Anybody working in primary care knows how hard it is, right?
You're doing a knee injection on one patient, then you're managing their diabetes, then someone comes in with hyperlipidemia, we do it all.
But with that, it's hard to keep up with what's new in the research world or with new guidelines.
And boy, did we just have some new guidelines that dropped.
The ACC AHA just dropped a 123-page clinical practice guideline.
On the management of dyslipidemia.
And I know what you're thinking.
Who has time to look through all that?
Well, you're in luck because I'm a sucker for punishment and I went through the guidelines, so you don't have to.
Obviously, this is an enormous document, so I will barely be scratching the surface, but I'm going to kind of provide an overall summary of what's new and how primary care clinicians are going to be expected to treat dyslipidemias going forward.
So, once again.
Big document.
We're going to touch a little bit on the big important things, I think, kind of the overall view.
So, first, we're kind of changing how we look at targets.
So, we're looking to treat earlier and treat to target.
So, the 2026 guidelines are a fundamental shift.
Compared to what we learned back in 2018.
So 2018, we kind of had this vague, hey, treat for a percentage drop when you start a medication.
You expect that, but we had no real endpoints.
And so I actually remember back in my residency talking about with my attendings, asking, like, well, like,
What's like the end game here?
And everyone just kind of shrugged and said, Oh, you just started medication, and that's that.
So, those days are no more.
We now have a much more proactive approach.
The core reality driving this is that we think the big thing is you have these prolonged exposure to atherogenic lipoproteins, like the lifelong exposure, what drives the risk.
So we think that this is a disease of a lifelong exposure.
Just like blood pressure, the earlier we can handle it, the better we will be long term.
And we are assessing risk differently as well, measuring new biomarkers routinely, treating two different targets.
And escalating to non-statins much faster.
And so, here are the four main steps in this process.
And we'll talk more about each one in depth here.
But the first is we assess risk.
We have different tools to do that as well.
Then we measure appropriate labs, which includes some new ones that we'll talk about.
Then we treat two specific goals, which we will specifically give you, and then escalate and use additional tools as needed.
So, those are kind of the big four things going forward.
But first, before we dive into it, let's talk specifically what's changed, like kind of some big overarching changes.
There's lots of changes.
If you go in there, there's like
Pages of what's actually changed.
So there's a lot of changes, but these are kind of the big things.
So I want to kind of compare and contrast the old and new approaches directly to see what's going on, how this changes our daily workflows.
So, we're officially retiring, first of all, the pooled cohort equations in favor of the new prevent calculator.
The pooled cohort equations, if you remember, everyone's calculated AS CBD risk.
That's what we used to use.
Now that is no more.
We are not using that, and we are using the prevent calculators.
It was found that the old pooled cohort equations were lacking and didn't take into consideration things like socioeconomic status, kidney function, or other important things as well.
So, with this new equation, the prevent equation, we now have a more sophisticated and accurate assessment, and it actually lowers the percentage for most people.
But that doesn't mean less people will be on medication.
What they actually did was lower the intermission threshold down from five to three, and we'll talk more about that in a little bit.
But they do so that overall the same amount of people will hit the criteria for treatment, and they don't necessarily say their goal is to have more people on meds.
But I can already see how that will be a big thing people will talk about.
They'll be like, they lowered the threshold, everyone's on med.
We'll talk more about that.
We're also banning the vague percentage reduction and focusing on hard numerical goals.
So previously, it'd be: hey,
50% reduction is the goal, and then we just kind of left it.
But now we actually have actual targets.
The big baseline numbers we're going for, most people is about 100 for pretty much everybody, and then 70 or 55 milligrams per deciliter, depending on other risk factors.
And on top of that, we also have advanced testing like APOB and LP Little A.
They're no longer kind of fringe things that I just talk about because I'm a nerd.
No, they're going to be big and kind of mainstream.
That's a big thing.
And on top of that, we're adding and talking about medications that are not just statins as well, right?
So we're kind of broadening the horizon, broadening the toolbox.
And one thing I do want to mention here specifically is we talked about those prevent equations, right?
And retiring the pool cohort.
What's going on?
Like, why does this matter?
Well,
It's important because the underlying math has changed.
The new prevent equations are derived from 3.
3 million contemporary U.
S.
adults, making them much more accurate for the patients we actually see.
We have a very different population from when the initial pool cohort equations were calculated, so it was time for an update.
So, the prevent estimates the 10-year and also will give you a 30-year risk factor.
So, that's very important to know.
