Why Does Adderall Feel Different on a GLP-1? What We Know—and What We Don’t
Written by Dan Cripe, RN, BSN & Marcia Cripe, RN
Why Does Adderall Feel Different on a GLP-1? What We Know—and What We Don’t
You take your Adderall the same way you always have, but something feels different. Maybe it takes longer to kick in. Maybe the effect feels flatter, weaker, less predictable, or strangely delayed. You may even have days when you wonder whether you took it at all, followed by other days when it seems to work normally again.
If that started after semaglutide, tirzepatide, or another GLP-1-based medication, it is reasonable to wonder whether the two are connected. GLP-1 medications can slow gastric emptying and potentially affect the absorption of oral medications, so there is a biologically plausible reason Adderall could feel different for some people. What we do not have, however, is good clinical evidence showing exactly how GLP-1 medications change Adderall absorption, blood levels, onset, or effectiveness.
That distinction matters. Your experience can be real without science yet being able to tell us precisely why it is happening.
The First Thing to Know: There Is No Well-Established Adderall–GLP-1 Interaction
There is currently no established drug interaction showing that semaglutide or tirzepatide consistently raises or lowers amphetamine concentrations in a predictable way. There are also no strong clinical trials specifically measuring Adderall pharmacokinetics before and after starting a GLP-1 medication.
That means we cannot accurately say that a GLP-1 makes Adderall weaker, blocks Adderall, or causes Adderall not to absorb. Those statements go beyond the available evidence.
What we can say is that GLP-1 medications alter gastrointestinal motility, particularly gastric emptying, and both semaglutide and tirzepatide prescribing information warn that this can potentially affect concurrently administered oral medications. Because Adderall is taken by mouth and its timing matters to how you experience its effect, that creates a reasonable pharmacologic question.
The frustrating part is that the question has not yet been adequately studied.
GLP-1 Medications Can Slow How Quickly Your Stomach Empties
One of the established effects of GLP-1 receptor agonists is slower gastric emptying. Instead of a meal moving from your stomach into your small intestine at its usual rate, that process can take longer, particularly during certain phases of treatment.
A 2026 systematic review and meta-analysis of prospective studies found that GLP-1 receptor agonists significantly prolonged gastric emptying time. Across the included studies, the average prolongation in gastric emptying half-time was approximately 74 minutes, although the magnitude varied considerably depending on the drug, timing, patient, and method used to measure it.
That does not mean everything you swallow sits in your stomach exactly 74 minutes longer. Gastric emptying is much more complicated than that, and liquids, solids, medications, and different formulations may behave differently.
It does establish something important for this conversation: GLP-1 medications can meaningfully alter the timing of gastrointestinal transit.
Why Gastric Emptying Could Matter for Adderall
When you swallow Adderall, the medication has to move through your gastrointestinal tract before the active amphetamine reaches your bloodstream. Anything that changes the timing of that process could theoretically change when you begin noticing the medication's effects.
Immediate-release Adderall reaches peak plasma concentrations at approximately three hours under fasting conditions. Adderall XR is designed to release medication over a longer period and reaches its peak concentration later, at roughly seven hours.
That difference is important because what you experience as “kick-in time” is partly related to how quickly enough amphetamine reaches your circulation and brain to produce a noticeable clinical effect. If gastrointestinal transit changes, the timing of absorption could potentially feel different even if the total amount of medication eventually absorbed remains similar.
That is the key hypothesis.
It is not yet proof that this is what happens to Adderall when you start a GLP-1.
Delayed Absorption Does Not Necessarily Mean Less Absorption
This is one of the most important distinctions in the entire discussion.
If a medication reaches your bloodstream later, you may experience it as weaker simply because the effect does not appear when you expect it to. But a delayed peak concentration does not automatically mean that your body ultimately absorbs less medication.
We already know this can happen with Adderall XR under other circumstances. Food does not meaningfully reduce the overall amount of amphetamine absorbed from Adderall XR, but a high-fat meal can delay the time to peak concentration by several hours.
In other words, the same total exposure can feel different because the timing has shifted.
This is one reason a person could reasonably say, “My Adderall takes forever to start working now,” without the medication necessarily being completely malabsorbed.
Whether GLP-1-induced gastric slowing produces this exact effect with Adderall has not been directly demonstrated, but the pharmacologic concept is plausible.
