May 23, 2025 • 13 mins
In this episode of Daily Value, we look inside the NAD+ wars - breaking down the science, the hype, and the controversy surrounding Nicotinamide Riboside (NR) and Nicotinamide Mononucleotide (NMN). These two molecules have been promoted as keys to longevity, but the story is far more complex. We’ll look at the biochemistry of NAD+ metabolism, compare what the research really says about NR and NMN, and dig into the regulatory drama that’s shaped their (NMN’s) availability. Most importantly, we’'ll look at a bigger-picture strategy for restoring NAD+, one that goes beyond precursors alone.
00:00 the NAD Wars
01:02 Understanding NAD+ and Its Importance
01:52 The Role of NR and NMN in NAD+ Replenishment
02:29 Biochemical Pathways of NAD+ Production
04:14 Challenges and Regulatory Issues with NMN and NR
05:44 Clinical Research and Safety Profiles
07:13 Complexities in Boosting NAD+ Levels
09:04 Multi-Targeted Strategies for NAD+ Restoration
13:25 Conclusion: Embracing Complexity in Aging
PMID: 35134387
PMID: 39026037
doi:10.1002/fft2.511
Mark as Played
Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:00):
There's a molecular battle raging at the heart of
aging, fought between twomolecules that promise to
restore youth from the insideout.
That's nicotinamide riboside,also called NR, and nicotinamide
mononucleotide, also called NMN.
While NR boasts clinical trialsand regulatory stability, nmn
faces scrutiny from scientistsand regulators alike.
(00:23):
But, as recent researchhighlights, replenishing NAD
plus is far more complex thanchoosing sides.
Today we're going to dig deepinto the biochemical realities,
clinical data and regulatorydrama behind the NAD wars and
ask if either molecule alone istruly enough to combat aging.
Hello everyone, welcome back toDaily Value.
(00:53):
I'm William Wallace, and todaywe're taking a look at a
molecule whose depletion hasprofound effects on our health
nicotinamide adeninedinucleotide, nad+.
As many of us know it.
It's not an exaggeration to saythat NAD+ is fundamental to
life itself.
It serves as an essentialcoenzyme for hundreds of
(01:13):
enzymatic reactions thatregulate metabolism, maintain
mitochondrial function andfacilitate DNA repair.
But here's the issue Our NADplus levels are not stable
throughout our lives.
Research consistently showsthat NAD plus concentrations
decline sharply as we age,starting notably around middle
age and into later years.
(01:34):
This decline does not justcorrelate with aging.
It may actively drive manyaspects of the aging process.
Lower NAD plus levelscompromise cellular energy
production, reduce theefficiency of DNA repair
mechanisms and weaken cellularresilience against inflammation.
This is where our molecularcontenders, nicotinamide
(01:55):
riboside, nr, and nicotinamidemononucleotide, nmn, enter the
picture.
Both have surged into thespotlight because of their
ability to replenish cellularNAD plus levels.
However, as recent researchreviews emphasize, boosting NAD
plus levels isn't as simple asjust taking a precursor.
It's a complex biochemicaldance influenced by multiple
(02:15):
enzymes, transporters andpathways.
To truly understand how NR andNMN stack up against each other,
we need to briefly understandhow NAD plus metabolism works
and why restoring NAD plus isboth promising and challenging.
Nad plus productionpredominantly occurs through the
salvage pathway, which accountsfor roughly 85% of total NAD
(02:37):
plus biosynthesis.
This pathway efficientlyrecycles nicotinamide back into
NAD+, highlighting the criticalimportance of precursor
molecules like NMN and NR.
Nmn, a vitamin B3 derivative,occurs naturally within the
human body as well as in variousfruits and vegetables.
Importantly, nmn exists in twoforms, a-type and B-type, but
(03:00):
only the B-type has demonstratedactual biological activity.
Its primary physiological roleis serving as an intermediary in
NAD plus production.
Specifically, nicotinamidephosphoribosyltransferase, or
NAMPT, a rate-limiting enzyme,converts nicotinamide to NMN,
which is subsequentlytransformed into NAD plus by NMN
(03:23):
adenyl transferases or NMNAT.
Nr, another NAD+ precursor, hasa simpler biochemical pathway,
discovered as a directcontributor to NAD+ metabolism
in 2004.
Nr bypasses the NAMPT-dependentstep, converting directly into
NMN via enzymes callednicotinamide riboside kinases.
(03:45):
This makes NR uniquelyefficient as it does not rely on
the rate-limiting enzyme NAMPT.
