Archive for category Pharmacological

[WEB SITE] Dopamine deficiency: Symptoms, causes, and treatment

    1. Symptoms
    2. Causes
    3. Diagnosis
    4. Treatment
    5. Dopamine vs. serotonin
    6. Outlook



Dopamine is a chemical found naturally in the human body. It is a neurotransmitter, meaning it sends signals from the body to the brain.

Dopamine plays a part in controlling the movements a person makes, as well as their emotional responses. The right balance of dopamine is vital for both physical and mental wellbeing.

Vital brain functions that affect mood, sleep, memory, learning, concentration, and motor control are influenced by the levels of dopamine in a person’s body. A dopamine deficiency may be related to certain medical conditions, including depression and Parkinson’s disease.

A dopamine deficiency can be due to a drop in the amount of dopamine made by the body or a problem with the receptors in the brain.



Sad and depressed woman with low dopamine levels. alone in thought.

A dopamine deficiency is associated with depression, but researchers are still investigating this complex link.


The symptoms of a dopamine deficiency depend on the underlying cause. For example, a person with Parkinson’s disease will experience very different symptoms from someone with low dopamine levels due to drug use.

Some signs and symptoms of conditions related to a dopamine deficiency include:

  • muscle cramps, spasms, or tremors
  • aches and pains
  • stiffness in the muscles
  • loss of balance
  • constipation
  • difficulty eating and swallowing
  • weight loss or weight gain
  • gastroesophageal reflux disease (GERD)
  • frequent pneumonia
  • trouble sleeping or disturbed sleep
  • low energy
  • an inability to focus
  • moving or speaking more slowly than usual
  • feeling fatigued
  • feeling demotivated
  • feeling inexplicably sad or tearful
  • mood swings
  • feeling hopeless
  • having low self-esteem
  • feeling guilt-ridden
  • feeling anxious
  • suicidal thoughts or thoughts of self-harm
  • low sex drive
  • hallucinations
  • delusions
  • lack of insight or self-awareness



Dopamine model 3D render.

 Dopamine deficiency may be influenced by a number of factors. Existing conditions, drug abuse, and an unhealthy diet may all be factors.


Low dopamine is linked to numerous mental health disorders but does not directly cause these conditions.

The most common conditions linked to a dopamine deficiency include:

In Parkinson’s disease, there is a loss of the nerve cells in a specific part of the brain and loss of dopamine in the same area.

It is also thought that drug abuse can affect dopamine levels. Studies have shown that repeated drug use could alter the thresholds required for dopamine cell activation and signaling.

Damage caused by drug abuse means these thresholds are higher and therefore it is more difficult for a person to experience the positive effects of dopamine. Drug abusers have also been shown to have significant decreases in dopamine D2 receptors and dopamine release.

Diets high in sugar and saturated fats can suppress dopamine, and a lack of protein in a person’s diet could mean they do not have enough l-tyrosine, which is an amino acid that helps to build dopamine in the body.

Some studies have found that people who are obese are more likely to be dopamine deficient too.


There is no reliable way to measure levels of dopamine in a person. However, a doctor may look at a person’s symptoms, lifestyle factors, and medical history to determine if they have a condition related to low levels of dopamine.



Omega-3 fatty acid supplements.

Omega-3 fatty acid supplements may help to boost dopamine levels naturally.


 Treatment of dopamine deficiency depends on whether an underlying cause can be found.

If a person is diagnosed with a mental health condition, such as depression or schizophrenia, a doctor may prescribe medications to help with the symptoms. These drugs may include anti-depressants and mood stabilizers.

Ropinirole and pramipexole can boost dopamine levels and are often prescribed to treat Parkinson’s disease. Levodopa is usually prescribed when Parkinson’s is first diagnosed.

Other treatments for a dopamine deficiency may include:

  • counseling
  • changes in diet and lifestyle
  • physical therapy for muscle stiffness and movement problems

Supplements to boost levels of vitamin Dmagnesium, and omega-3 essential fatty acids may also help to raise dopamine levels, but there needs to be more research into whether this is effective.

Activities that make a person feel happy and relaxed are also thought to increase dopamine levels. These may include exercise, therapeutic massage, and meditation.

Dopamine vs. serotonin

Dopamine and serotonin are both naturally occurring chemicals in the body that have roles in a person’s mood and wellbeing.

Serotonin influences a person’s mood and emotions, as well as sleep patterns, appetite, body temperature, and hormonal activity, such as the menstrual cycle.

Some researchers believe that low levels of serotonin contribute to depression. The relationship between serotonin and depression and other mood disorders is complex and unlikely to be caused by a serotonin imbalance alone.

Additionally, dopamine affects how a person’s moves, but there is no clear link to the role of serotonin in movement.


Dopamine deficiency can have a significant impact on a person’s quality of life, affecting them both physically and mentally. Many mental health disorders are linked to low levels of dopamine. Other medical conditions, including Parkinson’s disease, have also been linked to low dopamine.

