Howdy Folks today is a special episode rather than giving you an interview in this episode. I'd like to take a shot at instead giving you guys the full
lay of the land on a topic we've continually
touched on across multiple episodes, which is all things NAD.
We've brushed up against this topic in many interviews, the most obvious of which being the conversation. I had with dr. David Sinclair,
but also others like a prior episode with dr. Eric Burdon. Both great episodes which
You should definitely listen to those
episodes were however
conversations, which means that in each case, while certainly educational, they weren't
necessarily structured to strictly be a primer.
Today's episode is different, instead my goal in this one is to structure it in a way
as to give you an overview that can lay the framework. Towards your understanding, the relevance, the questions that still need to be answered by the field. And also
just my sort of concluding thoughts when it's all said and done. Not only on any
D. But also on the so-called NAD boosters
which are the NAD precursors nicotinamide, right beside and nicotinamide
mononucleotide before we kick this thing off, a quick mention about this episode it's actually been out for almost an entire week surprised you shouldn't be. This is one of the new elements of the engine that keeps found my fitness. Not only running, but thriving by offering a few solid concrete perks for supporting memories, I'm able to keep this
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Without further Ado, on to the podcast today I'm going to talk about a molecule that has
become in recent years, extremely relevant to the field of Aging. Specifically, I'm referring to nad+, which I will refer to as NAD for short and some of the related precursor molecules nicotinamide Rye beside often referred to as NR and nicotinamide mononucleotide, often referred to, as nmn these
two.
Precursor molecules are called NAD boosters which can both be
found as consumer available supplements. Just in
case you've never heard of NAD, it's
probably one of the most important molecules on the
planet. So important, in fact, that without it, life would cease to exist the NAD boosters nicotinamide, right beside and nicotinamide mononucleotide at very high doses. In animal Studies, have both
been shown to improve the way multiple tissues and cell types age including
skeletal and heart muscle brain and stem cells. They have
I have been to preliminary clinical
trials, in humans, showing nicotinamide, Rye beside May raise NAD levels in white blood cells,
which is pretty darn cool. However, I still think there are many open questions
that need to be answered regarding NAD boosters and I will touch on some of these concerns in this episode. But the
possibility that intracellular NAD may be increased from a supplement or several types of supplements
is awfully interesting.
If not downright exciting
for one simple reason
NAD levels decrease with age
and a decrease in
In NAD levels across a variety
of types of tissues is
associated with many. And I mean
many Hallmarks of Aging these
Hallmarks of Aging that are associated with
age-related changes in the NAD pool. Either directly or
indirectly include things like loss of Proteus. Stasis mitochondrial, dysfunction glucose intolerance insulin resistance, cellular senescence, altered epigenetics and more. This is partly because the availability of NAD promotes DNA repair
capacity while its decline.
Associated with the accumulation of DNA damaging reactive oxygen species.
Another reason is because NAD is required for energy production. So when NAD levels decline, as they do with age
this results, in less energy production, in many tissues like the brain, immune cells, muscle Etc. That means those organs do not work as well as they once did during youth. When energy levels
were maintained, NAD is also required
for the activation of a very important family of enzymes involved in longevity called
Ruins. The
complete answer to why NAD levels fall with age is still an
open question but there's a few things we
do know as we age chronic inflammation and immune activation two processes that consume NAD tend to go up. And with them our need for DNA repair
placing an immense Demand on our NAD
pool. Meanwhile, our
ability to produce and recycle NAD tends to fall with age.
We're going to cover a lot of ground in this episode but I want to start with an overview of NAD.
NAD has a very important role in energy metabolism NAD can be synthesized in the
body, from a variety of dietary sources, including the amino acid tryptophan, which is in tons of healthy foods like salmon, spinach and nuts. And the three forms of niacin, which is
vitamin B3. Also
found in Dutch in foods, like lean meats, legumes, veggies.
