DEE-SWAS (Night Terrors, Sleep EEG Abnormalities etc.) masquerading as Regressive Autism

  

 

One of the key points in understanding "autism" is that it is not a single biological condition. It is just a behavioral diagnosis based on observed developmental patterns involving language, social communication, repetitive behaviors and sensory differences.

That means very different biological conditions can produce children/adults who all outwardly appear some version of “autistic.”

A striking example of this was recently shared with me by one of our readers.

 

A Child Diagnosed with "autism"

The parents noted severe developmental regression accompanied by unusual sleep disturbances and night terrors. Over time they also observed something very interesting, that changes in valproic acid (VPA) dosing appeared to significantly affect symptoms.

Their neurologist had performed EEGs which reportedly showed abnormalities and yet despite this, no further major investigations were ordered:

• no epilepsy-protocol MRI
• no prolonged 24-hour EEG
• and no comprehensive workup for epileptic encephalopathy.

Meanwhile, the family pursued extensive genetic testing searching for answers.

This is unfortunately an increasingly familiar story in developmental medicine, a child receives a behavioral autism diagnosis, and the diagnostic process effectively stops there.

 

Seeking a second opinion

The family eventually attended a specialized pediatric neurology clinic at a major children’s hospital.

The difference was immediate.

After reviewing EEGs, videos before regression, videos after regression and recordings of the child’s sleep terrors, the specialists concluded that the child fit the modern framework of:

DEE-SWAS
(Developmental and Epileptic Encephalopathy with Spike-and-Wave Activation in Sleep)

The older terms for overlapping conditions include:

• ESES (Electrical Status Epilepticus in Sleep)
• CSWS (Continuous Spike-Wave During Sleep)
• Landau-Kleffner syndrome

The clinic immediately ordered:

• epilepsy-protocol MRI
• prolonged 24-hour EEG
• metabolic investigations
• ophthalmologic evaluation
• orthopedic assessment

Most strikingly, they reportedly stated that this looked like:

“DEE-SWAS masquerading as autism.”

 

What Is DEE-SWAS?

DEE-SWAS is increasingly understood as a disorder of abnormal brain network synchronization during sleep.

The key issue is not simply seizures. Some children have obvious seizures, others do not.

In many children, pathological spike-wave activity during deep non-REM sleep may interfere with:

• language development
• memory consolidation
• emotional regulation
• cognition
• attention
• and developmental plasticity itself.

Some primarily present with:

• regression
• loss of speech
• autistic behaviors
• sensory abnormalities
• emotional dysregulation
• fluctuating cognition
• sleep disturbance
• night terrors.

In many cases, the child outwardly appears to have classic regressive autism.

 

Why night terrors matter

Night terrors are usually benign in ordinary children.

However, in the context of

• developmental regression
• abnormal EEGs
• fluctuating cognition
• or epileptiform activity

they become much more significant.

DEE-SWAS specifically affects deep slow-wave sleep — the same sleep stage associated with night terrors and abnormal arousal phenomena.

This does not mean every child with night terrors has epileptic encephalopathy.

But regression plus unusual sleep phenomena should raise suspicion that a prolonged sleep EEG may be warranted.

 

Treating the EEG to treat the child

One of the most interesting concepts in modern DEE-SWAS research is:

“Treating the EEG to treat the patient.”

The concern is that the abnormal sleep spike-wave activity itself may drive the developmental deterioration.

Treatments used include:

• valproic acid
• clobazam
• clonazepam
• steroids
• ketogenic diet
• acetazolamide (Diamox)
• ethosuximide
• and in some cases surgery.

Ethosuximide is particularly interesting because it is a T-type calcium channel blocker that affects thalamocortical spike-wave synchronization.

The thalamus appears to play a major role in generating these pathological sleep oscillations.

Ketogenic therapies and ketone esters are also fascinating because they may:

• stabilize neuronal metabolism
• reduce hyperexcitability
• alter glutamate/GABA balance
• and improve network stability during sleep.

