How Diets High in Seafood Lead to EHS
It is well-established, common wisdom that overconsumption of anything, natural or unnatural, can and does lead to consequences. While we can all agree that maximizing our exposure to nature, whether it be increased sun, walking barefoot, clean eating, or avoidance of man-made electrosmog, leads to positive benefits, there is a flip-side to natural approaches as well.
One such example is seafood.
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The truth about seafood
Many today are on the fence about ocean or river sourced living foods, primarily because of their potential for metal and toxin accumulation. It is well known that the higher up in the water-based food chain we look, the higher probably for such accumulation, especially with regard to methylmercury. But this post is not about this well-trodden issue. The real (but well hidden) problem with seafood consumption is its high Omega-3 fatty acid content, specifically EPA and DHA, and the manner in which they increase vulnerability to electromagnetic hypersensitivity syndrome (EHS).
You read that right: eating too much seafood will make you more sensitive to EMF and, with enough time, induce full-blown EHS.
EHS: real or placebo?
EHS is still an outlier in human pathologies. Associated symptoms spread a very wide gamut and are consistent in their ability to confound concrete diagnoses. Complaints range from sleep disturbances, burning sensations / rashes, stress, fatigue, headache, prickling skin, and cognitive dysfunction. Taken together, such symptoms could be the result of an enormously varied range of diseases and ailments. Due to the fact that they overlap with other functional somatic syndromes and idiopathic environmental intolerance, formal study of EHS has been unable to make firm correlations. Nonetheless, clinicians and scientists gifted with the ability to connect dots are beginning to uncover the complex mechanisms which underlie this disorder.
One such mechanism is demyelination and resulting hypersensitivity of the central and peripheral nervous systems.
Demyelination of nerves
Myelin is the lipid-rich insulating sheath around nerve cell axons. It is formed in the central nervous system (CNS) by glial cells, also known as oligodendrocytes, and in the peripheral nervous system (PNS) by Schwann cells. This fatty sheath increases the traveling speed of electrically coded information between nerve cell bodies by reducing axonal membrane capacitance. The electrical signal induces the release of additional chemical messages or neurotransmitters that bind to receptors on the adjacent post-synaptic cell. This can be either a nerve cell in the CNS or a muscle cell in the PNS.
Myelin is absolutely essential for normal motor function, sensory function, and cognition. With degradation and destruction of these sheaths come significant issues with walking, hearing, seeing, increased pain sensation, and memory recall, among other things. This destruction is most frequently correated with autoimmune disorders such as multiple sclerosis or other inflammatory peripheral neuropathies characterized by numbness, prickling or tingling in the feet or hands which often spreads upward into the arms and legs. It is well known that anti-myelin antibodies in multiple sclerosis can be responsible for the breakdown of the fatty-acid sheaths. In the case of peipheral neuropathy, high blood sugar associated with diabetes damages the nerves.
But there is another less well-known origin to demyelination…
It begins with chronic fatty acid imbalances
No one can contest the importance of Omega-3 fatty acids, particularly DHA, in both intrauterine and neonatal brain development. An estimated 35-60% of neural tissue is composed of lipids, 35% of which are polyunsaturated fatty acids (PUFAs) located in brain neurons and glial cells. 40-50% of those PUFAs, in turn, are considered to be DHA. The most rapid and complex growth occurs primarily in the last trimester of pregnancy and first two years of life. Fetal and infant brains are incapable of converting plant-based alpha-linolenic acid (ALA) into DHA, making a baby entirely dependent on the mother for its supply.
Even into adulthood, DHA plays a vital role in supporting the overall structure and proper function of the brain through its integration into phospholipids such as phosphatidylethanolamine (PE), phosphatidylserine (PS) and, to a lesser degree, phosphatidylcholine (PC). As the most unsaturated cell membrane fatty acid, DHA is also essential for membrane fluidity. It has been not only implicated in optimal brain function but also in the reduction of cardiovascular risk, improved outcomes in autoimmune diseases, and decreased inflammation.
The problem lies not in the widely applicable utility of Omega-3 fatty acids in the human body and brain, but in the human tendency to excessively leverage compounds for their biological benefit, creating imbalances that would not typically be found in nature. Looking at the undeniable benefits of adequate dietary DHA (and EPA) intake, it is hard to imagine that too much of a good thing could be potentially harmful. But this is precisely what happens in individuals that overconsume seafood products such as wild herring, salmon, halibut, mackerel, sardines, oysters, mussels and other shellfish. People regularly ingesting these foods (i.e. more than 2-3 times per week), are inducing a complex cascade of metabolic changes that can have far-reaching implications for neurological health. Let me explain…
You see, Omega-3s are not the only player in neurobiology. Omega-6 essential fatty acids, though often demonized for their role in inflammatory responses, are also critical to the cessation of cell damage and promotion of cell repair by conversion to eicosanoids that bind to receptors in every tissue of the body, including the brain. Arachidonic acid (AA), in particular, is one of the most abundant fatty acids in the brain in almost identical quantities to DHA. As a matter of fact, without sufficient arachidonic acid levels in the brain, multiple functions may be disrupted including, but not limited to, the maintenance of hippocampal cell membrane fluidity. Absence of AA leads not only to a lack of PPAR-gamma mediated protection from oxidative stress1 but also deficits in neuronal growth and repair via syntaxin-3.2 For this reason, essential fatty acids must be understood in parallel rather than in isolation.