But the prevent estimates 10-year risk about 40 to 50% lower than the old pool cohort equations did for the exact same patient.
And so, because the calculator gives us lower numbers, the guidelines lower the intervention threshold to 3% to make sure we don't undertreat.
Right, so let's take for an example: they're the exact same person who used to be five percent, right?
It was five percent, is now at three percent.
So, they wanted to keep the threshold for treatment the same, um, and at first glance.
Treating people at three percent might sound crazy, right?
Like it sounds like they're just trying to get everybody on a statin medication, they're owned by big pharma, right?
And that was my first initial reaction: oh, like they just want to have it in the water supply.
But there were two main reasons why they made this decision.
This is their
Justification for it.
And the first is their new calculator, and the second is something called the net clinical benefit.
We'll tackle each one of those.
So, as mentioned before, the new calculator lowers the risk threshold by lowering the threshold to 3%.
The ACC and HA wanted to ensure that a similar number of at-risk adults remain eligible for what they describe as life-saving treatment.
So they wanted to say, hey,
If you wanted to, we want to be able to have the same amount of people make that decision, right?
They're not saying you have to be on this.
They're saying, hey, this threshold of three now, we're saying you could classify for that and qualify for a medication.
And for some people who want to be more aggressive,
That's what the option they wanted to give them.
So that's what they're saying.
And understand their recommendations have big things when it comes to insurance and coverage.
And so that's what they're doing.
This and giving people the option, that's fine
But how do we know for sure that treating someone with a 3% risk is actually beneficial?
Well, that brings us to our second point: the net clinical benefit.
So, to figure out who should get a statin
Researchers weighed the good against the bad.
So, for the good, they wanted to look at how many people do we really need to treat to prevent one major heart attack or stroke.
This is the number needed to treat.
And for the bad, and when they were asked, they asked, how many people do we need to treat to accidentally cause one new case of diabetes?
And this is the number needed to harm.
As we know with satins, there is an increased risk of diabetes with patients.
So they're using that as their harm, saying, How many patients do we have to treat that will cause diabetes?
That's the number needed to harm.
And so, overall, I don't mean this to bore you, but they use previous trial data to kind of figure out this math.
And so, they have seen in previous trials that moderate intensity statins typically reduce a patient's relative risk of cardiovascular events by 35%.
And so, on top of that, we know that if you treat 100 people for 10 years with a statin medication, the medication will cause about one case of diabetes.
So, those are like the baseline numbers they've looked at previously.
This is what we have.
So let's pretend there's a room full of 100 people, and all of them have exactly a 3% 10-year risk of having a heart attack or stroke.
Without any treatment, we expect three of those 100 people to have some sort of event, right?
So three out of 100.
If we give everyone a moderate intensity statin and we reduce those events then by 35%, right?
Because that's the expected relative risk.
And 35% of three is roughly one.
Roughly one.
And so we prevented exactly one major event.
But because we've treated 100 people as well with these statins, we've also caused one case of diabetes.
So, therefore, a 10-year rate of 3% is the exact intersection point of where the benefit of preventing one heart attack equals the harm of causing one patient to have diabetes.
And so, overall, the committee felt that because strokes and heart attacks
Obviously, they have lots of morbidity and mortality.
They figured that was a trade-off that is worth it when compared to one case of chronic diabetes.
If that's for you, that's not for me to decide, but that was their logic.
And it was a tangent.
I apologize.
Thanks for sticking with me, but it was a tricky thing.
And
Initially, the first thing I read, I was like, whoa, like, where did that come from?
So, I want to make sure we all understood that.
And before I dug into it, it pretty much sounded like they want everyone on a statin, which is not great for building trust with patients, right?
They think we're just pill pushers and we're trying to do this.
No, there's some method behind the madness.
Whether you agree with it or not, that's totally up to you, but that's where that came from.
So, just a side tangent, I apologize, but that's it.
Next, let's talk about something called the CPR framework.
So, they've given us this neat little framework to help develop personalized care.
And I love that.
For me, honestly, this is the best part of the new guidelines: we no longer have to just like
Follow orders blindly.
Not that we should have been, you should always be using your brain.
That's kind of how it felt before.
And so we're using our brain, working collaboratively with patients to help figure out the best course of action.
And this CPR framework is practical, right?
It helps you lead a discussion with your patients.
So, the C is calculate.
So, you calculate first, you run the prevent equation to get the baseline 10-year risk.
Maybe you can even look at the third year if you want to do it.
That's fine.
It's a good activity as well.
