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Dr.Kats posted an update
Sugar cravings indicate low serotonin (consuming carbohydrates can temporarily boost serotonin levels) and ergo, low tryptophan and coupled to that, deficient nicotinic acid.
lamaeh and faysia9 Comments-
Can you comment on the relationship between low serotonin and low tryptophan? I’ve never been able to tolerate it and am a massive sugar addict, and on SSRI’s most of my life; wondering if it’s related. Thanks!
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Just saw the article below but it’s way too much for me to synthesize. 😋
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@lamaeh – not a problem! To address this, I will delineate these details beyond just l-tryptophan being the biological precursor for serotonin to make it more relatable and understandable in your personal case, while considering your previous (but not current?) SSRI-use and how this all plays into your unfavorable past experiences with tryptophan supplementation (i.e., what you will realize soon, was too high of amounts of it and further improper by not taking into account nicotinic acid necessary alongside).
Please check back later tonight or by tomorrow morning for my breakdown of all this for you!1
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Most people think: “Tryptophan → serotonin → melatonin, so I’ll just take more tryptophan.”
That’s chemically true, but physiologically incomplete — because tryptophan metabolism is hierarchy-based, not democratic.
The body assigns tryptophan to three competing pathways:
1. NAD⁺ (niacin) synthesis via kynurenine — primary survival use
2. Protein synthesis — maintenance use
3. Serotonin/melatonin synthesis — luxury use
So unless the NAD⁺ pool is already adequate, growingly and eventually, ultimately, nearly all free-form L-tryptophan is siphoned to regenerate NAD⁺ via the kynurenine/’de novo’ route, while also in consideration of the lacking nicotinic acid exogenously incoming, thereby leaving more insufficient tryptophan for serotonin or melatonin, as well as its other roles such as protein synthesis/anabolism.
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⚙️ Why NAD⁺ balance comes first
* Chronic stress, inflammation, and heavy amino-acid oxidation all drain NAD⁺ (basically protons / H+ proton motive force to process forward the breakdown of energy consumed into being usable for growth/function and resilience).
* This requirement ensues unchecked without consideration of pure, free-form nicotinic acid exogenously, i.e., the most efficient, direct precursor biologically in more ‘higher-ordered’ animals such as most mammals.
* As with so many other entities that without rhyme or reason systematically remain consumed in populations, SSRIs and other psychotropics increase serotonin turnover, which uses NAD⁺ at multiple redox steps (tryptophan hydroxylase, monoamine oxidase).
* Over years of SSRI exposure or high metabolic stress, baseline NAD⁺ falls; the brain can’t convert tryptophan efficiently to serotonin anymore.
* Result: sugar cravings, poor sleep, mood flattening — the brain signals for glucose because glucose metabolism transiently boosts NAD⁺ and serotonin synthesis.
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🔄 Why pairing free-form L-tryptophan with nicotinic acid matters
Supplementing tryptophan alone can worsen this imbalance:
* The body sees it as a substrate to rebuild NAD⁺ first.
* By way of enough flux to indicate directly biosynthesizing the NAD+, L-tryptophan is still automatically used as a substrate to rebuild NAD⁺ first as it was before.
* Serotonin production barely rises — sometimes even falls as the kynurenine pathway dominates.
Adding nicotinic acid (niacin) in the proper ratio replenishes NAD⁺ directly, so the body no longer has to “sacrifice” tryptophan for survival metabolism.
Only then can the 5-HTP → serotonin → melatonin arm receive adequate substrate flow.
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🌙 What “secondary improvement” means
Once NAD⁺ sufficiency is restored:
* Tryptophan hydroxylase and aromatic amino-acid decarboxylase regain redox capacity (they both depend on NADPH/NAD⁺ cycling).
* More of each ingested milligram of free-form L-tryptophan now reaches the serotonin pathway.
* Brain serotonin rises gradually and the pineal gland’s melatonin output normalizes—sleep onset improves, cortisol rhythm stabilizes.
* These effects are secondary benefits of metabolic restoration, not direct pharmacologic serotonin loading.
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🗣️
> The serotonin and melatonin effects of tryptophan depend on your NAD⁺ status first. When NAD⁺ is low (after stress, inflammation, or long SSRI use), compounded with lacking exogenous (direct-precursor) NAD+ supplementation by way of nicotinic acid, the body diverts nearly all tryptophan towards meeting the growing demand for rebuilding NAD⁺ instead of for serotonin (or for its other roles including for protein synthesis).
