Antidepressants vs Neurofeedback

Growing old healthily: Why you should avoid antidepressants

A recent study from Sweden has investigated how antidepressants affect dementia, fracture risk and mortality. The results are alarming: there is a significant link between taking antidepressants and a worsening of dementia, an increased risk of bone fractures and a higher mortality rate.

Antidepressants and their risks

The study shows that selective serotonin reuptake inhibitors (SSRIs) in particular, such as citalopram, sertraline and escitalopram, are associated with accelerated cognitive decline. Patients taking these drugs lose their mental abilities more quickly and have a higher risk of severe dementia. In addition, higher doses are associated with an increased risk of fractures and increased overall mortality.

The scientists therefore recommend choosing antidepressants very carefully and reviewing their use regularly.


Alternatives to antidepressants

Instead of relying on medication, there are effective natural methods to prevent or treat depression and cognitive decline.

1. orthomolecular medicine

This therapy relies on a targeted supply of vitamins, minerals and trace elements that are essential for brain function. Studies show that an adequate supply of vitamin D, B vitamins, omega-3 fatty acids and magnesium can alleviate depressive symptoms and promote cognitive health.

2. traditional Chinese medicine (TCM)

TCM methods such as acupuncture, herbal medicine and Qi Gong help to stabilize emotional balance and have been shown to reduce stress and depression.

3. neurofeedback – the revolution in brain research

Neurofeedback is one of the most promising non-drug methods for treating depression and dementia. This method works by specifically training brain waves to bring brain activity into a healthy state.

📌 Advantages of neurofeedback:
Reduces depressive symptoms threefold compared to conventional methods.
Delays cognitive decline in dementia patients.
Can improve cognitive function in some cases.
Strengthens motor skills and spatial awareness to prevent falls.

Neurofeedback starts where medication often fails – it actively improves the self-regulation of the brain and thus offers a sustainable solution without side effects.


Summary of the study

A Swedish long-term cohort study (Mo et al., 2025) with 18,740 dementia patients investigated the relationship between antidepressants, cognitive decline and health risks. The most important results:

DrugAnnual deterioration in cognition (MMSE points)Increased risk of fractures and mortality
Citalopram (SSRI)-0,41Yes
Sertraline (SSRI)-0,25Yes
Escitalopram (SSRI)-0,76Yes
Mirtazapine (other)-0,19Yes
Amitriptyline (TZA)No significant deteriorationNo

🔍 Higher doses of SSRIs led to faster cognitive decline and increased health risks.

🔍 The researchers recommend that antidepressants should only be used with caution and that regular checks should be carried out.


Conclusion: opt for natural alternatives!

This study shows that antidepressants are not the best choice for older people with depression or dementia. Natural methods such as orthomolecular medicine, TCM and above all neurofeedback offer a sustainable solution without side effects.

📌 My personal advice:
👉 Avoid antidepressants if there are alternatives!
👉 Rely on neurofeedback – a highly effective, scientifically proven method.
👉 Support your mental health with targeted nutrition and natural healing methods.

Antidepressants ❌Neurofeedback ✅
Side effects: Fatigue, weight gain, dependenceWithout medication: no chemical stress for the body
Increased risk of falling: weakens motor skills & balanceBetter fine motor skills: strengthens coordination & body control
Accelerates dementia: Increases cognitive declineSlows down dementia: promotes brain plasticity & memory
Increased mortality: higher risk of fractures & diseasesLive healthier for longer: Supports the brain & nervous system

If you would like to find out more about neurofeedback and natural forms of therapy, please let me know! 😊


Summary of the study “Antidepressant Use and Cognitive Decline in Patients with Dementia: A National Cohort Study”

Authors: Minjia Mo et al. (2025)
Source: BMC Medicine, DOI: 10.1186/s12916-025-03851-3
Study period: 2007-2018
Data source: Swedish Register for Cognitive and Dementia Disorders (SveDem)