These three forms of vitamin B3 include nicotinamide. Also called
niacin amide.
Nicotinic acid and nicotinamide, right beside
they are commonly referred
to as niacin equivalents but dietary sources of NAD are not the major source of NAD. The major source of NAD is through a recycling mechanism that we will discuss later. The reason for that is because our organs require such large quantities of NAD that it would be impossible to consume enough from our
diet. So why do we require such
large quantities of NAD? First and foremost, energy plays a critical role in energy
metabolism
Critical meaning without it, you can't make energy NAD, participates in back and
forth, processes of reduction and oxidation often referred to as redox
reactions. These alternating conversions of nids, oxidized
form, which is NAD to its reduced form. Nadh
are crucial for the metabolism of glucose
and fatty acids and the formation of ATP.
Since both oxidized and reduced forms of NAD are essential
for these linked sets of reactions cells need to maintain massive
concentrations of
Both NAD and nadh basically without these molecules Not only would we cease
to exist but life on our planet would cease to
exist NAD is also a
cofactor for many different important enzymes in
this context. A
cofactor means something that is required for an enzyme to work. It has to bind to the enzyme and this activates the enzyme so it can perform its function.
So let's talk about a few of these enzymes, several of these and NAD required. Enzymes are inside the mitochondria.
And this is another
Way NAD participates in the generation of energy, aside from itself, being a type of energetic
currency. It also acts as a
cofactor for enzymes involved in the production of energy from glucose outside of the mitochondria. This is referred to as
glycolysis, many types of cells use look like hollis's as their
primary source of energy. For example, red blood cells do not have any mitochondria,
so a hundred percent of the energy
they require to perform their function of delivering oxygen and other goodies to other tissues in the body comes from glycolysis.
Calluses NAD plays a very important role
in mitigating DNA damage Uniden a deed repair damage to DNA.
That is because NAD is a
cofactor for one of the most important enzymes involved in repairing. DNA damage called parp one, the activation of part one requires an enormous amount of NAD. For example. Excessive DNA damage in subsequent part 1. Activation have been shown to decrease NAD levels to 20 to 30 percent of its normal levels. The ability to repair DNA damage is important for longevity.
Lymphoblastoid cell lines established from blood
samples of humans who were centenarians hundred years or older
have significantly higher part. One activity than cell lines established from younger individuals that are 70 years old park. One activity has also been correlated with
maximum lifespan in
mammals the higher. The
part one activity, the longer the lifespan. For example, the activity of part 1 was measured across multiple mammalian, species,
and the difference in PowerPoint
activity between the longest-lived mammals tested.
Which were humans and the shortest-lived mammals tested, which were rats was
fivefold. So not too much of a surprise but genomic stability, which relies on NAD in general and
part one, specifically may be very important for
longevity and AD is required to
activate. Signaling proteins known as sirtuins, which are highly conserved enzymes that play roles in health span and Longevity. And multiple organisms. Sirtuins are linked to the regulation of a variety of
metabolic processes like the response to stress and the
Nation of Life Span. The way they do this is through epigenetic regulation sirtuins utilize NAD to remove specific chemical structures called acetyl groups. A
process called deacetylation from cellular proteins to control the activation of genes involved in energy metabolism at apogee. Circadian rhythm DNA
repair, cell, survival and more
when cellular energy levels are low
such as during exercising fasting or caloric.
Restriction, NAD levels rise which also means the
A ratio of
NAD to its reduced form, nadh
increases. And this serves as a
sensor to switch on sirtuin expression and subsequent activity Resveratrol a naturally occurring, compound found in red grapes and other plants is a potent, sirtuin activating compound and
it's beneficial effects on
health span. Some of which is now showing up in human research are thought to
result from sirtuin activation, alright, so that is NAD in a nutshell, it's important stuff. Unfortunately,
Becomes
depleted across various tissues, including the brain, as we age.