Both NMN and NR can be obtainedfrom dietary sources, either in
their free forms or asmetabolites produced during NAD
plus catabolism.
Precursors such as tryptophan,nicotinamide and niacin also
(04:05):
contribute to NAD plus synthesisbut face limitations like side
effects at higher doses, makingNMN and NR particularly
appealing as supplements to many.
While NMN and NR have gainedattention for their potential
health benefits, significantdebate and regulatory
uncertainty have emerged,particularly around NMN.
Critics argue that NMN facessignificant challenges regarding
(04:27):
its cellular entry andbioavailability.
Specifically, they note thatNMN's structure as a nucleotide
carrying an additional phosphategroup limits its ability to
freely cross cellular membranes.
This characteristic maynecessitate specific
transporters, potentiallylimiting its effectiveness
across various tissues.
(04:48):
Adding to that complexity, nmnhas recently been subject to
regulatory scrutiny.
Initially marketed as a dietarysupplement, nmn faced
regulatory action due to itsprior investigation as a
pharmaceutical drug, triggeringthe FDA's drug preclusion cause.
This led to the temporaryexclusion of NMN from the
dietary supplement market in theUnited States.
(05:09):
However, recent legal actionshave resulted in a temporary
stay, complicating its currentstatus and leaving its market
position uncertain as of rightnow.
In contrast, nr maintains itsgenerally recognized as safe
also called grass status withoutregulatory interruption,
supported by a more establishedbody of actual human clinical
(05:32):
data.
These regulatory and structuralconsiderations show important
distinctions between NMN and NR,which seems to be influencing
consumer perceptions as well asmarket dynamics.
Clinical research has providedevidence supporting the safety
of both NMN and NR.
In humans.
Studies have shown NMN to besafe at oral doses ranging from
(05:54):
100 to 1,250 milligrams per day.
For instance, clinical trialshave demonstrated that a single
doses of 100, 250, and 500milligrams of NMN produced no
notable clinical changes in bodytemperature, heart rate, blood
pressure or oxygen saturation.
Moreover, prolonged dosing ofNMN at 1,250 milligrams daily
(06:16):
for four weeks was also found tobe safe and well-tolerated,
further confirming NMN's safetyprofile, at least short-term.
Nr has been extensively studiedin human clinical trials.
Safe daily doses of up to 2,000mg have been established, with
studies consistentlydemonstrating dose-dependent
increases in blood NAD pluslevels following administration.
(06:38):
Specifically, clinical trialsreport increases in whole blood
NAD plus levels by 22, 51, and142% after daily NR doses of 100
, 300, and 1,000 milligramsrespectively, sustained over
multiple weeks.
Further benefits associatedwith NR supplementation include
reduced fatty liver, decreasedoxidative damage indicators and
(07:02):
enhanced neuronal NAD pluslevels when taking 1,000
milligrams of NAD.
These clinical outcomes providesome support for the safety of
NR and NMN supplements.
However, boosting NAD pluslevels is not as simple and
straightforward as simplyincreasing precursor intake, due
to several interconnectedbiochemical bottlenecks and
(07:24):
regulatory factors.
Firstly, the NAD plus consumingenzymes like CD38, parps, also
known as polyADP, ribosepolymerases and sirtuins, become
increasingly active with ageand inflammation significantly
elevating NAD plus turnover.
This heightened consumption canrapidly offset any potential
gains made throughsupplementation with precursors.
(07:46):
Secondly, the efficiency of NADplus recycling via the salvage
pathway decreases with age.
The enzyme NAMPT, necessary forrecycling nicotinamide back
into NAD plus, declinessignificantly over time, making
the process less effective andlimiting NAD plus replenishment.
Additionally, the body respondsto excessive nicotinamide
(08:09):
accumulation by activatingnicotinamide and methyl
transferase NNMT.
This enzyme methylates andexcretes excess nicotinamide,
further depleting available NADplus precursors and leading to
methyl donor depletion.
Available NAD plus precursorsand leading to methyl donor
depletion, which can negativelyimpact all kinds of functions.
These interconnected factorsheightened NAD plus consumption,
(08:32):
diminished recycling capacityand active removal of precursor
molecules create a challengingbiochemical environment.
Effective strategies for NADplus restoration thus require a
multi-targeted approach thatsimultaneously addresses these
underlying issues, rather thanrelying solely on precursor
supplementation.
