's just telling people to avoid ultra-process foods and seed oils. Is it really that bad? Yeah, great question. And what I always say is misinformation always has unintended consequences even if the intentions are good.
So I don't really care about people's intentions because Hitler had good intentions. You know, like, I realize this is a non-equivalence fallacy, but the point is nobody believes they're doing the wrong thing. Very few people do the wrong thing and say, I know I'm doing the wrong thing. They twist it around in their mind is how it's the right thing. Now in this case, I think the problem is you create this fear around these foods and again, you get people focusing on the wrong things.
You know that, well, I'm not going to have seed oils, but you know butter and bacon and a bunch of saturated fat is fine. And I don't have to worry about calories because it's all about insulin and you get, I mean, I'm not sure if you're familiar with Ethan Sucly, but he's a Hollywood actor who lost over 300 pounds and he'd been on every different diet. And he said, you know, I went down the low carb rabbit hole and I got stuck and couldn't lose weight.
And I thought it was the veggies in my salad that were keeping me from losing weight. And looking back, I feel like such a moron because it was all the oil and butter and bacon that I was having that was stopping me from losing fat because I was over consuming calories. And so I really, I try to emphasize, hey, every different approach works. Like you don't, like these people who are so dogmatic about this is the only way they can work. I'm like, do you have eyes?
Because like you can just go look at other people who have lost weight from every different methodology out there, you know? And so what that says is everything works, but it's important for us to be honest about why it works. Otherwise, people start making these weird associations in their heads. And I see the downstream effects of that largely in just kind of disordered eating patterns. I realize that's not really a popular thing to talk about, but I mean, I work with a lot of people.
I have worked with a lot of people over the course of my career. My wife's worked with a lot of people over the course of her career. And I mean, maybe they wouldn't be diagnosed like a, like a, like a DSM, but I would say that they were, you know, had some kind of form, like 50% of them probably had some form of disordered eating or disordered eating habits. And a lot of it was based around misinformation that they had heard and they'd formed weird associations with food in their mind.
I'll never forget. I had somebody who was convinced that gluten made them fat. And then I always say, well, I'll fight you to a bunch of gluten. I gain, I always gain weight. And like, well, when do you, when do you typically gluten? And it's, it'd be like, well, you know, last week I, I caved on my diet and I ate a pizza and I'm like, so you ate the whole pizza and you were surprised that you didn't feel good afterwards and that you gained weight.
Do you think it was the gluten or do you think it was, you know, the, the 2000 calories in the pizza? And so I said, you know, here, do me a favor. I like have two slices of bread tonight before you go to bed. Let me know if, you know, if you have a response. And I said, like, oh my gosh, I'm not gluten tolerant. I'm like, yeah, no kidding, you know, so it's like people can draw these weird associations in their mind if, you know, we're not careful about how we present the information.
Right. Yeah. It's the, the old case of the absolute selling and the oversimplified message sometimes, sometimes I kind of understand where people are coming from because I think they think if they speak with a lot of nuance, then it's too hard for someone to sort of grab a hold of. But then the flip side of that is an oversimplified message as you say, which is then conflicting with the next oversimplified message, which conflicts with the next one.
And, you know, people just end up not knowing who to trust or believe. So back to, back to Bigmen here. What do you think the primary motive is behind his position, that insulin and little egg acid are uniquely a problem? Do you think that as a scientist, he genuinely believes that position or is he sort of trying to find mechanistic evidence to support a diet of choice that may have worked for him and work for people in his community? Both things can be true.
So I would, I would, I've kind of, kind of changed my tune over the years, which I used to think like the people that did this sort of stuff, that they were all just money hungry and this was a pl- you know, this was a way for them to make money. But what you realize is not everybody's motivated by money necessarily. For some people, they, you know, it's a fame thing or like just the positive feedback they receive from that community.
Because I mean, you probably know this, like if you're kind of in the extreme plant-based community, if you pander to that audience, and that's most of your audience, I mean, you get a lot of really positive feedback, you know what I mean? And so that's very motivating for some people. When you sit in the middle, is when you tend to get a lot of the criticism, you know? So I think, you know, it's impossible for me to know what kind of his motivations are.
I would suspect, because I've been guilty of cognitive dissonance before when I was younger. And a lot of it was driven by just what you said. I found something that kind of worked for me, and just assumed that that would work for everybody else. And then I've just kind of started retroactively trying to find, you know, the studies that confirmed what I already believed to be true, and we, that's called confirmation bias. And that's how most people go about it.
It's they form a belief based on their own personal experience. And then they look for the science to support that. And what I'll always say is, if you're so positive about it, why do you even need science to support it? If you liked it and it worked for you, what's, why do you feel the need to prove that it's the best thing since sliced bread? You know it works for you. Fantastic. But just don't assume it's going to work for everybody else.
And I'm not saying, you know, people say all this worked for me or that didn't work for me. And they think physiological and really want to boils down to and we know this from the data very clearly. It's an adherence thing. They just found a diet that quote unquote felt easy to them. I had a conversation with Christopher Gardner about diet fits. And that seemed to be where he was leaning as well.
Like they looked at genetics, they looked at insulin resistance to see if any of that could explain why did someone do better on low carb or high carb and as a team, they were left thinking this is likely behavior or you know at home. Why could someone at home do well on a low carb diet or maybe their family didn't give them a hard time about it and other people in the family were eating like that and it was accepted in their friendship group, et cetera, et cetera.
So I think that's a great point. Lane, thank you so much for doing this. I think I might have to get you back on next time to chat about fructose. Yeah. And metabolic health. Fantastic. We'll schedule you back in. Sounds great Simon. Thank you for having me. Thank you for joining me for this episode and your interest in science based conversation. I hope you enjoyed it and found the information covered, interesting and instructive.
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