There is limited evidence that diet and lifestyle can affect the levels of dopamine a person creates and transmits in their body. Certain medications and some therapies may help relieve symptoms, but a person should always speak to a doctor first if they are concerned about their dopamine levels.


via Dopamine deficiency: Symptoms, causes, and treatment


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[ARTICLE] Eslicarbazepine acetate as a replacement for levetiracetam in people with epilepsy developing behavioral adverse events – Full Text



Psychiatric and behavioral side effects (PBSEs) are a major cause of antiepileptic drug (AED) withdrawal. Levetiracetam (LEV) is a recognized first-line AED with good seizure outcomes but recognized with PBSEs. Eslicarbazepine (ESL) is considered to function similarly to an active metabolite of the commonly used carbamazepine (CBZ). Carbamazepine is used as psychotropic medication to assist in various psychiatric illnesses such as mood disorders, aggression, and anxiety.


The aim was to evaluate the psychiatric profile of ESL in people who had LEV withdrawn due to PBSEs in routine clinical practice to see if ESL can be used as a possible alternative to LEV.


A retrospective observational review was conducted in two UK epilepsy centers looking at all cases exposed to ESL since its licensing in 2010. The ESL group was all patients with treatment-resistant epilepsy who developed intolerable PBSEs to LEV, subsequently trialed on ESL. The ESL group was matched to a group who tolerated LEV without intolerable PBSEs. Psychiatric disorders were identified from case notes. The Hamilton Depression Scale (HAM-D) was used to outcome change in mood. Clinical diagnoses of a mental disorder were compared between groups using the Fisher’s exact test. Group differences in HAM-D scores were assessed using the independent samples t-test (alpha = 0.05).


The total number of people with active epilepsy in the two centers was 2142 of whom 46 had been exposed to ESL. Twenty-six had previous exposure to LEV and had intolerable PBSEs who were matched to a person tolerating LEV. There was no statistical differences in the two groups for mental disorders including mood as measured by HAM-D (Chi-square test: p = 0.28).


The ESL was well tolerated and did not produce significant PBSEs in those who had PBSEs with LEV leading to withdrawal of the drug. Though numbers were small, the findings suggest that ESL could be a treatment option in those who develop PBSEs with LEV and possibly other AEDs.

1. Background

Epilepsy is a neurological condition with an enduring predisposition to generate seizures and is associated with cognitive, psychological, and social issues [1]. Neuropsychiatric disorders are also more prevalent in people with epilepsy than in the general population [2] ;  [3]. There is, however, still ambiguity as to whether these comorbidities are the result of a direct link such as a genetic predisposition or structural cause leading to seizures and psychiatric problems or if seizures over time lead to psychiatric symptoms [4].

Treatment strategies in epilepsy need to be tailored to the individual and in particular, clinicians when choosing the appropriate antiepileptic drug (AED) medication need to pay attention not only to seizure patterns but also to a number of different parameters such as age, gender, comorbidities, and cognitive state.

Up to 75% of people with epilepsy may at some point have mental health issues. Antiepileptic drugs also have the potential to impact on mental health and cognition [5] ;  [6], and treatment with some AEDs is associated with the occurrence of psychiatric and behavioral side effects (PBSEs) while other may have beneficial psychotropic effects [7][8][9] ;  [10]. The PBSEs are often overlooked in epilepsy management and, withdrawal of an AED occurs only if the impact of these symptoms is significant and usually a risk to self or others.

Understanding psychotropic effects of (AEDs) is crucial but knowledge is limited. Carbamazepine (CBZ)-purported mode of action is via the modulation of voltage-sensitive sodium channels. Apart from antiepileptic action, CBZ is also used as a mood stabilizer and has proven efficacy in affective disorders. Oxcarbazepine (OXB) is structurally related to CBZ and is a prodrug that is converted into licarbazepine. The active form licarbazepine is the S enantiomer, known as eslicarbazepine (ESL). The presumed mechanism of action is as for CBZ. Conversely, OXB has never been proven to work as a mood stabilizer. In view of similarities of the postulated mechanism of action but a better tolerability profile, OXB has been used “off label” in mood management.