The brain skeletal muscle of the heart. These are all tissues with a very high metabolic demand and thus require a lot of NAD. So what happens when you can't meet that metabolic demand things? Start to generate and fall apart, they don't work as well. As I mentioned before NAD, depletion has been associated with the Hallmarks of Aging, such as decreased Futaba, G increased, DNA damage, increased mitochondrial, dysfunction and dysregulated.
Did metabolism depletion of NAD. May predispose
organisms to the development of a variety of age-related diseases, including neurodegenerative diseases, such as Alzheimer's disease, and Parkinson's disease,
cardiovascular disease and muscle. Atrophy, it may also increase the susceptibility
to infections since the immune system requires tons of Edna NAD
in contrast NAD levels, increase under
conditions. That many of us already think of as generally healthspan promoting
such as exercise. And also,
Fasting or in the case
of Lab Rats, full-blown lifelong caloric restriction. Furthermore NAD restoration through a, variety of different
methods has been shown to increase lifespan in lower-level
organisms such as yeast and worms, as well as in rodents
taken together. These findings suggest that NAD plays a
critical role in aging specifically, the reduction of NAD levels commonly insert observed in
aging is thought to be a combination
of decreased synthesis and recycling as
well.
Well, as increased consumption and degradation increased DNA damage and inflammation. As seen in aging May decrease NAD and potentiate aging. So the question that's been on everyone's mind is, can I erase NAD levels in my body? And if so, will that give me superpowers
or at the very least, help me to live healthier and free of disease longer.
The answer isn't just supplements though. That's a possibility and one some
labs are very excited about and pursuing. In
fact, any D levels are heavily influenced by lifestyle and particularly things that
Energy stress like fasting, caloric, restriction, and exercise which all raised NAD. Remember NAD can be made
from things in the diet like tryptophan or nice and equivalent but these nice and equivalents are not the major source of NAD. The reason for that is because the body's
demand for NAD exceeds, its capacity to produce it from these
forms of vitamin B3. So the
body recycles, nicotinamide using a recycling pathway called the NAD. Salvage pathway.
This is
the predominant source of NAD.
Let me explain how we get NAD from this recycling pathway, the consumption of NAD. From enzymes that use
it. Generates nicotinamide as
a by-product, nicotinamide is converted into
nicotinamide, mononucleotide and subsequently into NAD. There are two important
things to know about the NAD. Salvage pathway first nicotinamide has been shown to inhibit the activity of sirtuins which is not necessarily
a good thing.
Second, the enzyme that converts
nicotinamide into nicotinamide
mononucleotide is subject to feedback inhibition by NAD levels. That means at a certain concentration of NAD. Nicotinamide will no longer be converted
into nicotinamide mononucleotide and subsequently NAD, rather it will remain
nicotinamide which is unfortunate because as I just mentioned some Studies have
shown nicotinamide inhibits
sirtuin activation
Remember sirtuins are involved in longevity, that means you want them to be activated. The other source of NAD is from
nicotinamide, right beside, which is converted into nicotinamide mononucleotide and subsequently NAD.
Both nicotinamide right beside and nicotinamide
mononucleotide are found in low concentrations in many foods,
but they are also found in supplements
and are referred to as NAD boosters.
So let's talk NAD. Boosters these, two NAD, precursors nicotinamide.
And nicotinamide mononucleotide are referred to as NAD boosters. Because in supplement form, they have been shown to be. Well, tolerated at high
doses and to effectively raise
NAD levels and to ameliorate age Associated diseases in rodents the most extensively. Studied NAD, booster is nicotinamide, right? Beside
several animal Studies have shown
that when nicotinamide Rye beside is orally administered, at high doses, it
can counteract an obesogenic diet by improving insulin
sensitivity. It can improve endurance and strength.
