So to me, the best use of this self discipline in a syringe is to look at it as a temporary enhancement to overcome addictions rather than this is your new normal and you're going to be drugged for life.

Welcome to the Metabolic Mind Podcast.

I'm your host, Dr. Bret Scher.

Metabolic Mind is a nonprofit initiative of Bouzouki Group where we're providing information about the intersection of metabolic health and mental health and metabolic therapies such as nutritional ketosis as therapies for mental illness.

Thank you for joining us.

Although our podcast is for informational purposes only and we aren't giving medical advice, we hope you will learn from our content and it will help facilitate discussions with your healthcare providers to see if you could benefit from exploring the connection between metabolic and mental health.

What if we're using GLP1 medications all wrong?

Look, the GLP1 medications, WeGovy, Manjaro, Ozempic, they are revolutionizing the medical profession of weight loss.

Right?

Like the medical weight loss is beyond anything we've ever seen.

But what if we're using them incorrectly?

What if to get optimal metabolic health and long term safety and long term weight loss, there was a better way to use them?

I'm joined today by Dr. Ben Bickman, who's a professor and researcher at BYU and and he specializes in insulin and metabolic health and he has a really interesting theory about using these medications as microdoses to help curb cravings for carbohydrates, which will then allow a transition to a healthy low carb diet to allow for longer term success with weight loss, but more importantly, improved metabolic health with very low risk for any side effects and lower cost.

Sounds intriguing.

Let's get into the details with Professor Ben Bickman.

Many of the interventions we discuss can have potentially dangerous effects if done without proper supervision.

Consult your healthcare provider before changing your lifestyle or medications.

In addition, it's important to note that.

People may respond differently to ketosis and.

There isn't one recognized universal response.

Well Ben, welcome back to Metabolic Mind.

It's great to see you again.

Yeah.

Hey Brett, glad to connect with you.

Yeah, I enjoy every opportunity to sit down and chat with you.

We had a great interview a while back here on Metabolic Mind, which I highly recommend people check out.

But I reached out to you to circle back and talk to you again because of this really interesting article you wrote, this op ed about the use of GLP1s, sort of microdosing to address cravings.

So I want to get into all that.

But before we get into the details tell us a little bit about, you know, what got you interested in metabolic health to begin with and maybe how that led you to think about GLP1s and so forth.

Yeah, my journey in towards the.

Well to the point I'm at now.

All of which of course always a means to an end.

As a young married guy thinking about how to provide for a future family, I during my master's degree in exercise science or exercise physiology, which really had me thinking that I would have a career devoted to muscle tissue and muscle metabolism.

But in the course of that thesis work I stumbled on a paper that had just recently been published and this is 25 years ago ish at this point.

And the paper documented a phenomenon that was an absolute revelation to me, which is that the fat cells can aggressively secrete pro inflammatory hormones which in and of itself was fascinating.

The fact that the fat cell was an active endocrine organ.

I had no idea of that at the time.

I'd never learned that.

But during the course then of my dissertation, which was my dissertation work with a man named Linus Dome, my work was looking at the degree to which inflammation contributes to insulin resistance.

And in fact Linus at the time my mentor, whom I love and revere to this day, he had one of the first grants funded by Johnson and Johnson to look at the effects of these incretins.

And all of the conversation around these gut derived hormones with GLP1 then and even now still being the most famous, was focused on its role as an anti diabetic.

But there was this side effect, there was this known phenomenon that people on these drugs tended to just eat a little less and would thus lose a little weight.

And that became of course the fervor that we find the world enraptured with now, which is this idea that the drugs are weight loss drugs.

So I've had my finger on the pulse of these drugs for over 20 years now.

But I never could have predicted, in fact indeed Brett, if I had, I would have made some more prudent investments to secure my family's financial future.

I never could have imagined the, the obsession that has come to surround what was what had long been known as just a pretty effective anti diabetic.

Yeah, I think it's so interesting to go back in your history and the, the concept of fat being an endocrine organ and actually being able to secrete pro inflammatory marker or pro inflammatory hormones and chemicals and.

And you're right, that's not how we're taught in medical school or, or undergrad or you know, fat is just something that is stored calories.

Basically.

You don't, it's not thought of so much as being active.

And really interesting concept about, you know, GLP1s have been on the radar screen for a long time, haven't they?

