Information Theory of Ageing

Is it possible to stop or reverse ageing, and with it the multitude of chronic and degenerate conditions we tend to succumb to with time?  The new “Information Theory of Ageing”, proposed by researcher David Sinclair, seems to hold such a promise.  Great strides have already been made with mice, where old mice rapidly regain their youthful strength and stamina and organ damage is reversed.  Simultaneously human studies are on the way.

By understanding the workings of the Information Theory of Ageing we can start applying some of its principles in order to activate and fuel our longevity genes.

For people suffering from any degenerate conditions this may be especially interesting to apply.  (Do also read the article on Glyphosate and GMO’s if you suffer from any chronic disease, as it is of key importance for the healing process.)

So, what is the Information Theory of Ageing?

The Information Theory of Ageing

To better understand the context of Information Theory let us take a look at how digital and analogue information are coded in humans and go from there.

Digital Information

We find what can be named as digital information in our genome.  The digital information is the ATCG coding of the DNA.  In computers we have 0 and 1, and using these we can write down information as sequences of 0’s and 1’s.  Our DNA has four basic letters namely the nucleobases A (adenine), T (thymine), C (cytosine), and G (guanine).  The sequences of these contain the genetic information in a digital form.

Half a century ago it was hypothesised that mutations in this digital coding, due to environmental factors such as radiation, led to ageing.  However, this theory does not really hold up, as experiments with mice with large amounts of mutations did not show signs of early ageing.

Analogue Information

Then, we have the epigenetic information.  This has to do with how the DNA strands are packaged.  Usually they are tightly fixated together with proteins called histones.  The way they are packaged decides which genes will be expressed and which will be silenced.  When they are packed tightly the genes are silenced.  When they are opened up, they can be expressed.

Here  is where the so called “longevity genes” come in.  They are named Sirtuins.  They package the DNA and silence certain genes.  In fact, the name “sirtuins” comes from SIR2, which was first found in yeast in the 1970’s and thus given the name “Silent Information Regulator 2”.  And so, as indicated through their name, an important job of the sirtuins is to silence certain information.  In the 1990’s sirtuins were found in worms, and then in the beginning of the 2000’s much of what we know about them was discovered.  The particular information that sirtuins silence has to do with the ageing process, hence the nick-name “longevity genes”.

So, the epigenome is what controls how the DNA is packaged and thereby what is expressed.  This information is not recorded in a digital form.  Instead it has been proposed by researcher David Sinclair that it can be seen as an analogue form of information.  It is analogue because it has to be able to change and adapt quickly, as the environment changes.  As such, it is highly affected by noise, over time.

And so, the new theory, proposed by David Sinclair is that ageing is loss of analogue information, over time.

In other words, we lose some of the epigenetic information over time, and genes that should be silenced, that we relate to ageing, are not silenced efficiently.

The question related to staying young now becomes:  How do you maintain the analogue information, or even re-gain lost analogue information?  How do we make sure that the Sirtuins work properly?

Researchers are working on re-gaining lost information and are making progress.  This involves being able to control the process of taking any cell back to a pluripotent stem cell.   This involves using three of of four Yamanaka transcription factors (Oct4, Sox2, and Klf4), which can be activated through viruses and in other ways.  With these proceedings one is able to restore lost organ functions and such.  On September 10th 2019 David Sinclair and Matthew LaPlante will be coming out with their book Lifespan:  Why We Age and Why We Don’t Have To.  Surely, it will contain all of this information in detail.

You can read about how mice are re-gaining their optic nerves based on the reversal of the three above mentioned Yamanaka factors.

When it comes to making the sirtuins work properly we already know some crucial details.  These tell us how we can activate them and provide them with what they need to work.  Knowing this we can work on making sure they function in our bodies.  This will be the focus of the rest of the article.


Sirtuins are proteins that are also enzymes.  In humans we have found 7 types of sirtuins.  In the picture you can see where they are found in the cell (in the nucleus, cytoplasm, and mitochondria) and what general functions they have (information gotten from Wikipedia):

 Apart from silencing certain genes some of them also have the job of repairing damaged DNA.  When they do this they leave the site, where they are silencing genes, do their repair work, and should later come back to continue silencing.  However, sometimes they cannot find their way back.  When this happens with the sirtuins, and some other proteins, over time, the cell tends to lose its youthfulness, because the ageing related genes are not being silenced properly.  The more DNA damage, the greater the chances of the sirtuins to lose their way back to the silencing site.