Study structure and methodology

Study design

  • Type: National cohort study
  • Location: Sweden
  • Inclusion criteria: Patients with newly diagnosed dementia, recorded in SveDem
  • Observation period: From the time of diagnosis until October 16, 2018
  • Sample: 18,740 patients (54.5 % women, average age 78.2 years)

Measurements

  • Main variable: Antidepressant use (defined as at least one prescription)
  • Assessment of cognitive decline: Mini-Mental State Examination (MMSE)
  • Primary outcome: Cognitive change over time
  • Secondary outcomes:
    • Severe dementia (MMSE < 10)
    • Fractures
    • Mortality
  • Statistical analyses:
    • Linear mixed models for analyzing the MMSE progression
    • Cox proportional hazard models for calculating the risk of dementia deterioration, fractures and death

Results

Antidepressant use in the cohort

  • Number of patients on antidepressants: 4,271 (22.8 %)
  • Most common class: Selective serotonin reuptake inhibitors (SSRIs) (64.8 %)
  • Most commonly used medication:
    • Citalopram (SSRI)
    • Mirtazapine (other antidepressants)
    • Sertraline (SSRI)
    • Escitalopram (SSRI)
    • Amitriptyline (TZA)
    • Venlafaxine (SNRI)

Influence on cognitive changes

Drugβ-value (annual change in MMSE points)Significance
All antidepressants-0,30p < 0,001
Sertraline (SSRI)-0,25p = 0,011
Citalopram (SSRI)-0,41p < 0,001
Escitalopram (SSRI)-0,76p < 0,001
Mirtazapine (other)-0,19p = 0,014
  • Patients on antidepressants showed faster cognitive deterioration than non-users.
  • The strongest negative effect was observed for escitalopram (-0.76 MMSE points per year).
  • The effect was particularly strong in patients with severe dementia (MMSE 0-9).

Influence on other health risks

OutcomeHazard Ratio (HR)Significance
Severe dementia (MMSE < 10)1,35p = 0,035
Fracture risk1,18p < 0,001
Mortality (all causes)1,07p = 0,016
  • Higher SSRI doses were associated with an increased risk of severe dementia, fractures and death.

Dose-response relationship

Dose range (DDD = defined daily dose)β-value (annual change in MMSE points)
≤ 0.5 DDD-0,20
> 0.5 / ≤ 1.0 DDD-0,33
> 1.0 DDD-0,37
  • Higher doses of SSRIs led to greater cognitive decline.

Conclusions

  • Antidepressants accelerate cognitive decline in dementia patients.
  • SSRIs (especially escitalopram) have the strongest negative effects.
  • Higher SSRI doses increase the risk of severe dementia, fractures and mortality.
  • Regular monitoring of antidepressant use in dementia patients is necessary.

This study underlines the need for cautious and individualized use of antidepressants in patients with dementia, as their benefit may be questionable and the risk may be high.

Mo, M., Abzhandadze, T., Hoang, M. T., Sacuiu, S., Grau Jurado, P., Pereira, J. B., Naia, L., Kele, J., Maioli, S., Xu, H., Eriksdotter, M., & Garcia-Ptacek, S. (2025). Antidepressant use and cognitive decline in patients with dementia: a national cohort study. BMC Medicine, 23(82). https://doi.org/10.1186/s12916-025-03851-3


Terms and abbreviations

p-value (p-value)

The p-value indicates how likely it is that a certain result occurred by chance.

  • Small p-value (e.g. p < 0.05) → The result is statistically significant. It is very unlikely that it was only due to chance.
  • Large p-value (e.g. p > 0.05) → The result is not significant, it could have arisen by chance.

Example: If there is a p-value of 0.001, this means that the probability that the result is just chance is 0.1%.


β-value (beta coefficient)

The β value shows how strongly one variable influences another.

  • Negative β-value → The variable causes a decrease.
  • Positive β-value → The variable causes an increase.

Example:

  • β = -0.30 for antidepressants means that patients taking antidepressants lose 0.30 points per year faster on the MMSE scale (Mini-Mental Status Test) than patients not taking antidepressants.