> In this process, especially as requirements grow unchecked, most of the input tryptophan as free-form even, if without accommodating, sufficient nicotinic acid, gets oxidized into toxic chemicals that are by the oxidative environments of excess electrons, broke down into intermediate metabolites along this not-meant-to-be primary route of biosynthesis of what we put into our mouths to become nicotinic acid mononucleotide (the molecule l-tryptophan in herein route as substitute inefficiently expended for and nicotinic acid immediately converge into) — the degree of this re-route of L-tryptophan — whether liberated from protein of diet by stomach-pancreas-small intestine-bloodstream and/or directly through its free-form isolated supplementation (usually at too high of amounts, a fact that is not realized until you know this info that I am disseminating!) — essentially depending on how inflammatory/oxidative the situation has become to that point (meanwhile engrained within this the whole time, how much nicotinic acid supplied exogenously, in coupling)!
> That’s why many people feel no benefit—or even agitation—from tryptophan alone and/or most accurately, without nicotinic acid at ideal dose together. Pairing it with proper accompanying exogenous amount of free-form, pure nicotinic acid restores NAD⁺ directly, freeing tryptophan to serve its intended role in serotonin and melatonin synthesis, in this arena of that pathway for this conversation.
> Once this redox balance is re-established (see below for more on that), the brain’s 5-HTP → serotonin → melatonin pathway “reawakens,” improving mood stability, sugar craving control, and sleep rhythm—not because more tryptophan forces serotonin higher, but because metabolism is finally unblocked. You feel, eat, sleep, get, and thereon stay better only then with more progress via proper biochemical modulation back towards such aspects of homeostatic metabolism and regulation, as biochemically measured in the tryptophan–serotonin–meltonin pathway.
Key Points Summary:
* The serotonin and melatonin effects of tryptophan depend on your NAD⁺ status first. When NAD⁺ is low (after stress, inflammation, or long SSRI use), the body diverts nearly all tryptophan toward rebuilding NAD⁺ instead of serotonin.
* That’s why many people feel no benefit—or even agitation—from tryptophan alone. Pairing it with a small, balancing amount of nicotinic acid restores NAD⁺ directly, freeing tryptophan to serve its intended role in serotonin and melatonin synthesis.
* Once that redox balance is re-established, the brain’s 5-HTP → serotonin → melatonin pathway “reawakens,” improving mood stability, sugar craving control, and sleep rhythm—not because more tryptophan forces serotonin higher, but because metabolism is finally unblocked.
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Objectives Forward…
When NAD⁺ levels fall, enzymes like tryptophan-2,3-dioxygenase (TDO) and quinolinate phosphoribosyltransferase (QPRT) are activated, pulling L-tryptophan away from its serotonin/melatonin role of interest herein, and en re-route, in lieu of nicotinic acid simultaneously, increasingly expending its capacity by leaving no choice but burning it to rebuild NAD⁺ — exerting detrimental, accumulatively imminently fatal consequences to the system over its life course, the junction of which towards such fate will not be overcome let alone ever be enabled for clinically meaningful counter to take place, sans identification and grasp of how to chemically manipulate the logistics to do so, unless in this ultimate case, how to do that is found, which appears to be harnessed through realizing the optimal way of combined supplementation of adequate amounts of these two nutrient factors that serve as the limiting precursors to provide that ability to power a flux in our favor to switch sides back towards to eventually thereon remaining at health/homeostasis.
In its compounding of these two identified limiting nutrient factors, by synthesizing what relevant information and evidence has been demonstrated thankfully already per the findings of previous investigations, whilst further consistently shown and hopefully in this way, further confirmed in more recent observations — specifically in terms of what it comes down to in how it combines the relative amounts of niacin and tryptophan (~30.5x as much mass [in mg. or g.] of nicotinic acid as the amount of free-form L-tryptophan) — InfinaLife delivers the optimal “medicine.”
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Wow, thank you! It’s interesting because I’ve tried oral and nasal NAD supplementation with no results, but when I tried IV I literally couldn’t tolerate (metabolize?) it and had to stop the drip. I’m just back on the NA, using up the last of the NA/AA combo and then will try the new combo.