What is needed in order for the sirtuins to do their work and find their way back to silence the proper genes?

In their work the sirtuins indirectly control hundreds of other enzymes.  Some of the sirtuins work by removing acetyl-groups of other proteins, deacetylating them.  They remove acetyl-groups from histones, the proteins that DNA is wrapped around.  When they do this the DNA ends up being winded up tightly.  When it is wound up tightly the genes are silenced and the DNA is protected from exposure to damage.  However, in order to do this work, or deacetylation, the sirtuins require something called NAD, nicotinamide adenine dinucleotide.

What is NAD?

NAD is Nicotinamide Adenine Dinucelotide and it is a co-enzyme.  A co-enzyme is a compound that an enzyme needs to function.  An enzyme is a protein that functions as a catalyst, and makes a particular chemical reaction happen.  Enzymes are essential for the function of our bodies.

We have NAD in the NAD+ form and the NADH form.  It changes from one to the other.  It plays an essential role in cell metabolism, particularly in the mitochondria.

In the picture below we can see how NAD works inside of the mitochondria to produce energy in the form of ATP:

Apart from being required for energy production, NAD is also consumed by some enzymes, like PARPs (poly-(ADP-ribose)-polymerase), CD38 (Cluster of Differentiation 38, cyclic ADP ribose hydrolase), and sirtuins.  In fact, NAD is essential for some sirtuins to work.  As we age we tend to get lower and lower levels of NAD.  This affects the work of the sirtuins negatively.  So, if we could keep our NAD-levels high, the sirtuins could do their job better.

How Do We Raise NAD-levels?

Taking NAD itself orally is not an efficient way of raising NAD-levels as the molecule is rather large and does not get into the cells as easily where it is needed. It is, however, possible to do direct infusions of NAD molecules and this is done in some clinics.  In those cases it is interesting to first take betaine (trimethyglycine) to reduce the flush-like side-effects of the infusions and improve the efficacy of the procedure.  Doing NAD IVs is currently quite expensive, around a thousand USD per IV, and so that may be a disadvantage.  There are also companies working on super NAD-boosters in the form of drugs, like MIB626, but these not available quite yet.

There are also ways of stimulating the body to make more NAD and it is possible to take pre-cursors to NAD.  Avoiding actions that lead to rapid NAD consumption can sometimes also be incorporated.

Some types of stress raise the NAD-levels.  This is called hormesis, and it induces a hormetic stress response.  These are:

  •  Physical exercise
  •  Heat
  •  Cold
  •  Lack of nutrients

By doing some physical exercise, exposing ourselves to some heat or cold, or fasting at times, we will increase our NAD production as a result.

Physical Exercise

It may be of interest to do the Nitric Oxide Release Exercise three times a day.  It was developed by the medical doctor Zack Bush and has a number of benefits.  It quickly releases NO, Nitric Oxide, in the blood lining, makes it possible to build muscle, and relaxes the blood vessels.   It also leads to biogenesis of mitochondria.  When we do very intense exercise we will tend to stimulate the production of new mitochondria.  The exercise itself takes less than 4 minutes and it is recommended that one do it three times a day, waiting at least 2 hours between the different sessions (so that the nitric oxide may be restored and re-released).  All together this will amount to about 10 minutes of exercise per day.  The idea is that this may be all the cardio you need in a day.

Here is a video showing how to perform the nitric oxide release exercise:

Heat and Cold

The taoists recommend 3 minutes of hot water followed by 3 minutes of cold water, experienced repeatedly.  For beginners this may be a challenge so you may start with 20 seconds of hot water, as hot as one can stand, followed by 30 seconds of cold water, as cold as one can stand.  This should be repeated a number of times and one should finish with 2 minutes of cold water.

Immediately after the shower one will feel quite invigorated and general well-being will be felt throughout the body.  This will in part be due to the hormones released from the cold shower.