Levetiracetam (LEV), a commonly prescribed AED in the UK, is associated with PBSEs including irritability, depression, and anxiety [9] ;  [11]. A study suggested that PBSEs occurred in around 17% of people exposed to commonly used AEDs. Nearly 1 in 5 study participants on LEV reported PBSEs to LEV. However for CBZ the reported PBSEs were significantly lower [11]. The ESL did not figure in this study. Another study suggested that PBSEs with ESL were < 2.5%. While side effects such as irritability, anxiety, and aggressive behavior have been associated with other AEDs, rates of aggression and agitation were comparable between ESL and placebo [12]. […]

Continue —> Eslicarbazepine acetate as a replacement for levetiracetam in people with epilepsy developing behavioral adverse events

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[ARTICLE] Cost-Effectiveness of Treating Upper Limb Spasticity Due to Stroke with Botulinum Toxin Type A: Results from the Botulinum Toxin for the Upper Limb after Stroke (BoTULS) Trial – Full Text


Stroke imposes significant burdens on health services and society, and as such there is a growing need to assess the cost-effectiveness of stroke treatment to ensure maximum benefit is derived from limited resources. This study compared the cost-effectiveness of treating post-stroke upper limb spasticity with botulinum toxin type A plus an upper limb therapy programme against the therapy programme alone. Data on resource use and health outcomes were prospectively collected for 333 patients with post-stroke upper limb spasticity taking part in a randomized trial and combined to estimate the incremental cost per quality adjusted life year (QALY) gained of botulinum toxin type A plus therapy relative to therapy alone. The base case incremental cost-effectiveness ratio (ICER) of botulinum toxin type A plus therapy was £93,500 per QALY gained. The probability of botulinum toxin type A plus therapy being cost-effective at the England and Wales cost-effectiveness threshold value of £20,000 per QALY was 0.36. The point estimates of the ICER remained above £20,000 per QALY for a range of sensitivity analyses, and the probability of botulinum toxin type A plus therapy being cost-effective at the threshold value did not exceed 0.39, regardless of the assumptions made.

1. Introduction

Stroke is a major cause of mortality and morbidity and imposes a significant burden on both health services and society [1,2,3]. In the United Kingdom (UK) it is estimated that the annual direct costs of stroke are approximately £4 billion, which constitutes around 5.5% of the total UK expenditure on health care [3]. If the costs of lost productivity and informal care are taken into account, the total annual societal costs of stroke are estimated to be around £9 billion [3]. In England, over 900,000 people are living with the consequences of stroke, 300,000 of whom are moderately or severely disabled [4]. As the proportion of older people in society increases, so the burden of stroke is likely to grow.

Upper limb spasticity after stroke is an important clinical problem and its identification and treatment are key components of stroke rehabilitation [5]. Upper limb spasticity may cause deformity, reduced function and pain [6]. Botulinum toxin type A, which when given by intramuscular injection causes temporary local muscle paresis by blocking neuromuscular transmission [7], has become an established treatment for spasticity due to stroke. Randomised controlled trials have shown that botulinum toxin reduces muscle tone [8] and improves the performance of basic upper limb functional tasks such as hand opening for cleaning and ease of dressing [9,10,11]. However, the impact on active upper limb function (e.g., reaching and grasping) and the efficacy of repeated treatment is less clear.

The BoTULS trial was a pragmatic multi-centre randomised controlled trial to evaluate the clinical and cost-effectiveness of botulinum toxin type A plus an upper limb therapy programme in the treatment of post stroke upper limb spasticity. The clinical results indicated that botulinum toxin type A did not improve active upper limb function (as measured by the Action Research Arm Test (ARAT)), but that there may be benefits in terms of decreased muscle tone, improved upper limb strength, improved ease of performance of basic upper limb functional activities and reduction in pain [12]. This article describes the results of the cost-effectiveness analysis. […]

Continue —> Toxins | Free Full-Text | Cost-Effectiveness of Treating Upper Limb Spasticity Due to Stroke with Botulinum Toxin Type A: Results from the Botulinum Toxin for the Upper Limb after Stroke (BoTULS) Trial | HTML

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[ARTICLE] Efficacy and Safety of AbobotulinumtoxinA (Dysport) for the Treatment of Hemiparesis in Adults With Upper Limb Spasticity Previously Treated With Botulinum Toxin: Subanalysis From a Phase 3 Randomized Controlled Trial – Full Text



To assess the efficacy and safety of abobotulinumtoxinA in adults with upper limb spasticity previously treated with botulinum toxin A (BoNT-A).


post hoc analysis from a Phase 3, prospective, double-blind, randomized, placebo-controlled study (NCT01313299).


A total of 34 neurology or rehabilitation clinics in 9 countries.


Adults aged 18-80 years with hemiparesis, ≥6 months after stroke or traumatic brain injury. This analysis focused on a subgroup of subjects with previous onabotulinumtoxinA or incobotulinumtoxinA treatment (n = 105 of 243 in the total trial population) in the affected limb. The mean age was 52 years, and 62% were male.


Study subjects were randomized 1:1:1 to receive a single injection session with abobotulinumtoxinA 500 or 1000 U or with placebo in the most hypertonic muscle group among the elbow, wrist, or finger flexors (primary target muscle group [PTMG]), and ≥2 additional muscle groups from the upper limb.

Main Outcome Measurements

Efficacy and safety measures were assessed, including muscle tone (Modified Ashworth Scale [MAS] in the PTMG), Physician Global Assessment (PGA), perceived function, spasticity, active movement, and treatment-emergent adverse events.