Length. Another animal studies showed at high-dose nicotinamide, right beside, could reverse mitochondrial damage, it could increase mitochondrial, biogenesis and reverse muscular. Atrophy and animals that had a severe muscle wasting disease. Nicotine, and my driver's side has also been shown to have positive effects on the brain and animals.
It increase neurogenesis, it's decreased cognitive
deterioration and amyloid-beta
production. It's also been shown to increase his synaptic plasticity in mice nicotinamide. Mononucleotide has not
Studied as extensively as nicotine, my right beside, but there have been several animal Studies have. Also shown nicotinamide, mononucleotide can have health benefits for example. Injection, with high-dose nicotinamide, mononucleotide has been shown to counter an obesogenic diet and improved several markers, of metabolic Health, high-dose injection of nicotinamide mononucleotide has been shown to improve heart function in animals, with heart problems, and to improve cognition, and memory and animals with neurodegenerative disease.
A long-term study found that
dietary administration of nicotinamide. Mononucleotide mitigated, the age Associated physiological, decline in mice that have an accelerated aging phenotype.
Specifically starting at five months of age. Mice were
fed either a hundred or 300 milligrams per kilogram body weight.
Nicotinamide,
mononucleotide for 12 months, these animals had improved
skeletal muscle function, mitochondrial function, increased energy expenditure, increase bone density, and also decreased insulin.
And these benefits occurred in a
dose-dependent manner. So the higher the dose of nicotinamide mononucleotide, the greater the benefit
while this all sounds great. There is another important point that I want to mention. While many animal Studies have found that nicotinamide right beside and nicotinamide mononucleotide can
ameliorate age-related Disease by increasing energy levels in different
tissues. There is always one disease context
that throws a curve ball cancer.
In a recent study nicotinamide
mononucleotide was shown to accelerate cancer growth in
Mice with a type of pancreatic cancer where pro-inflammatory senescent cells Drive tumor growth. When mice were injected with 500 milligrams per kilogram, body weight of nicotinamide mononucleotide for 13 days. They exhibited significant increases in precancerous and cancerous lesions in the pancreas. So, let's talk about this. A little more because nicotinamide, mono nucleotides effect on accelerating tumor. Growth was dependent on senescent cells, which can disrupt normal
Functions and ironically
also Drive the progression of cancer over time as well. This
is in spite of the fact that senescence is a
program that usually prevents cancer more immediately in the short term,
the reason this happens is that when cells become senescent, they can
secrete molecules that tend to have the following
qualities. They are pro-inflammatory. They're involved in immune activation and evading. The immune
system, they're involved in growth signaling and also involved in angio Genesis which plays
A role in cancer.
Metastasis NAD. Seems to increase this
quality of senescent cells likely because it's being used in terms of energy
metabolism. So it's making these cells even the senescent cells even more tumorigenic. And while this study only looked at nicotinamide,
Mana nucleotides effect on cancer
growth, it's quite possible that nicotinamide right beside may
show similar results in this very, very specific context, which is a type of cancer. Where pro-inflammatory
Senescent cells Drive tumor growth.
That does not mean that nicotinamide, mononucleotide,
or nicotinamide, rye beside supplementation will cause cancer or even drive, tumor progression and other types of cancer.
But I will say it would be nice to see
long-term animal studies to confirm. I'm sure those are underway
now. Let's focus our attention on whether translation of all. This preclinical data to humans is likely with the exception of the cancer study. I just mentioned
much of the preclinical data seems pretty
You promising.
But there are a couple of
important points to make with respect to these animal studies that are very relevant for translating this data to humans.
First, let's talk about dose
a majority of the rodent studies which to use nicotinamide, right beside orally used a
very high dose
of nicotine in my right beside in the range of 400 milligrams per kilogram body weight, which translates to a human equivalent dose of 32 milligrams per kilogram body weight. So for a hundred and eighty pounds,
Person. That would be approximately two point six grams of nicotine and my dry beside per day.