These showers will increase the number of mitochondria you have and your NAD-levels.  You will probably notice how the first couple of days the cold showers will be rather painful, but already on your 4th day it will not seem as big of a deal.  You will be killing off not so efficient mitochondria and generating new.

We know that Sirt3 responds to cold and helps make more mitochondria, creating brown fat (fat that is full of mitochondria).

Saunas can also be of benefit.  There are some Finish studies showing some health benefits.  The sauna benefits seem comparable to benefits gotten through exercise.


It is good to feel hunger each day.  One way of achieving this is through intermittent fasting.  This means one has a window of eating that is shorter than 12 hours.  The rest of the time one is not eating or drinking anything other than water.  Having an 8 hour window of eating, thus 16 hours of fasting per day, one will usually go into the phase where the body uses glycogen and possibly even starts running out of it (depending on what one had as a last meal and what activities one has engaged in).  This will trigger the stress response that stimulates the NAD production and have long list of other benefits, including the start of autophagy.

It is good to combine your first cardio exercise with a fasted state.  So, you can do your first NO release exercise before you start eating.

To also get stronger detox benefits and a good sleep, with all the benefits that accompany good sleep, it is advisable to not eat for four hours before going to sleep.  If this is not something you can do each day, do try to do it at least two times a week and notice how it affects your sleep and general wellbeing.

Another useful way of fasting is to have one or two days a week without food.  This should leave the body without food for around 36 hours.  This way one will be able to go into the process of autophagy and experience a deeper cleansing.  It will also stimulate the synthesis on NAD.

We can also increase NAD-levels by ingesting:

  •  Substances that produce a stress-response, and mimic lack of nutrients
  •  Pre-cursors to NAD

Often we will find that the pre-cursors to NAD work better when the body is also exposed to some type of stress (as the types described above).  For instance, when the precursor NMN is taken up by cells it is converted into NAD in one single step, but that step depends on the stress response.


Substances That Induce Stress - Xeno Hormeses

There is a number of natural substances that can induce a stress response, xeno hormeses, that may lead to a synthesis of NAD within the body.


Resveratrol is a plant stress response.  It is found in fruits like grapes, blueberries, mulberries, and raspberries as they ripen to protect them from problems like fungus infections, or lack of water.  It is primarily found in grape skin.

It mimics a lack of nutrients in animals, including humans.  It has been shown to activate Sirt1.  Let us do a brief aside:  How does resveratrol mimic the fasted state?  This is interesting.  It actually mimics free fatty acids, which is what is released when we are fasting, particularly oleic acid (18:1).  However it does not have the calories of fat.  This may also further explain why monounsaturated fats (basically free fatty acids) are healthy.  We find them among other places in olive oil, and the Mediterrenian diet, full of olive oil, is known to have positive effects on health.

It also seems to have significant and very positive effects on blood vessels, reducing arterial stiffness.

However, in nature it is found in very small quantities (5-10mg of resveratrol per 100g of grape skin and a glass of red wine will on average contain 0.3mg of resveratrol) and as a purified supplement is it not very bioavailable.  Taking a purified supplement with fat may increase its absorption.  In mice fat increased the amount of resveratrol taken up five- to tenfold.

Taken together with an NAD-precursor such as NMN there will be a synergetic response, as the resveratrol induced stress response will stimulate the conversion of NMN into NAD.  The researcher David Sinclair takes 500mg of resveratrol with yoghurt in the morning (wishing to take that amount in wine would require 1666 glasses of wine).


Pterostilbene is a polyphenol that is also found in red wine and some berries and it is quite similar to resveratrol, but it appears to be 80% more bioavailable.  However to get significant amounts from regular food seems rather difficult.  To get 3 mg one would have to eat 140 cups of blueberries And so, this may be a substance that may require supplementation in a purified form.  It is probable that the different substances may work better together when coming from whole foods.   It seems that resveratrol and pterostilbene may complement each other.


This is also a sirtuin activating substance.  It is a polyphenol that is found in small quantities in strawberries.  It is also an anti-cancer agent and a senolytic.  A senolytic gets rid of senescent cells, damaged cells that affect other nearby cells negatively in the body.  Its senolytic properties are only activated when taken at sufficiently large doses.  But in small doses it still has positive influence.  It has the capacity to cross the blood-brain barrier and is a neurotropic.  It is neuroprotective, increases glutathion, and reduces inflammation.