At week 4, more subjects had ≥1 grade improvement in MAS for the PTMG with abobotulinumtoxinA versus placebo (abobotulinumtoxinA 500 U, 81.1%; abobotulinumtoxinA 1000 U, 75.0%; placebo, 25.0%). PGA scores ≥1 were achieved by 75.7% and 87.5% of abobotulinumtoxinA 500 and 1000 U subjects versus 41.7% with placebo. Perceived function (Disability Assessment Scale), spasticity angle (Tardieu Scale), and active movement were also improved with abobotulinumtoxinA. There were no treatment-related deaths or serious adverse events.


The efficacy and safety of abobotulinumtoxinA in subjects previously treated with BoNT-A were consistent with those in the total trial population. Hence, abobotulinumtoxinA is a treatment option in these patients, and no difference in initial dosing appears to be required compared to that in individuals not treated previously.



Upper limb spasticity (ULS) is common after stroke or traumatic brain injury (TBI). The impact can be highly significant, including abnormal hand and arm positions, impaired self-care, and limited passive/active range of motion, as well as additional burden to the caregiver [1-5].

The effectiveness of treatment with intramuscularly injected botulinum toxin A (BoNT-A) in reducing muscle tone in patients with ULS is well established [5-8]. Several guidelines now recommend BoNT-A injections as a first-line treatment option in these patients [6,7,9-11].

AbobotulinumtoxinA (Dysport; Ipsen Biopharm, Wrexham, UK) is a BoNT-A preparation approved in the United States and Europe for the treatment of ULS in adult patients [12,13]. A recent clinical trial examined the efficacy and safety of a single injection session of abobotulinumtoxinA (500 or 1000 U) in 243 adults with ULS who had hemiparesis at least 6 months after stroke or TBI [14]. The effects observed included improvements in muscle tone, perceived function, spasticity, and active range of motion. Furthermore, the treatment was well tolerated, and all treatment-related adverse events (AEs) were mild or moderate in severity.

Among the subjects enrolled in this study, 105 had previously undergone treatment in the upper limb with onabotulinumtoxinA or incobotulinumtoxinA. The aim of the present analysis was to assess the efficacy and safety of abobotulinumtoxinA in adults with ULS who had been previously treated with a BoNT-A, and to describe the doses of abobotulinumtoxinA administered to these subjects. […]

Continue —> Efficacy and Safety of AbobotulinumtoxinA (Dysport) for the Treatment of Hemiparesis in Adults With Upper Limb Spasticity Previously Treated With Botulinum Toxin: Subanalysis From a Phase 3 Randomized Controlled Trial – ScienceDirect

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[WEB SITE] Top 3 Vitamins for Stroke Recovery

Top 3 Vitamins for Stroke Recovery (and Some Honorable Mentions)

During stroke recovery, proper nutrition is essential. A healthy diet can help you maintain a healthy weight – which can help reduce your risk of a second stroke – and provide your body with the fuel it needs to heal itself.

These essential vitamins for stroke recovery can be found in supplements, or they can be found in whole foods – which is a much better way to go. We’ll cover how to do that at the end.

Important Note: Vitamins Can Interfere with Medication and Create Complications!

The purpose of this article is to inform you of vitamins that can help promote health and wellbeing.

We ABSOLUTELY recommend running new supplements by your doctor first because they can interfere with any medication you’re taking.

For example, ginko biloba is an herb that is widely used to help prevent ischemic stroke because it’s a natural blood thinner. Meaning, complications can arise if you’re already on blood thinning medication.

Be safe and be sure to run everything by your doctor. We cannot stress this enough!

Now, onto the top 3 vitamins.

1. Coenzyme Q10 (CoQ10)

CoQ10 is powerful antioxidant that helps protect your tissues from the damage that toxic molecules, also known as free radicals, cause. Bodily stress caused by these free radicals is believed to play a role in many diseases, including cardiovascular disease, a precursor to stroke.

Supplementation with CoQ10 can reduce your risk of developing cardiovascular disease and therefore reduce your risk of a second stroke. Also, low CoQ10 levels have been associated with greater tissue damage to the brain during stroke.

CoQ10 can be found in most liver organs like heart, liver, and kidney… But if you’re not too keen on organ meats (and if you’re not, we don’t blame you) then you can also find smaller amounts of CoQ10 in spinach, broccoli, and cauliflower.

2. Vitamin B3 (Niacin)

This one is simple: Vitamin B3 can help you recover brain function after stroke. Sweet! And if that isn’t reason enough to love this B vitamin, it also helps boost ‘good’ cholesterol levels, which are typically very low in stroke survivors.

You can find vitamin B3 in tuna, chicken, turkey, and salmon. For some meatless options, you can also find vitamin B3 in peanuts and brown rice – just in lesser quantities.