Semaglutide and Tirzepatide Do Not Have Identical Gastric Effects
It is also worth separating semaglutide from tirzepatide rather than treating every GLP-1-based medication as pharmacologically identical.
The current Wegovy prescribing information states that semaglutide delays gastric emptying and therefore has the potential to influence oral medication absorption. However, clinical pharmacology studies with once-weekly injectable semaglutide generally did not find clinically meaningful changes in absorption for the oral medications that were tested.
That is reassuring, but Adderall was not one of those medications. It therefore cannot be used to conclude that semaglutide definitely has no effect on Adderall timing.
Tirzepatide's labeling includes a similar warning about oral medications. Its prescribing information also notes that the gastric-emptying delay is greatest after the first dose and tends to diminish with continued treatment.
That pattern may matter if you notice your stimulant feels most unpredictable shortly after starting tirzepatide or increasing the dose. It provides a biologically plausible explanation, but again, this has not been specifically tested with Adderall.
The Effect on Gastric Emptying Can Change Over Time
Another reason the experience may feel inconsistent is that the gastrointestinal effects of GLP-1 medications are not necessarily identical from week to week.
With tirzepatide, delayed gastric emptying is strongest after the first dose and diminishes after subsequent doses. Researchers also describe a phenomenon known as tachyphylaxis, in which some gastric-emptying effects become less pronounced with continued GLP-1 exposure.
That could theoretically explain why an oral medication seems dramatically delayed during the first few weeks of treatment and then becomes more predictable later. It could also help explain why dose escalations temporarily seem to change the way another medication behaves.
But individual responses vary considerably. Some people continue to have substantial early fullness, nausea, retained gastric contents, or other evidence of slowed gastrointestinal motility well into treatment.
That variability is exactly why your experience may not match someone else's.
Immediate-Release and Extended-Release Adderall May Not Feel the Same on a GLP-1
If you take immediate-release Adderall, you are accustomed to a relatively discrete onset and shorter period of action. When that onset changes, it can be especially noticeable because you know roughly when you normally expect the medication to begin working.
A delay that would be subtle with another medication may feel obvious with a stimulant. You may take your dose at 7:00 a.m. expecting to be focused by 8:00 or 9:00, then realize it is almost lunchtime before you notice much effect.
Adderall XR adds another layer because its formulation is specifically designed to release amphetamine in stages. The capsule contains beads that create an immediate-release component followed by a delayed-release component, producing a longer overall concentration curve.
Anything that changes gastrointestinal transit, luminal conditions, food timing, or release timing could theoretically alter how that experience feels. That does not mean the XR formulation is necessarily more affected by GLP-1 therapy, but it does mean its pharmacokinetics are more complicated than simply swallowing an immediate-release tablet.
Food Can Already Change How Adderall XR Feels
You may also be changing how and when you eat without realizing that this could affect the subjective timing of your stimulant.
The Adderall XR prescribing information notes that a high-fat meal can delay peak amphetamine concentrations by roughly 2.5 hours without meaningfully changing overall absorption. That is a significant shift in timing.
Now consider what commonly happens after starting a GLP-1. Breakfast may disappear, your first meal may move several hours later, portion sizes may shrink dramatically, or you may alternate between taking medication on an empty stomach one day and with food the next.
Those changes can introduce another variable into an already complicated system. If your Adderall suddenly feels inconsistent, it is worth looking not only at your GLP-1 injection but also at when you take your stimulant relative to food and how that routine has changed since starting treatment.
Eating Much Less Can Change How a Stimulant Feels Too
There is another possibility that has nothing to do with absorption.
GLP-1 treatment can dramatically reduce caloric intake. Adderall can also suppress appetite, which means taking both medications together may make it surprisingly easy to go much of the day without eating.
You may then experience fatigue, weakness, shakiness, headache, difficulty concentrating, or a general sense that your brain is not functioning normally. Those symptoms can easily be interpreted as “my Adderall isn't working.”
Sometimes the stimulant may be working pharmacologically while your body simply does not have enough energy, fluid, or nutrition to feel mentally sharp.
That is an important distinction because increasing a stimulant dose would not correct inadequate intake.
Dehydration Can Mimic Poor Stimulant Effect
Hydration deserves similar attention.
