Antidepressant Peptides: Facts to Consider

For decades, the scientific and medical communities have assumed that a “chemical imbalance” in the brain is to blame for depressive disorders. We have put together this guide on facts to consider about antidepressant peptides to help you out. Depression has long been thought to result from an imbalance in the neurotransmitters Serotonin, Norepinephrine, and Dopamine. To treat depression, it seemed sensible to restore these levels, often by increasing them.

An abundance of medications, including SSRIs like Prozac and Zoloft, monoamine oxidase inhibitors (MAOIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants, and medications that affect norepinephrine and dopamine levels, have been developed as an outcome of the “chemical imbalance” hypothesis. Some promoted these substances as 80-90% effective in the early 1990s for treating depression and associated disorders. Therefore, they rapidly became among the most often prescribed medications in the West. Unfortunately, consumers and their medical providers gave these wonder medications much more credit than they deserved in an attempt to combat the symptoms of depression.

Recent research, however, has disproven the idea that antidepressants like Prozac have any noticeable advantage over a placebo. Everyone avoided the topic for a while, and for a good reason, there wasn’t a good way out. But as time went on, medical professionals had to confront the reality that SSRIs and other medications with similar mechanisms of action weren’t very effective at treating depression. This discovery, far from marking a low point in the study of depression, led to the testing of many novel therapeutic approaches, such as peptides, electroconvulsive therapy, and even medicines like ketamine.

Antidepressant Peptides

The etiology and pathophysiology of depression probably include neuropeptides or peptides that are active in the central nervous system. Studies have shown that peptides, including Vasopressin, Galanin, and neuropeptide Y, play an essential role in regulating monoaminergic receptor transmission. In other words, peptides presumably regulate neurotransmitters like Serotonin and Dopamine at the molecular level. Incorrect chemical control and signaling, rather than a “chemical imbalance,” is the root of the depression issue.

Multiple neuropsychiatric disorders may include neuropeptide systems, implying that many psychiatric symptoms are caused by a genuine physical failure of specific receptors or their ligands. Changes in neuropeptide systems such as Arginine-Vasopressin, cholecystokinin, corticotropin-releasing factor, neuropeptide Y, and others have been linked to schizophrenia.


The hunger hormone Ghrelin may help alleviate depression in certain subjects. High cortisol levels are associated with an increase in this peptide, which controls growth hormone and energy balance. High amounts of the stress hormone cortisol are linked to diseases like sadness and anxiety, but it’s not entirely apparent that cortisol is to blame.

In rats, reducing depressive-like behavior and hypomotility by stimulating the ghrelin receptor (growth hormone secretagogue receptor) reduced cortisol levels. Tryptophan metabolism is also affected when Ghrelin is deleted in mice. Many neurotransmitters have been linked to the pathophysiology of depression, and tryptophan is a precursor to several chemicals. Ghrelin analogs like Ipamorelin, GHRP-2, and GHRP-6 may have the same antidepressant effects as Ghrelin. Although anecdotal evidence points in this direction, researchers still lack complex data. Most research on these peptides has focused on their capacity to promote growth hormone production, tissue healing, and bone formation. Only lately has there been any genuine concern about their effects on the brain and spinal cord.


Short peptides like Pinealon have been shown to interact with DNA and cause changes in gene expression directly. Animal studies have demonstrated that administering Pinealon may alter behavior and significantly affect circadian rhythm problems. Pinealon has shown some potential in animal models of depression, which is not surprising given the strong correlation between sleep and sadness.

Evidence suggests that Pinealon increases 5-tryptophan hydroxylase expression in the brain. Because of its central function in serotonin biosynthesis, this enzyme may affect brain serotonin levels. Pinealon has also been proven to alleviate neuropsychiatric symptoms from disturbed sleep and sleep deprivation.


Anxiety and depression are so closely connected that they are commonly diagnosed together. According to studies involving people suffering from anxiety and depression, the inflammatory cytokine IL-6 may have a role in both disorders. Patients with anxiety-asthenic disease and other psychosomatic illnesses when depression is accompanied by symptoms such as nerve pain, exhaustion, headache, heart palpitations, and high blood pressure may benefit significantly from IL-6 therapy. Fibromyalgia and chronic fatigue syndrome studies have shown an interest in IL-6. Both illnesses seem to have high IL-6, and it is essential to note that antidepressants may help in certain situations for both. Researchers are interested in Selank for treating anxiety and depression since it can inhibit the expression of the gene that produces interleukin 6 (IL-6).


Studies have indicated that depressed patients have lower levels of BDNF (brain-derived neurotrophic factor). BDNF is critical in neurons’ development, maturation, survival, and synaptic connections. Abnormalities in BDNF levels and BDNF receptors have been closely connected to depression and suicidality. It is unclear whether reduced BDNF levels are a result of depression or a cause of depression.

Upregulating BDNF has been suggested as a therapy for depression. A short synthetic derivative of ACTH called Semax has been demonstrated to increase BDNF in some rat brain regions (including the basal forebrain). As a bonus, rat exploration activity is boosted by BDNF treatment, and anxiety and depressive-like behaviors are mitigated. Research has also shown that Semax may help treat attention-deficit hyperactivity disorder (ADHD), adding to the mounting evidence that BDNF may serve as a final standard route in various neuropsychiatric disorders.

Conclusions Regarding Peptides for Depression

As was said above, peptides for depression research are only getting started. Researchers have focused extensively on medications that affect these three neurotransmitters, which suggests that they are more likely to be successful. Despite the relative scarcity of knowledge in this area, there are nonetheless convincing studies to show that peptides like Ghrelin, MIF-1, and others may give vital insights into the genesis of depression. More than a few animal studies have also shown that these peptides may provide powerful and largely side-effect-free therapeutic alternatives for depression, anxiety, and other neuropsychiatric diseases. While more work has to be done, the existing data speaks well for future studies into peptides for depression. Visit Biotech Peptides’ website for more articles on various compounds and where you can buy them.

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