We think they're like a brand new drug, but it's a brand new formulation and a brand new use.

And there was actually a podcast I heard not too long ago about the GLP1s, about sort of the history of their development and how it was almost scrapped.

Like they couldn't quite get it for a long enough half life and a high enough dose and like it sounded like it was so close to being scrapped, but then of course turns into the blockbuster medication that it is.

And, and a very effective one.

Like, we have to be be honest, like people are losing more weight on these medications than they've lost on any medication in the past.

Now the question, I would even argue that's.

That's all absolutely amen.

They're very effective.

In fact, that's really why I think we need a little bit of a nuanced view.

They're too effective.

Right, Right.

So let's talk about that.

So I was just.

So the fact that you can say people are losing more weight on these drugs than any other drug in the history, most people would take that as a positive thing, was to say you don't necessarily see that as an overwhelming positive statement.

So help us clarify that.

Yeah, yeah.

So a lot of my view on the current use of these drugs is, is that they are, they are a little too much of a good thing.

So with, with the use of the drug, we need to appreciate what GLP1 does.

And GLP1 has myriad effects throughout the body.

Yes.

On the alpha cells of the pancreas regulating glucagon.

Yes.

Receptors on the intestine regulating the movement of the smooth muscle, or in other words, the rate at which food is moving through the gut.

But also too, there are effects at the hypothalamus in the brain which influence satiety and hunger, in fact, reducing hunger, promoting a sense of satiety.

And when you combine that central brain effect of promoting a sense of fullness with the slower movement of food through the intestines, that is a dynamite combination of helping someone just want to eat less now, it is a little too much of a good thing where you are starting to get.

There are enough consequences that have been revealed in the published literature that I've, I've tried to be a voice of, of caution.

But I, I somewhat regret that some people have, have assumed that I am just universally opposed.

I'm actually not universally opposed.

I just think that I am opposed to how they're currently used, which is that the dose is too high and that they are used, they are prescribed with the language being this is a weight loss drug.

When, when I actually think we, we don't do the patient any good when we describe it as a weight loss drug because we ought to be helping using it in a, in a way to improve habits.

Now before I even mention the habit part of it and my ideal use of the drug, if used at all, I just want to mention that there are consequences to the currently prescribed use of these drugs, including a significantly elevated risk of blindness that just came out within the last month, a twofold increased risk of blindness and the consequences on overall body mass where a two year trial found that of the total weight lost, roughly 40% was coming from fat free mass.

Now that doesn't mean it's all muscle and bone, but it certainly means some of it is muscle and bone.

That is sobering in light of the fact that over 70% of patients in the United States get off the drug at two years for whatever reason, cost or access or they get tired of feeling a little nauseous, which is how a person feels when the stomach slows down as much as it does.

And what do they gain back?

Well, the human body will readily gain back fat, but depending on the age and even the sex of the individual, they may never gain back that muscle and bone mass, even as modest as it was, that's gone probably for good.

And one last nail in the coffin I would say is with, with regards to why I'm opposed to these drugs as they're currently used is it's the, the effect on emotional well being where we often hype up the effects of the food noise, where the person's cravings are gone for, for junk food, for various foods.

And we'll revisit that in a moment.

But what if the reality is that their cravings for many things they used to enjoy are gone?

And what I mean by that is there is an over about a 200% increased risk of major depression in these individuals on the drug versus placebo as well as an over 100% increased risk of anxiety and even suicidal behaviors.

So one way of perhaps more honestly describing the reduced cravings for food they shouldn't be eating may be to say that you just aren't going to like anything as much as you used to like, in other words, you have a dude who is less interested in getting together with his guys, his, his friends to go bowling or you have a gal who's less interested in going for a walk around the block with her, with her girlfriends from her neighborhood or something.

And so you have people who just may be less interested in all of the things that used to find them, to bring them joy.

And this may be the reality that explains the significant effect of, on mood disorders.

So that's why those are some of my main concerns that really I think justify some heavy caution with the current use of the drugs.

Yeah, it's a very interesting point about just less interest in everything and not just food.

I hadn't seen so much about that.

So that's very interesting to hear about.

And we've done content here about the psychiatric potential impacts with some studies showing no worsening.

But all those studies exclude anybody with any kind of a psychiatric history.