 

For more information on treatment:

Treatment of Developmental/Epileptic Encephalopathy With Spike-Wave Activation in Sleep

Is DEE-SWAS Rare?

Officially, yes. But many experts suspect it is significantly under-recognized.

Why? Because many children with:

• regression
• autism
• language loss
• or sleep problems

never receive a prolonged sleep EEG monitoring.

A short daytime EEG may miss much of the pathology.

This is especially important because some children may improve substantially when the abnormal sleep-related epileptiform activity is treated.

DEE-SWAS is likely a spectrum from mild to severe. The underlying cause varies, but often is thought to be an anomaly in an ion channel (calcium, sodium, potassium).  

Autism is just a behavioral phenotype

Cases like this reinforce an increasingly important idea.

“Autism” represents a common behavioral phenotype arising from many different biological mechanisms.

For one child:

• synaptic dysfunction may dominate.

For another:

• mitochondrial dysfunction.

For another:

• immune dysregulation.

And for another:

• sleep-activated epileptiform encephalopathy.

The behavioral presentation may look similar, while the biology underneath is profoundly different. The treatment will also be different, although there are surprising overlaps.

 

Conclusion

DEE-SWAS is not just a case of a bad night’s sleep.

The concern is months or years of abnormal electrical activity repeatedly disrupting the brain during one of its most critical developmental states.

In DEE-SWAS the brain spends large portions of deep sleep in a pathological synchronized firing mode instead of normal developmental processing.

Over time this may interfere with language acquisition, cognition, emotional regulation and developmental plasticity itself, potentially leading to developmental regression and a child who outwardly appears to have regressive autism.

This post is not suggesting that most regressive autism is actually DEE-SWAS, but some clearly is.

However, children with:

• clear regression
• fluctuating abilities
• sleep deterioration
• night terrors
• language loss
• episodic worsening
• or unusual EEG findings

deserve more extensive neurological investigation than they often receive.

The father who contacted me persisted despite initial dismissal and eventually reached a centre experienced in developmental epileptic encephalopathies.

That persistence may prove extremely important for their child’s future outcome.

Excitatory/Inhibitory (E/I) imbalances as a unifying, treatable, feature of severe autism that cause Cognitive Impairment, Self-Injurious Behavior (SIB) and ultimately seizures in some

 

Autism is a complex condition that manifests in a range of symptoms, from social and communication challenges to sensory sensitivities and repetitive behaviors. Researchers long ago identified a key neurobiological mechanism that underlies many of the core and associated features of autism: excitatory/inhibitory (E/I) imbalances in the brain.

These imbalances, where the delicate interplay between neuronal excitation and inhibition is disrupted, offers a unifying framework to explain certain severe manifestations of autism, including cognitive impairment, self-injurious behavior (SIB), and seizures. Understanding E/I imbalance not only sheds light on the biology of autism but also opens new avenues for targeted therapies.

 

The Role of E/I Balance in the Brain

Neuronal circuits rely on a finely tuned balance between excitatory and inhibitory signals to function properly. Excitatory neurons promote the firing of signals, enabling processes like learning, memory, and sensory integration. Inhibitory neurons, on the other hand, dampen excessive activity, ensuring stability and preventing overstimulation.

In individuals with autism, this balance is often disrupted. Overactive excitatory signaling or insufficient inhibitory control can lead to hyperexcitability in certain brain regions, contributing to behavioral and neurological symptoms. This imbalance is influenced by a range of factors, including:

• Genetic mutations in key synaptic proteins (e.g., SHANK3, SCN1A, GABA receptor subunits).
• Neuroinflammation and oxidative stress.
• Developmental disruptions in synaptic pruning or circuit formation.

 

How E/I imbalances drives severe autism symptoms

 

Cognitive Impairment

E/I imbalance affects the prefrontal cortex and hippocampus, regions critical for cognitive functions like problem-solving, memory, and attention. Disrupted neural signaling in these areas impairs synaptic plasticity—the brain’s ability to adapt and learn—which can manifest as intellectual disability in some individuals with autism.

