The dopamine dream team (DDT) stack: Try this for laser-sharp focus and euphoria

This stack is unlike any other stack you’ve heard of. It’s called the DDT stack.

3 of the 4 ingredients aren’t typically known for boosting dopamine, yet they work so well in that regard.

The purpose with the stack is firstly to optimize cellular function and energy production. This is the foundation that we’re building on. When we have that in place, we can throw in a dopaminergic if that’s still really needed.

Our 4 ingredients are:

  • Piracetam
  • Pyruvate
  • Creatine
  • PRL-8-53

#1 Piracetam

Piracetam was the first racetam made, followed by phenylpiracetam, oxiracetam, pramiracetam, aniracetam, etc (in no perticular order).

Piracetam was first made around the 1950s Corneliu E. Giurgea and it was used around that time for epilepsy in the 1950s.

Piracetam is in the racetams group, with the chemical name 2-oxo-1-pyrrolidine acetamide. It is a derivative of the neurotransmitter GABA and shares the same 2-oxo-pyrrolidone base structure with pyroglutamic acid.

As we all know, GABA is sedative and calming. Pyroglutamic acid on the other hand facilitates ATP synthesis by stimulating de novo synthesis of purines. Pyroglutamic acid is found in Metadoxine and Cardenosine and contains some interesting properties.

Piracetam influences neuronal and vascular functions and influences cognitive function without acting as a sedative or stimulant and restores cell membrane fluidity (which decreases with aging due to lipid peroxidation), mitochondrial function and ATP production.

At a neuronal level, piracetam modulates neurotransmission in a range of transmitter systems (including cholinergic and glutamatergic), has neuroprotective and anticonvulsant properties, and improves neuroplasticity. At a vascular level, it appears to reduce erythrocyte adhesion to vascular endothelium, hinder vasospasm, and facilitate microcirculation. This diverse range of physiological effects is consistent with its use in a range of clinical indications. Its efficacy is documented in cognitive disorders and dementia, vertigo, cortical myoclonus, dyslexia, and sickle cell anemia. While high doses are sometimes necessary, piracetam is well tolerated.

Reference

And this is why I like this compound so much. It doesn’t directly boost certain neurotransmitters, but rather optimizes cellular function and energy production which then leads to better functioning of neurotransmitters. It’s the dysfunction of neurotransmitters that’s responsible for mental disorders so trying to modulate certain individuals neurotransmitters isn’t the most effective strategy.

Here are some of the great benefits of piracetam. Piracetam:

  • Influences membrane fluidity, particularly when normal fluidity is compromised, as is often seen during aging. Piracetam has been shown to alter the physical properties of the plasma membrane by increasing its fluidity and by protecting the cell against hypoxia. This effect of piracetam doesn’t just make it great for the brain, but for the whole body as well. Piracetam is an agent with antithrombotic, neuroprotective and rheological properties.
  • Significantly decreases the destabilizing effects of the amyloid peptide. Amyloid peptide was shown to cause lipid disorganization within the cell membranes.
  • Increases locus coeruleus firing, which increases noradrenaline levels in the brain (R). This effect can enhance focus, alertness and libido. Some people who use piracetam report an increase in libido.
  • Has been found to increase oxygen consumption in the brain, apparently in connection to ATP metabolism. Piracetam, while in the brain, appears to increase the synthesis of cytochrome b5, which is a part of the electron transport mechanism in mitochondria. This effect combined with the improvement in cell fluidity can greatly increase cellular function and energy production.
    • Mitochondrial stabilization and protection might be an important mechanism to explain many of piracetam’s beneficial effects in elderly patients (R).
  • Protect neurons against endotoxin damage (R). In alcohol-treated rats, piracetam administration is associated with a decrease in lipofuscin, a marker of neuron membrane damage. Furthermore, piracetam promotes neuroplasticity when neural circuits are recoverable.
  • Inhibits stress-induced increase in prolactin (R).
  • Influences neurotransmitter function as follows. Piracetam:
    • Enhances the efficacy of AMPA (a glutamate receptor)-induced calcium influx in brain cells. It also increases the maximal density of AMPA receptors in synaptic membranes from rat cortex due to the recruitment of a subset of AMPA receptors which do not normally contribute to synaptic transmission. At larger doses, piracetam potentiates potassium-induced release of glutamate from rat hippocampal nerves.
    • Modifies hippocampal acetylcholine levels in the rat and increases the population of muscarinic cholinergic receptors in the frontal cortex of aged but not young mice by up to 40%. Furthermore, carbachol-induced accumulation of inositol-monophosphates (a measure of muscarinic cholinergic receptor function that decreases with age) was elevated following piracetam treatment suggesting that piracetam can normalize functional deficits associated with aging.
    • In the glutamatergic system, significantly increased N-methyl-D-aspartate (NMDA) receptor density in the forebrain of aging mice by approximately 20% after 14 days of treatment. Furthermore, piracetam treatment normalized the age-related elevated affinity of L-glutamate for the NMDA receptor, suggesting that it can restore NMDA receptor function.
    • Affect the dopaminergic system, which can be blocked with a dopamine receptor antagonist (R, R).
    •  Piracetam stimulates an antidepressant action of a single dose of ketamine in cases of behavioral depression, though it has no antidepressant effect when administered at a single dose (only chronically) (R). Piracetam seems to potentiate the effect of other compounds, such as ketamine or other anti-depressants.