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@lamaeh
### Why IV / “pre-made” NAD feels so strange
NAD⁺ inside the body is not really a nutrient; it’s an internal cofactor that your cells continuously **break down and rebuild** from smaller precursors.
When you infuse NAD⁺ in a vein, your cells do **not** simply absorb it intact and snap it into place. Most of that IV NAD⁺ has to be **broken apart at the vessel wall and in the circulation**, and then reassembled via the same enzymatic machinery that was already struggling in the first place. So IV NAD⁺ is like dumping assembled engines into a factory whose bottleneck is *metal and workers*, not finished engines. The system gets hammered with a pharmacologic load, which is exactly why a lot of people feel awful and can’t tolerate the drip.
The real solution, in my view, is to remove the bottleneck on **your own ability to make and recycle NAD⁺**, not to force-feed the finished molecule.
### Why I center everything on nicotinic acid (NA)
Among the various “vitamin B3” forms, **nicotinic acid** is the classic, direct vitamin precursor that feeds new NAD⁺ (and NAADP⁺) synthesis. The other B3-type compounds – niacinamide, NR, etc. – can contribute, but they are more dependent on **additional conversion steps and rate-limited salvage enzymes**, which are exactly what get stressed in chronic inflammation and disease.
Nicotinic acid is the form that most cleanly expresses the “vitamin” property here: when you give enough NA, you give cells **unrestricted substrate to build NAD⁺ and NAADP⁺**, without leaning so heavily on those already-strained salvage loops.
So your pattern – **no benefit from oral/nasal NAD, can’t tolerate IV NAD, but do fine with NA** – is exactly what I would expect. Your system is saying: “Let me build NAD⁺ myself from a proper vitamin precursor; don’t shove the finished nucleotide into my bloodstream.”
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### What InfinaLife actually does (NA + proportional free L-tryptophan)
InfinaLife is built around two pieces working together:
1. **Nicotinic acid (NA)** as the heavy lifter for NAD⁺ and redox;
2. A **small but precisely proportional dose of free-form L-tryptophan**, riding alongside the NA.
That free-form tryptophan is the “signal” piece. Here’s what that means in practice.
#### 1. Before InfinaLife: chronic tryptophan drain into oxidative degradation
In modern chronic inflammatory states, the body tends to:
* Be **short on NAD⁺**, and
* Respond by **driving tryptophan hard through oxidative degradation in the liver** (the kynurenine pathway).
In textbooks that pathway is often framed as a way to “make NAD⁺ from tryptophan,” but under chronic stress that’s not what really happens in a useful way:
* Large amounts of tryptophan are pulled into the liver and **oxidized / broken down**,
* A lot of that flux stalls in intermediate, oxidative catabolites,
* You get **depletion of tryptophan** and accumulation of these degradation products,
* Without a proportionate, clean rise in NAD⁺ to show for it.
So practically, a lot of the tryptophan you eat is being **siphoned into a degrading, oxidative sink** in the liver in an *attempt* to cover NAD⁺ needs, but it doesn’t actually restore NAD⁺ efficiently. You lose the tryptophan and don’t really fix the NAD⁺ problem.
That means:
* **Free tryptophan pools** inside cells stay low and tightly guarded,
* Less is available for protein repair, serotonin, melatonin, etc.,
* You live in a state of both **NAD⁺ shortfall and tryptophan depletion.**
#### 2. First move: NA supplies NAD⁺ directly and “clears the backlog”
When you take InfinaLife, the nicotinic acid component:
* Directly feeds **new NAD⁺ synthesis** via the proper NA pathway,
* Improves the **NAD⁺/NADH redox balance**,
* Begins to **relieve the pressure** that was forcing tryptophan into that oxidative degradation sink.
In other words, NA steps in as the appropriate, high-capacity substrate for NAD⁺, and over time:
* The body no longer needs to shove so much tryptophan into that dysfunctional degradation route,
* The system can gradually **“clear” that overload state** where tryptophan is being wasted in the liver without solving the NAD⁺ problem.
#### 3. Second move: the proportional free-Trp dose as a **signal**
On top of that, InfinaLife gives you a **small, carefully scaled dose of free-form L-tryptophan**, tied proportionally to the NA dose.
That matters because:
* This is **unbound, free tryptophan**, not slow-release protein-bound Trp.
* It reaches the bloodstream and liver as a **clean, immediate free-Trp pulse** right when NA is supplying robust NAD⁺ substrate.