Given the complexities andmultiple bottlenecks outlined,
(08:55):
effective NAD plus restorationrequires interventions that
targets various pathwayssimultaneously rather than
relying solely on precursorsupplementation simultaneously
rather than relying solely onprecursor supplementation.
Firstly, addressing excessiveNAD plus consumption by
inhibiting the activity of majorNAD plus consumers is critical.
Natural compounds such as theflavonoid apigenin commonly
(09:15):
found in parsley and chamomilehave demonstrated the ability to
inhibit CD38, leading tonotable increases in NAD plus
levels in some models.
Another promising naturalcompound, quercetin, widely
available as a dietarysupplement, has also shown
potential in preclinical studiesfor CD38 inhibition.
Similarly, targeting the PARPenzymes, particularly PARP1, can
(09:39):
significantly preserve NAD pluslevels, at least it has in
preclinical models.
Luteolin, a flavonoid found inbroccoli, and EGCG, found in
green tea, exhibit naturalPARP-inhibiting properties,
potentially contributing to thepreservation of NAD+.
Enhancing NAD+ recycling throughactivation of NAMPT is another
(10:00):
viable strategy.
Lifestyle interventions such ascalorie restriction, occasional
intermittent fasting andregular exercise significantly
boost NAMPT activity, enhancingNAD synthesis naturally.
Additionally, certain dietarycompounds such as curcumin found
in turmeric, have beensuggested to support NAMPT
(10:20):
activity indirectly throughanti-inflammatory pathways.
Lastly, activity indirectlythrough anti-inflammatory
pathways.
Lastly, inhibiting niacinamideand methyltransferase to prevent
nicotinamide methylation andsubsequent precursor loss can
also be targeted.
Naturally Dietary methyl donorssuch as trimethylglycine that's
, betaine and cholinesupplementation, can support
methylation processes, helpingmaintain balanced methyl donor
(10:42):
pools while potentially reducingexcessive nicotinamide
excretion.
A combined strategyincorporating precursor
supplementation, for instance NRor NMN, dietary and lifestyle
modifications to target CD38 andPARP activity, like consuming
apigenin, quercetin, luteolin,enhancing recycling pathways via
(11:03):
things like calorie restrictionand exercise, and supporting
methylation, presents a moreholistic and synergistic
approach to raising NAD pluslevels and sustaining that A
multi-pathway strategy may bewhat's needed to counteract NAD
decline with age.
Nr, supported by substantialclinical evidence and a clear
(11:24):
regulatory status, emerges as areliable and reasonably
well-studied NAD plus precursor.
Clinical studies suggest dosesranging from 300 milligrams to
100 milligrams daily effectivelyelevate NAD plus levels, with
doses up to 2,000 milligramsdaily shown to be safe.
But again, it's important tonote that most studies done in
(11:47):
humans with NR have not resultedin the same clinical outcomes
that we see in preclinicalmodels.
At least that's not the case inpeople that are semi-healthy or
already healthy, but there doesseem to be some benefit in
models like those of Parkinson's.
Conversely, nmn offerspromising preclinical data and
(12:09):
reasonably robust safetyprofiles from early clinical
studies, with oral doses rangingfrom 250 mg to 1,250 mg daily
demonstrating good tolerabilityand significant NAD plus
increases.
However, nmn faces significantregulatory uncertainty and
bioavailability challenges dueto its molecular structure,
potentially limiting widespreaduse, as well as effectiveness
(12:48):
pathways involved in NAD plusdecline.
True efficacy in NAD plusrestoration likely demands a
multi-targeted approachcombining precursor
supplementation and strategicdietary and lifestyle
interventions.
Compounds like apigenin dosedat 50 to 100 milligrams daily,
quercetin at 250 to 500milligrams daily, luteolin at
100-200 mg daily and curcumin at500-1500 mg daily, coupled with
(13:10):
supportive lifestyle practiceslike exercise and calorie
restriction, offer a synergisticmethod for enhancing NAD plus
synthesis, reducing excessiveNAD plus consumption and
improving precursor recyclingand the NAD Plus wars.
The real winner is not found ina single molecule, it's found
in synergy.
Remember aging isn't a battlewe win molecule by molecule.
(13:34):
It's a war won by embracingcomplexity.
So arm yourself wisely, choosecomprehensively and thrive at
every age.
Thank you for joining me todayon Daily Value.
Until next time, stay healthy.
There's a molecular battle raging at the heart of
aging, fought between twomolecules that promise to
restore youth from the insideout.
That's nicotinamide riboside,also called NR, and nicotinamide
mononucleotide, also called NMN.