Piracetam has been shown to increase reading comprehension and accuracy in dyslexic
children, improve alertness, socialization and IQ in elderly psychiatric patients and even has promise for treating alcoholism.

Oral absorption of piracetam is close to 100% and peaks in your blood at around 30 min.

While food does not affect the extent of absorption of piracetam, it does decrease the maximal plasma concentration of the drug by 17% and prolongs t-max to 1.5 hours.

Piracetam crosses blood-brain and placental barriers and is found in all tissues, except adipose tissue. The uptake into the brain is less rapid than into the circulation, and the half-life in cerebrospinal fluid is nearly 8 hours, whereas in plasma it’s about 5 hours.

Piracetam is remarkably well tolerated. In preclinical trials, no irreversible toxicity was
reported in mice, rats or dogs receiving single oral doses of up to 10 g/kg (R).

The dosing of piracetam varies according to indication. For cognitive disorders and vertigo, it is 2.4–4.8 g daily, for dyslexia it is 3.2 g daily, for cortical myoclonus, it is 7.2–24g daily, for prophylaxis of vaso-occlusive crises in sickle cell anemia it is 160 mg/kg/day, and for remission of vaso-occlusive crises, it is 300 mg/kg/day i.v. in four divided doses (R).

In one study, 162 patients with age-associated memory impairment received piracetam 2.4g/day, piracetam 4.8g/day, or placebo for 3 months. All patients were also enrolled in a memory training program. The improvement with piracetam 4.8g/day was significantly greater than with placebo alone on a range of memory tests including immediate, global, and delayed recall. Piracetam 2.4g/day produced a significantly greater improvement than placebo in immediate recall (R).

So a minimum dose of 1-2.5g should suffice.

What about the other racetams?

Other racetams, such as phenylpiracetam also have other functions than piracetam, such as being a dopamine and noradrenaline reuptake inhibitors which can cause receptor desensitization. Also, I can’t find evidence that the modified racetams have the same mitochondrial and energy stabilizing effects as piracetam. Plus, you can take piracetam daily even in very high doses without having to cycle, whereas with the others, you might have to cycle.

#2 Pyruvate

Pyruvate is the end product of the 10 step process called glycolysis. Pyruvate can then be transported in the mitochondria by the mitochondrial pyruvate carrier, where it’s then turned into acetyl-CoA by pyruvate dehydrogenase (PDH). PDH is the rate limited step in energy production from carbohydrates.

Pyruvate dysmetabolism, because of excessive inhibition of PDH by PDK (pyruvate dehydrogenase kinase; the main antagonism to PDH), contributes to progressive diseases such as chronic obstructive pulmonary disease (COPD), obesity, diabetes, mental disorders and aging.