I'm calculating some sort of risk.
Then the P is personalized.
Acknowledge that the calculator doesn't know everything, right?
That's the big thing.
It's not perfect.
It doesn't cover every scenario in life, and the patient in front of you is not a
You know, a research subject is your patients, we have to figure it out, so we have to look for risk-enhancing factors as well.
In the guidelines, they now use the term CKM syndrome, which stands for cardiovascular kidney metabolic syndrome.
And it's based on a bunch of different things like abdominal obesity, insulin resistance, dyslipidemia, increased blood pressure, and kidney issues.
But they also look at other things too, like
If you went through premature menopause or have an inflammatory autoimmune disease or a strong family history, so here you get to really talk with patients to figure out what their risk tolerance is and can come up with a plan moving forward.
Then the R stands for reclassify.
And if you and the patient are stuck in a gray zone, maybe, or have uncertainty, you can always order additional tests or imaging things like coronary arterialcium to break the tie.
So, overall, though, it's kind of this CPR framework to create a personalized plan for patients, which is wonderful.
And then, another thing that is kind of changes how we're viewing things and what we're looking for, and why things have shifted in terms of LDL, moving beyond that.
You know, the conversation used to be just like LDL, what's your LDL number?
That's it, that's all that matters.
But it's kind of moved to really understanding the overall burden of disease.
So, what they're looking at here.
Looking at the whole picture of all the molecules that can potentially cause atherosclerosis.
I have lots of content on this in previous videos, but essentially, athogenic lipoproteins are the lipoproteins that can get into the cell of endothelial space and cause atherosclerosis.
And all these atherogenic ones have something called an APO B100 attached to them.
So now we're focusing more on this because previously what we focused on was LDL.
It's actually measuring the mass of cholesterol that's carried by the LDL particles and not the actual particle numbers.
And now that we have APOB, which is a pretty standardized test, it measures the number of athogenic particles specifically, because there's one APO-B molecule per particle, right?
So one per one, that's an equivalent there.
That's easy to know.
And what they found is that this is an even better marker than just regular LDL cholesterol.
And it turns out the more particles you have, the higher risk you have as well.
And the reason we mention this is because some people are what we call discord, meaning they have a normal LDL, everything looks fine, but their APOB is actually very high.
And traditional labs would not catch this, but these patients are still at risk without ever knowing it if we just use LDL.
So that's why we care.
And so let's kind of use a car analogy or a highway analogy.
LDL is the cargo that's being carried.
It's the mass of stuff.
It doesn't tell you how many trucks or cars it takes to carry that cargo.
It just tells us how much cargo is there.
And so you could be incredibly inefficient and have a hundred Uber drivers carrying a little bit of cholesterol each, or you could have one single truck carrying all the cholesterol.
In terms of particles, having one truck would be much better than having hundreds of vehicles, as just having a single particle would be way better than having multiple particles.
Obviously, that's simplistic.
I understand that.
But the more particles, typically the higher risk.
However, they're not recommending APOB for everybody.
They typically recommend it for people after you start a treatment, indicating that you can kind of start with LDL.
And then once you're kind of tweaked and you're maybe at goal, you can further order these lab tests to help guide additional treatments.
And then, one thing they're also recommending that everybody get one time in their life is LP little.
So, I also have more videos about this topic, but LPA is essentially a specific type of LDL particle that is particularly atherogenic.
It has an additional protein strand attached to it, known as apo-lipoprotein A, and it's almost entirely driven by our genetics, unfortunately.
However, we found that it has a really, really high risk for cardiovascular disease, and it's an independent risk multiplier.
And it is incredibly athergenic and inflammatory.
It also increases cardiovascular risk independent of LDL cholesterol.
So, this topic has been talked about for years as part of the European guidelines, and now it's a part of the American guidelines as well.
And so, moving on next, though, let's talk about those biomarkers a little more.
So, the practical clinical side of APOB and LP little A.
So, ApoB, once again, not recommended day one necessarily by the guidelines.
You can if you want to.
I don't know if it'll be covered by insurance, but you're not wrong to do it, but it's not.
Strictly in the guidelines, but you can use it as a guide after therapy to see and make sure you hit your overall goals, right?
Specifically, patients who have diabetes or high triglycerides.
You can have that discordance, right?
And we're about these populations.
It's really difficult to calculate LDL sometimes based off of if you have really high triglycerides.
And so these.
Specific populations may benefit from getting additional like APOB testing.