Studies have shown that restoring E/I balance in animal models can improve cognitive deficits, highlighting its central role in intellectual development.

 

Self-Injurious Behavior (SIB)

Self-injurious behaviors, such as head-banging or skin-picking, are often linked to dysregulated sensory processing and impaired impulse control. Hyperexcitability in brain regions like the amygdala can heighten stress responses, while altered pain thresholds caused by E/I imbalance may make some individuals less sensitive to injury.

Addressing the underlying imbalance can reduce the neural hyperactivity driving these behaviors and improve emotional regulation.

 

Seizures

Seizures are a common comorbidity in autism, affecting up to 30% of individuals. They arise directly from hyperexcitability in neural networks, where excessive excitation leads to abnormal, synchronized firing of neurons. Genetic conditions like Dravet syndrome, linked to mutations in sodium channel genes (e.g., SCN1A), exemplify the connection between E/I imbalance and epilepsy.

Therapies that stabilize E/I balance, such as GABA-enhancing drugs or ion channel modulators, have shown promise in reducing seizure frequency and severity.

 

Targeting E/I Imbalance: A Path Toward Better Treatments

Given its central role in severe autism symptoms, E/I imbalance represents a promising target for therapeutic intervention. Approaches to restore balance include:

 

Pharmacological Therapies

Bumetanide

Bumetanide is a diuretic that also affects neuronal chloride homeostasis by inhibiting the NKCC1 transporter. In autism, elevated intracellular chloride levels impair the function of GABA, shifting its action from inhibitory to excitatory. Bumetanide lowers intracellular chloride, restoring GABA’s inhibitory effect and reducing hyperexcitability. Clinical trials have shown improvements in social behaviors and reduced severity of core autism symptoms in some individuals.

 

L-Type Calcium Channel Blockers

L-type calcium channels play a role in synaptic plasticity and neuronal excitability. Excessive calcium influx can contribute to hyperexcitability and oxidative stress. Blockers like nimodipine and verapamil may help stabilize neuronal activity and have shown potential in reducing seizures and hyperactivity in preclinical studies.

 

T-Type Calcium Channel Blockers

T-type calcium channels are involved in regulating burst firing and thalamocortical oscillations. Dysregulation of these channels can contribute to sensory processing abnormalities and seizures. Agents like zonisade, traditionally used for absence seizures, may also offer benefits in addressing E/I imbalances in autism.

 

Memantine

Memantine is an NMDA receptor antagonist that modulates glutamatergic signaling. By dampening excessive excitatory activity, it can reduce hyperexcitability and improve cognitive and behavioral symptoms. Clinical studies have shown mixed results, with some individuals experiencing notable benefits in areas like communication and social interactions.

 

Low-Dose Clonazepam

Clonazepam, a benzodiazepine, enhances GABAergic inhibition by increasing the activity of GABA-A receptors. At low doses, it can stabilize neural circuits without causing significant sedation. It has been used off-label to manage anxiety, hyperactivity, and seizures in autism.

 

Valproate

Valproate is an anticonvulsant and mood stabilizer that enhances GABAergic signaling and reduces excessive excitation. It has shown efficacy in managing seizures and may also improve irritability and aggression in some individuals with autism.

 

Baclofen and R-Baclofen

Baclofen is a GABA-B receptor agonist that enhances inhibitory signaling. It can modulate overactive NMDA receptor activity, which may be beneficial in cases of excitatory dysfunction. Baclofen has been studied for its role in reducing repetitive behaviors and improving social interaction in preclinical models.

 

Taurine

Taurine is an amino acid with inhibitory properties that can enhance GABAergic activity and reduce excitatory signaling. It also acts as an antioxidant, mitigating oxidative stress linked to hyperexcitability.