The greater the magnitude of the β value, the stronger the effect.


DD (Defined Daily Dose, DDD = Defined Daily Dose)

  • The DDD is the amount of a drug that an average adult needs daily to achieve a normal effect.
  • This unit of measurement helps to make different drugs comparable.

Example:

  • 1.0 DDD means that a patient takes exactly the recommended daily dose.
  • >1.0 DDD means a higher than recommended dose, which is often associated with more severe side effects.

SSRIs (selective serotonin reuptake inhibitors)

SSRIs are a group of antidepressants that are often prescribed for depression and anxiety disorders.

  • They increase the serotonin level in the brain, a “happiness hormone” that stabilizes the mood.
  • Well-known SSRIs are citalopram, sertraline and escitalopram.

According to the study, SSRIs are associated with faster cognitive decline in dementia patients.


Hazard ratio (HR, risk ratio)

The hazard ratio (HR) shows how much an event (e.g. death or fracture) changes in one group compared to another group.

  • HR = 1 → No difference between the groups.
  • HR > 1 → Higher risk for the event.
  • HR < 1 → Lower risk for the event.

Example:

  • HR = 1.18 for fractures means that people taking antidepressants have an 18% higher risk of fractures than people not taking antidepressants.
  • HR = 1.35 for severe dementia means that the risk of severe dementia is increased by 35%.

Summary for laypersons

  • p-value: Shows whether the result is random. A value below 0.05 means that it is very likely a real effect.
  • β-value: Shows how much a medication changes something. Negative values mean a deterioration, e.g. faster memory loss.
  • DDD: A standard dose indication for drugs to make different doses comparable.
  • SSRI: A type of antidepressant that is often used but was associated with faster cognitive decline in the study.
  • Hazard ratio: Shows how much a risk increases or decreases. Values above 1 mean a higher risk of a certain event (e.g. death or fractures).
Cerebrolysin and Barain

Cerebrolysin in traumatic brain injury (TBI): A systematic review and meta-analysis

A look at the current study situation on cerebrolysin in the treatment of TBI

Introduction

Traumatic brain injury (TBI) is one of the most common causes of permanent neurological damage and long-term disability. Every year, millions of people worldwide suffer a TBI, ranging from mild concussions to severe traumatic brain injuries. Treatment options are limited and many patients struggle with long-term cognitive and motor deficits.

Cerebrolysin, a neuropeptide preparation derived from porcine brain protein, has been discussed for years as a potential neuroprotective and neurorestorative therapy for various neurological diseases. In a recent systematic review and meta-analysis published in Brain Sciences (Jarosz et al., 2023), the efficacy of cerebrolysin in TBI was investigated. The results are promising, but also raise new questions about the optimal application.


What is cerebrolysin?

Cerebrolysin is a low molecular weight peptide preparation made from purified porcine brain proteins. It contains biologically active peptides that have been shown to have neuroprotective and neurorestorative properties. Previous preclinical and clinical studies indicate that Cerebrolysin:

  • can modulate inflammatory reactions in the brain,
  • supports the regeneration of nerve cells,
  • promotes synaptic plasticity and
  • improves cognitive abilities after neurological damage.

These properties have sparked interest in Cerebrolysin as a potential treatment for patients with TBI.


Study overview: Methodology of the meta-analysis

The systematic review by Jarosz et al. (2023) analyzed 10 clinical trials with a total of 8749 patients who received cerebrolysin after a TBI. The studies were extracted from PubMed, Cinahl, Web of Science and Embase and selected according to strict scientific criteria.

Inclusion criteria for the analysis:

✅ Adult patients (>18 years)
✅ Diagnosis of mild, moderate or severe TBI
✅ Treatment with cerebrolysin in a clinical setting

Parameters analyzed:

🔹 Glasgow Outcome Scale (GOS) → Assessment of functional recovery
🔹 Glasgow Coma Scale (GCS) → Measurement of the state of consciousness
🔹 Mortality (death rate)
🔹 Length of stay in hospital (LOS – Length of Stay)

The studies used different doses of Cerebrolysin (10-50 ml per day) over a period of 5 to 30 days.