And as I mentioned before, diabetics are, they're known to have discordance, meaning they have lots of small LDL particles, but if you looked at the LDL, it may look normal.
So, once again, that is the discordant pattern.
That's why APOB can be very helpful.
And it helps you risk stratified patients a little better, right?
And if you just want to get this right away, once again
It's fine.
Not sure if insurance will cover it, but can be useful.
And then for APOB, the gold is less than 90 milligrams per deciliter for most, or less than 70 for high-risk, or 55 for very high-risk people.
For LP little A, this is measured, as I mentioned, one time in your life.
It's one and done, and since it's pretty much genetic.
And an L P little A of greater than 125.
Of nanomoles per liter or 50 milligrams per deciliter is a risk enhancer.
And so that's kind of the threshold I give.
The higher you go, the worse it gets.
And so it's not just like, oh, binary, it's like the higher, the worse it is, but that's what it is.
And it's hard though because we don't have any great options currently to treat LP little A.
It's still good to know, right?
So we can make sure everyone understands the risks and all the other risk factors are optimized.
But we don't have a lot of great medications for it.
Statins don't decrease it and actually may bump it up a little bit.
PCSK9 hitters do seem to reliably decrease it just a little bit, but nothing's out for primary treatment of LP little A yet.
I know it's coming down the pipeline, but not there yet.
But once again, it's more just an understanding of: hey, I have this risk factor, so I might be more aggressive in treating my other risk factors.
That's really what we're doing for it.
And then now let's talk about CACS.
So it's time to talk about coronary artery calcium.
A much bigger emphasis placed on these guidelines as it helps us decide whether or not someone would qualify for treatment in these kinds of intermediate situations, right?
So here's exactly
You know what we do if this CAC comes back to your inbox, what does it mean?
Well, a CAC of zero makes you feel pretty good, right?
So, meaning you can kind of defer treatment and repeat the scan in three to seven years unless they have high-risk conditions, risk factors, or diabetes, or smoker, something like that.
Uh, CAC zero makes you feel generally pretty good for a CAC of 1 to 99.
Then you say, Hey, you might consider starting a statin with a goal of less than 100.
So it's not like fluorid disease, but saying, Hey, you'd qualify, we might consider there's something going on in there.
A CAC of 100 to 999 means established disease, requiring aggressive therapy as they recommend and trying to get LDL less than 70.
And then a CAC greater than 1,000
Is really bad.
It's not good.
That requires aggressive, aggressive treatment, essentially treating it like secondary prevention with aggressive combination therapy to get LDL less than 55.
And so, overall, hopefully, this can be helpful when you're talking with patients to kind of help stratify the risk.
Here's the most common way I see it: patients don't want to start a medication, then you get the CAC to determine if there's visible hard plaque or not.
And of course, we have to remember that the CAC just shows calcified plaque and not soft plaque, right?
We're not seeing into the lumen of the arteries.
So statistically,
They're low risk with a zero CAC, which is great, but it doesn't mean they're zero risk, right?
So you can still have soft plaque, which is actually the plaque that breaks off and causes heart attacks.
That can still happen.
So you're not at zero risk with a zero CAC.
But you are at a lower risk.
So that's nuance there.
And the world's not perfect, I understand that.
But just for clarification, it doesn't mean like, oh, nothing could happen.
It could, depending on the plaque, but just wanted to mention that.
Next, I want to talk about the return of hard treatment targets.
So we have to get comfortable treating to a specific numerical value instead of just percentages now.
I think overall, this makes sense because it gives us actual targets instead of just this nebulous like, hey, drop it by thirty five percent or whatever.
But there's going to be different targets depending on you and your patient's level of risk, tolerance, and personal preferences.
However, overall,
For the average person walking around, the general goal is less than 100 milligrams per deciliter from an LDL perspective, and the non-HDL would be less than 130.
This is a general goal for pretty much anybody.
It also works for intermediate risk patients.
And ultimately, this level is achievable with or without pharmacotherapy, depending on factors like genetics, diet, and lots of things.
Once again, I'm trying to make it very clear that in no way, shape, or form am I or anyone recommending, hey, you have to have medications, but they're saying, hey, generally, 100 is kind of the goal, and that's like where we're going for.
On top of that, though, there are obviously different thresholds.
So, for those who have higher baselines or really high cholesterol, or maybe hypercholesterolemia, or are a higher risk.
Usually, here we're going to be a little more aggressive, and they're going for less than 70 in terms of the LDL or 100 for the non-HDL.
And as you note, you'll see that the non-HDL is always 30 more than the LDL.