 

Pioglitazone

Pioglitazone, a PPAR-gamma agonist, has anti-inflammatory effects that can indirectly stabilize neural circuits by reducing neuroinflammation associated with E/I imbalances. Preliminary studies suggest it may have benefits for behavioral symptoms in autism.

Other agents including

• Anti-inflammatory Drugs: Minocycline and mefenamic acid reduce neuroinflammation, which can exacerbate E/I imbalances.
• Ion Channel Modulators: Sodium channel blockers like lamotrigine and carbamazepine stabilize hyperexcitable neurons and may reduce both seizures and behavioral dysregulation.

 

Neuromodulation Techniques

• Transcranial Magnetic Stimulation (TMS): A non-invasive method to modulate cortical excitability.
• Transcranial Direct Current Stimulation (tDCS): Targets specific brain regions to enhance or suppress neural activity.

 

 

The Role of NMDA and GABA Receptors in E/I Imbalance

Excitatory NMDA receptors and inhibitory GABA receptors play central roles in maintaining E/I balance. NMDA receptor dysfunction, characterized by either hyperactivity or hypoactivity, is implicated in autism. Overactive NMDA receptors can amplify excitatory signaling, while underactive NMDA receptors can impair synaptic plasticity. Both scenarios disrupt neural communication and contribute to autism-related symptoms.

GABA receptors, particularly GABA-A and GABA-B subtypes, are essential for inhibitory control. Dysfunctional GABAergic signaling reduces the brain’s ability to counterbalance excitation, leading to hyperexcitability.

Baclofen’s modulation of GABA-B receptors exemplifies how targeting these systems can restore balance. By reducing NMDA receptor overactivation and enhancing GABAergic inhibition, baclofen addresses multiple aspects of E/I dysregulation.

 

NMDA receptor dysfunction

Addressing NMDA receptor dysfunction requires a nuanced approach because the receptor can be either hypoactive/underactive or hyperactive/overactive in autism, depending on the individual and the specific neural circuits involved. Treatments vary based on the direction of dysfunction:

 

Treating NMDA Hypofunction

In cases where NMDA receptors are underactive, excitatory signaling is insufficient, leading to impairments in synaptic plasticity, learning, and memory. Strategies to enhance NMDA receptor activity include:

1. D-Cycloserine
• Acts as a partial agonist at the glycine site of the NMDA receptor.
• Enhances receptor activity without overactivation, making it useful for improving social and cognitive functions in some individuals with autism.
2. Sarcosine
• A glycine transport inhibitor that increases synaptic glycine levels, promoting NMDA receptor activation.
• Preclinical studies suggest potential improvements in behavioral symptoms.
3. Glycine Supplements
• Directly increase the availability of a co-agonist required for NMDA receptor activation.
• May improve signaling in circuits where glycine levels are suboptimal.

 

Treating NMDA Hyperfunction

Excessive NMDA receptor activity can lead to excitotoxicity.  When there is too much glutamate or an overactive NMDA receptor, the influx of calcium ions into the neuron becomes excessive. This causes a series of harmful processes contributing to neuronal damage, increased oxidative stress, and seizures. Strategies to dampen NMDA receptor overactivity include:

1. Memantine
• An NMDA receptor antagonist that reduces overactivation without completely shutting down receptor function.
• Clinical trials in autism have reported mixed results but some individuals benefit in areas like hyperactivity and irritability.
2. Magnesium Supplements
• Magnesium acts as a natural blocker of the NMDA receptor under resting conditions.
• Supplementation can stabilize receptor activity and reduce hyperexcitability.
3. Low-Dose Ketamine
• At sub-anesthetic doses, ketamine modulates NMDA receptor activity and enhances synaptic plasticity.
• Emerging research suggests potential benefits for specific autism symptoms, although risks and side effects must be carefully managed.
4. Antioxidants (e.g., N-Acetylcysteine, Vitamin E)
• Reduce oxidative stress caused by NMDA receptor hyperactivity.
• Support neuronal health and may mitigate excitotoxicity.