GLP-1 medications can reduce food intake, and meals are one of the times many people naturally drink fluids. Nausea, vomiting, diarrhea, constipation, and early fullness can further reduce fluid intake, while stimulants themselves can contribute to dry mouth and sometimes make people less aware of ordinary eating and drinking cues.
If you become even mildly dehydrated, you may feel tired, foggy, dizzy, headachy, or less able to concentrate. Once again, that can feel like your ADHD medication has suddenly stopped doing its job.
Before assuming the problem is entirely pharmacokinetic, look at the larger picture. If you are taking Adderall with coffee and then realizing at 2:00 p.m. that you have barely eaten or drunk anything else, your brain may be dealing with more than medication timing.
Major Weight Loss Could Potentially Change Medication Response
Substantial weight loss adds another variable.
Amphetamine pharmacokinetics show meaningful variability among individuals, and body weight is one factor associated with differences in plasma exposure. That does not mean stimulant dosing should simply be adjusted according to pounds lost, because Adderall dosing is individualized according to response and tolerability rather than routinely calculated by body weight in adults.
Still, if your body has changed dramatically since your stimulant regimen was originally established, it is reasonable for your prescriber to reassess how the medication is working. The dose and formulation that felt ideal at one point in your treatment may not necessarily continue to feel identical after major physiologic changes.
Weight loss is unlikely to provide one neat explanation for every change, but it belongs on the list of variables worth considering.
Your GLP-1 May Also Be Changing the Experience of Reward
This is where the discussion becomes much more interesting—and much less certain.
GLP-1 signaling interacts with brain systems involved in motivation, reinforcement, and reward. Research into food reward, alcohol use, and other behaviors suggests that these medications may reduce how compelling some rewards feel.
Amphetamine works differently. Its central nervous system effects involve dopamine and norepinephrine signaling, and those systems contribute to attention, motivation, arousal, and reinforcement.
That raises an obvious question: Could a GLP-1 change the subjective experience of a stimulant even if blood levels remain normal?
At the moment, we do not have strong human evidence answering that question.
A “Flatter” Adderall Effect Is Not the Same as Proven Reduced Absorption
Some people describe their stimulant after starting a GLP-1 as less noticeable rather than simply delayed. They may still function better on it than without it, but they no longer feel the same sense of activation, drive, focus, or motivational push that they previously associated with the medication.
That experience could theoretically involve central reward processing rather than gastrointestinal absorption. GLP-1 pathways interact with brain regions involved in motivation, and there is growing research on how these drugs alter responses to rewarding stimuli.
But we should be careful here. There is not currently good evidence showing that semaglutide or tirzepatide directly blocks Adderall's dopamine or norepinephrine effects in people taking both medications.
So if your stimulant feels flatter, it is reasonable to report that experience to your clinician. It is not accurate to conclude that your GLP-1 is “canceling out dopamine.”
“My Adderall Doesn't Kick In Anymore” Can Mean Several Different Things
When you describe your medication as not working, try to be as specific as possible because different patterns point toward different explanations.
Maybe the medication eventually works but starts two or three hours later than it used to. That pattern makes altered timing or absorption more plausible.
Maybe it starts normally but seems to wear off sooner. That is a different pharmacologic question.
Maybe it lasts the usual amount of time but feels less motivating or stimulating. That could reflect a change in subjective response rather than straightforward delayed absorption.
Or maybe your attention is poor all day while you are also barely eating, sleeping poorly, dehydrated, nauseated, or experiencing significant fatigue.
All of those experiences can sound like “Adderall isn't working,” but they are not the same clinical problem.
Injection Timing May Be Worth Paying Attention To
If you take a weekly GLP-1 medication, you may notice that your Adderall feels different at particular points in your injection cycle.
For example, it may seem more delayed during the first day or two after your injection when nausea, fullness, and gastrointestinal effects are strongest, then feel more predictable later in the week. That pattern would be useful information to give your prescriber because it suggests the problem is varying alongside your GLP-1 exposure or gastrointestinal symptoms.
Do not assume the relationship just because the timing seems to match, though. Weekly changes in food intake, sleep, hydration, caffeine, work demands, and other factors can create similar patterns.
The useful approach is to observe the pattern rather than immediately assigning a mechanism to it.
Dose Escalations May Be Another Clue
If your stimulant seemed normal at one GLP-1 dose and noticeably different immediately after moving to a higher dose, that is worth documenting.