We will discuss human studies in a
minute, but that is a very high
dose and it is a dose that is
orders of magnitude higher that has ever been clinically tested regarding the nicotinamide mononucleotide animal studies. The majority of them all used, very high dose about 500 milligrams per kilogram body weight, and typically it was injected into the abdominal region.
In of animals
which makes it quite
difficult to translate findings to humans. The oral dose that was used in the long-term aging, study used a dose range on the low end. The dose was a hundred milligrams per kilogram
body weight, which is
a human equivalent dose of around, eight milligrams per kilogram body weight.
So for a hundred eighty pound
person that translates to about. 650 3 milligrams of nicotinamide mononucleotide which seems pretty doable.
Of course, the mitigation of age Associated physiological.
Decline was much more robust at the high dose of 300 milligrams per kilogram body weight, which is a human equivalent dose of 24 milligrams per kilogram body weight, or approximately 2 grams of nicotinamide mononucleotide per day for a hundred, and eighty pound person. Again, that's a pretty high dose.
The next point of concern is
the bioavailability of either, nicotinamide? Right beside or
Nicotinamide mononucleotide, the important point to address is whether nicotinamide right beside or nicotinamide mononucleotide
can reach other tissues intact and directly form NAD.
Without going through that NAD recycling, pathway that I mentioned earlier
called the Salvage pathway. The Salvage pathway would mean that nicotinamide rye
beside or nicotinamide. Mononucleotide were first metabolized into just nicotinamide before
Forming NAD, instead of directly forming NAD.
This is an important point because NAD produced from the
Salvage pathway
is subject to feedback inhibition
and therefore cannot raise NAD levels in tissues above a certain level.
So let's talk about some details. An animal study using isotope tracers allowed NAD made directly from
nicotinamide right beside or directly from nicotinamide mononucleotide versus n.
NAD made from nicotinamide
via the Salvage Pathway to be measured. What the study found was that I at a
low oral dose of around, 50 milligrams, per kilogram
body weight of either,
nicotinamide, right beside or nicotine Ahmad nicotinamide, mononucleotide.
They produced very low levels of a name NAD,
May directly from those precursors, but only in the liver, not in other tissues, low levels of nicotine, in my drive NAD. On the other hand were found in the kidneys and very low levels of nicotine in my drive and AD were found in the muscles and also in the
brain, the human equivalent dose of 50
milligrams per kilogram. Body weight is roughly four point zero, seven milligrams per kilogram body weight. So for
An 80 pound person that is
approximately 330. 2 milligrams of either nicotinamide, right beside or nicotinamide - mononucleotide, which is a pretty doable dose,
but very little increases in NAD,
were found at least in animals at that dose.
A higher oral dose was also done but only for nicotine, my dry beside a dose of
200 milligrams per kilogram, body, weight of nicotinamide, Rai beside showed no difference compared to a low dose in terms of making NAD, direct from nicotinamide right beside in any other tissues other than the liver. However, more of the NAD. Derived from the Salvage pathway was found in the kidney muscle and the Brain then at the lower dose,
so 200 milligrams per kilogram
To wait, translates to around a human equivalent dose of 13.6. Sorry, 16.3 milligrams per kilogram body weight,
which for a hundred, and eighty pound person is about one
point three grams, which is
pretty high, when nicotinamide Rye beside or
nicotinamide, mononucleotide were given intravenously at a time, varying doses. So 50 milligrams per kilogram body weight, or 500 milligrams per kilogram body. Weight directly produced NAD was
Found in the liver kidney and muscle in a dose-dependent manner.
However, the only NAD detected in the brain was that, which was
salvaged from nicotinamide suggesting that neither nicotinamide right beside nor nicotinamide. Mine are nucleotide cross, the broad blood-brain barrier,
it is noteworthy that head-to-head
comparison of identical doses of injected nicotinamide, right beside and nicotinamide mononucleotide produced more NAD made directly from nicotinamide right beside it.