 

Balancing NMDA Dysfunction

In some cases, the same individual may show hypoactivity in some circuits and hyperactivity in others.

Combining treatments tailored to the specific functional state of NMDA receptors in different brain regions. For example, Low-dose ketamine or memantine may help dampen excessive NMDA activity in the amygdala or basal ganglia, while D-cycloserine might be used to enhance NMDA function in areas like the prefrontal cortex.

  

Calcium, Sodium and Potassium Channels

Calcium signaling is critical for excitatory neurotransmission, as calcium ions mediate glutamate release and synaptic plasticity. Dysregulated calcium channels, such as overactive L-type or T-type channels, contribute to hyperexcitability and sensory abnormalities.

Sodium channelopathies, involving mutations in genes like SCN1A, directly impact neuronal firing rates. Excessive sodium influx leads to hyperactive neurons, causing seizures and other excitatory-driven symptoms. While calcium channels influence neurotransmitter release, sodium channel dysfunction primarily affects action potential generation.

Potassium channels, responsible for repolarizing neurons after firing, also play a key role in maintaining neural stability. Mutations in potassium channel genes can prolong neuronal firing and contribute to hyperexcitability.

 

Conclusion

While E/I imbalance is not the sole cause of autism, it is a key unifying feature that connects many severe symptoms. By targeting this imbalance, clinicians can develop more precise and effective treatments tailored to the individual’s needs. Early intervention, particularly during critical periods of brain development, holds the greatest potential for improving outcomes.

As we continue to unravel the complexities of autism, the concept of E/I imbalance serves as a key nexus to understand, and more importantly, treat the challenges faced by individuals with severe autism and their families. By restoring balance, to the extent possible, both in the brain and in daily life, we can empower those with severe autism to reach their full potential. 

People with mild autism are likely affected by less extreme E/I imbalances, but they may be more aware of them. They are likely easier to treat. The principles are the same. 

The issue of sound sensitivity can affect autism from level 0 (including self-diagnosed and ADHD) all the way to level 3; it is complex because it involves both an E/I imbalance and further issues. There will be a summary post on this subject. 

 

Alpha-lactalbumin Whey Protein – Treating Neurological Dysfunction, including Epilepsy and Autism, via the Gut (Eubiosis)

 

Moo! α-Lactalbumin is a whey protein constituting 22% of the proteins in human milk and 3.5% of those in cow milk.

 

Most parents love the idea of treating their child with autism or epilepsy with diet.

Diet is so popular because you do not need a doctor - no drugs, no prescriptions, just healthy food.

This blog is about the science, which often takes us to drugs that need a prescription, but when talking about using the gut to fine-tune how the brain works, much can be achieved with nutraceuticals.

We previously saw how the ketogenic diet, which has been reducing epilepsy for one hundred years, actually works by modifying which bacteria grow in the gut.  The super high fat diet encourages specific bacteria to flourish and it is these bacteria which indirectly cause the cessation in seizures. You can replicate the effect with probiotic bacteria, without needing the highly restrictive diet at all.

Today I will introduce Alpha-lactalbumin, which is a commercially available whey protein found in mother’s milk and to a lesser extent in cow milk. 

Alpha-lactalbumin when combined with another regular in this blog, sodium butyrate, has been shown to improve autism, epilepsy and indeed depression.

The research also suggests that Alpha-lactalbumin may improve sleep and mood disorders.

  

Whey protein vs NAC

I recall reading about whey protein as an antioxidant back in 2013, when I was deciding what to try next after Bumetanide, as I developed by son's personalized polytherapy for autism. I did choose NAC, but I still recall the surprising option of whey protein.

Whey protein is popular among athletes and body builders.

Whey protein is a mixture of proteins isolated from whey, the liquid material created as a by-product of cheese production. The proteins consist of α-lactalbumin (ALAC), β-lactoglobulin, serum albumin and immunoglobulins.