3. Fish Oil

Fish oil is a great source of EPA and DHA – two omega-3 fatty acids that are excellent for a healthy brain.

Fish oil can help you in two ways.

First, fish oil can help lower elevated triglyceride levels, which are a stroke risk factor. Second, the DHA in fish oil helps promote healthy brain function.

This makes fish oil helpful for both stroke prevention and stroke recovery. Score!

Other Important Vitamins (and One Non-Vitamin)

Update: This article has become one of most popular! As a thank you for taking the time to read our blog, we added some honorable mentions.

Other important vitamins that can help boost stroke recovery are:

Omega 3’s are essential for healthy brain function because they’re an essential fat and, well, your brain is made of 60% fat! Vitamin B12 plays a strong role in both brain and nerve health while vitamin D plays a strong role in brain and muscular health.

Vitamin C can help boost your stroke prevention efforts – and your immune system!

Probiotics are interesting because they aren’t a vitamin or a mineral. Instead, probiotics are bacteria that comprise your microbiome, which consists of 100 trillion little microbes that live inside your gut. Your microbiome has a nervous system of it’s own called the enteric nervous system where it communicates with your brain through the gut-brain axis.

When this communication is impaired, all sorts of health problems can arise, including depression and impaired brain function.

It’s a thick topic and a recent discovery, so refer to this series for more information.

How to Get These Vitamins without Spending Tons of Extra Money

As you can see, many vitamins and nutrients play a vital role in protecting your health – and it can seem a little overwhelming. If you’re not too keen on going out and buying all these supplements, there’s actually a better alternative:

Eat a variety of whole foods every day.

The two keys here are variety and whole.

Whole foods are foods that most resemble their true form and are minimally touched by processing. When foods are processed, it can strip them of many essential vitamins and minerals.

For example, rice is a much better choice than processed white pasta; roasted vegetables pack way more nutrients than fried potatoes; and a blueberry/banana/yogurt parfait is much healthier than blueberry cheesecake.

When we eat a wide variety of whole foods, we’re much less likely to develop a deficiency because you have a higher chance of eating foods with the particular nutrients you need. The easiest way to do this: Listen to your body. It will tell you what you need.

Craving fish tacos?

You probably need the omega 3’s and vitamin D that fish contains. So go for it! But skip the processed restaurant version. Enjoy a nice home-cooked dinner with fish and other whole foods and your body will be satisfied and prepared to recover from stroke with all the resources it needs.

And if impaired hand function is keeping you out of the kitchen, here are some tips on how to cook one-handed after stroke.

We hope this article has helped you better understand how proper nutrition can take your recovery to the next level.

Related Reading:

via Top 3 Vitamins for Stroke Recovery – Flint Rehab

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[BLOG POST] Tryptophan in Mood, Anxiety, and Depression


Deficiency of monoamines, such as dopamine, epinephrine, and serotonin, is the most widely accepted theory explaining mood disorders. Among these neuromediators, serotonin deficiency is considered as most significant in relation to anxiety and depression. This theory has been proven by the effectiveness of drugs that help to increase monoamines levels in the brain, although research in this direction has been hampered by the limitations of present-day technology in measuring the levels of specific monoamines and their properties. However, studies do indicate that their deficiency plays a role in individuals prone to mood swings.

Tryptophan as precursor for serotonin

Tryptophan is one of the essential amino acids. It can’t be produced by our body and has to come through food products rich in proteins. It is required for both anabolic processes and production of various hormones. Tryptophan is a chemical precursor for the synthesis of the neurotransmitter serotonin. This means that the amount of serotonin produced in our body is dependent on the dietary intake of tryptophan. Since serotonin is related to mood regulation, it is entirely possible that tryptophan deficits may have a negative effect on our mood state. On the other hand, its supplementation may be helpful in disorders like anxiety or depression. Multiple investigations seem to support the idea that decreased levels of tryptophan lead to a reduction in serotonin and changes in mood. Some studies have indicated that higher intake of tryptophan may improve social interactions by improving mood and decreasing aggression and dominant behavior.

Serotonin in mood and cognition

Serotonin is important for both mood regulation and regulation of cognitive functions like learning and memory. The effect of monoamine inhibitors called serotonin reuptake inhibitors in various disorders of mood supports this theory. However, it is important to keep in mind that antidepressants are only partially effective in treating mood disorders since monoamine deficits are just one of the factors influencing mood. Most of the serotonin in our body is produced outside the brain, indicating that this compound has a much broader role in our normal physiology. It is possible that many functions of serotonin are still not understood.

Tryptophan depletion and mood regulation

To understand the role of serotonin, and more specifically tryptophan, many tryptophan-depletion studies have been done in recent times. In one simple crossover study, 25 healthy adults were studied for mood changes like anxiety and depression after consuming either a high tryptophan diet or a low tryptophan diet for four days. Tryptophan consumption seems to affect mood even in such a short interval. The study showed that those on a high tryptophan diet had much better mood as compared to those on a low tryptophan diet, although the negative effects of a low tryptophan diet were less pronounced. If such a quick and straightforward analysis can show the difference, it is entirely possible that long-term low tryptophan consumption or depletion may have much graver consequences for mental health.