Dose escalation often brings a temporary increase in nausea, early fullness, reduced intake, and gastrointestinal effects. Tirzepatide's effect on gastric emptying is also particularly notable during early exposure, which makes changes around initiation or escalation biologically plausible.
That still does not prove the GLP-1 altered your Adderall pharmacokinetics. It simply gives your clinician more useful information than saying, “My medication feels weird.”
Patterns are valuable because they can help distinguish an isolated bad day from a consistent treatment-related change.
Could Switching From Immediate-Release to XR Fix It?
Not necessarily.
It can be tempting to reason that if immediate-release Adderall feels unpredictable, extended-release must solve the problem—or the reverse. But because we do not know exactly what mechanism is causing the change, there is no universal answer.
Immediate-release and extended-release amphetamine products have different absorption and release profiles. Some people may find one formulation more predictable than another, but that is an individualized prescribing decision rather than a GLP-1-specific rule.
The same applies to lisdexamfetamine, commonly known as Vyvanse. Lisdexamfetamine is a prodrug that is converted to active dextroamphetamine after absorption, which gives it different pharmacokinetic characteristics from mixed amphetamine salts.
Those differences may matter clinically, but there is not enough evidence to say one stimulant formulation is automatically “better” for people taking GLP-1 medications.
What About Vyvanse?
Vyvanse often enters this conversation because its activation process differs from Adderall.
Lisdexamfetamine itself is absorbed and then converted primarily in the blood to active dextroamphetamine. That conversion process helps produce a relatively consistent pharmacokinetic profile and is one reason its effect may feel smoother for some people.
Studies comparing lisdexamfetamine with immediate-release d-amphetamine show that lisdexamfetamine reaches peak amphetamine concentrations later while producing similar overall exposure. Research has also shown that certain changes in gastric conditions can alter the timing of extended-release mixed amphetamine salts more than lisdexamfetamine.
That makes Vyvanse scientifically interesting in this context, but it still does not prove it is unaffected by GLP-1 therapy. There have not been adequate studies specifically comparing Vyvanse and Adderall in people taking semaglutide or tirzepatide.
If your medication response has become unpredictable, formulation is something to discuss with your prescriber—not something to switch on your own.
What About Caffeine?
Caffeine can make the picture even harder to interpret.
You may start drinking more coffee because your stimulant feels weaker, only to develop jitteriness, anxiety, palpitations, reflux, or disrupted sleep. The next day you feel more tired and unfocused, which makes the stimulant seem even less effective and encourages more caffeine.
GLP-1 treatment can also change your relationship with coffee. Some people suddenly tolerate less of it, dislike the taste, or experience more reflux when they drink it.
If you are trying to figure out what changed, keeping caffeine relatively consistent for a few days may help you see the pattern more clearly.
Acidic and Alkaline Substances Can Affect Amphetamine Levels
Amphetamine pharmacokinetics are also influenced by pH.
The Adderall XR prescribing information notes that acidifying agents can reduce amphetamine blood levels while alkalinizing agents can increase them. Changes in urinary pH alter how quickly amphetamine is eliminated from the body.
That does not mean ordinary dietary fluctuations explain every change in your stimulant response, and you should not intentionally manipulate pH to try to make your medication stronger.
It does mean Adderall already has several pharmacokinetic variables before a GLP-1 is added to the picture. When you combine food timing, gastrointestinal motility, hydration, weight change, sleep, caffeine, and pH effects, it becomes clear why the subjective response can be difficult to reduce to one explanation.
Why Online Answers Often Sound More Certain Than the Science Is
If you search this question online, you will often encounter very confident answers.
One person says GLP-1 medications definitely prevent Adderall from absorbing. Another says delayed gastric emptying has absolutely no effect on oral medications. Someone else says GLP-1s lower dopamine and therefore stimulants stop working.
None of those broad statements accurately reflects the evidence.
We know GLP-1 medications can delay gastric emptying. We know their prescribing information specifically warns about the potential to affect oral drug absorption. We also know that studies involving semaglutide and several other oral drugs often did not show clinically important changes in total exposure.
What we do not know is exactly what happens to Adderall's onset, peak concentration, total exposure, or clinical effectiveness in people taking specific GLP-1 medications.