Results of the meta-analysis

The most important findings from the analysis are:

Improvement in neurological functions: Patients who received Cerebrolysin showed a significant improvement in GCS and GOS compared to the control group(p < 0.05). This indicates that Cerebrolysin can positively influence functional recovery after TBI.

No significant reduction in mortality: Treatment with Cerebrolysin had no significant effect on the mortality rate(p = 0.111).

No reduction in the length of hospital stay: The patients who received Cerebrolysin did not have to stay in hospital for a shorter period of time than the control group(p = 0.634).

Interpretation of the results

The improvement in GOS and GCS shows that cerebrolysin can support neurological recovery after TBI. However, the lack of effect on mortality and length of hospitalization means that the therapy cannot be considered an acute life-saving measure.


How does cerebrolysin work? – Mechanisms of neuroprotection

Cerebrolysin unfolds its effect through several mechanisms:

🧠 Neuroprotection: Reduction of inflammation, inhibition of free radicals and protection of neurons from oxidative stress.
🧬 Neuroplasticity: Promotion of synapse formation and maintenance of neuronal communication.
🔬 Regeneration: Activation of signaling pathways such as the Sonic Hedgehog (Shh) pathway, which stimulate the growth of new nerve cells.
Influencing neurotransmitters: modulation of the GABA and cholinergic systems, which can lead to improved cognitive functions.

Of particular interest is the finding that Cerebrolysin can show positive effects even months after the original injury. This could make it a valuable addition to the long-term rehabilitation of TBI patients.


Critical view and open questions

Despite the positive results, there are some unanswered questions:

🔹 Optimal dosage and treatment duration: In the studies analyzed, dosages between 10 and 50 ml per day were used. However, there is no consensus on which dose is most effective.

🔹 Timing of treatment: Some studies started treatment within 24 hours of the injury, others only after several months. Previous research suggests that early administration could be more effective.

🔹 Long-term effects: There is not yet enough data on how long the positive effects of Cerebrolysin last and whether repeated treatment cycles are necessary.

🔹 Side effects: While most patients tolerate Cerebrolysin well, there is a small risk of allergic reactions, including anaphylactic shock.


Conclusion and future research

The systematic review by Jarosz et al. (2023) shows that cerebrolysin has promising neuroprotective properties in TBI. In particular, the improvement in GCS and GOS suggests that cerebrolysin may promote functional recovery.

However, it remains unclear which patients benefit most from the therapy and which dosage is optimal. Future randomized, multicenter trials are needed to clarify these questions and possibly establish cerebrolysin as a standard treatment for TBI.


Sources:

Jarosz, K., Kojder, K., Andrzejewska, A., Solek-Pastuszka, J., & Jurczak, A. (2023). Cerebrolysin in Patients with TBI: Systematic Review and Meta-Analysis. Brain Sci. 2023, 13, 507. DOI: 10.3390/brainsci13030507


Did you like this article?

💬 Share your opinion in the comments! Do you have experience with Cerebrolysin or other questions about TBI? Discuss with us! 😊

Neurofeedback as a therapeutic intervention for ADHD: current evidence and practice.

This is a summary of the study “Neurofeedback as a Treatment Intervention in ADHD: Current Evidence and Practice” which also emphasizes the topic of metabolic performance (brain brightening).

The study deals with neurofeedback as a treatment approach for ADHD. It describes various protocols, the number of sessions and the associated successes. It mentions that neurofeedback could be interpreted as a form of “brain whitening”, which presumably means improving brain performance through training. Different methods have their own advantages and disadvantages, and the success of the treatment varies depending on the application.

