Does NAD+ Actually Give You More Energy?

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All right, so we are going to fire away with a quick Q&A 17, and the question I want to spend the most time on is the one about NAD plus, because the answer depends almost entirely on who is asking it.

And what NAD plus is, is it works as a coenzyme that carries electrons down this electron transport chain inside of your mitochondria so that you can produce ATP, which is ATP is basically just the raw form of energy that your entire body uses to function.

That sentence has a lot packed into it, so walk the chain from the top.

You eat food, your body breaks it into smaller molecules, and those molecules get stripped of electrons inside the mitochondria, which are the small structures inside your cells where most of your energy gets made.

Those loose electrons have to go somewhere, and the thing that picks them up and carries them to the next station in the line is NAD plus.

It hands them off down a series of protein complexes, and the energy released at each handoff gets used to pump protons across a membrane, and the pressure from those protons drives a tiny molecular turbine that assembles ATP.

NAD plus is not energy itself, but rather the delivery truck that makes energy production possible, and if you run out of trucks, the whole loading dock backs up no matter how much food you put on it.

Now, here is where the supplement question gets interesting, because your body recycles NAD plus constantly. The same molecule picks up electrons, drops them off, and goes back for more, thousands of times a day, which means you are not burning through some finite reservoir buried somewhere in your cells. What you are running, instead, is closer to a fleet of delivery trucks that cycle the same route over and over.

So the question is not whether you have NAD plus, since every living person carries some amount of it already. The real question is whether the size of your fleet has shrunk enough that it has become the limiting factor.

As you age, depending upon what you eat, how well you take care of your body, drug use, diet, sleep habits, et cetera, basically how hard you are on your body paired with aging is going to dictate whether or not your body has the ability to sustain this pool of NAD plus that's available to transport these electrons that considered to answer your question.

A twenty eight year old who trains four days a week, sleeps seven hours, eats enough protein, and does not drink much is almost certainly not NAD plus limited. His mitochondria are already producing as much ATP as his cells are asking for, and adding more raw material to a system that is not running short of raw material does nothing you can feel.

But a person who's in their 50s or 60s, who doesn't exercise, who doesn't diet, who doesn't have a long history of taking care of themselves, they could take something like NAD plus and be like, holy shit, like the world is a new place.

Why? Because over time, paired with age and all the other variables I discussed, they probably have a much lower available pool of NAD plus, which means that it's basically the blocker that your body has that's not giving it the ability to transport these electrons and produce the ATP that it needs to produce.

This is what makes the research so frustrating for anyone looking for a clean yes or no.

In Elhassan et al., Cell Reports, 2019, older men took nicotinamide riboside, a precursor your body converts into NAD plus, at 1000 milligrams a day for 21 days, and muscle NAD plus itself did not rise in a statistically meaningful way even though downstream metabolites clearly did, which tells you the compound got in and got used but the muscle pool was not what was short.

Martens et al., Nature Communications, 2018, ran 500 milligrams twice daily for six weeks in healthy middle aged adults and did raise blood NAD plus by about 60 percent, and still found no change in exercise performance or most of the measures you would expect to shift if energy production had improved.

The compound worked exactly as designed and pushed the number up considerably, yet that number simply was not what had been holding those particular people back.

That is the whole lesson of NAD plus supplementation. If your habits are where they should be, you're doing the right things. Very unlikely that you're going to need to add something like NAD plus to help you feel your best.

And so what I'll say is this is if you want to know, like do a small dose, 50 milligrams, 25 milligrams, see if you feel a difference. There's no need to wait around for weeks, because the effect, if there is one, tends to show up fast, within days rather than a month, since restoring a pool that is genuinely the limiting factor does not require some slow accumulation phase.

The same logic applies to every injectable protocol, which is why I want to cover the timing question before we leave this.

Now, there's also another consideration that we make when it comes to pharmacology, which is it takes typically about five half lives of a drug for it to be fully saturated in your system.

Testosterone cypionate has roughly an eight day half life, so five half lives puts you around forty days before your blood level stops climbing and settles into a steady range, which is why pulling labs at week two tells you almost nothing about where you will land.

Behre et al., Journal of Clinical Endocrinology and Metabolism, 1999, tracked this directly with testosterone undecanoate and showed how long serum levels take to plateau across repeated injections rather than after a single dose.

Snyder et al., Journal of Clinical Endocrinology and Metabolism, 1980, showed the other half of the problem, which is that even at steady state, levels swing substantially between the peak after an injection and the trough before the next one.

When we take blood, we are capturing one point on that curve. Draw at the peak and you look supraphysiological. Draw at the trough and you look undertreated. Same protocol, same person, two completely different conclusions.

And then the other consideration would be something like your fasting glucose, right? Typically when we send people to get labs done, we ask that they fast 12 hours before, they don't eat anything until after their lab work is done because we want to get a baseline level of what your fasting glucose is, what your blood sugar levels are when you haven't eaten.

Eat a bagel two hours before the draw and your glucose reading describes your breakfast, not your metabolism.

The whole thing comes back to the same principle. A number only means something if you know what conditions produced it, and most people chasing a supplement are reacting to a number they captured under the wrong conditions.

On the mechanics side, a lot of the frustration people have with peptides is pressure, not product.

Vials are sealed under vacuum, so when you push water in without letting anything out, the pressure fights you on the way back. Then what will happen is when I add more water into it, more of a thing in there, it doesn't displace the air that's already in there.

So then when I go to draw, it's not creating problems for me where I'm having to wait like 10 minutes to watch it drip, drip, drip, but worst case scenario in between injections, let's say you reconstitute it, you come back the next day or the next week, just fill your insulin syringe full of air, then draw it, inject the air into the peptide, flip it back over, draw out the amount that you want, and you'll never have problems with being able to extract your peptide from the vial or losing anything.

If you experience a situation where you draw it and you get a lot of bubbles and it's all crazy, most of the time it's because you pulled it too fast, you squirted into the syringe, that's not what you want to do.

Research: Elhassan et al., Cell Reports, 2019 (PMID: 31412242); Martens et al., Nature Communications, 2018 (PMID: 29599478); Behre et al., J Clin Endocrinol Metab, 1999 (PMID: 10229906); Snyder et al., J Clin Endocrinol Metab, 1980 (PMID: 6777395); Kraemer et al., J Appl Physiol, 2002 (PMID: 12831709); Helms et al., JISSN, 2014 (PMID: 24864135).

References

Behre et al., Journal of Clinical Endocrinology and Metabolism, 1999. PMID: 10229906. https://pubmed.ncbi.nlm.nih.gov/10229906/

Snyder et al., Journal of Clinical Endocrinology and Metabolism, 1980. PMID: 6777395. https://pubmed.ncbi.nlm.nih.gov/6777395/

Elhassan et al., Cell Reports, 2019. PMID: 31412242. https://pubmed.ncbi.nlm.nih.gov/31412242/

Martens et al., Nature Communications, 2018. PMID: 29599478. https://pubmed.ncbi.nlm.nih.gov/29599478/

Kraemer et al., Journal of Applied Physiology, 2002. PMID: 12831709. https://pubmed.ncbi.nlm.nih.gov/12831709/

Helms et al., Journal of the International Society of Sports Nutrition, 2014. PMID: 24864135. https://pubmed.ncbi.nlm.nih.gov/24864135/