The most scientifically accurate answer therefore lives somewhere between “there is no possible interaction” and “your GLP-1 is blocking your Adderall.”
A Simple Way to Track What Is Actually Happening
If your Adderall suddenly feels different, you do not need to turn your day into a pharmacology experiment. A few simple observations can make your conversation with your prescriber much more useful.
For several days, note what time you take your stimulant, when you first notice an effect, when you feel it is working best, and when you think it wears off. Also notice whether the pattern changes according to your GLP-1 injection day.
It can help to document food timing, major nausea or fullness, hydration, caffeine, and sleep as well. You are looking for obvious patterns rather than trying to measure every variable perfectly.
You may discover that the stimulant always seems delayed the morning after your injection, or that the days it “doesn't work” are also the days you have eaten almost nothing.
That information is much more clinically useful than simply reporting that Adderall feels weaker.
From a Nurse: What I’d Pay Attention To
If your stimulant feels different after starting a GLP-1, I would focus first on what exactly changed rather than assuming the medication has stopped working.
- Is the onset delayed? If it eventually works but takes much longer to start, timing and gastrointestinal absorption deserve consideration.
- Does it feel weaker all day? That is different from delayed onset and may require a broader review of dose, sleep, nutrition, hydration, ADHD symptoms, and other medications.
- Did the change happen after starting or increasing your GLP-1? That timing is useful information for your prescriber.
- Does the effect vary across your injection week? A consistent pattern may help identify whether gastrointestinal symptoms or GLP-1 timing are contributing.
- Are you eating enough? Severe appetite suppression plus stimulant-related appetite reduction can leave you trying to concentrate on very little fuel.
- Are you hydrated? Headache, fatigue, dizziness, and brain fog can easily feel like poor stimulant response.
- Has your caffeine intake changed? More caffeine can temporarily mask fatigue while making anxiety, sleep, heart rate, and reflux worse.
- Has your weight changed substantially? Major physiologic changes are another reason for your prescriber to reassess medication response.
- Are you having significant nausea, vomiting, prolonged fullness, or difficulty tolerating oral intake? Those symptoms deserve attention independently of how your stimulant feels.
- Do not double doses or take extra stimulant because the first dose feels delayed. If absorption is simply slower, taking additional medication could create excessive exposure later when both doses are active.
That last point is particularly important. A medication that feels absent at 9:00 a.m. may not actually be gone—it may simply be arriving later than expected.
When You Should Talk to Your Prescriber
A consistent change in stimulant effectiveness is worth discussing, particularly if it is affecting your ability to work, drive, study, manage responsibilities, or function safely.
Your prescriber may want to look at the timing of your symptoms, stimulant formulation, dose, GLP-1 dose changes, food intake, other medications, blood pressure, heart rate, sleep, and other possible contributors.
You should also contact your healthcare team if you develop significant palpitations, chest pain, fainting, severe agitation, marked blood pressure changes, persistent vomiting, inability to maintain hydration, or other concerning symptoms.
Do not independently increase, repeat, crush, alter, or change the timing of prescribed stimulant medication in an attempt to “overcome” delayed gastric emptying.
Why Adderall May Feel Different on a GLP-1
There is a plausible reason your Adderall may feel different after starting semaglutide, tirzepatide, or another GLP-1 medication: these drugs can slow gastric emptying, and changes in gastrointestinal transit can potentially alter the timing of oral medication absorption. What we do not currently have is direct clinical evidence proving exactly how GLP-1 treatment changes Adderall concentrations or ADHD symptom control.
If your stimulant now takes longer to kick in, delayed gastrointestinal transit is one possible explanation. But it is not the only one.
Your eating schedule may have changed. You may be consuming far fewer calories or fluids. Your weight may have changed substantially. Your sleep, caffeine use, gastrointestinal symptoms, or stimulant formulation may also be contributing.
There is also a more speculative possibility that GLP-1-related changes in reward and motivation could alter how the stimulant feels even when its pharmacokinetics remain adequate. That hypothesis is scientifically interesting, but it is not yet established in human studies.
So the most accurate answer is not “GLP-1 medications make Adderall stop working.”
It is this:
GLP-1 medications change enough about gastrointestinal physiology, eating behavior, and possibly reward processing that a change in how your stimulant feels is plausible—but the Adderall-specific science has not caught up with the patient experience yet.