Pyruvate is neuroprotective by reducing oxidative stress

Reactive oxygen species (ROS) produced from the electron transport chain (ETC), through hypoxia, lipid peroxidation, NOX, iNOS, etc., inhibit glucose oxidation and contribute to brain disorders, such as Alzheimer’s (accumulation of amyloid Beta (Aβ)), Parkinson’s disease, etc. Pyruvate quenches ROS (including hydrogen peroxide, superoxide, and peroxynitrite) and can help to protect against neurological damage (R).

In a mouse model of Parkinson’s disease, the administration of ethyl pyruvate, an ethyl ester of pyruvate that is hydrolyzed into pyruvate and ethanol, protects substantia nigra neurons from oxidative neurotoxicity, which is attributed to metabolic protection provided by pyruvate metabolism. Additional studies have shown that ethyl pyruvate administration inhibits RNS (reactive nitrogen species) and ROS damage and protects neurons from peroxide-induced damage.

A potential hypothesis explaining the protective effect of pyruvate relies on the oxidation of pyruvate and subsequent generation of NADH, which can be converted into mitochondrial NAPDH via NADP-transhydrogenase, which reduces ROS levels by replenishing reduced glutathione (R).

Pyruvate enhances neuronal energy levels

Many mental disorders are due to reduced cellular health and low energy levels.

The development of a hypometabolic state, a key feature observed in Alzheimer’s disease and Parkinson’s disease, may be corrected by the administration of pyruvate. In one study, exogenous administration of pyruvate and 3-beta-hydroxybutyrate directly into the cerebrospinal fluid was shown to ablate excitatory neurotoxicity and corrected neuronal energy deficiency in a mouse model of Alzheimer’s disease.

Reference

Alzheimer’s disease and Parkinson’s disease share many similarities: increased ROS production, hypometabolic states, and overall metabolic dysfunction in their respective regions of the brain.

ATP is needed for the uptake of glutamate and when astrocyte glucose uptake and oxidation is impaired, astrocytes lack the energy to sufficiently clear glutamate from the synapse. This leads to excitatory neurotoxicity, defined in part by increased ROS and mitochondrial dysfunction, and neuronal death. Astrocytes in mice fed pyruvate and 3-beta-hydroxybutyrate had twice the glycogen stores compared to standard diet controls (R).

Pyruvate protects against a variety of degenerative conditions

Pyruvate can be helpful for a variety of conditions exactly because it stimulates glucose oxidation and rescues low ATP levels.

Pyruvate:

  • In this case, ethyl pyruvate, protected against diabetic nephropathy, regardless of blood glucose levels (R).
  • Protected against cataract formation and increased cellular ATP levels in a mouse model of diabetes (R).
  • Prevented zinc-induced islet β-cell death in a mouse model of diabetes by protecting cellular ATP levels (R).
  • Enhances exploratory behavior and brain glycogen in mice (R). Exploratory behavior can include meeting new people, trying out a new hobby, thinking of new ideas to help your business grow faster, talking about/listening to new topics, etc.
  • Activates brown adipose tissue (BAT) with an increase in the level of uncoupling protein-1 (UCP1) (R). 
  • Improves memory (R)

The reason why pyruvate works so well is because it stimulates PDH and can be used as a substrate for that enzyme as well. It lowers lactate and increases the pyruvate:lactate and NAD:NADH ratio.

Two studies in Caenorhabditis elegans concluded that a long lifespan is dependent on PDH activity, noting that inhibition of PDH reduced lifespan and that inhibition of PDK increased lifespan (R). So based on this, pyruvate, ethyl pyruvate and other compounds that increase PDH (such as vitamin B1, calcium and magnesium) should be able to enhance lifespan or at least health span.

Pyruvate increases dopamine

Apart from improving energy production, pyruvate can also increase dopamine release. Although I can’t find a study showing that pyruvate increases dopamine, it’s ability to increase PDH is able to increase dopamine.

TTFD (Fursultiamine, a disulfide derivative of thiamine, structurally similar to allithiamine.), increases dopamine release in the medial prefrontal cortex (mPFC) through energetic and signaling roles in enhancing Na+ permeability (R). These effects are likely exerted by TTFD, a coenzyme of PDH, which supports glucose metabolism in skeletal muscles.

