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Advanced Neurology A novel approach to mitigate muscle atrophy in GBS

Polyunsaturated fatty acids, such as omega-3s, are 4. Practical considerations and future
essential constituents of all cellular membranes that direction of omega-3 fatty acid
cannot be adequately synthesized endogenously . Myelin supplementation and GBS
[80]
sheaths are formed from the membranes of Schwann cells
(PNS) or oligodendrocytes (CNS) wrapping themselves With mounting evidence of the efficacy in mitigation of
around neuron axons . The omega-3 fatty acid, DHA, muscle atrophy and their theoretical value in promoting
[80]
has been found to constitute 5.8% of Schwann cells remyelination, omega-3 fatty acids, when co-ingested with
membranes and 5.1% of oligodendrocyte membranes . appropriate nutritional building blocks , have a strong
[67]
[81]
Within the Schwann cell, omega-3 fatty acids have been potential to become a low-cost, low-risk adjunct treatment
shown to augment the expression of anti-oxidant enzymes to existing therapeutic measures in the management
and prevent oxidative stress-induced cell death , further of GBS. Studies have promoted their potential use in
[82]
supporting their importance in the remyelination process. mitigating muscle atrophy in other clinical conditions,
Given the role of omega-3 fatty acids as a physical building such as prolonged immobilization or cancer cachexia [60,86] .
block constituting the myelin sheath, and cell membranes In addition, there also has been the emergence of COVID-
in general, ensuring adequate supply may help facilitate the 19-associated GBS, which may also benefit from omega-3
remyelination process. A facilitated remyelination process supplementation; however, the specific details are beyond
[87]
could potentially improve the overall recovery phase of the scope of this paper .
GBS. However, this question has yet to be specifically The recommended dosage and ratio of omega-3 fatty
addressed experimentally. acids in the literature varies broadly, depending on target

3.2.2. Neuroprotection through mitigation of population and intended effect. In the general population,
excitotoxic-like effects the recommended daily intake for males and females
is 1.6 and 1.1 g/day, respectively . There is still a lack
[62]
Excitotoxicity refers to the pathologically depolarized state of consensus of optimal dosage for the prevention and
of a damaged neuron eventually leading to neuronal cell treatment of generalized peripheral neuropathy . For the
[88]
death . The underlying mechanism of cell death is related GBS population specifically, in any initial investigation,
[83]
to a glutamate-associated, rapidly increased intraneuronal it could be appropriate to follow a regimen similar to the
calcium concentration, triggering a cascade of inter-related previous RCTs studying the effects of omega-3 fatty acids
intracellular events ultimately ending in neuron death. on muscle atrophy, which included a total dose ranging
This includes the uncontrolled activation of nucleases, between 2.2 and 5 g/day, at an approximate EPA: DHA
cytosolic proteases, protein kinases, and lipases . This ratio of 3:2 [63,68,70] . It should also be noted that one of the
[83]
process is analogous to one of the key mechanisms of published randomized trials demonstrating omega-3 fatty
neuronal death in GBS, as outlined above. Within the acid attenuation in muscle atrophy supplemented their
CNS, omega-3 fatty acids have been shown effective in experimental group 4 weeks before immobilization .
[63]
neutralizing excitotoxicity through their mitigative effects In the case of GBS, dietary supplementation would likely
on inflammation and oxidation . DHA pre-treatment only begin once a diagnosis is confirmed, forgoing the
[84]
within hippocampal neurons was shown to be associated opportunity to prophylactically raise baseline omega-3
with rapid recovery of calcium concentrations on an fatty acid levels. It is unknown how this could impact
experimental rodent model . the expected benefit of supplementation. This adjunctive
[85]
Although excitotoxicity is classically described within dietary intervention would theoretically continue until
the CNS, severe GBS demyelination is believed to share the functional recovery was obtained, with the potential
same underlying mechanism when it involves motor axon benefit maximized in those with the greatest degrees of
loss: A direct influx of extracellular calcium and subsequent weakness and immobilization.
enzyme cascade activation . However in GBS, calcium Future studies are required to test the direct effects of
[47]
influx is secondary to complement-mediated membranous omega-3 fatty acid supplementation on muscle volume,
pores formation rather than high intracellular glutamate muscle strength, rates of electrophysiologically-assessed
[47]
levels . It seems possible that unchecked calcium- nerve recovery (e.g., nerve conduction velocities and
[83]
activated lipases and proteases may further promote amplitudes), as well as their effects on overall function
demyelination, delaying GBS recovery. Omega-3 fatty and long-term morbidity, within the GBS population.
acids could potentially have a neuroprotective role in Concurrently, further studies can be performed to explore
the PNS through normalization of intracellular calcium the potential positive effects of omega-3 supplementation
concentrations, neutralization of reactive oxygen species, in other demyelinating conditions beyond that of GBS
and provision of an environment ideal for remyelination. (e.g., polyneuropathy, organomegaly, endocrinopathy,

Volume 2 Issue 2 (2023) 7 https://doi.org/10.36922/an.280