Liver kidney and particularly in the muscle tissue compared to nicotinamide mononucleotide.
So what does this all mean? And should we care what this data from the
isotope? Tracer studies means,
is that even at very high oral doses. Neither nicotinamide,
right beside or nicotinamide, mononucleotide appeared to directly be transported to other tissues other than the liver
at least again at those
doses that were measured
Ever nicotinamide, right beside and
nicotine Ahmad mononucleotide were converted into nicotinamide which was then transported to other tissues. And some of that nicotine mind was then converted into NAD and at the
end of the day,
isn't raising cellular energy levels, what is most important anyway?
The other animal studies a previously mentioned that showed positive health benefits and tissues like
the muscle, or the brain were at a very high oral dose of nicotine, in my dry beside
and nicotinamide mononucleotide. In fact, in some cases, they were double the dose. So
they were about 400 milligrams per kilogram body weight.
So, it's possible that nicotinamide right
beside and nicotine Ahmad mononucleotide can be transported to other tissues other than the liver at very, very high.
Oral doses
that that's yet to be shown. However, it's also possible that at very, very high doses, the NAD, derived from the Salvage pathway was high enough to do something beneficial, the isotrope the isotope data also suggests that if nicotinamide,
right beside or nicotinamide adenine, dinucleotide is administered, intravenously. Both of those compounds are able to be transported to other tissues and directly form NAD and not.
Be subject to feedback inhibition. This also raises NAD levels in multiple tissues to a much higher concentration than otherwise would be,
of course IV. Injection of these NAD
boosters is very challenging to translate to
humans. You may be wondering why all the
messing around with NAD boosters like nicotinamide, right beside and nicotinamide minor nucleotide in the first place. The reason nicotinamide right beside and nicotinamide mononucleotide are popular is because they can be transported into multiple tissue types including the liver kidney Moss.
And heart. The brain is the
exception. Neither
nicotinamide right beside nor nicotinamide mononucleotide seem to be able to directly cross the blood-brain barrier, but both form nicotinamide, which can be transported into all tissue types including the brain where it can then form NAD.
So why not just go to the source and take or inject NAD directly? Well for starters NAD has
poor
bioavailability animal Studies have shown that upon
ingestion, oral oral.
We administered NAD is primarily digested into the precursor nicotinamide but also to nicotinamide right beside and nicotinamide mononucleotide before being
absorbed while oral bioavailability of NAD is low, the hope is that intravenous NAD. Infusion May bypass that digestive system
The problem is that no mammalian NAD. Transporter has been identified. And with the exception of the brain and the Heart
extracellular NAD, has not been shown to be taken up into tissues.
When NAD was injected into the
abdominal region of mice. It was able to raise NAD levels in some brain regions.
Similarly mice. That were injected with a high dose
of NAD. Had increased levels of NAD in the
heart and also protection from cardiac hypertrophy. This suggests that Direct
Of NAD at a high-dose, maybe doing something
beneficial, at least in the brain, and in the
heart.
I would like to mention that just because no data exists, that does not mean that
NAD. Delivered intravenously, cannot raise NAD levels and other tissues other than the brain or the
heart. It's possible that extracellular NAD. Could be metabolized to nicotinamide and that could be transported to
other tissues like muscle. And also be transmitted be converted into NAD.
While there is very little, little
preclinical data and 0, clinical data on Direct IV, injection of
NAD it
I seem like this maybe also be a good
idea or a good area to explore as a potential way to Boost energy levels and tissues.