Tryptophan and gut-brain axis

When we talk about the gut-brain axis we are not just discussing the digestive role of the gut and its effect on overall health, something that has been well known for many years. Our digestive system is also involved in neuro-hormonal signaling, through which it can have an impact on brain functioning. Recently, the influence of gut health on the brain has been the subject of many studies and for good reason. Our gut has more nerve cells than our spine, and it produces many hormones that have various implications for health. Further, it is now well understood that the neural relationship between the gut and brain is dual-sided, and there are more nerve fibers sending information from the gut to the brain rather than from the brain to the gut. Thus, due to the effect of nerves, hormones, and other neurologically active compounds, the gut plays a prominent role in mental wellbeing. Even small changes in the gut could directly affect our behavior. Gut microbiota and their relationship to mood have also recently received lots of attention.

When it comes to tryptophan, the digestive system is not solely involved in its absorption or metabolism. Now it is well-established that serotonin is mostly produced in the gut rather than in the brain, further strengthening the theory of gut-brain interrelation. This theory explains the mood alterations in irritable bowel syndrome (IBS). Further, the development of IBS has been shown to be connected to tryptophan depletion.

The studies show that tryptophan depletion, due to its relationship with serotonin, is undoubtedly one of the most essential elements to consider when analyzing altered mood and cognition. Low serotonin could generally cause a state of lowered mood, impaired cognition, poor working memory, and lower reasoning. Conversely, high tryptophan supplementation could have a positive effect on mood, memory, energy level, and emotional processing.

Low dietary consumption of tryptophan could be one of the elements leading to chronic conditions like depression and anxiety. Bowel conditions like IBS that disturb tryptophan metabolism and alter serotonin levels may also modify our behavior and feelings.

The search for effective therapeutic approaches to the treatment of mood disorders, anxiety, and depression has gained lots of attention in the last few decades. Understanding the role of tryptophan may open up new possibilities for managing mood and cognition problems. It is quite possible that a high tryptophan diet may not only help to prevent mood disorders but also increase the effectiveness of existing drug therapies.


Delgado, P. L. (2000) Depression: the case for a monoamine deficiency. The Journal of Clinical Psychiatry61 Suppl 6, 7–11. PMID: 10775018

Jenkins, T. A., Nguyen, J. C. D., Polglaze, K. E., & Bertrand, P. P. (2016) Influence of Tryptophan and Serotonin on Mood and Cognition with a Possible Role of the Gut-Brain Axis. Nutrients8(1). doi: 10.3390/nu8010056

Lindseth, G., Helland, B., & Caspers, J. (2015). The Effects of Dietary Tryptophan on Affective Disorders. Archives of Psychiatric Nursing29(2), 102–107. doi: 10.1016/j.apnu.2014.11.008

Young, S. N., & Leyton, M. (2002) The role of serotonin in human mood and social interaction. Insight from altered tryptophan levels. Pharmacology, Biochemistry, and Behavior71(4), 857–865. PMID: 11888576

Young, S. N., Smith, S. E., Pihl, R. O., & Ervin, F. R. (1985) Tryptophan depletion causes a rapid lowering of mood in normal males. Psychopharmacology87(2), 173–177. doi: 10.1007/BF00431803

Image via freeGraphicToday/Pixabay.

via Tryptophan in Mood, Anxiety, and Depression | Brain Blogger


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[WEB SITE] Treating Levetiracetam-Induced Behavioral Effects With Vitamin B6

Data showed that 11.8% of levetiracetam-treated patients experienced behavioral side effects.

Data showed that 11.8% of levetiracetam-treated patients experienced behavioral side effects.

Daily pyridoxine (vitamin B6) was found to be an effective treatment for the behavioral adverse effects seen with the antiepileptic drug levetiracetam, according to a poster presented at the AES Annual Meeting 2017.

Treatment with levetiracetam (Keppra; UCB) has been shown to cause non-psychotic behavioral effects (eg, aggression, anger, emotional lability, anger, depression, anxiety) in clinical studies (13% in levetiracetam-treated patients vs 6% in placebo-treated). Currently, there is a lack of data regarding the treatment of behavioral effects of levetiracetam, which represents a key cause of treatment discontinuation.

For the retrospective study, Creighton University School of Medicine researchers evaluated whether pyridoxine supplementation could benefit patients who are experiencing behavioral adverse effects due to levetiracetam. The team reviewed electronic medical records of all patients in the Creighton University Epilepsy Center Clinic (2011–2015) for those taking levetiracetam. Forty-five of the 380 total patients receiving levetiracetam (median dose 1000mg daily; highest dose 4000mg daily) were initiated on pyridoxine 100mg daily for symptom control.