And those that don't, sort of the real world evidence suggests something completely different, that there could be an increased risk for those who are predisposed to depression or suicidality or whatever the case may be.

So that's really interesting.

But just to go back to the muscle loss or the lean body mass loss, you know, it sort of highlights that weight loss isn't necessarily the goal, but improved metabolic health is the goal.

And losing fat and gaining muscle is a perfect combination for improving metabolic health.

But losing fat and muscle can still improve metabolic health as these studies have shown.

But makes me wonder about the long term consequences of that with, with decreased muscle mass.

And then to throw on top of that though, some people are saying, well it's the same thing with weight loss surgery.

It's the same thing with severe caloric restriction.

You see the same percentage of lean mass loss.

So that makes it okay.

So I want to get your impression on those two things, both, you know, justifying it that way and also the impact on long term metabolic health.

Yeah, so I, I do think it is appropriate to compare the use of the GLP1 drugs to other very often relied on weight loss interventions like gastric bypass.

And the, the other one you mentioned.

It was gastric bypass, severe caloric restriction.

Very, very low calorie diet.

Yeah, yeah, that actually the reason I mentioned that is just from the scientific perspective, which is that it helps us understand how a person is losing this weight, even this good weight, if you will, the lean mass potentially on the drug because it does suggest that it's not a direct effect of the drug itself.

But rather an artifact of the fact that they're just not really eating as much as they were before.

And even maybe what they are eating is being very poorly absorbed.

That's certainly part of the consequence of so significantly slowing the rate at which food is moving through the intestine.

And so that's an interesting just point for people to take away from how you phrased the question, which is that it does at least bring some comfort to the fact that it's not a direct effect of the drug, for example, or in other words, it doesn't mean the semaglutide is somehow directly damaging muscle tissue, but again, it's rather just a feature of the overall metabolic milieu of someone, of someone who is perhaps poorly nourishing their body.

Yeah, but further, it's not like, it's not like those interventions severely, severely restricting calories and undergoing gastric bypass don't have a rebound themselves, that we know that the people who attempt to lose weight just through calorie restriction alone, with that being the intention, that's also the intention, that is the mechanism whereby people lose weight on the Biggest Loser game show.

And there's a reason you never see these people again, because once they're off the air, they can't continue this starvation induced model.

And then hunger always wins.

Moreover, even the rate at which people regain weight with gastric bypass is quite sobering.

Where they can start to out eat the physical restrictions of the gut, what was once a very small little stomach because of the surgical restriction of it, the intestines have this remarkable ability to be somewhat dynamic or plastic, if you will, and then they can start to stretch out again with repeated stretching and before the person knows they're back to eating how they were before with the use of the drug.

It's actually even simpler than that, which is that this phenomenon of diminishing returns where you have too much of a signal, in fact there is evidence to suggest this, although it's in animals that with repeated GLP1 activation, the signal starts to decay.

In other words, too much of a signal will result in a resistance to the signal, which is a fundamental principle of biology, whether it's cancer biology and chemotherapeutics, whether it's antibiotics to treat infections and even hormones, too much of a signal will result in the decay or the loss of that signal over time.

And GLP1 would be no exception to this.

So we see the diminishing returns of the drug, which is one of the reasons why I would imagine people are getting off it at such a high rate because it just has.

It stops working like it used to.

Right.

If you're still getting the side effects and the.

And the bill to have to pay for it, but not seeing the benefits, why would you continue it?

Yeah, well, so obviously here at Metabolic Mind, we focus on metabolic health and mental health.

And the reason why I like to talk so much about these medications is because they do have an impact on metabolic health, but also that, as you mentioned, they have direct brain effects.

And part of that could be for cravings.

Like we know a big part of overeating leading to obesity and type 2 diabetes and poor metabolic health is cravings is just, you could say the brain going haywire, so to speak.

And it's not necessarily willpower, it's not necessarily just, you know, white knuckle it, but your brain is almost being hijacked.

So a lot of what you wrote in this article of maybe a new way to use these GLP1s focused on cravings.

So tell us about, about that.

How, how you got into that.

Yeah, yeah, it was a paper.

So I need to give some credit to Arnie Ostrup, who is in Denmark, and he has been really at the forefront of GLP1 research maybe since its inception.

