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.
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.
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.