 

Improved glutathione status in young adult patients with cystic fibrosis supplemented with whey protein

We sought to increase glutathione levels in stable patients with cystic fibrosis by supplementation with a whey-based protein.

 After supplementation, we observed a 46.6% increase from baseline (P<0.05) in the lymphocyte GSH levels in the supplemented group. No other changes were observed. 

Conclusion: The results show that dietary supplementation with a whey-based product can increase glutathione levels in cystic fibrosis. This nutritional approach may be useful in maintaining optimal levels of GSH and counteract the deleterious effects of oxidative stress 

 

The Antioxidant Effects of Whey Protein Peptide on Learning and Memory Improvement in Aging Mice Models

The results showed that WHP could significantly improve the accumulation of MDA and PC, increase the activities of SOD and GSH-Px, resist oxidative stress injury, and enhance the potential of endogenous antioxidant defense mechanisms. WHP can significantly improve the decline of aging-related spatial exploration, body movement, and spatial and non-spatial learning/memory ability. Its specific mechanism may be related to reducing the degeneration of hippocampal nerve cells, reducing the apoptosis of nerve cells, improving the activity of AChE, reducing the expression of inflammatory factors (TNF-α and IL-1β) in brain tissue, reducing oxidative stress injury, and improving the expression of p-CaMKⅡ and BDNF synaptic plasticity protein.

These results indicate that WHP can improve aging-related oxidative stress, as well as learning and memory impairment.

 

 

 α-lactalbumin (ALAC)

Today we are really focused on one specific whey protein, α-lactalbumin (ALAC), which is actually sold commercially as a nutraceutical.

 

https://www.arlafoodsingredients.com/health-foods/our-ingredients/alpha-lactalbumin/?downloadUrl=%252F4908eb%252Fglobalassets%252Frestricted%252F2017%252F_ho_alpha20_wellbeing_0317_v2.pdf

 

 

Applications for α-lactalbumin in human nutrition

α-Lactalbumin is a whey protein that constitutes approximately 22% of the proteins in human milk and approximately 3.5% of those in bovine milk. Within the mammary gland, α-lactalbumin plays a central role in milk production as part of the lactose synthase complex required for lactose formation, which drives milk volume. It is an important source of bioactive peptides and essential amino acids, including tryptophan, lysine, branched-chain amino acids, and sulfur-containing amino acids, all of which are crucial for infant nutrition. α-Lactalbumin contributes to infant development, and the commercial availability of α-lactalbumin allows infant formulas to be reformulated to have a reduced protein content. Likewise, because of its physical characteristics, which include water solubility and heat stability, α-lactalbumin has the potential to be added to food products as a supplemental protein. It also has potential as a nutritional supplement to support neurological function and sleep in adults, owing to its unique tryptophan content. Other components of α-lactalbumin that may have usefulness in nutritional supplements include the branched-chain amino acid leucine, which promotes protein accretion in skeletal muscle, and bioactive peptides, which possess prebiotic and antibacterial properties. This review describes the characteristics of α-lactalbumin and examines the potential applications of α-lactalbumin for human health.

 

α-Lactalbumin constitutes approximately 22% of total protein and approximately 36% of the whey proteins in human milk and approximately 3.5% of total protein and approximately 17% of whey proteins in bovine milk (Figure 1)¹,². It has an amino acid composition that is high in essential amino acids and comparatively rich in tryptophan, lysine, cysteine, and the branched-chain amino acids (BCAAs) leucine, isoleucine, and valine.³ (Table 1)⁴. Because of its unique amino acid profile, α-lactalbumin has potential for multiple uses: (1) as a component of infant formulas, to make them more similar to breast milk; (2) as a supplement to promote gastrointestinal health or modulate neurological function, including sleep and depression; and (3) as a therapeutic agent with applications in conditions or diseases such as sarcopenia, mood disorders, seizures, and cancer. 