The study describes three standard protocols for neurofeedback for ADHD: theta/beta (TBR), sensorimotor rhythm (SMR) and slow cortical potentials (SCP). TBR requires 30-40 sessions and is as effective as methylphenidate. SMR probably requires a similar number of sessions and helps reduce inattention and hyperactivity. SCP requires about 35 sessions and improves reaction time and memory. Successes include improvements in academic performance, sleep quality and cognitive function.

The study examines neurofeedback-based approaches for the treatment of ADHD. It describes three standard protocols: TBR, SMR and SCP. Each has its own advantages and disadvantages.

30-40 sessions, effective as medication, improves academic performance. Advantages: Lasting effect, no side effects. Disadvantage: High number of sessions.

Same as TBR, with additional improvement in sleep. Advantage: Positive effects on sleep, disadvantage: Further research required.

35 sessions, improves reaction time and memory. Advantage: Improved cognitive functions, disadvantage: High training effort.

Enriquez-Geppert S, Smit D, Pimenta MG, Arns M. Neurofeedback as a Treatment Intervention in ADHD: Current Evidence and Practice. Curr Psychiatry Rep. 2019 May 28;21(6):46. doi: 10.1007/s11920-019-1021-4. PMID: 31139966; PMCID: PMC6538574.

The effect of training different neurofeedback protocols on aspects of cognitive performance.

Here is a translation of the abstract of the study “The effect of training distinct neurofeedback protocols on aspects of cognitive performance”

Summary
The use of neurofeedback as an operant conditioning paradigm has shown that participants are able to gain some control over specific aspects of their electroencephalogram (EEG). Based on the link between theta activity (4-7 Hz) and working memory performance and between sensorimotor rhythm activity (SMR, 12-15 Hz) and attentional processing, we investigated the possibility that training healthy individuals to specifically increase one of these frequencies might have a specific impact on certain aspects of cognitive performance compared to a non-neurofeedback control group. The results showed that after eight neurofeedback sessions, the SMR group was able to selectively increase their SMR activity as evidenced by increased SMR/theta and SMR/beta ratios. In contrast, the subjects who were trained to selectively increase theta activity showed no changes in their EEG. In addition, the SMR group showed a significant and clear improvement in recall performance in a semantic working memory test and also improved to a lesser extent accuracy in focused attention processing in a 2-sequence continuous performance test task. These results suggest that healthy individuals can learn to increase a specific component of their EEG activity and that this increased activity can promote semantic processing in working memory tasks and, albeit to a lesser extent, focused attention. Possible mechanisms that could mediate these effects are discussed and several approaches for future research are outlined.

Translation of the abstract from: Vernon, D., Egner, T., Cooper, N., Compton, T., Neilands, C., Sheri, A. & Gruzelier, J. (2002). The effect of training distinct neurofeedback protocols on aspects of cognitive performance. PMID: 12543448, DOI: 10.1016/s0167-8760(02)00091-0.

The influence of neurofeedback on HRV and gastric activity

Here is the summary of the study with the title:

The Impact of Alpha-Neurofeedback Training on Gastric Slow Wave Activity and Heart Rate Variability in Humans

Background:

The study investigates the possibility of influencing gastric function through targeted neurofeedback training (EEG-NF). Previous research has shown a coupling between the alpha-band activity of the insula in the EEG and gastric slow wave (GSW) activity.

Methods:

  • Design: Randomized crossover design with 20 healthy volunteers
  • Interventions: Two sessions of different EEG neurofeedback training:
    • Active training: increase in alpha activity in the left posterior insula (LPIns)
    • Control training: increasing activity in the primary visual cortex (PVC)
  • Data recording: EEG, electrogastrogram (EGG) to record gastric slow wave activity, ECG to record heart rate variability (HRV)
  • Test after training: 5-minute water load test (5WLT)

Procedure

1. electrode placement for EEG neurofeedback training

  • The EEG signals were recorded with a 21-channel cap in the 10/20 system.
  • Neurofeedback training was performed using a specific electrode or a combination of electrodes that best represent the activity of the left posterior insula (LPIns).
  • As a rule, a lead via P3, CP3 or T5/P7 (depending on the individual head model) is used to approximate LPIns activity, as these electrodes cover the nearest surface representations of the insula.
    (comment not part of the study)
  • As the training aimed to increase alpha-band activity (8-12 Hz) in the LPIns, feedback was generated based on real-time EEG data from this region.