While NR boasts clinical trialsand regulatory stability, nmn
faces scrutiny from scientistsand regulators alike.
(00:23):
But, as recent researchhighlights, replenishing NAD
plus is far more complex thanchoosing sides.
Today we're going to dig deepinto the biochemical realities,
clinical data and regulatorydrama behind the NAD wars and
ask if either molecule alone istruly enough to combat aging.
Hello everyone, welcome back toDaily Value.
(00:53):
I'm William Wallace, and todaywe're taking a look at a
molecule whose depletion hasprofound effects on our health
nicotinamide adeninedinucleotide, nad+.
As many of us know it.
It's not an exaggeration to saythat NAD+ is fundamental to
life itself.
It serves as an essentialcoenzyme for hundreds of
(01:13):
enzymatic reactions thatregulate metabolism, maintain
mitochondrial function andfacilitate DNA repair.
But here's the issue Our NADplus levels are not stable
throughout our lives.
Research consistently showsthat NAD plus concentrations
decline sharply as we age,starting notably around middle
age and into later years.
(01:34):
This decline does not justcorrelate with aging.
It may actively drive manyaspects of the aging process.
Lower NAD plus levelscompromise cellular energy
production, reduce theefficiency of DNA repair
mechanisms and weaken cellularresilience against inflammation.
This is where our molecularcontenders, nicotinamide
(01:55):
riboside, nr, and nicotinamidemononucleotide, nmn, enter the
picture.
Both have surged into thespotlight because of their
ability to replenish cellularNAD plus levels.
However, as recent researchreviews emphasize, boosting NAD
plus levels isn't as simple asjust taking a precursor.
It's a complex biochemicaldance influenced by multiple
(02:15):
enzymes, transporters andpathways.
To truly understand how NR andNMN stack up against each other,
we need to briefly understandhow NAD plus metabolism works
and why restoring NAD plus isboth promising and challenging.
Nad plus productionpredominantly occurs through the
salvage pathway, which accountsfor roughly 85% of total NAD
(02:37):
plus biosynthesis.
This pathway efficientlyrecycles nicotinamide back into
NAD+, highlighting the criticalimportance of precursor
molecules like NMN and NR.
Nmn, a vitamin B3 derivative,occurs naturally within the
human body as well as in variousfruits and vegetables.
Importantly, nmn exists in twoforms, a-type and B-type, but
(03:00):
only the B-type has demonstratedactual biological activity.
Its primary physiological roleis serving as an intermediary in
NAD plus production.
Specifically, nicotinamidephosphoribosyltransferase, or
NAMPT, a rate-limiting enzyme,converts nicotinamide to NMN,
which is subsequentlytransformed into NAD plus by NMN
(03:23):
adenyl transferases or NMNAT.
Nr, another NAD+ precursor, hasa simpler biochemical pathway,
discovered as a directcontributor to NAD+ metabolism
in 2004.
Nr bypasses the NAMPT-dependentstep, converting directly into
NMN via enzymes callednicotinamide riboside kinases.
(03:45):
This makes NR uniquelyefficient as it does not rely on
the rate-limiting enzyme NAMPT.
Both NMN and NR can be obtainedfrom dietary sources, either in
their free forms or asmetabolites produced during NAD
plus catabolism.
Precursors such as tryptophan,nicotinamide and niacin also
(04:05):
contribute to NAD plus synthesisbut face limitations like side
effects at higher doses, makingNMN and NR particularly
appealing as supplements to many.
While NMN and NR have gainedattention for their potential
health benefits, significantdebate and regulatory
uncertainty have emerged,particularly around NMN.
Critics argue that NMN facessignificant challenges regarding
(04:27):
its cellular entry andbioavailability.
Specifically, they note thatNMN's structure as a nucleotide
carrying an additional phosphategroup limits its ability to
freely cross cellular membranes.
This characteristic maynecessitate specific
transporters, potentiallylimiting its effectiveness
across various tissues.
(04:48):
Adding to that complexity, nmnhas recently been subject to
regulatory scrutiny.
Initially marketed as a dietarysupplement, nmn faced
regulatory action due to itsprior investigation as a
pharmaceutical drug, triggeringthe FDA's drug preclusion cause.
This led to the temporaryexclusion of NMN from the
dietary supplement market in theUnited States.
(05:09):
However, recent legal actionshave resulted in a temporary
stay, complicating its currentstatus and leaving its market
position uncertain as of rightnow.
In contrast, nr maintains itsgenerally recognized as safe
also called grass status withoutregulatory interruption,
supported by a more establishedbody of actual human clinical
(05:32):
data.