Just a quick way you can remember that.
The non-HDL, always 30 more than the LDL.
And that's actually really important because non-HDL is kind of like another proxy for APOB.
So APOB is all the astrogenic lipoproteins, non-HDL.
Is that as well?
It's LDL, it's VLDL, it's IDL.
It should be technically the remnants, all the things that can cause atherosclerosis.
That's what it's looking for.
And honestly, it might even be a better number than LDL, but LDL is just easier, and we understand that.
And so that's what the targets are.
It's always usually 30 more.
And so that's very useful to understand.
And on top of that, for other primary prevention, like I mentioned before, if we're looking for higher-risk patients for primary prevention, it is less than 70.
With the non-HDL of 100.
And then finally, getting into our secondary prevention group, meaning they've already had some sort of event and their targets are less than 55 or less than 85 for non-HGL.
So that's super low.
And of course,
We always have to remember that if we're getting to these targets, once we're at the target, it's reasonable to check that ApoB to make sure that we don't have discordance as well and are making sure we understand the true risk that patients have.
And so, on top of this, we've talked about goals, right?
Like where are we going to, what are these targets?
Well, how do we get there?
Well, we kind of have a new expanded toolkit.
We'll talk about the medications for lowering lipids.
And I have lots of information on previous videos all about this as well, so I don't want to go into too much detail.
But essentially, they're given permission for primary care clinicians and everybody treating this condition to open up the toolbox and use the resources they have available.
So they still recommend statins as first line because they're cheap and everywhere.
But in a world where people are more aware of statin side effects or are having issues with it, it's good to have other options.
The first option they recommend is adding on azetamive.
So it's an oral medication taken daily and works synergistically usually with statins as it blocks cholesterol absorption, whereas we know statins limit cholesterol synthesis.
Most of the studies, though, are looking at this from an add-on perspective, not in and of itself.
But at the end of the day, if someone can't tolerate a statin, you could absolutely be on azetia or azetamib monotherapy.
That's no problem.
There's just less data that necessarily improves hard outcomes on its own, but that's there.
Next, we have the newer player called Bempidoic Acid, which is an inhibitor of cholesterol synthesis, but it's different than a statin.
And it's actually really come to light over the past few months because it seems to be a great option for those who are statin intolerant.
What's cool about it is it's a prodrug.
So actually, it's activated in the liver, and it's much more specific to the liver.
So we have way fewer skeletal muscle side effects.
So, if your patient is intolerant to statin medications because of muscle symptoms, this might be a great option.
And although they have similar mechanisms, they are different, and guidelines say you can use them together.
So, you can do a statin and membidogas as well.
Next, we have the PCSK9 inhibitors.
These are monoclonal antibodies currently that require an injection ranging anywhere from bi-weekly to monthly.
These are really strong, very potent, and are currently our big guns for lowering lipids aggressively.
Usually, you have to have a prior off to get there with failure to get to goal targets with other medications.
But these ones drop at anywhere from 40 to 60 percent, what I've seen.
And then finally, we have inclizarin, which is a small interfering RNA injection that is only given twice per year after your loading dose.
So, usually, you do a couple of loading doses.
A couple months apart and then every six months.
And they're also very effective at lower LDL.
Once again, going to require prior off.
This is not nearly as common as a PCSK9.
Maybe we'll get there, I'm not sure, but that is an option in FDA approved as well.
And so you can see now we have lots of tools in the toolbox, and it's nice that we have specific goals so we can use these medications to judiciously hit our goal targets.
End of note, the overall recommendations are that people do not take supplements or for lowering LDL specifically as the data is insufficient.
That's what part of the guidelines say.
We can't make any formal recommendations.
That's a whole different thing, and I kind of have a potential problem with like just talking about pharmacotherapy.
There's lots of things we can do, but just to mention, hey, there are things you can do from a lifestyle perspective, right?
So, maintaining, you know, as best we can.
Normal body composition, that's really, really important.
But from a diet perspective, a higher fiber diet, like the higher you go with your fiber, the lower your LDO goes.
Can your gut handle it?
Who knows?
That's the big question.
That's one big thing you can do.
Also, decreasing saturated fat intake, the overall dietary recommendations for the guidelines are less than 10%.
That's just like the national nutrition guidelines.
But that can help as well.
And they're not really talked about too much in here.
They do mention diet and lifestyle, but I want to specifically plug those because for me, that's super important that we have to lock those in if at all possible.
But if we need to do medicines, we can do that too.