The data showed 11.8% of levetiracetam-treated patients experienced behavioral side effects with agitation, insomnia, and irritability being the most commonly observed. These behavioral changes were typically seen within the first month of starting levetiracetam therapy. Nearly all of the patients who received pyridoxine (42/45; 93.3%) remained on levetiracetam therapy as they saw significant improvement in their behavioral symptoms.

“This benefit is seen across the entire range of levetiracetam dosing,” lead author Kalyan Sajja noted. Supplementation with pyridoxine 100mg daily enabled continued treatment with levetiracetam in these patients. The authors added that a large multicenter, prospective, randomized-controlled trial can further validate this clinical benefit.


Sajja K, Sankaraneni R, Galla K, Singh SP. Role of Pyridoxine (Vitamin B6) in the Treatment of Levetiracetam Induced Behavioral Effects in Epilepsy Patients. Presented at: AES annual meeting in Washington, DC. Abstract 1.308.

via Treating Levetiracetam-Induced Behavioral Effects With Vitamin B6

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[WEB SITE] Neurontin and Lyrica are a Death Sentence for New Brain Synapses : Shocking Study

Image result for Neurontin and Lyrica are a Death Sentence for New Brain Synapses : Shocking Study

by Ann Blake-Tracy

A shocking study shows that these two drugs block the formation of new brain synapses1, drastically reducing the potential for rejuvenating brain plasticity – meaning that these drugs will cause brain decline that apparently robs one of the ability to rebuild. The study demonstrating this type of brain damage with these two drugs came out in 2009 but apparently the media has been very lax in getting any of this information to the public – most likely because they do not want to jeopardize their advertising income from this company.
But the patients are not the only ones not getting this information because the doctors are apparently clueless as well. I say that because first our Facebook group for these two drugs “Neurontin (Gabapentin) & Lyrica (Pregabalin) Should Be Illegal” is growing so quickly. Then this past Spring my brother working on some things in the backyard pulled a muscle in his back. I was shocked to learn that he had gone to the doctor for that and the doctor gave him a prescription for Neurontin!

When I asked when he had started having seizures that he would need an anti-seizure medication for he said, “What?!”
I had to explain to him that Neurontin is an anti-seizure medication and that the company had received two huge fines, totaling billions, from the FDA for prescribing it for anything else. And in 2010 they were even found guilty of RICO, yes racketeering, for encouraging doctors to prescribe this drug off label – for things it is not approved for-like pulling a muscle in your back! Then I shared with him the information in this study indicating the brain damage from the drug at which point he understandably decided not to take the drug.
Although I have included the full article on this below this is the link to the article which you need to follow to find the full research study if you want to take it to your doctor to educate him:

Now my question is why on earth has the FDA not pulled these drugs from the market in light of this study? I ask that because before this study the worst I had seen in producing brain damage were the diet pills Fen-Phen and Redux which were pulled from the market due to the brain damage they produced … even though the media convinced the world those drugs were pulled because of the heart and lung damage. It was the brain damage the FDA was concerned about and had required studies from the maker to prove its safety. Something they had not yet done before Dr. Una Mc Cann at NIH put out a study showing the most horrific brain damage. Those drugs were pulled only days later.

Neurontin and Lyrica are a Death Sentence for New Brain Synapses

Neurontin and its newer more potent version, Lyrica, are widely used for off-label indications that are an outright flagrant danger to the public. These blockbuster drugs were approved for use even though the FDA had no idea what they actually did in the brain. A shocking new study shows that they block the formation of new brain synapses1, drastically reducing the potential for rejuvenating brain plasticity – meaning that these drugs will cause brain decline faster than any substance known to mankind.

The problem of these drugs is compounded by their flagrant illegal marketing. Neurontin was approved by the FDA for epilepsy back in 1994. The drug underwent massive illegal off-label promotion that cost Warner-Lambert 430 million dollars (the very first big fine for off-label promotion). The drug is now owned by Pfizer. Pfizer also owns Lyrica, a super-potent version of Neurontin. It has been approved by the FDA for various types of pain and fibromyalgia. Lyrica is one of four drugs which a subsidiary of Pfizer illegally marketed, resulting in a $2.3 billion settlement against Pfizer.

Even though the marketing of these drugs has been heavily fined, they continue to rack up billions in sales from the off-label uses. Doctors use them for all manner of nerve issues because they are good at suppressing symptoms. However, such uses can no longer be justified because the actual mechanism of the drugs is finally understood and they are creating a significant long-term reduction in nerve health.

The researchers in the above study try to downplay the serious nature of the drugs by saying “adult neurons don’t form many new synapses.” That is simply not true. The new science is showing that brain health during aging relies on the formation of new synapses. Even these researchers managed to question the common use of these medications in pregnant women. How is a fetus supposed to make new nerve cells when the mother is taking a drug that blocks them?

