Use this Stroop test to lower your brain serotonin levels

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Use this Stroop test to lower your brain serotonin levels

Serotonin is one of the five primary neurotransmitters, also popularly associated with “happiness” and depression.

This view of serotonin as the “happy hormone” is blatantly false…

Many things suffer when you have high brain serotonin — one of those is focus and cognitive ability which falls.

Think of what you need attention for:

Reading, writing, hiking, walking down stairs, driving, work-related tasks…

Professionals need focus for studying and performing their tasks be it engineering, law, surgery or what-have-you.

All these require high engagement and high focus — they are best done with undivided attention.

But brain serotonin levels interfere with focus and attention.

Brain serotonin is actually under the influence of diet, which it controls in so many ways you might think it’s a molecular signal for food.

This particular amino acid appears to have been chosen throughout evolution to help control and signal-for food intake, positively inducing the pleasure derived from eating yet also the motivation to seek more.

‘This finding also indicates that serotonin liberated from the axon terminals exerts a tonic inhibitory effect on acetylcholine release.’ ―Vizi

Fenfluramine (a.k.a. fen–phen) — a popular diet treatment — highlights the intimate link between serotonin and eating.

This treatment acts to increase brain serotonin, giving overeaters that certain “feeling” they crave without them having to eat something.

Yet not all foods are equal in this respect.

It has been found that brain serotonin depends directly on the plasma tryptophan ratio (Fernstrom, 1971), and for this reason the food’s specific amino acid profile can certainly make a difference:

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Whey and egg-white are the two most serotonergic foods.

Yet their whole-food counterparts — i.e. whole eggs and whole milk — provide a more balanced amino acid profile that doesn’t have the effect.

And also…unsaturated fatty acids are known to displace tryptophan from high-affinity binding sites on serum albumin, thereby tending towards:

  1. The displacement of free tryptophan
  2. An increase of the plasma Fernstron ratio
  3. An enhancing brain tryptophan uptake
  4. An increase of brain serotonin synthesis through the enzyme tryptophan hydroxylase

Although all fatty acids displace tryptophan, to some extent, oleic acid does so with the highest potency.

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So after eating a fish pan-fried in olive oil, you can forget all about assembling that ship-in-a-bottle you had planned on…

…or finishing that 10,000 piece jigsaw puzzle, lengthy essay or book, or that manual transmission rebuild on the aging sports car.

We also have many pharmacological options in which brain serotonin can either be increased or decreased at whim, such as ergolines and amino acids, often quite reliably depending on the treatment or supplement employed.

So manipulating brain serotonin is actually a routine occurrence, one accomplished daily through the ingestion of food. This process should be understood due to its widespread practice and serotonin’s ability to disrupt higher brain functions.

‘Memory function, particularly long-term memory retrieval and storage, was impaired following intravenous administration of 7g tryptophan.’ ―Schmitt

But first you must become convinced that serotonin can actually be detrimental, at least at times, becoming disruptive when engaged in complex tasks.

This effect is most reliably demonstrated by acute tryptophan depletion:

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Acute tryptophan depletion is accomplished by drinking a mixture of several amino acids, fifteen in this case, while excluding tryptophan of course.

Drinking such a cocktail substantially lowers the Fernstrom ratio by diluting plasma tryptophan with its competitors:

Valine, leucine, isoleucine, phenylalanine, and tyrosine all compete with tryptophan for brain uptake.

This method had been made reliable through small, incremental adjustments made since its inception in the ’70s.

This refinement of technique eventually yielded a mixture that keeps all other neurotransmitters, and notably dopamine, at a more-or-less constant concentration in the brain.

‘The ratio of tyrosine (the precursor of catecholamines) to other LNAAs does not change significantly with ingestion of either drink, and thereby excludes possible dopaminergic effects.’ ―Gallagher

So this was tailored to isolate tryptophan, eliminating confounding effects from other neurotransmitter precursors.

Below is a table that was published in another article also using the same dose level, and also studying the same effect:

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Both studies noted a reduction of certain tasks, most notably incorrect responses in the Stroop color test.

The Stroop test measures the ability to correctly name the color of ink used to print words.

This would seem a simple task were it not for the color-printed words being adjectives denoting different colors — i.e. orange, purple, red, etc.. .

‘For example, when analysed post hoc, all 6 outcome measures on which significant interactions were observed showed significantly improved performance following acute tryptophan depletion when administered on the second visit.’ ―Gallagher

A somewhat confusing task, to be sure, yet perhaps more difficult yet was the dichotic listening trial.

This test measures the ability to listen to stereo headphones in which each channel plays different sounds.

The dichotic listening task measures focused attention when just one of the two channels is relevant — the other being a distraction — or the ability to integrate two sets of information simultaneously.

Performance on this task was significantly enhanced by low serotonin in another article on tryptophan-depletion (Schmitt, 2000), as was the Stroop color test.

‘The finding of an improvement in attentional performance following acute tryptophan depletion in the present study is in keeping with the literature and the role of 5-HT [serotonin].’ ―Gallagher

Other articles analyzing the opposite effect, i.e. tryptophan loading, reported the expected decrements in cognitive tasks (Sobczak, 2003)…

As did the experiments using serotonergic treatments:

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This study compared paroxetine (Paxil™) and sertraline (Zoloft™) against a control group, both being SSRIs yet the latter also enhancing dopamine a bit.

The experimenters took note of this fact, and had apparently used sertraline for that very reason.

Sertraline also causes a lower prolactin spike than all other SSRIs, an observation explained by its minor yet significant dopaminergic activity.