Quercetin is a flavanoid found in food.  We find 173 mg/100g i capers, 55 mg in dill, 53 mg in coriander, 32 mg in red onion, 15 mg in cranberries, and 13 mg in lingonberries.

Quercetin is mostly known as a senolytic, clearing senescent cells in the body, reducing senescent toxicity, especially when taken together with other agents, like the chemodrug dasatinib.  As a senolytic it may be seen as an anti-ageing agent.  But is also makes resveratrol more efficient by reducing the rate of resveratrol sulfation in the liver.

It appears to activate Sirt1 and perhaps through it suppress the pro-inflammatory pathways.

Furthermore it is also a CD38-inhibitor, which means that it inhibits the enzyme that degrades the NAD-synthesis as well as the age-related NAD-decline.

It is also able to get into the brain and there it protects against neurodegenerative diseases like Parkinson’s.  It protects the dopamine producing cells.  Dopamine tends to drop off after age 45.  It also protects against brain herpes.  This is relevant because 70% of the population over 50 years old who have the herpes virus in their body will have a brain invasion and the herpes will infect the neurons.

What Are Some Pre-Cursors to NAD?

There are several pathways through which NAD is produced.  One is called a de novo pathway and in it one starts with the amino acid tryptofan.   Another is the salvage pathway, which entails certain vitamins B3, and B3 precursors.   The one starting with nicotic acid (NA) is called Preiss-Handler pathway, and the one starting with nicotinamide riboside (NR) is the Nkr-pathway.  In the picture we see what the pathways look like and what the different substances are.

These pathways are not always available to all cells.  Some cells may use some pathways more than others.

Which of these precursors are best at raising NAD levels?  The best options seem to be NMN and/or NR.  But let us take a look at them one by one.


NMN, nicotinamide mononucelotide, is perhaps the quickest way as it gets into the cells and only requires one step to be converted into NAD.  The conversion happens with the help of the enzyme Nmnat, nicotinamide mononucleotide adenylyltransferase, of which there are three types in humans.  This enzyme is also neuroprotective, perhaps in part due to its role in NAD production.  It is up-regulated when exposed to stress such as heat shock or lack of oxygen.  So, it means that more NMN can be turned into NAD when we also expose the body to some stresses.  Resveratrol also appears to activate Nmnat.

The downside of NMN is that the human studies on its efficacy and safety are still on the way (some results should be available in December of 2019) and it is a very expensive supplement to get and perhaps impossible to get in large enough quantities from whole food.  It is important to keep NMN cool and dry, so that it does not degrade into nicotinamide, which is not desirable as it may end up having the opposite effect of what we are looking for.

NMN is found only in tiny quantities in some foods.  Broccoli has 0.25-1.12 mg/100g, cabbage may have up to 0.9 mg, avocado up to 1.6 mg, tomatoes 0.3mg.  And so, to efficiently raise NAD levels one would require a purified supplement.  David Sinclair is taking 1000 mg in the morning.



NAM, nicotinamide, is a sort of vitamin B3, that unlike niacin does not produce a flush when taken in larger quantities.  Taking NAM may produce some effect in raising NAD levels but not as significantly as NMN or NR.  As we see in the picture depicting the production of NAD, NAM needs the enzyme Nampt to be turned into NMN.

Just like NAD levels decline with age, so do Nampt levels.  Because of this, due to ones age, one might not have enough Nampt to significantly raise NAD levels.  Also, it has been found that outside of the body NAM can be a sirtuin inhibitor when taken in large doses, but not necessarily inside the body.  So, NAM is not the best option when it comes to raising NAD levels.  It seems to inhibit sirtuins and PARPs.

Nampt has also been seen to be over-expressed in some cancers and may assist in the formation of new blood vessels.  However, we do not have studies showing that supplementation with NAD precursors leads to cancer.  In fact, the contrary seems more plausible, the body seems to be more capable of defending itself and restoring itself as a result of raised NAD levels.