2. training protocol: real-time feedback for alpha neurofeedback

  • During the 30-minute neurofeedback session, participants received auditory feedback when alpha activity in the target region (LPIns) increased above a threshold.
  • Reward mechanism: An audio signal was triggered when alpha activity within the LPIns (based on the 10/20 electrodes) was enhanced.
  • Comparison condition: In a control group, the primary visual cortex (Brodmann area 17, near Oz) was trained instead of the LPIns.

Summary:

  1. EEG recording via the 10/20 system with a 21-channel cap.
  2. Neurofeedback training presumably via P3, CP3 or P7/T5as these electrodes are closest to the left posterior insula.
    (comment not part of the study)
  3. Real-time audio feedback based on alpha-band activity (8-12 Hz) in these channels.
  4. Subsequent source localization with eLORETA to check whether the activation really took place in the LPIns.

Results:

  • heart rate variability (HRV): Longer successful neurofeedback duration was associated with increased parasympathetic activation (RMSSD: r = 0.59; p = 0.005) and decreased stress response (SI: r = -0.59; p = 0.006).
  • Gastric slow wave activity: There was a significant correlation between successful neurofeedback duration and the stability of gastric rhythmicity in the control training, but not in the LPIns group.
  • EEG activity: Correlations were found between the successful duration of LPIns training and different EEG frequency bands in the insula (e.g. beta-band activity in the left and right anterior insula).
  • Functional connectivity: Beta-band connectivity between LPIns and RAIns was negatively correlated (r = -0.54; p = 0.013), while gamma-band connectivity between LPIns and RPIns was positive (r = 0.46; p = 0.04).

Conclusion:

  • EEG neurofeedback training of LPIns had significant effects on HRV, EEG activity and functional connectivity.
  • Training efficiency should be given greater consideration in the future, especially the duration of successful neurofeedback training.
  • The results suggest that targeted EEG neurofeedback training may be a non-invasive method to modulate the brain-gut axis and autonomic function.
  • The study only examined the acute effects of alpha neurofeedback training on HRV. This means that the improvement in HRV was measured directly after the 30-minute training session, but no long-term study was carried out.

Mathew, J., Galacgac, J., Smith, M.L., Du, P. and Cakmak, Y.O. (2025), The Impact of Alpha-Neurofeedback Training on Gastric Slow Wave Activity and Heart Rate Variability in Humans. Neurogastroenterology & Motility e15009. https://doi.org/10.1111/nmo.15009

Can a long-term improvement in HRV be expected?

As this study only looked at the acute effects, no direct statement can be made about long-term effects. However, there is some evidence from neurofeedback research that suggests that regular training can lead to lasting improvements:

  1. Neuroplasticity & Repetitive Training:
    • Neurofeedback can bring about lasting changes in neuronal networks through operant conditioning.
    • Previous studies have shown that regular EEG neurofeedback (over several weeks) can bring about long-term changes in HRV.
  2. Mechanism: Improvement of vagus activity:
    • Since alpha training in the left posterior insula (LPIns) is associated with higher parasympathetic activity and vagus tone, regular training could stabilize this effect.
    • The insula is a central modulator of the autonomic nervous system, so a long-term increase in alpha activity could improve vagus function and thus HRV in the long term.

Recommendation for long-term effect:

Since this study only examined a single session, it would be useful to conduct future studies with a multi-week training program. Based on previous neurofeedback studies, 6 to 8 weeks of training (2-3 sessions per week) may be required to achieve a lasting improvement in HRV.

Dipl. Ing. Michael Schiffer MBA, 22-Feb-2025, Baden-Baden