‘As for vigilance, the overall pattern of results is in line with the general hypothesis that the dopaminergic activity of sertraline was able to at least partially attenuate a serotonergically induced vigilance decrement.’ ―Schmitt

And in line with the foregoing considerations, sertraline caused less performance decrements in the Mackworth clock test.

This was apparently due to its ability to increase dopamine, a neurotransmitter shown to promote focused attention and vigilance:

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The Mackworth clock test was created during WWII as a screening device for radar operators.

This test involves attentively watching a display similar to a clock where the second-hand markings are progressively illuminated in a clockwise fashion.

The display is predictable save for a few random instances where a marking is skipped, after which the subject is instructed to press a button.

As can be seen above, paroxetine significantly increased the number of errors and had slowed reaction time.

So these are consistent effects, induced either by serotonergic treatments or tryptophan manipulation.

Although many other tests showed no consistent effect, the ones having to deal with focused attention and vigilance nearly always did.

Focused attention and vigilance are characteristics of acetylcholine.

‘Noradrenaline is mainly involved in rapid but transient changes in cortical arousal in response to outside stimuli, whereas dopamine and acetylcholine are thought to be primarily associated with an internally driven energetic state, which varies more slowly and is not readily modulated by external stimulation. Serotonin is thought to dampen the activity of each of these neurotransmitter systems, thereby promoting behavioural inhibition and cortical dearousal.’ ―Schmitt

The raphe nucleus is the specific region responsible for synthesizing the majority of the brain’s serotonin.

This region distributes serotonin to many others using long projections, where biochemical studies show they are actively inhibited:

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This study used seven individual treatments and physical ablation to study the effects of serotonin on the striatum.

This brain region is very important and involved in decision making, planning, and motivation. This region sits at the junction between the midbrain and forebrain.

They found that in every case:

  1. Serotonergic treatments decreased acetylcholine release
  2. Anti-serotonergic treatments increased acetylcholine release
  3. Treatments that increase brain dopamine also increased acetylcholine release
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From the cumulative data gathered from this study you can draw only one logical conclusion:

Serotonin actively inhibits brain metabolism in the striatum, and dopamine increases it.

This could be the very reason, or at least a partial one, for the cognitive deficits seen in the above attention and vigilance tasks.

This one study showed that the one neurotransmitter most associated with focus and vigilance is actively inhibited by serotonin, and in a brain region related to those abilities.

‘In serotonin-deficient slices the release of acetylcholine enhanced by ouabain was significantly higher, independent of how serotonin deficiency was produced (raphe nuclei lesion, p-CPA pretreatment, 5,7-DHT pretreatment).’ ―Vizi

And there is verification from many other studies besides.

Three years before was one showing serotonin’s tonic inhibitory effect by partial ablation of the raphe nuclei, preventing the distribution of serotonin only to the examined area (Olpe, 1977).

Add to the seven treatments that were used, the three serotonin reuptake inhibitors fluoxetine, paroxetine, and sertraline…

As well as acute tryptophan depletion and raphe ablation

And you have over a dozen modalities all tending towards the same conclusion:

Serotonin actively decreases focused attention and vigilance, perhaps by decreasing acetylcholine release in the striatum.

Obviously, we all must eat and cannot do without serotonin entirely.

Yet by understanding its origin and function we can use it — or decide NOT to use it — to our advantage.

Keeping serotonin towards the low-end of the normal range could take a bit of sacrifice, and this is because the serotonergic state is somewhat pleasant by design and because so many good-tasting foods can induce it.

Foods such as gelatin, cheese, beef, leaves, and fruit — with the exception of avocado — are all more-or-less safe to eat in this regard.

‘Methysergide, which is considered to be a 5-HT blocking agent, antagonized this inhibitory effect.’ ―Olpe

Corn is notoriously deficient in tryptophan and is used experimentally for this reason, yet most corn sold these days is genetically modified and now has an enhanced immunogenicity.

Alternatively: serotonin can be antagonized either directly by treatments that inhibit it or more indirectly through dopaminergic treatments.

Increasing the dopamine∶serotonin ratio also keeps prolactin from being released from the pituitary, leading to a more masculine form to match the more consequential mindstate.

‘Since prolactin release is stimulated by serotonergic input but inhibited by dopaminergic input, the DA activity of sertraline may have attenuated the serotonergic effects on prolactin release.’ ―Schmitt

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Matt Cook is editor-in-chief of Daily Medical Discoveries. Matt has been a full time health researcher for 26 years. ABC News interviewed Matt on sexual health issues not long ago. Matt is widely quoted on over 1,000,000 websites. He has over 300,000 daily newsletter readers. Daily Medical Discoveries finds hidden, buried or ignored medical studies through the lens of 100 years of proven science. Matt heads up the editorial team of scientists and health researchers. Each discovery is based upon primary studies from peer reviewed science sources following the Daily Medical Discoveries 7 Step Process to ensure accuracy.
Booij, Linda. "The effects of high-dose and low-dose tryptophan depletion on mood and cognitive functions of remitted depressed patients." Journal of Psychopharmacology (2005)

Olpe, Hans-Rudolf. "The response of striatal cells upon stimulation of the dorsal and median raphe nuclei." Brain research (1977)

Schmitt, J. A. "Serotonin and human cognitive performance." Current pharmaceutical design (2006)

Schmitt, Jeroen. "Additional dopamine reuptake inhibition attenuates vigilance impairment induced by serotonin reuptake inhibition in man." Journal of psychopharmacology (2002)

Gallagher, Peter "Effects of acute tryptophan depletion on executive function in healthy male volunteers." BMC psychiatry (2003)

Vizi, E. S. "Evidence of the modulatory role of serotonin in acetylcholine release from striatal interneurons." Brain research (1981)