These are the kind of situations the FDA should be all over. As usual, the FDA is sitting around pondering a suicide warning for Lyrica while its off-label uses include bi-polar disorder and migraine headaches. The FDA is likely to twiddle its thumbs for the next decade on the brain damage issue. Consumer beware.

Referenced Studies
^ Neurontin and Lyrica are Highly Toxic to New Brain Synapses Cell Çagla Eroglu, Nicola J. Allen, Michael W. Susman, Nancy A. O’Rourke, Chan Young Park, Engin Özkan, Chandrani Chakraborty, Sara B. Mulinyawe, Douglas S. Annis, Andrew D. Huberman, Eric M. Green, Jack Lawler, Ricardo Dolmetsch, K. Christopher Garcia, Stephen

Via- Drugawareness

via Neurontin and Lyrica are a Death Sentence for New Brain Synapses : Shocking Study – Your Health Guide

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[Abstract] Post-Injury Administration of Galantamine Reduces Traumatic Brain Injury Pathology and Improves Outcome


Acetylcholine is an excitatory neurotransmitter in the central nervous system that plays a key role in cognitive function, including learning and memory. Previous studies have shown that experimental traumatic brain injury (TBI) reduces cholinergic neurotransmission, decreases evoked release of acetylcholine, and alters cholinergic receptor levels. Galantamine (U.S. Food and Drug Administration approved for the treatment of vascular dementia and Alzheimer’s disease) has been shown to inhibit acetylcholinesterase activity and allosterically potentiate nicotinic receptor signaling. We investigated whether acute administration of galantamine can reduce TBI pathology and improve cognitive function tested days after the termination of the drug treatment. Post-injury administration of galantamine was found to decrease TBI-triggered blood-brain barrier (BBB) permeability (tested 24 h post-injury), attenuate the loss of both GABAergic and newborn neurons in the ipsilateral hippocampus, and improve hippocampal function (tested 10 days after termination of the drug treatment). Specifically, significant improvements in the Morris water maze, novel object recognition, and context-specific fear memory tasks were observed in injured animals treated with galantamine. Although messenger RNAs for both M1 (Nos2, TLR4, and IL-12ß) and M2 (Arg1, CCL17, and Mcr1) microglial phenotypes were elevated post-TBI, galantamine treatment did not alter microglial polarization tested 24 h and 6 days post-injury. Taken together, these findings support the further investigation of galantamine as a treatment for TBI.

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The Impact of Traumatic Brain Injury on Later Life: Effects on Normal Aging and Neurodegenerative Diseases

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Jing ZhaoJonathan HuynhMichael J. HylinJohn J. O’MalleyAlec PerezAnthony N. MoorePramod K. Dash

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Minocycline plus N-acetylcysteine reduce behavioral deficits and improve histology with a clinically useful time window

Michael SangobowaleNatalia M. Grin’kinaKristen WhitneyElena NikulinaKarrah St. Laurent-ArriotJohnson S. HoNarek BazyanPeter Bergold

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[Abstract] Treatment of Traumatic Brain Injury with Vepoloxamer (Purified Poloxamer 188)


Vepoloxamer is an amphipathic polymer that has shown potent hemorrheologic, cytoprotective, and anti-inflammatory effects in both pre-clinical and clinical studies. This study was designed to investigate the therapeutic effects of vepoloxamer on sensorimotor and cognitive functional recovery in rats after traumatic brain injury (TBI) induced by controlled cortical impact. Young adult male Wistar rats were randomly divided into the following groups: 1) sham; 2) saline; or 3) vepoloxamer. Vepoloxamer (300 mg/kg) or saline was administered over 60 min via intravenous infusion into tail veins starting at 2 h post-injury. Sensorimotor function and spatial learning were assessed using a modified neurological severity score and foot fault test, and Morris water maze test, respectively. The animals were sacrificed 35 days after injury and their brains were processed for measurement of lesion volume and neuroinflammation. Compared with the saline treatment, vepoloxamer initiated 2 h post-injury significantly improved sensorimotor functional recovery (Days 1–35; p < 0.0001) and spatial learning (Days 32–35; p < 0.0001), reduced cortical lesion volume by 20%, and reduced activation of microglia/macrophages and astrogliosis in many brain regions including injured cortex, corpus callosum, and hippocampus, as well as normalized the bleeding time and reduced brain hemorrhage and microthrombosis formation. In summary, vepoloxamer treatment initiated 2 h post-injury provides neuroprotection and anti-inflammation in rats after TBI and improves functional outcome, indicating that vepoloxamer treatment may have potential value for treatment of TBI. Further investigation of the optimal dose and therapeutic window of vepoloxamer treatment for TBI and the mechanisms underlying beneficial effects are warranted.

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Correlation of Concussion Symptom Profile with Head Impact Biomechanics: A Case for Individual-Specific Injury Tolerance

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