To the system, the combined state – **“NAD⁺ demand is now properly met by NA” + “free Trp is actually present and not scarce”** – is interpreted as:
> “We are no longer in a tryptophan-depletion emergency.
> We do not need to keep pushing tryptophan into that oxidative degradation track.”
Mechanistically, that tends to:
* **Downshift the drive** to keep oxidizing Trp in the liver just to chase NAD⁺,
* Reduce the chronic flux of Trp into those degradation products,
* Shift the balance from **catabolism → anabolism** with respect to tryptophan.
That’s the “signal”: the free-Trp fraction, when it arrives alongside adequate NA, is a clear biochemical message that the old pattern – “drag Trp into the liver and burn it up while still not fixing NAD⁺” – can be switched off.
#### 4. What happens to the rest of the tryptophan you eat
Once NA is covering NAD⁺ properly, and the free-Trp pulse has told the system to back off the oxidative sink, something important changes:
* The tryptophan you get from normal dietary protein – which previously was **getting pulled into the liver and degraded** – can now increasingly be **preserved and redirected** to its intended roles:
* **Protein synthesis and tissue repair**,
* **Serotonin → melatonin** (mood, circadian rhythm, sleep),
* Other constructive pathways that were starved when Trp was chronically treated as sacrificial fuel.
So InfinaLife is not “just more tryptophan.” It is:
* NA: supplying NAD⁺ directly and **displacing the need** to waste Trp in oxidative degradation,
* Free-Trp (in a controlled ratio): providing the **signal** that Trp is no longer to be sacrificed like that,
* Together: shifting your whole tryptophan economy from a **degrading sink → restored, anabolic use.**
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### Why I want you to skip more NA/AA and move straight to InfinaLife
The original NA/AA combo (nicotinic + ascorbic acid) came from an older view where some of the “vitamin C benefits” were likely **indirect niacin benefits** – vitamin C helping niacinamide-type scraps feed back toward nicotinic acid and NAD⁺. That made sense when nicotinic acid itself wasn’t being pushed hard, and when the full NA story wasn’t clear.
The flip side we now see is:
* Ascorbic acid interacts chemically with the same nicotinyl ring that both niacinamide and nicotinic acid share.
* At higher levels, this means ascorbic acid can **interfere with nicotinic acid’s own smooth conversion into NAD⁺**, exactly where we want a clean, high-capacity flux.
Given that:
* You’re precisely the phenotype that does **poorly** with forced NAD⁺ and **best** when NAD⁺ is built endogenously from NA, and
* We now have a formulation (InfinaLife) that couples NA with the **right amount of free-Trp “signal”**,
…it’s simply a better use of your time and biology to transition fully to InfinaLife rather than keep pouring money into NA/AA.
To soften the financial hit for members who previously bought NA/AA, I’m effectively doing a **buy-one-get-one** on the first InfinaLife order (doubling the amount on that first shipment) so this pivot isn’t punished financially.
**In short:**
* IV / pre-made NAD⁺ overloads the system without fixing the bottleneck.
* Nicotinic acid fixes the bottleneck by restoring NAD⁺ from the proper vitamin precursor.
* Under chronic stress, tryptophan is mostly being **dragged into oxidative degradation in the liver, not productively turned into NAD⁺**.
* The small, proportional free-Trp fraction in InfinaLife is the **signal** that lets the body stop wasting tryptophan this way and reallocate it back into serotonin, melatonin, and protein synthesis.
* That’s why I’d rather have you not finish what you already have, and instead just move fully onto InfinaLife and let that NA + Trp pair do what your IV NAD never could.
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Ok, thank you! Ordering.
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Will be interesting because I’ve never tolerated tryptophan either, but it’s making sense!
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@lamaeh well, without niacin coming making NAD+ meanwhile taking too large of doses solo of tryp, it’s quite a rush I imagine to have all that extra dump down the kynurenine pathway of oxidative metabolites that have already been compiling! Also, without Certificates of Analysis documentation from manufacturers, how can we know the “tryptophan” you were taking in the past was pure? Albeit, given the bullshit pathogen scare in the 90s, that is the ONE molecule that if it is being taken solo, it’s likely from the doctor prescribed so UPS-grade that their pharmacy issues.
I think you will see MUCH preferable results here calibrated to and with niacin!
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