Sorry! We Meant To Say Lower Serotonin.

TheDopamines The simplistic idea that mood disorders like depression or anxiety – and numerous other conditions of the mind – predominantly result from insufficient serotonin levels in the brain, has never been properly experimentally demonstrated and contradicts basic physiological principles.

Regardless, extremely profitable drugs like the very popular SSRI’s (Selective Serotonin Reuptake Inhibitors) and other related so called anti-depressant drugs – many of which are prescribed with the intention of increasing levels of serotonin – are still the first line of defense for the majority of doctors and psychiatrists.

“Our…claim…is that the direct pharmacological effects of SSRIs are not responsible for symptom reduction…SSRIs cause…a worsening of symptoms…symptom reduction is due to…the brain’s homeostatic mechanisms that attempt to restore energy homeostasis…which explains why symptoms fail to alleviate for several weeks after the initiation of SSRI treatment…”

“The time differential between the onset of 5HT [serotonin] reuptake inhibition by SSRIs (minutes) and onset of their antidepressant efficacy (weeks to months), when considered with their overall poor therapeutic effectiveness, has cast some doubt on the role of 5HT in depression.”

There is, on the other hand, a growing body of scientific evidence which suggests that increased levels of serotonin are actually central to the processes which promote learned helplessness-like symptoms, including many of those associated with anxiety and depression.

“While the literature on depressed patients is necessarily limited due to the methodological difficulties measuring serotonin…in the human brain, the most pertinent studies support the high serotonin hypothesis…that serotonin transmission is elevated in…depression.”

“We demonstrate invariably increased serotonin synthesis and transporter availability in patients with SAD [social anxiety disorder] relative to healthy controls, which supports an overactive presynaptic serotonin system.”

Anxiety and depression very often go hand in hand and there is plenty of evidence which suggests that reduced levels of serotonin (in the body and the brain) go along with improvements in biological function – as well as the reduction of issues related to inflammation and degeneration – and that this understanding can be used in the creation of effective approaches to treatment of mood disorders in general.

“Individuals with social phobia make too much serotonin. The more serotonin they produce, the more anxious they are in social situations…patients with social phobia produced too much serotonin in a part of the brain’s fear centre, the amygdala.”

It is important to remember that the vast majority of serotonin found in the body is produced in the intestines. A sub-optimal digestive system commonly results in an overproduction of bacteria – and its toxic byproducts such as endotoxin – and this has been shown to be directly connected to rising levels of serotonin, as well as other inflammatory substances (including estrogen, nitric oxide and histamine).

“More than 90% of the body’s 5-HT is synthesized in the gut…gut microbiota plays a key role in promoting levels of colon and blood 5-HT…Interestingly, the indigenous microbiota also modulates hippocampal levels of 5-HT……revealing a role for the microbiota in regulating the brain serotonergic system.”

Many of the stress related substances which increase alongside serotonin – and are promoted by excess bacterial growth – have been found to play a causative role in the promotion of systemic inflammatory issues, making the well known link between digestive distress and mood dysregulation more explainable.

“Regarding depression-related onset of diseases of the digestive system…experimental and clinical studies have demonstrated that acute and chronic stress have impacts on the gastrointestinal system, being permissive in the development of gut diseases.”

When stress goes up – particularly in combination with insufficient provision and availability of sugar – this then leads to a rise in levels of cortisol and adrenalin as well as the release of fat out of storage as free fatty acids for fuel. When the fat entering circulation is polyunsaturated, it then powerfully interferes with energy metabolism and thyroid function.

“When patients with depression were compared with healthy controls, depression was associated with higher oxidative stress MDA levels [malondialdehyde – resulting from lipid peroxidation of polyunsaturated fats]…suggest[ing] that oxidative stress plays a role in depression and that antidepressant activity may be mediated via improving oxidative stress/antioxidant function.”

“…depressed patients have enhanced levels of adrenal hormones and corticotropin-releasing factor (CRF) in the blood…it is clear that serotonin and adrenal hormones may contribute to the symptoms of depression.”

Although it is still a commonplace argument that SSRI’s – and other so called serotonin increasing antidepressants – improve mood regulation by raising serotonin levels in the brain, evidence that the positive effects which sometimes result from their use do not actually arise in this manner, is building.

“we propose that the brain is attempting to restore energy homeostasis rather than serotonin homeostasis…the upward trajectory in serotonin during initial ADM [antidepressant medication] treatment is often associated with a worsening of symptoms…the downward trajectory…with symptom reduction.”

“the effects of…inactivation of the 5-HTT [serotonin transporter or SERT] on anxiety-like behavior in mice are robust and provide an independent line of evidence supporting a link between the low-expressing 5-HTT…with anxiety in humans.”

When stress is high and resources are limited, one way of understanding the role of serotonin – in relation to depression – would be to see it as part of an attempt by the body to survive on less, shutting down whatever it can get away with. Although from an evolutionary perspective this can be helpful, there are potentially serious metabolic and degenerative consequences.

Many people now understand depression to be one of the results of a hypometabolic state, and the relationship between serotonin, the polyunsaturated fats and animal hibernation – in some ways similar to depression – is not coincidental.

“Participants…received heating…until their core body temperature reached 38.5°C…the current study found that WBH [whole-body hyperthermia] was associated with a substantial reduction in depressive symptoms…WBH holds promise as a safe, rapid-acting, antidepressant modality with a prolonged therapeutic benefit.”