But I always wanted to mention that.
And then now I want to take it all, bring it all together.
So, looking at this kind of primary care algorithm, see what it looks like when a patient comes to your clinic.
So, you know, now we've kind of expanded
The ages as well, right?
So it used to be 40 years old, now it's starting at 30.
So anybody 30 years old, all the way up to 79, we can follow these guidelines.
So the first step would be to, once again,
Use the prevent calculator, right?
We're going to try to look at their 10-year risk and we're checking to make sure where they're at.
And on top of this, maybe you're capturing them for the first time.
So you're also checking their LP little A as well.
That's a one-time check, as we mentioned, but we're first of all assessing their risk.
Risk.
And then from there, we're looking at their risks and we try to figure out: do they fall into low risk?
Are they borderline, intermediate, or high?
And once we have this information, we can start making a customized decision.
So, if you have a patient who wants to be very aggressive and start a medication prophylactically, that's great.
You can do that.
Or maybe you have a patient who just does not want to start any sort of medication, wants lifestyle changes, that's fine too.
We just can talk about the risks and
Let them know.
Or maybe you have someone who's on the fence and really doesn't know what to do, not quite sure.
They don't really want to start a medication.
So you decide to get a CAC and see.
That's great too.
There's lots of options.
The biggest thing now is that we can change and customize treatments to patient and clinician desires, which I love.
From here, then, ideally, after that, we check labs and act on them, right?
So, after we do this, we checked it, we started a treatment.
Well, we want to recheck, right?
It's no longer good enough just to start a medication.
We want to make sure that we're hitting our target.
And the current recommendations are to recheck labs anywhere from four to 12 weeks after initiating therapy or lifestyle changes, and that's when we can check them.
And then, if things are good and settled, they recommend repeating every six to 12 months to assess the ongoing efficacy.
I think it's really important too, right?
Because I know previously it was kind of said and forgetting it, but now we actually have targets, and patients are individualized people and not just numbers.
And so it's important that we're always reconsidering, reassessing, and figuring out what's best for them.
And finally, once we're at goal, depending on the level of risk and other factors, we can add on additional tests like APO-B Iptizard.
And so, overall, I really love this algorithm in that the main goal here is to have a conversation with patients to determine everyone's level of comfort and risk.
I tell my residents,
The best part of being a physician is you get to use your brain and think critically.
And that's kind of what this is.
It's providing a framework for you.
We get to decide how we best want to treat people, work with patients in a nuanced fashion, and kind of work together to figure it out.
I think this is less dogmatic and kind of understanding, hey, overall risk.
It goes into many, many more things.
It talks about risk-enhancing factors and lots of other stuff that we can go deeper into.
But it really kind of, I thought, was a nice step in the right direction of saying, hey, let's look at this from a more holistic perspective rather than just focusing on like one specific number.
Obviously, that's the easiest thing for us to treat:
LDL cholesterol, like it's easy with medications, that's what you do, and that's why we've done it historically.
But I think this is a step in the right direction of looking at the patients as more holistically.
Like, what can we do to overall decrease your risk?
And so, as we wrap it up, these are the things that we're going to be able to implement right away in primary care, right?
So, the first is to ditch the old pooled cohort equation.
And start using the prevent calculator to get a more accurate risk assessment for patients.
Once we have that, we can make shared decisions for treatment, and we can order additional biomarkers as needed.
And finally, it's important that we are tight trading treatments to our specific individualized goals and are no longer just doing a set and forget a thing.
And so, as I mentioned before, that is just barely scratching the surface of this enormous document.
But I think this should cover the biggest changes.
However, if you're interested in diving deeper into this document, I'd be more than happy to make a video series going through the major sections because I'm a huge nerd and I enjoy that stuff.
But I don't have unlimited free time, so I would love to know if someone actually would want that.
If that's the case, let me know in the comments below.
Otherwise, that's going to be it for today.
Thank you so much for stopping by.
If you found this helpful, it would mean the world to me if you share this with a friend or colleague of yours.
But that's going to be it for today.
Now get off your phone, get outside, have a great rest of your day.
We'll see you next time.
Disclaimer, this podcast is for entertainment, education, and informational purposes only.
The topics discussed should not solely be used to diagnose, treat, or prevent any condition.
The information presented here was created with an evidence-based approach, but please keep in mind that science is always changing, and at the time of listening to this, there may be some new data that makes this information incomplete or inaccurate.
Always seek the advice of your personal physician or qualified healthcare provider for questions regarding any medical condition.