If the change is consistent or interfering with your functioning, document the pattern and bring it to your prescriber. The goal is not simply to make your stimulant feel more noticeable again—it is to understand what has changed and find a treatment pattern that remains effective, predictable, and safe.
Medical Disclaimer
Adderall and Adderall XR are Schedule II prescription stimulants with risks including misuse, dependence, cardiovascular effects, psychiatric adverse effects, appetite suppression, and other medication-specific warnings. Semaglutide, tirzepatide, and other GLP-1-based medications also have medication-specific indications, warnings, contraindications, interactions, and adverse effects.
This article provides general educational information and does not determine whether a change in stimulant response is caused by altered absorption, inadequate dosing, GLP-1 therapy, ADHD progression, nutritional intake, another medication, or another medical condition.
Do not increase, repeat, split, crush, change, stop, or otherwise alter prescribed stimulant or GLP-1 medication because the stimulant feels delayed or less effective without discussing the change with the clinician managing your treatment.
Seek appropriate medical care for chest pain, fainting, severe or persistent palpitations, severe agitation, inability to maintain hydration, persistent vomiting, or other concerning symptoms.
Sources
1. Eli Lilly and Company. Zepbound (tirzepatide) U.S. Prescribing Information. Revised 2026.
https://pi.lilly.com/us/zepbound-uspi.pdf
2. Novo Nordisk. Wegovy (semaglutide) U.S. Prescribing Information. Revised 2026.
https://www.novo-pi.com/wegovy.pdf
3. Takeda Pharmaceuticals USA, Inc. Adderall XR (mixed salts of a single-entity amphetamine product) U.S. Prescribing Information. Revised 2026.
https://www.accessdata.fda.gov/drugsatfda_docs/label/2026/022063s007lbl.pdf
4. DailyMed. Adderall—dextroamphetamine saccharate, amphetamine aspartate, dextroamphetamine sulfate, and amphetamine sulfate tablet. U.S. National Library of Medicine.
https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=f22635fe-821d-4cde-aa12-419f8b53db81
5. Chen A, Zhao K, Ceban F, et al. Glucagon-like peptide-1 receptor agonists and gastric emptying time: a systematic review and meta-analysis of prospective studies. Canadian Journal of Anesthesia. 2026;73(4):345-356. PMID: 42087044. doi:10.1007/s12630-026-03114-6.
https://pubmed.ncbi.nlm.nih.gov/42087044/
https://doi.org/10.1007/s12630-026-03114-6
6. Jalleh RJ, Jones KL, Rayner CK, et al. Clinical Consequences of Delayed Gastric Emptying With GLP-1 Receptor Agonists and Tirzepatide. Journal of Clinical Endocrinology & Metabolism. 2025. PMID: 39418085.
https://pubmed.ncbi.nlm.nih.gov/39418085/
7. Hooper L, Liu S, Pai MP. GLP-1RA-induced delays in gastrointestinal motility: Predicted effects on coadministered drug absorption by PBPK analysis. Pharmacotherapy. 2025. PMID: 39989027. PMCID: PMC11998891. doi:10.1002/phar.70007.
https://pubmed.ncbi.nlm.nih.gov/39989027/
https://pmc.ncbi.nlm.nih.gov/articles/PMC11998891/
https://doi.org/10.1002/phar.70007
8. Ermer J, Homolka R, Martin P, et al. Pharmacokinetics and Pharmacodynamics of Lisdexamfetamine Compared with D-Amphetamine in Healthy Subjects. Pharmacopsychiatry. 2017. PMID: 28936175.
https://pubmed.ncbi.nlm.nih.gov/28936175/
9. Haffey MB, Buckwalter M, Zhang P, et al. Effects of omeprazole on the pharmacokinetic profiles of lisdexamfetamine dimesylate and extended-release mixed amphetamine salts in adults. Postgraduate Medicine. 2009. PMID: 19820270.
https://pubmed.ncbi.nlm.nih.gov/19820270/
10. Patrick KS, Straughn AB, Perkins JS, González MA. Evolution of amphetamine pharmacokinetics in the treatment of attention-deficit/hyperactivity disorder. Clinical Pharmacokinetics. Background pharmacokinetic evidence summarized in later reviews.
https://pubmed.ncbi.nlm.nih.gov/28910145/