So just by increasing glucose oxidation and brain energetics, pyruvate is able to increase dopamine.

#3 Creatine

By now we all know that creatine is great for increasing brain energy.

Creatine is neuroprotective by maintaining mitochondrial bioenergetics, evident by increased mitochondrial membrane potential, reduced intra-mitochondrial levels of reactive oxygen species and calcium and maintained adenosine triphosphate levels were maintained. Induction of mitochondrial permeability transition was significantly inhibited in animals fed creatine (R).

Creatine most effective enhances cognitive performance when the brain is fatigued, which is very easy to do with a low carb diet, sleep loss, stress, overwork, low protein diet, etc.

Furthermore, creatine activates the adenosine and dopamine D1 and D2 receptors, which is known to have anti-depressant and pro-energizing effects (R).  Creatine is also a potent natural survival and neuroprotective factor for developing nigral dopaminergic neurons (R).

As a side note, taurine pairs very well with creatine to exert anti-depressant effects.

#4 PRL-8-53

Once we have established the foundation with piracetam, pyruvate and creatine, we can throw in another substance that boost dopamine to a great extent.

All three of these first compounds will enhance cellular function and energy production and the piracetam specifically can potentiate the effect of PRL-8-53, thus reducing the dose necessary for a strong effect.

I like PRL-8-53, because, in addition to its dopaminergic effects, it also has anti-serotoninergic effects, which can help to reduce fatigue and enhance working memory, focus, etc. (R, R)

You can pick any other dopaminergic for this stack, such as Catuaba bark extract, Mucuna Pruriens, uridine, etc if you can’t source PRL-8-53.

Check out my Instagram post here.

Stack summary

My experience so far

I’ve been using this stack for quite some time now and I always get the same effect from it.

I feel very good, light and in a state of euphoria. If I’m feeling slightly off or distract one day, then this stack helps to restore my baseline, which is when I’m able to focus and motivated for many hours of end.

As many of you might know, I tend to feel relatively insensitive to most supplement, but for this stack, I definitely notice great improvements. And the beauty of this stack is that it doesn’t have to be cycled.

This stack is great for euphoria as well, but if you want something else to make you feel even better once a week or so, through in some Kratom. I wouldn’t use Kratom too frequently since it’s an opioid agonist and can increase prolactin and lower testosterone (as shown in this case report (R)). But I think that once a week at about 2-3g should be totally fine.

Please share this stack with your friends

I’d like to ask that if you use it and experience good effects from it, to share the DDT stack with your friends as well. I usually tell my friends what I’m taking and then I give them a serving or three of mine so that they can try it for themselves. This then also gives you the opportunity to talk to them about the stack as I can guarantee you that they probably haven’t heard of it from this perspective before. If they then want to learn more about it, please share the link to the article for more information.

How to share it:

  • Share this article or the stack on all your social media where your friends might be interested
  • Email this article to your friends that have high demand jobs
  • Tell your online and offline friends that you’re using the DDT stack and they can just google the DDT stack or you can share the link with them

DDT stack for ultimate focus and euphoria. Piracetam, pyruvate, creatine and PRL-8-53. Super simple, but very effective.

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8 Replies to “The dopamine dream team (DDT) stack: Try this for laser-sharp focus and euphoria”

  1. these products are taken all together at the same time or have different schedules from each other,
    When would you take each one and can you take it every day or how is it?

    1. Hey Diego,
      I take it all together in the morning every day. Sometimes I take 1 day a week off.

  2. What do you think about AMPAkine (For example coluracetam)?Do you use them?

    1. Hey Andrey,
      I have not researched that compound specifically yet, but restoring AMPA signaling in certain situations can be very helpful for sure.

  3. Great post Hans! Will try the DDT stack out soon. Do you use all of the listed products in the morning on a empty stomach all together?

    1. Hey Michel,
      I don’t take it on an empty stomach, but you can do that if you want. I don’t want to stimulate my body too much right after waking without enough carbs.

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