These regulatory and structuralconsiderations show important
distinctions between NMN and NR,which seems to be influencing
consumer perceptions as well asmarket dynamics.
Clinical research has providedevidence supporting the safety
of both NMN and NR.
In humans.
Studies have shown NMN to besafe at oral doses ranging from
(05:54):
100 to 1,250 milligrams per day.
For instance, clinical trialshave demonstrated that a single
doses of 100, 250, and 500milligrams of NMN produced no
notable clinical changes in bodytemperature, heart rate, blood
pressure or oxygen saturation.
Moreover, prolonged dosing ofNMN at 1,250 milligrams daily
(06:16):
for four weeks was also found tobe safe and well-tolerated,
further confirming NMN's safetyprofile, at least short-term.
Nr has been extensively studiedin human clinical trials.
Safe daily doses of up to 2,000mg have been established, with
studies consistentlydemonstrating dose-dependent
increases in blood NAD pluslevels following administration.
(06:38):
Specifically, clinical trialsreport increases in whole blood
NAD plus levels by 22, 51, and142% after daily NR doses of 100
, 300, and 1,000 milligramsrespectively, sustained over
multiple weeks.
Further benefits associatedwith NR supplementation include
reduced fatty liver, decreasedoxidative damage indicators and
(07:02):
enhanced neuronal NAD pluslevels when taking 1,000
milligrams of NAD.
These clinical outcomes providesome support for the safety of
NR and NMN supplements.
However, boosting NAD pluslevels is not as simple and
straightforward as simplyincreasing precursor intake, due
to several interconnectedbiochemical bottlenecks and
(07:24):
regulatory factors.
Firstly, the NAD plus consumingenzymes like CD38, parps, also
known as polyADP, ribosepolymerases and sirtuins, become
increasingly active with ageand inflammation significantly
elevating NAD plus turnover.
This heightened consumption canrapidly offset any potential
gains made throughsupplementation with precursors.
(07:46):
Secondly, the efficiency of NADplus recycling via the salvage
pathway decreases with age.
The enzyme NAMPT, necessary forrecycling nicotinamide back
into NAD plus, declinessignificantly over time, making
the process less effective andlimiting NAD plus replenishment.
Additionally, the body respondsto excessive nicotinamide
(08:09):
accumulation by activatingnicotinamide and methyl
transferase NNMT.
This enzyme methylates andexcretes excess nicotinamide,
further depleting available NADplus precursors and leading to
methyl donor depletion.
Available NAD plus precursorsand leading to methyl donor
depletion, which can negativelyimpact all kinds of functions.
These interconnected factorsheightened NAD plus consumption,
(08:32):
diminished recycling capacityand active removal of precursor
molecules create a challengingbiochemical environment.
Effective strategies for NADplus restoration thus require a
multi-targeted approach thatsimultaneously addresses these
underlying issues, rather thanrelying solely on precursor
supplementation.
Given the complexities andmultiple bottlenecks outlined,
(08:55):
effective NAD plus restorationrequires interventions that
targets various pathwayssimultaneously rather than
relying solely on precursorsupplementation simultaneously
rather than relying solely onprecursor supplementation.
Firstly, addressing excessiveNAD plus consumption by
inhibiting the activity of majorNAD plus consumers is critical.
Natural compounds such as theflavonoid apigenin commonly
(09:15):
found in parsley and chamomilehave demonstrated the ability to
inhibit CD38, leading tonotable increases in NAD plus
levels in some models.
Another promising naturalcompound, quercetin, widely
available as a dietarysupplement, has also shown
potential in preclinical studiesfor CD38 inhibition.
Similarly, targeting the PARPenzymes, particularly PARP1, can
(09:39):
significantly preserve NAD pluslevels, at least it has in
preclinical models.
Luteolin, a flavonoid found inbroccoli, and EGCG, found in
green tea, exhibit naturalPARP-inhibiting properties,
potentially contributing to thepreservation of NAD+.
Enhancing NAD+ recycling throughactivation of NAMPT is another
(10:00):
viable strategy.
Lifestyle interventions such ascalorie restriction, occasional
intermittent fasting andregular exercise significantly
boost NAMPT activity, enhancingNAD synthesis naturally.
Additionally, certain dietarycompounds such as curcumin found
in turmeric, have beensuggested to support NAMPT
(10:20):
activity indirectly throughanti-inflammatory pathways.
Lastly, activity indirectlythrough anti-inflammatory
pathways.