Because the polyunsaturated fats are known to suppress digestion and interfere with liver function, they have the effect of further encouraging bacterial overgrowth, increasing exposure to the damaging effects of endotoxin. These factors then promote the circulation through the system of serotonin and estrogen, dramatically increasing levels of stress.

“Ovarian hormones have also been shown to affect numerous factors regulating serotonin synthesis and serotonin levels…ovarian hormones promote…tryptophan hydroxylase, the rate-limiting enzyme in the synthesis of serotonin, and reduce serotonin reuptake transporter…expression…numerous serotonergic receptor subtypes are reportedly regulated by ovarian steroids, as well as implicated in depression…”

“estrogen may increase the capacity for serotonin synthesis…and…contribute to distinct components of anxiety behavior.”

As cortisol levels continue to rise, more and more muscle tissue is broken down causing an increase in the release of the inflammatory amino acids, in particular tryptophan. Rising levels of stress and the associated interaction between greater amounts of tryptophan and polyunsaturated fats throughout the system further raise levels of serotonin.

“The rate of serotonin synthesis was reduced by ATD [acute tryptophan depletion] by a factor of about 9.5 in males and of about 40 in females.”

“The administration of amino acid…mixtures that are selectively deficient…in tryptophan…can decrease serotonin…synthesis…Neuroimaging, cerebrospinal fluid, microdialysis and postmortem tissue punch studies indicate that this magnitude of decline decreases brain 5-HT”

Estrogen, serotonin and endotoxin as well as some other inflammatory substances released in the body under stress, interact powerfully with the polyunsaturated fats suppressing metabolism and causing many of the symptoms of depression and anxiety.

Rising levels of estrogen and serotonin have been shown to be important factors causing many kinds of degeneration and disease, including cancer.

“…this report makes…a parallel between induced tumorigenicity by expression of the 5-HT2B receptor in nontransformed fibroblasts and its expression by spontaneous tumors…”

The high stress inflammatory state – where thyroid is under active and tryptophan and cortisol are rising – encourages an increase in serotonin throughout the body and in the brain, and it would be illogical (even based solely on this information) to suggest that it makes sense for mood dysregulation to be the result of some kind of serotonin lack.

A diet removing the polyunsaturated fats and limiting intake of difficult to digest starches and fibers, whilst providing sufficient protein from milk, cheese and gelatin and plenty of sugar from sweet ripe juicy fruits, fruit juice, honey and white sugar, is one way to help limit serotonin and protect against depression and anxiety.

Maintaining blood sugar stability can help by reducing stress and preventing the excessive release of polyunsaturated free fatty acids into the blood. This protects against interference with energy metabolism and can go a long way towards improving mood stability.

Regular snacks throughout the day – made up of a combination of the above sources of protein and carbohydrate in varying ratios depending on individual metabolic needs – can help to achieve this.

Although the relationship between mood and serotonin is not always black and white, protection from the disorders of the mind appears to come from improvements in the functioning of overall thyroid systems and metabolism as well as an increase in the provision of energy, enhanced by – and resulting in – a lowering of serotonin.

What do most doctors understand about the biological role of serotonin in relation to depression (and many other mood disorders and conditions), and how would a change in perspective influence the treatment approaches recommended by them?

See More Here

Serotonin Synthesis and Reuptake in Social Anxiety Disorder

Individuals with social phobia have too much serotonin – not too little

Serotonin engages an anxiety and fear-promoting circuit in the extended amygdala

Is serotonin an upper or a downer? The evolution of the serotonergic system and its role in depression and the antidepressant response.

Mice Genetically Depleted of Brain Serotonin Do Not Display a Depression-like Behavioral Phenotype

Cyproheptadine for prevention of neuropsychiatric adverse effects of efavirenz: a randomized clinical trial.

Effects of the 5HT antagonist cyproheptadine on neuropsychological function in chronic schizophrenia.

Indigenous Bacteria from the Gut Microbiota Regulate Host Serotonin Biosynthesis

Differences between males and females in rates of serotonin synthesis in human brain

Maternal Inflammation Disrupts Fetal Neurodevelopment via Increased Placental Output of Serotonin to the Fetal Brain

A new method for rapidly and simultaneously decreasing serotonin and catecholamine synthesis in humans

miR-1202: A Primate Specific and Brain Enriched miRNA Involved in Major Depression and Antidepressant Treatment

Estrogen-mediated effects on depression and memory formation in females

Oxidative Stress and Antioxidant Parameters in Patients With Major Depressive Disorder Compared to Healthy Controls Before and After Antidepressant Treatment: Results From a Meta-Analysis

Elevated morning cortisol is a stratified population-level biomarker for major depression in boys only with high depressive symptoms

Social Behavioral Deficits Coincide with the Onset of Seizure Susceptibility in Mice Lacking Serotonin Receptor 2c

An epigenetic mechanism links socioeconomic status to changes in depression-related brain function in high-risk adolescents

Ras Involvement in Signal Transduction by the Serotonin 5-HT2B Receptor

Chronology of Onset of Mental Disorders and Physical Diseases in Mental-Physical Comorbidity – A National Representative Survey of Adolescents

Whole-Body Hyperthermia for the Treatment of Major Depressive Disorder

Genetics of emotional regulation: the role of the serotonin transporter in neural function.

Reducing peripheral serotonin turns up the heat in brown fat

Estrogen selectively increases tryptophan hydroxylase-2 mRNA expression in distinct subregions of rat midbrain raphe nucleus: association between gene expression and anxiety behavior in the open field.

Suppression of transcriptional drift extends C. elegans lifespan by postponing the onset of mortality


Artist: walmazan: “Serotonin & the Dopamines”

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