The downfalls of serotonin & SSRIs

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Paul Saladino20m · 2022-12-26

Claims Made

46

Claims Supported

39

Support Rate

85%

Support rate

39 of 46 claims supported

39 supported7 partial / not

Claims from this content

44

Well SupportedSSRIs inhibit the activity of the serotonin transporter, slowing serotonin deactivation and increasing extracellular serotonin.Well SupportedIncreased free-floating tryptophan readily enters the brain and promotes serotonin production when unopposed by other large neutral amino acids.Well SupportedThe stomach and small intestine should ideally be free of bacteria before reaching the colon for proper nutrient absorption.Partially SupportedSymptoms of very high serotonin include diarrhea, flushing, mental changes, psychosis, and depression.Partially Supported

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Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.

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Increasing serotonin with SSRIs or SNRIs can lead to a state of being unfeeling or chemically lobotomized.

Partially SupportedIndividuals with diarrhea-predominant IBS may not tolerate spicy foods due to high serotonin.

Partially SupportedElevated extracellular serotonin can lead to blood clotting and fibrosis, and it inhibits the synthesis of dopamine by reducing tyrosine hydroxylase.

Well SupportedApproximately 90% of serotonin is produced in the gut.

Partially SupportedTlr4 activation triggers tryptophan hydroxylase, leading to serotonin production, with 90% of serotonin produced in the GI tract.

Partially SupportedInsufficient digestive enzymes or stomach acid can lead to undigested food reaching the colon, which is a pathological state.

Partially SupportedThe German FDA initially refused Prozac due to concerns about suicide, an admitted side effect in the first two weeks of SSRI use.

Partially SupportedProzac increases the brain synthesis of the neurosteroid allopregnanolone, which is a potent antidepressant.

Partially SupportedFree fatty acids can displace tryptophan from albumin, increasing free-floating tryptophan and potentially affecting brain entry.

Not SupportedProzac elevates extracellular serotonin while blocking the 5-HT2C receptor, potentially causing systemic damage like fibrosis.

Partially SupportedActivation of TLR4 by endotoxin triggers a cascade involving iNOS, leading to increased nitric oxide production.

Partially SupportedEndotoxin absorption into the bloodstream activates the TLR4 receptor, mimicking a direct bacterial injection.

Partially SupportedHigh serotonin levels can lead to a 'zombified' state by blunting the body's response to environmental stimuli, which is not a cure for depression but a suppression of reaction.

Partially SupportedPost-mortem studies show elevated serotonin levels in depressed individuals who committed suicide.

Partially SupportedSerotonin lowers metabolic rate, particularly in the brain.

Partially SupportedHigher cognitive functions, including mood, are dependent on brain energy levels (ATP).

Partially SupportedThe beneficial effects of Prozac are primarily seen at microdosing levels before it inhibits the serotonin transporter.

Partially SupportedTlr4 activation stimulates NF-kappa B, which activates COX and LOX enzymes, triggering inflammatory mediators when sufficient lipids are present.

Not SupportedMainstream medicine's approach to depression involves blunting emotional responses.

Partially SupportedA 20% drop in brain ATP levels can lead to violent aggression, and excessively high serotonin levels can cause psychosis.

Partially SupportedSerotonin produced in the gut can affect the brain via the vagus nerve and by crossing the blood-brain barrier.

Partially SupportedSerotonin is a pro-fibrotic mediator.

Partially SupportedAllopregnanolone, a derivative of progesterone, is a fast-acting antidepressant for postpartum depression and may be effective for all types of depression.

Partially SupportedSelective serotonin antagonists, such as turbo (acting on 5-HT2B receptors), are being developed to treat conditions potentially caused by serotonin.

Partially SupportedProzac acts as a partial antagonist at the serotonin 5-HT2C receptor, which blocks serotonin's role in driving cortisol production.

Partially SupportedSerotonin primarily functions as a metabolic regulator and inhibits the inflammatory cascade, particularly in the brain.

Partially SupportedElevated extracellular serotonin inhibits the synthesis of tyrosine hydroxylase, leading to reduced dopamine synthesis.

Partially SupportedMany SSRI drugs are no more effective than placebo, with Prozac and Lexapro being exceptions.

Partially SupportedBlocking the 5-HT2C receptor can help treat conditions like Cushing syndrome.

Partially SupportedElevated serotonin levels are a poor prognostic indicator, typically associated with carcinoid syndrome.

Partially SupportedConsuming protein with food can lead to other amino acids outcompeting tryptophan for brain entry, unlike during fasting.

Partially SupportedSerotonin metabolites like 5-HIAA can be measured in blood and urine.

Partially SupportedTlr4 activation increases nitric oxide production, a free radical that attacks tissues and generates toxic aldehydes contributing to cardiovascular disease.

Partially SupportedLarge-scale, long-term clinical trials have shown that SSRI drugs are generally no more effective than placebo for depression.

Partially SupportedGram-negative bacteria's endotoxin can irritate tissues and increase intestinal wall permeability over time.

Partially SupportedIt is not possible to measure serotonin levels directly in the brain of living patients.

Partially SupportedSerotonin can cause psychosis, including schizophrenia-type diseases.

Partially SupportedFibrosis, often driven by serotonin, can be a precursor to cancer in solid organs.

Partially SupportedHigh serotonin levels can lead to irritability and aggression.

Partially SupportedDuring fasting, increased lipolysis leads to higher levels of free fatty acids, which can displace tryptophan from albumin.