Lastly, inhibiting niacinamideand methyltransferase to prevent
nicotinamide methylation andsubsequent precursor loss can
also be targeted.
Naturally Dietary methyl donorssuch as trimethylglycine that's
, betaine and cholinesupplementation, can support
methylation processes, helpingmaintain balanced methyl donor
(10:42):
pools while potentially reducingexcessive nicotinamide
excretion.
A combined strategyincorporating precursor
supplementation, for instance NRor NMN, dietary and lifestyle
modifications to target CD38 andPARP activity, like consuming
apigenin, quercetin, luteolin,enhancing recycling pathways via
(11:03):
things like calorie restrictionand exercise, and supporting
methylation, presents a moreholistic and synergistic
approach to raising NAD pluslevels and sustaining that A
multi-pathway strategy may bewhat's needed to counteract NAD
decline with age.
Nr, supported by substantialclinical evidence and a clear
(11:24):
regulatory status, emerges as areliable and reasonably
well-studied NAD plus precursor.
Clinical studies suggest dosesranging from 300 milligrams to
100 milligrams daily effectivelyelevate NAD plus levels, with
doses up to 2,000 milligramsdaily shown to be safe.
But again, it's important tonote that most studies done in
(11:47):
humans with NR have not resultedin the same clinical outcomes
that we see in preclinicalmodels.
At least that's not the case inpeople that are semi-healthy or
already healthy, but there doesseem to be some benefit in
models like those of Parkinson's.
Conversely, nmn offerspromising preclinical data and
(12:09):
reasonably robust safetyprofiles from early clinical
studies, with oral doses rangingfrom 250 mg to 1,250 mg daily
demonstrating good tolerabilityand significant NAD plus
increases.
However, nmn faces significantregulatory uncertainty and
bioavailability challenges dueto its molecular structure,
potentially limiting widespreaduse, as well as effectiveness
(12:48):
pathways involved in NAD plusdecline.
True efficacy in NAD plusrestoration likely demands a
multi-targeted approachcombining precursor
supplementation and strategicdietary and lifestyle
interventions.
Compounds like apigenin dosedat 50 to 100 milligrams daily,
quercetin at 250 to 500milligrams daily, luteolin at
100-200 mg daily and curcumin at500-1500 mg daily, coupled with
(13:10):
supportive lifestyle practiceslike exercise and calorie
restriction, offer a synergisticmethod for enhancing NAD plus
synthesis, reducing excessiveNAD plus consumption and
improving precursor recyclingand the NAD Plus wars.
The real winner is not found ina single molecule, it's found
in synergy.
Remember aging isn't a battlewe win molecule by molecule.
(13:34):
It's a war won by embracingcomplexity.
So arm yourself wisely, choosecomprehensively and thrive at
every age.
Thank you for joining me todayon Daily Value.
Until next time, stay healthy.
Popular Podcasts
On Purpose with Jay Shetty
I’m Jay Shetty host of On Purpose the worlds #1 Mental Health podcast and I’m so grateful you found us. I started this podcast 5 years ago to invite you into conversations and workshops that are designed to help make you happier, healthier and more healed. I believe that when you (yes you) feel seen, heard and understood you’re able to deal with relationship struggles, work challenges and life’s ups and downs with more ease and grace. I interview experts, celebrities, thought leaders and athletes so that we can grow our mindset, build better habits and uncover a side of them we’ve never seen before. New episodes every Monday and Friday. Your support means the world to me and I don’t take it for granted — click the follow button and leave a review to help us spread the love with On Purpose. I can’t wait for you to listen to your first or 500th episode!
Crime Junkie
Does hearing about a true crime case always leave you scouring the internet for the truth behind the story? Dive into your next mystery with Crime Junkie. Every Monday, join your host Ashley Flowers as she unravels all the details of infamous and underreported true crime cases with her best friend Brit Prawat. From cold cases to missing persons and heroes in our community who seek justice, Crime Junkie is your destination for theories and stories you won’t hear anywhere else. Whether you're a seasoned true crime enthusiast or new to the genre, you'll find yourself on the edge of your seat awaiting a new episode every Monday. If you can never get enough true crime... Congratulations, you’ve found your people. Follow to join a community of Crime Junkies! Crime Junkie is presented by audiochuck Media Company.
Ridiculous History
History is beautiful, brutal and, often, ridiculous. Join Ben Bowlin and Noel Brown as they dive into some of the weirdest stories from across the span of human civilization in Ridiculous History, a podcast by iHeartRadio.