NR, nicotinamide riboside, is actually a type of vitamin B3.  It is capable of raising NAD levels in humans and does so without any major downside, it seems for now.  In an 8 week double blind placebo controlled trial the amounts of 100, 300, and 1000mg of nicotinamide riboside chloride were given and blood levels of NAD were raised by 22, 51, and 142% respectively within two weeks and stayed at those levels throughout the trial.  In clinical trials on humans doses as high as 2000mg per day were administered without any side-effects.

In one of the trials it was also discovered that NAAD (nicotinic acid adenine dinucleotide) seems to be created when NR is supplemented.  It has been shown that NR boosts NAD more than do NA or NAM and that NR is orally bioavailable.  See the differences of how NA, NAM, and NR boost NAD in mice in the picture.

It may be the case that there is a certain minimum dose one has to take to affect the NAD-levels throughout the body by taking NR.  If taking less ones body might simply remove it all.

It is very interesting to see that NR improves stem cell function and mitochondrial function in mice.  Stem cells are important in the regeneration of tissues.

NR does not need the enzyme Nampt to be converted into NAD, which otherwise is the rate-limiting enzyme, and tends to decline with age.  Instead it uses the nicotinamide riobse kinases NRK1,2.  They are up-regulated by stress.  NR also does not inhibit sirtuins.

A word of caution is to keep the supplement cool and dry.  Otherwise it will degrade into nicotinamide and have the opposite effect (inhibit sirtuins and PARPs).



NA, nicotinic acid, is usually called niacin and is the most common form of vitamin B3.  It leads to NAD production through the Preiss-Handler pathway.  The problem with taking niacin is that it causes a flush when larger amounts are taken.  The flush is usually experienced as heat and a sensation or itching and/or burning and lasts for a few minutes.  Even a dose of as little as 50mg may give rise to a flush, though starting out with lower doses and increasing incrementally one may develop a larger tolerance and be able to handle larger doses without flushing.  Also niacin has a short half-life and is not able to raise NAD levels as efficiently as other precursors.  As opposed to other precursors NA seems to be able to lower blood lipids.


It seems that tryptophan is the main NAD precursor in the liver.  When little tryptophan is present in the diet most of it is used to make NAD.  It has been suggested that 1mg of niacin is equivalent to 60mg of tryptophan.  When taking large quantities of tryptophan there is a series of possible side effects and so taking extra large doses of tryptophan to increase NAD levels may not be the best strategy

The NAD precursors should be taken in the morning as they may increase the energy and the peak NAD after taking say NR (Nicotinamide Riboside), is 8 hours.  The effects of taking a precursor only start kicking in after two to three hours of taking it orally.

We usually get NAD precursors from food.  The largest source is usually unprocessed food, where we break down the there present NAD and similar compounds (like NADH, NADPH, their metabolites, etc).

How do we avoid lowering NAD?

What if, instead of trying to boost NAD we could find the cause for its decline and address it?   Well, that just might be possible.  The cause has to do with an over-expression of NAD-consuming enzymes.

Apart from sirtuins there are also enzymes like PARPs and CD38 that consume NAD.  If we can make sure that they do not have to consume as much NAD, we will help preventing NAD drainage.  Also, it is important to avoid alcohol, as that too can drain NAD.

CD38 - Responsible for Age-Related Decline

Interestingly enough it currently looks like the expression of CD38 increases with ageing and that increase may be responsible for the age-related lowering of NAD.  The over-expression of CD38 eventually leads to unhealthy mitochondria.  The activity of CD38 itself seems to be in part mediated by Sirt3.

So, what is CD38?  It is an enzyme that acts on cell surfaces and is involved in immune response, inflammation, cancer, and metabolic diseases.  It is often on the surfaces of immune cells, like macrophags.  Perhaps its role is to protect against certain types of pathogens like certain types of bacteria, which need NAD to grow but cannot make it on their own.  The presence of CD38 would then lead to the demise of the metabolic system of the pathogen.  CD38 is also involved in calcium signalling.  A complete lack of CD38 in mice leads to some unwanted consequences, like a not so well working immuno-response, behavioural modifications, and some metabolic disturbances.

However, CD38 is also the main NAD-degrading enzyme in mammals.  With increasing age its expression increases 2-3 times in all tissues tested in mice and some tissues that were tested in humans. It is also important in the creation of Alzheimer’s disease and CD38 inhibition may be interesting in its prevention.