I was at an event with him and he had mentioned a compelling perspective, which now in hindsight seems obvious, but it's not one that I'd considered, which is that he had said, what if some people just don't have a sufficient GLP one response to Food and that's what's driving the obesity and that it was an offhand comment and I'm sure for him it wasn't.

And he was thinking of a dozen studies that he could readily cite, although none of which would have been familiar to me because it was such a novel view for me.

But to say all this another way, there was a paper published in the journal Gut by Ranganath et al.

And anyone could look this up.

It is fascinating what they did in 1996, which, Brett, was a wonderful year to graduate from high school, class of 96, but also also a fascinating year to make us a seminal discovery in the relevance potentially of GLP1 when it comes to obesity and its origins.

Neither you nor I are saying that calories don't matter, but you and I both have a more nuanced view, not to put words in your mouth, but that there needs to be an endocrine component that allows the fat cell or that enables the fat cell to even store that energy in the first place, and that would be the hormone insulin.

And so when you appreciate the necessity of insulin telling the fat cell to store that energy and then the need for sufficient calories to fuel that storage into the fat cell, it does leave you with a unique perspective that has you say, okay, well then what will spike insulin the most?

And of course that's going to be dietary carbohydrates.

Now, to bring all of this back to GLP1, in this Ranganath study in the journal Gut in 1996, they took people and separated them into two groups.

So imagine two people.

Now, I'm oversimplifying, but one is lean, one is obese.

They eat a carbohydrate, heavy meal.

The lean guy eats that same amount of carbohydrate and his brain has told him, you're done, you don't need more.

And so he pushes the plate away, he's done, he gets up and he leaves.

But his buddy, his roommate, his college roommate eats that same amount of carbohydrates.

And he does not get the signal telling him to stop.

In fact, not only does he not get the stop signal as GLP1 goes down, which it did at around two to three hours, not only did he not stop, he may want more.

And now we have this, this, I think an alternate, a different paradigm here when we look at GLP1 and its potential utility.

Because what if, based on that study and others like it, rather than saying we're going to give you this drug for weight loss, the individual thinking it is just a magic intervention, that they can still eat whatever they want, but the drug is going to help them lose weight, which is not true.

The drug helps the person lose weight as it changes habits.

And what is the habit that it perhaps changes the most when it comes to diet, it is controlling carbohydrate consumption or the cravings.

Because within the scope of all of the neurobiology research of cravings, there is no evidence that humans crave fat.

There is no evidence that they crave protein.

There is significant and consistent evidence that they crave carbohydrates.

Now someone say, well, with fat makes it even better.

Yeah, but still carbohydrates are the thing that they crave the most.

And we intuitively know this.

No one is sitting down and craving a hard boiled egg.

You know, a perfect balance of fat and protein.

We crave carbohydrates.

The saltier and crunchier, the better or the sweeter and the gooier.

The best of all perhaps, but it's going to be a carbohydrate.

And so what if our use of the drug influences the conversation that the clinician has with the patient?

And that's maybe to sum it all up in a crystallized way here.

It would be that I would imagine the best use of the drug being a clinician who sits down with the patient and then explain, you know, the patient doesn't need to be told they're overweight or unhealthy because of it.

They would know intuitively.

And it is important that the clinician acknowledge it and not pretend that having too much body fat is benign.

But they say you need to learn, you need to change the way you're eating.

And this even comes back to an earlier part of our conversation, Brett, where I said, as much as you and I can both acknowledge that calories matter, that should not be the beginning of the conversation, I believe, because that leads to hunger and just pure restriction.

What we ought to say is, let's put you on a program that's going to help lower your insulin, because when you lower insulin, the body will be burning more fat and metabolic rate will go up.

Thus we say, don't worry about your calories, just control your insulin.

And to do that, most effectively, control your carbohydrates, which is stop getting your carbs from bags and boxes with barcodes.

Whole fruits and vegetables.

Enjoy them liberally, eat them, don't drink them, but stop getting these refined ultra processed carbs.

And then the.

The seed oil crew would also shit.

Nod their heads to that because that's how we mostly get our seed oils at the same time, within those packages of refined carbs.

Right.

So that puts an extra layer on sort of what you were saying about this study, though, because, you know, same time we're saying that they were craving the.

Or that the, the GLP one did not go up with the carbs and they were craving carbs at the same time.

They're not craving probably broccoli and beans or lentils.

Right.