But let's move beyond what is plausible and talk about human data to date. There is no published evidence of oral
nicotinamide, mononucleotide supplementation in humans,
but there have been two
randomized, placebo-controlled, trials showing that nicotinamide, rye beside can increase NAD levels,
at least in white blood cells in a dose-dependent manner. So, let's talk about those
in an eight week, long randomized, double-blind placebo-controlled,
study involving a hundred and twenty healthy adults between the age
of 60 and 80 years
old a 250 milligrams, daily dose of nicotine in my drive aside and pterostilbene a natural compound. Found in blueberries, that activate sirtuin, similar to Resveratrol increased, participants whole blood and AD Levels by 40% compared to their Baseline levels. Just after four weeks, participants whole blood NAD levels increase by
90% when taking a double dose which was 500 milligrams, those who took the lower dose exhibited reduce diastolic, blood pressure and lower levels of the liver enzyme alanine aminotransferase, which is a marker of liver
damage. However, it is difficult to
know whether nicotinamide Rai beside pterostilbene or both are responsible for the effects on blood pressure and Liver Health. Previous clinical studies have found that Tara still being reduced blood pressure at least in adults.
Another randomized. Placebo-controlled, trial involving, 60, middle-aged and older adults between the ages of 55 and 79 years old demonstrated that a 500 milligram dose of nicotinamide, right beside twice daily for a total of one gram per day for six weeks was well, tolerated and increased energy levels in white blood cells by 60%.
The study participants also
experienced improvements in blood pressure and aortic stiffness. But these
effects were not statistically significant, possibly due to the size of the dose, or the
relatively small. Number of people in the study
nicotinamide, right? Beside had no effects on metabolic
function motor function or Exercise capacity and
performance. That's pretty much it for the randomized. Placebo-controlled, trials. The data seems to indicate that oral
nicotinamide, right? Beside can raise NAD levels and whole blood. And in
White
blood cells but that it is only a conclude that's the only conclusion that can be made. The highest dose tested was one gram per day administered as 500 milligrams, twice a day. If we Circle back to the
animal data on nicotinamide, right beside and all the benefits that we're seeing, that was a human equivalent dose of 32 milligrams per kilogram body weight, which is around 2.6 grams per day for a hundred and eighty pound person
while the short term clinical studies, show nicotinamide,
right beside given orally is safe at least in the short term
ERM. No long-term Studies have been done.
It's worth at least a small mention that nicotinamide, right beside and
nicotinamide mononucleotide both break down into nicotinamide over time,
especially in conditions of high humidity or high heat, somewhat perplexingly supplemental. Nicotinamide may even
reduce sirtuin
activation. The good news is that overall if these supplements are kept
cold, they are relatively stable and in
most cases the supplements will
contain very little nicotinamide.
So it's a good idea to make sure.
These
products. Stay cool as much as possible and get them from a manufacturer to make sure that they have not been laying around in a hot Warehouse somewhere longer than
necessary. Okay, just to recap NAD is crucial for our survival, it can be obtained in the diet but the body recycles it to get most of what it needs. Unfortunately day-to-day living plus
normal aging can cause any D levels to drop. This
causes metabolic and mitochondrial dysfunction as well as many of
the other problems and conditions associated with
aging like elevated.
Damage any D levels can go up when we exercise or fast, but NAD
boosters like nicotinamide, right beside and nicotinamide, mononucleotide can also and increase NAD levels in a dose-dependent manner.
However, most of the data on NAD
boosters comes from animal
studies, whether these boosters are effective and
safe. In humans is still a big
question, so those are my thoughts on NAD in a nutshell. I think the data on the NAD
precursors is very promising and
Exciting. But out of abundance of caution,
much more needs to be done before I'm ready to dive in with both
feet. That's it for today's episode. Thank you so much for listening. If you would like to learn more about
NAD nicotinamide, right beside and nicotinamide mononucleotide
check out the topic page is my team and I put
together remember earlier at the start of this
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This is one great example.
Now available
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Is we
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you can also just look them up on the topic pages and there's a really good
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illustrations, dozens of citations and more, literally everything we talked about today. I mean, everything sirtuins
NAD nicotinamide, right beside nicotinamide, mononucleotide, even the things, we barely mentioned like Resveratrol have a topic page. This is a powerful new resource made
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