 

Intestinal inflammation increases convulsant activity and reduces antiepileptic drug efficacy in a mouse model of epilepsy

We studied the effects of intestinal inflammation on pentylenetetrazole (PTZ)-induced seizures in mice and the effects thereon of some antiepileptic and anti-inflammatory treatments to establish if a link may exist. The agents tested were: alpha-lactoalbumin (ALAC), a whey protein rich in tryptophan, effective in some animal models of epilepsy and on colon/intestine inflammation, valproic acid (VPA), an effective antiepileptic drug in this seizure model, mesalazine (MSZ) an effective aminosalicylate anti-inflammatory treatment against ulcerative colitis and sodium butyrate (NaB), a short chain fatty acid (SCFA) normally produced in the intestine by gut microbiota, important in maintaining gut health and reducing gut inflammation and oxidative stress. Intestinal inflammation was induced by dextran sulfate sodium (DSS) administration for 6 days. Drug treatment was started on day 3 and lasted 11 days, when seizure susceptibility to PTZ was measured along with intestinal inflammatory markers (i.e. NF-κB, Iκ-Bα, COX-2, iNOS), histological damage, disease activity index (DAI) and SCFA concentration in stools. DSS-induced colitis increased seizure susceptibility and while all treatments were able to reduce intestinal inflammation, only ALAC and NaB exhibited significant antiepileptic properties in mice with induced colitis, while they were ineffective as antiepileptics at the same doses in control mice without colitis. Interestingly, in DSS-treated mice, VPA lost part of its antiepileptic efficacy in comparison to preventing seizures in non-DSS-treated mice while MSZ remained ineffective in both groups. Our study demonstrates that reducing intestinal inflammation through ALAC or NaB administration has specific anticonvulsant effects in PTZ-treated mice. Furthermore, it appears that intestinal inflammation may reduce the antiepileptic effects of VPA, although we confirm that it decreases seizure threshold in this group. Therefore, we suggest that intestinal inflammation may represent a valid antiepileptic target which should also be considered as a participating factor to seizure incidence in susceptible patients and also could be relevant in reducing standard antiepileptic drug efficacy.

  

Increased efficacy of combining prebiotic and postbiotic in mouse models relevant to autism and depression

Highlights 

·        Prebiotic/postbiotic combination is a suitable approach in manipulating the Microbiota Gut Brain Axis. 

·        Prebiotic/postbiotic combination is more effective than single drug administration. 

·        α-lactalbumin/sodium butyrate combination improves animal behaviour in autistic (BTBR) mice. 

·        α-lactalbumin/sodium butyrate combination improves animal behaviour in the depression chronic unexpected mild stress model.

   

Conclusion

It is not by chance that mother’s milk has evolved to be rich in Alpha-lactalbumin (ALAC).

ALAC has wide-ranging health benefits. People with gut dysbiosis would seem likely to benefit from it, particularly if they have co-occurring neurological symptoms (epilepsy, ASD, depression) that are made worse by GI inflammation.

NaB (Sodium Benzoate) has some overlapping benefits with ALAC and the research shows that the combined effect is better than either alone,

The increase in production of glutathione (GSH), the body’s main antioxidant is clearly a benefit of whey protein in general and we assume its effect extends to ALAC.

NaB seems to have an effect that can be very dose dependent.  Too little has no benefit and, at least in some people, too much and you lose the benefit.

NaB is producing butyric acid and depending on your fiber intake and gut bacteria you are already producing your own butyric acid.  As a result, it makes sense that the effective dose of NaB will vary from person to person.

This continues the earlier subject of eubiosis vs dysbiosis.  The graphic below looks nice, but really is an oversimplification.  You can modify the microbiome to produce a specifically targeted change in the brain, which has nothing to do with allergic diseases.  All  very clever and a little hard to believe at first.

 

 

Source : The Role of Prebiotics and Probiotics in Prevention of Allergic Diseases in Infants

I think ALAC is an interesting choice for autism and hopefully one day there will be a clinical trial.  In that trial do not exclude those with epilepsy, but collect data of the impact of ALAC on the frequency/intensity of seizures.