They're craving the more refined carbs and the processing, which is actually really interesting because now, you know, so many people are focusing on the processing itself and it's the processing and maybe focusing less on the fact that it's carbohydrate and its effect on insulin.

So there does seem to be like a little bit of a balance, but it seems like GLP1 might be the equalizer for that.

Do you think it.

Because it addresses both.

Yeah, yeah, that's.

I think so.

I think so, Brett.

I, in fact, that.

That Question sort of allows me to sort of complete that, that this whole long ranting thought, which is that I think the best use of the drug is when the clinician tells the patient, you need to control your carbs.

But there will be some people who will say back to the clinician, maybe even having, after, after having attempted, they will say, I just can't do it.

I am trying to control my carbs.

Then the clinician can, with nothing but empathy, say, all right, to some degree or another, you're addicted now let's help you with your addiction.

And so here's a drug at what we could call a microdose, you know, a fraction of what it's commonly used at now.

And then I'm going to cycle you on this for, I don't know, 90 days.

And then during this time will be checking in with you to determine how well you're doing at controlling your carbohydrate cravings.

The thing that humans crave the most when it comes to nutrition.

And many people I have known, this is anecdotal, which pains a scientist to invoke, but I've known individuals who do a 90 day protocol and when they wean themselves off, they cycle off the drug.

The habits have persisted.

And there is something powerful about that 90 days.

When it comes to changing habits and breaking addictions.

Some people will find that they can get off and they're, and they have a new normal.

They've, they've rewired their habits, if you will.

Some people will be good, but then they'll find the craving starting to come back.

Okay, no problems, cycle them back on.

And so overall, my view and the perspective that I attempted to articulate in that article, which was a good experience for me, a good exercise to actually crystallize these thoughts, it is that the drugs are very powerful and thus could be effective at a lower dose if framed in the context of this is a drug that's helping you control your cravings, not framed as a weight loss drug.

And then second, presenting the idea that this is a temporary intervention.

You're not on this forever, so you need to be deliberate about the habits that you're changing and the decisions you're making.

Because in 90 days I'm going to want to start to cycle you off this to see how well the habits have become a new normal for you.

So to me, the best use of this self discipline in a syringe is to look at it as a temporary enhancement to overcome addictions rather than this is your new normal and you're going to be drugged for life.

Right.

And not just, well here, now you're going to eat less of the standard American diet or now you're going to eat less of the very high carb diet, but rather this is the way to curb your cravings and your addiction so that you can transition to a lower carb.

Lower carb diet, which will then impact your insulin and your fat burning and lead you to better metabolic health.

And as, as you pointed out, and and so have I in numerous studies, the weight loss from a ketogenic diet is generally preserving of the lean mass or certainly losing a lot less of the lean mass.

So it seems like this is a way to really move towards greater metabolic health.

Is that how you see it as well?

Yeah, yeah, yeah, right.

In fact, that's a great ending there, as you said it, because earlier you'd sort of phrase this question of are all weight loss interventions going to result in the same degree of lean mass loss?

And no, if you can be adequately nourishing the body with all of what it needs, vitamins, minerals, et cetera, and not driving it into an an overt caloric deficit, but yet insulin is low, you are creating an environment that does facilitate uniquely fat loss versus muscle loss.

And, and so the, in fact my lab published a report finding that ketones are actually muscle preserving at a, as a direct signaling molecule that where beta hydroxybutyrate actually inhibited the, we gave it the muscles a chemical insult and beta hydroxybutyrate actually made the muscle cells more robust and resistant to injury.

So we have evidence right at the level of the cell.

Not to mention the significant commentary of decades of work from Dr. George Cahill, who would often refer to ketones as the great muscle preserving molecule, that they're muscle sparing.

But yeah, I think it's not a stretch to then say well with the, with a ketogenic low carb diet, with the intention being I'm just lowering my insulin, I'm not lowering my calories per se.

You're going to find I think yourself in a very superior metabolic environment to promote selectively greater fat loss.

Yeah, and I think that's so important to emphasize that it's not weight loss, it's fat loss, especially visceral fat, maintaining lean muscle mass.

And you just set it up perfectly for, for a way to do that.

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Now, you know, a lot of studies that involve pharmaceuticals and medications are sponsored and paid for by the pharmaceutical company.