Furthermore, CD38 seems to be involved in the degradation of the synthesis of NAD from NMN.  Taking NR (which is then converted to NMN) or NMN directly it was shown that the NAD synthesis becomes negatively impacted by CD38.  So, if one could find some way of partially inhibiting the action of CD38 more NAD could be synthesised from precursors and less NAD would be degraded.

Indeed, CD38-inhibition in animals has shown positive health effects on a number of diseases like obesity, kidney injury, heart ischemia, viral infections, and cancer.

There are artificial CD38-inhibitors as well as some plant molecules are CD38-inhibitors, some flavanoids.  It is interesting that one of the artificial inhibitors, called 78c, was used in animals to see if the age-related NAD decline could be counteracted, and it could.

Among the natural inhibitors we have quercetin.  Quercetin is a CD38 inhibitor both in the body and outside of the body.  It is also a direct sirt1 activator and potentiates resveratrol.  So, this may be an extra interesting option in terms of supplements for NAD-boosts.  There are other CD38 inhibitors like apigenin, but this one is not a direct sirt1 activator, like quercetin.  Others that have been identified are luteolinidin, kuromanin and luteolin.  The positive side is that the flavanoids do not seem to show any toxicity in humans (see this and this study).

Unfortunately, at this time, I do not know exactly how much quercetin one would have to take to inhibit CD38 sufficiently to stop the age-related NAD-decline and still get the benefits of CD38, or if it would work in humans.  But that would be an extremely interesting study to see.

PARPS - How to Avoid Over-Activating Them

PARPs also consume NAD but do not seem to be the cause of the age-related NAD-decline.  PARPs are important when we have double strain breaks of the DNA.  They come in and fix them.  But, as they do this they use up NAD.  And so, a healthy strategy is to keep the DNA breaks to a minimum.  We naturally often get DNA breaks in cell division but also when exposed to certain types of radiation.  Reducing our exposure to radiation is a health strategy that will help avoid NAD drainage.  This means avoiding non-essential x-rays and CT-scans.

Alcohol - Draining NAD

Each molecule of alcohol that is broken down in the body requires two molecules of NAD.   If we drink larger quantities or chronically, we will be lowering our NAD levels.

Methyl Donors

Taking supplements of NAD-precursors may lead to a depletion of methyl groups in the body.  This is because the pre-cursors need methyl groups to be excreted and when supplementing one would supplement with much more than one would be likely eat in regular food.   But we see that NAM seems to elevate homocysteine more than NA.  A short 8 week study of NR supplementation did not show increased homocysteine levels, but that was only an 8 week study.  Whether methyl-donor depletion really will be a problem we will probably see soon, as more studies in humans are concluded.

Some people already have problems with methylation without taking NAD precursors.  There are, for instance genetic variations often referred to as MTHFR (methylenetetrahydrofolate reductase) that may leave methyl-donor depletion.  Perhaps taking NAD precursors might exacerbate the problem for these persons.

Methyl donor depletion can lead to a number of problems because methylation is involved in a wide variety of processes.  Often one will see high homocysteine levels (which are related to circulatory disease) and low levels of certain B-vitamins may be common.  In some cases it may lead to a fatty liver when choline is low, or muscle weakness when creatine is not synthesised, or perhaps to low dopamine levels.

And so, as a precaution, it may be interesting to first measure some of the methyl donors or/and the homocysteine in the blood and after a month or two of taking NAD-precursors measure again in order to compare.

Here are some parameters in the blood that may be of interest to check in regard to how methylation is working in the body:

  •  Homocysteine  (becomes high when methyl donor are depleted)
  •  AST (liver)
  •  ALT (liver)
  •  Methionine
  •  Betaine
  •  Folate
  •  Choline
  •  B12
  • Methylomalonic acid

It is usually not absolutely necessary to take all these tests.  Some, like the melthylmalonic acid, may be more expensive.  But it is good to keep an eye on the homocysteine.

If taking NAD-precursors one may also consider taking some extra methyl donors.