Diets high in Omega-3 fatty acids such as DHA and EPA are thought to be universally anti-inflammatory and neuroprotective. In excess, however, there is a parallel supression of the arachidonic acid cascade. In the right balance, EPA, for example, competes with arachidonic acid to dampen its cyclooxygenase and lipooxygenase-mediated metabolism to thrombaxanes, prostaglandins, and leukotrienes which, in excess, can lead to excessive inflammation. EPA will also tend to promote the conversion of gamma-linolenic acid (GLA) to dihomo-γ-linolenic acid (DGLA) instead of AA, further improving the inflammatory profile. If seafood-derived Omega-3s are consumed in excess, however, we will will see an entirely different outcome: they will powerfully suppress arachidonic acid’s effects, systemically, leading to:
- Lower growth and repair of neurons3
- Downregulation of neurotransmitters / neurohormones / neuromodulators4567
- Disruption of ion channel and protein kinase activity89
- Reduced insulin sensitivity10
- Significant deficits in endocannabinoids1112
This effect will be further exacerbated if the seafood diet is also low in arachidonic acid or its precursors (e.g. nuts, seeds, or grain-fed animal meats). You heard that right: consuming seafood in excess in parallel with grass-fed meats will increase these effects.
Excess Omega-3s pour oil on the fire
So how does this skewed fatty acid profile increase vulerability to EHS?
The answer should be obvious. With the overconsumption of EPA and DHA, serum polyunsaturated fatty acid concentration can far outstrip the body’s natural defenses against lipid peroxidation. I am not talking about fish oils that have oxidized due to heat exposure or improper storage. This is something that happens in blood serum and in the brain when fat soluble antioxidants stores have been overutilized. This can easily happen with low-grade, chronic infection, exposure to electromagnetic fields, stress and trauma, and any other trigger for oxidative stress systemically. The result is an increase in DHA-derived lipid peroxides and, eventually, oxidative damage to myelin. The double-insult here is that in addition to lipid peroxidation and demyelination (potentially induced by EMF-exposure), the high levels of Omega-3 fatty acids have suppressed the arachidonic acid cascade, and damage to neurons cannot be sufficiently repaired nor grown with the help of neurotrophin-derived factors.
But the problem does not stop there. Cannabinoids, produced endogenously from arachidonic acid, play major neuromodulatory roles in the central nervous system by their inhibition (via cannabinoid receptor CB1R) of voltage-gated calcium channels.13
These cannabinoids have also been shown to modulate these channels directly by pulling back the reigns on not only high blood pressure, through lowered aldosterone, but also by mitigating excitotoxicity from intracellular calcium. When there is insufficient arachidonic acid from overconsumption of seafood high in DHA/EPA, the endocannabinoid system is no longer able to prevent calcium influx into cells — in particular, myelin. This causes the subsequent activation of cytosolic phospholipase A2 (cPLA2) and calpain, which degrade myelin lipids and proteins.14
In addition to the affects described above, an excessive DHA to AA ratio is also capable of inducing apoptosis through multiple mechanisms, including translocation of phosphatidylserine15, elevated BAX and CASP3 activity16 resulting from disruption of mitochondrial transmembrane potential17, and activation of PPARs via the p38 signaling pathway.18 With limited neuronal growth / repair and endocannabinoid deficits, calcium-induced oxidative stress can perpetuate neuroinflammation leading to further non-enzymatic oxidation of DHA. This produces extremely reactive neuroketals and additional toxic metabolites19, creating a potential demyelinating cascade. With increased demyelination and intracellular calcium, electromagnetic fields are capable of producing acute responses in the central and peripheral nervous systems characterized by the standard EHS symptomotology.
How much seafood can you allow?
Clearly, this is not a straightforward problem. Every individual has their own unique genetic expression for fatty acid desaturases and elongase activity with varying degrees of their required cofactors for induction.
Combined with wildly variable intake of essential fatty acids, the neurological decline induced by high-DHA/EPA diets may be undetectable for decades. Rare is the person that has the proper balance of EFAs and antioxidants combined with a pristine environment free of man-made electrosmog.
For the majority of us, the way forward is obvious: avoid diets excessively high in Omega-3 fatty acids, know your genetics, and quantify serum fatty acid levels at least annually. You may not be sensitive to electrosmog now, but come 2-3 years from now when every last patch of land around the globe is covered in 5G transceivers, you may find yourself spending more time with the canaries in the coalmine than you had bargained for.
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