And that's why they get done quickly and with, you know, thousands and thousands of people.

But for a study for what you're proposing, it probably wouldn't be to the benefit of the pharmaceutical company because it's a much lower dose and for a short time, as opposed to the current high dose, take it forever, see you later, which obviously benefits the pharmaceutical company.

So do you think labs will start doing research studies on this?

They'd have to get NIH funding or philanthropy funding or whatnot.

But do you think more will be doing it and will your lab be doing it?

Yeah.

Yeah, good question.

So we are currently actually analyzing a data set from a clinic.

So I had a clinician reach out to me who has been using low dose semaglutide with a combined low carb diet and their results outperform even the reported results of just semaglutide alone.

And, and again, what the patient finds so enjoyable is the fact that they're not expected to be on the drug indefinitely.

I think that is, I think that's common as as much as we have a culture, particularly in the US where people are able to see advertisements for drugs so much more readily than almost any other in any other country on the planet, we certainly have a more drug friendly culture in clinical care where the patient comes in asking for a drug, which is very odd in the rest of the world because they've seen an ad.

But even then I don't think a person would want to be on the drug indefinitely.

So this all comes back to what I mentioned earlier, that I think a lot of the value in this alternative paradigm of the use of the drug, namely microdosing and cycling, is that it changes the purpose of the drug, that the person is looking at it as you are a temporary tool, you little syringe, to help me learn to change my habits.

But that still requires some effort on their part.

It's not depriving them of the benefit of learning that self discipline, which I think is one of the points of life in a kind of grander sense, which is to just there's, you know, to me telling my body, hey, you fleshy tabernacle of clay, you're not in charge.

I am the part of me that is beyond this, this fleshy body.

And I don't like, and I think it's human nature, we don't like feeling addicted to things.

We don't like feeling dependent on things.

Even if it is the intervention that's helping us curb the addiction, we would like to get over both of them.

We want to stop using the intervention because we've learned to control our addictions.

Yeah, yeah, I think that's really well said.

And I think the way you're proposing it is, is almost like a, I don't know, like a no brainer, like why not?

Why wouldn't you try this first?

Right.

Rather than giving somebody a large dose of a medication that has serious potential side effects and can likely sort of commit them to lifelong use, why wouldn't you try a lower dose, safer, shorter term to see if it helps kickstart their, their own sort of lifestyle changes?

And I'm going to answer my own question here because I think part of that is doctors have sort of become jaded.

They're like, ah, diet doesn't work.

You know, lifestyle interventions don't work because what they've been taught and tried for so long, they eat less, move more low fat.

Yeah, it hasn't worked for 50 years.

So they get sort of jaded.

But, so that's the other part that's really important to emphasize of what you're saying is it's as a transition to reducing the carbohydrates.

So, so yeah, why wouldn't they do that?

I think people should do it more well.

And I think it's a combination.

You would know, of course, having gone through medical training.

I think it's a combination of the fatigue that a physician may experience, the fact that they can't bill that time.

You get paid for what you can bill.

And talking about nutrition might not be something a clinician, a physician is able to get compensated for.

So I really, I appreciate that.

But at the same time, they might not have even learned anything other than eat less, exercise more.

If that simplistic mantra worked, we would have solved the obesity problem before it ever started.

Because we've been saying that for 60 years.

Obviously a weight loss strategy that is based on just straight calorie deprivation and restriction and this sort of mistaken view of the laws of thermodynamics in a biological system, it does not, it does not lead to an actual successful intervention.

Well, I appreciate you coming on and giving us this insight and I think it's a very interesting thought and I hope some clinicians will embrace it and try it because it does seem like a much safer and potentially longer term effective solution.

So if people want to hear more about you, learn about all the work you're doing, where can we direct them to go?

Yeah.

Yeah.

Thanks again, Brett.

This was great.

Yeah.

I have two efforts that I really try to stay a high degree of involvement with.

One is my education arm, which is a professor.

Just thrills me.

I like teaching as many people as I can, but people, people can find me there@Ben Bickman.com and Bickman is just B I k M A n Ben Bickman.

Com and then I've also helped put together a coaching effort to help people get through these very kinds of things that we've been talking about.

And that's people can find that@insuliniq.com Great.

All right, well, thank you so much Ben.

I really appreciate it.

Yeah, my pleasure.

Thanks Brett.

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