Betaine anhydrous, or thrimethylglycine, is a natural substance found in foods like beets, spinach, or quinoa.  It is a small molecule with methyl groups and is a methyl donor.  As a methyl donor it may prevent homocysteine buildup in the blood.  Also, we had the added advantage of the amino acid glycine in thrimethylglycine.  This is an amino acid that is abundant in connective tissues, but if one does not eat connective tissues it may be on the low side.

Superfood Tip: Fermented Red Beets

Raw red beets contain 129mg of betaine per 100g beets.  An interesting way of eating beets is by fermenting them by cutting them into 2cm large cubes in a glass jar and filling it to the top with water with salt (1 table spoon of salt per litre of water).  You leave it for five days and then you can drink the juice or use the beets in your food.  For extra taste you can also add spices to the fermentation like lauryl leaves, all-spice, black peppar, and some garlic.  The red juice is kept in the fridge.

The fermentation process is extra interesting because it reduces the sugar content and provides us with a finished product that is also a probiotic and it is likely that the naturally occurring anti-nutrients like phytic acid and oxalates will be significantly reduced.  Beets also contain a lot of nitrates.  This is excellent because they will help you produce Nitric Oxide, which you will regularly release through the NO release exercise described above.  Beets also provide us with folate (100g give us 25% of a daily dose), which is also a methyl donor.

(Aside:  You can also release NO (Nitric Oxide) into your airways by humming.  You can actually get up to 250 ppm of NO in your nasal cavity.  This will help disinfect your airways, killing microbes, and assist the work of the mucosal respiratory cilia, which remove what should not be in the airways.  There is anectodal evidence of people curing chronic sinus problems in as little as 4 days by humming an hour a day.  This is also especially interesting in times of pandemics.)


Vitamin B12, in the form of methylcobalamin, as well as folate in the the form methylfolate may be useful vitamins to take.  B12 is especially important for those who follow a vegan diet and in the form of methylcobalamin it may provide extra advantages as a methyl donor.  Read more about B12 here and how the different types of B12 work in the body.

If one does not wish to take purified methyl-donor supplements it can be good to take nutritional yeast, as it contains several of the important B-vitamins, but usually not B12

Action Steps

In summary, we know that certain plant stress-response substances activate sirtuins when ingested, producing xeno hormeses.  We also know that certain stressful activities also tend to stimulate the production of NAD, through hormeses.  However, in order to produce NAD we will need some precursors to them.  And so, putting the three parts together (xeno hormeses, hormeses, and NAD-precursors) may prove to be a powerful youthfulness boost and important in assisting the recuperation from chronic illnesses.  Quercetin may also help in inhibiting the enzyme that leads to age-related NAD-drainage.

In terms of tips for food one would like to eat a lot of fresh (uncooked) food like salads and berries and this way get all sorts of polyphenols.  It is especially interested to get fresh food that has been stressed, not grown in perfect conditions, as that food will contain more stress-response molecules, like red grapes picked after a drought have more resveratrol, or bergamot is healthier after a nail has been driven into the trunk of the tree.  Further it is good to get monounsaturated fats like we find in olive oil and avocado.  Also it may be good to get in some fermented beets.

In order to naturally raise NAD levels and employ anti-ageing tactics you can:

  • Incorporate a short but intense work-out (like the “Nitric Oxide Release Exercise” above),
  • Take hot and cold showers (30 second of each repetitively, finishing with 2 min cold),
  • Let yourself feel hunger every day,
  • Do some intermittent fasting or 1 day a week without food,
  • Eat food containing resveratrol, pterostilbene, quercetin, curcumin, sulforaphane (or take whole food powders rich in them),
  • Make sure you are getting B-vitamins, for instance by adding nutritional yeast to your diet.

If you are willing to try supplements to raise NAD levels you can:

  • Take NAD-precursor supplements like NR or NMN (the fuel) but make sure you keep them cool and dry so they won´t degrade,
  • Consider also taking quercetin, pterostilbene or resveratrol (activates the fuel),
  • Check your blood to see homocysteine levels and possibly methyl donors,
  • Consider supplementing with methyl-donors like betaine, methylfolate, methylcobalamine,
  • Expose your body to fasting, heat/cold, and exercise (makes fuel useful).

Do not take any supplements before consulting with your health practitioner.  This article is only for informational purposes.  Consult with your health practitioner before making any changes.

How to Support This Work

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