|Arachidonic Acid and Caffeic Acid
In Health Secrets: Volume 2, under the chapter titled “Nutritional Protection from Electrosmog”, I discuss the potential of a particular compound for reducing the effects of mycotoxins (e.g. aflatoxins). These metabolic byproducts of mold are extremely dangerous to our health, and become more prevalent, and virulent, when exposed to electromagnetic pollution (thus its inclusion in that particular chapter).
That compound is known as “caffeic acid”, and it is a type of polyphenol, belonging to a class of food-derived antioxidants (other sources of polyphenols include grape seeds, green tea, cocoa, and berries). Caffeic acid has a variety of proven health benefits, including anti-inflammatory, anticancer, and antiviral properties, however, in this newsletter we are going to look at a different aspect of this compound.
A new study, using genetically engineered mice and human cell and tissue samples, was published in the November (2021) issue of Nature Neuroscience. This study, led by researchers from Johns Hopkins Medicine, set out to examine the relationship between arachidonic acid and ALS ( amyotrophic lateral sclerosis), also known as Lou Gehrig’s disease.
Arachidonic acid (AA) is an omega-6 fatty acid, involved in controlling the inflammatory response in the body, and a certain amount is required by the body to repair wounds or tissue damage. However, an excessive amount of this inflammatory enzyme has been found in the neuromuscular tissue of people with Alzheimer’s, Parkinson’s, and ALS. Given this relationship between AA and neurological/neuromuscular diseases, which are on the rise as the boomers age out, I thought it might be worthwhile to have a closer look at this particular study.
According to modern medicine, of the some 30,000 people with diagnosed ALS residing in the U.S., only about 10% of these cases are “attributed to heritable genetic alterations”. “The rest occur sporadically, and there is no known curative treatment.”
Now, as with many neurological/neuromuscular diseases that medicine has no explanation for, ALS may be caused by a variety of things: poor methylation (a DNA malfunction) (Source); a deficiency in methylcobalamin (a methylated form of vitamin B12); chronic vitamin D deficiency (Source); or demyelination (damage to the myelin sheath around nerves) (Source).
Or, such diseases may be caused by a combination of the aforementioned epigenetic malfunctions and nutritional deficiencies, in conjunction with a build up of toxins. This is especially likely since those who don’t methylate (epigenetic malfunction) cannot produce sufficient glutathione to remove toxins (heavy metals, molds, chemical pollutants) from their bodies.
That being said, let’s dive into the study.
These researchers began with the “established observation that though patients with ALS lose most of their muscle control because of damaged spinal motor neurons, generally they can still control their eye movements, which are guided by ocular neurons”.
By examining stem cells from lines cultivated from a person with ALS, the scientists searched for genetic pathways that might explain this “difference between disease-free ocular neurons and spinal motor neurons that bear the brunt of ALS”. What they found was “more activity in genes that control lipid metabolism: the process in which cells process fat”.
Further research, comparing ocular neurons and spinal motor neurons from 17 people with ALS, with control samples (from those without the disease), led to the conclusion “that spinal motor neurons of the people with ALS contained completely different amounts and types of lipids than did ocular neurons, compared to people without the condition”.
And the lipid pathway most different between the cells of those with ALS and the cells of those free of the disease, was that of arachidonic acid.
Remember that we are here not just to look at ALS, but for the fact that other ailments are also related to high levels of AA in the body. As most of you are aware, the ratio of omega-6 fatty acids to omega-3 fatty acids in the modern diet is horribly askew. (A healthy ratio of omega-6 to omega-3 fatty acids appears to be between 1-to-1 and 4-to-1, but studies suggest that people who follow a typical Western diet may consume a ratio of about 16-to-1.)
Of course the main problem is that omega-6 fatty acids, which AA is a member of, are the ones most associated with inflammatory diseases.
For example: “Elevated ratio of arachidonic acid to omega-3 fatty acid is associated with depression, and controlled intervention studies have found that decreasing this ratio through administration of omega-3 fatty acids can alleviate depressive symptoms.” (Source)
Now, while AA is an omega-6 fatty acid, we must realize that ” it is important in metabolism, especially in the synthesis of prostaglandins and leukotrienes, and is an essential constituent of the diet”.
Those two components, prostaglandins and leukotrienes, are derivatives of AA, and represent the link between AA and immunity and inflammation. Therefore, via inflammation (prostaglandins), AA plays ” a key role in the emergence and progression of frequent diseases such as obesity, diabetes, non-alcoholic fatty liver disease, and cardiovascular disease”. (Source)
And, via its effect on immunity (leukotrienes), AA is involved in autoimmune diseases. This is due to lipid pathways being a critical part of cell membrane integrity, which allows the flow of nutrients into cells and the removal of toxins. When there is too much inflammation, cell membranes will rupture, and if levels of AA are not tightly regulated this inflammatory messenger can mistakenly send signals to the immune system to attack itself. (Also discussed in Health Secrets: Vol 2, is the propensity of electromagnetic pollution to rupture cell membranes, when we are exposed to high levels of EMFs.)
Therefore, in cases of inflammatory and/or autoimmune diseases, one is advised by health professionals to limit their intake of AA (found mostly in dairy foods, eggs, fish, poultry and meat).
Now, back to caffeic acid.
As this study proceeded, the researchers fed caffeic acid to fruit flies genetically engineered to develop symptoms akin to ALS. “Flies fed caffeic acid were able to move around more, climb up the test tube more often and live longer than flies that did not receive the compound.”
Next, the scientists did the same experiment with mice bred to develop ALS,
By altering the AA pathway in these mice, with caffeic acid, the researchers ” were able to reduce the condition’s muscle-weakening symptoms in the mice – which experienced a 20%-25% increase in grip strength – and extend their survival by two to three weeks”.
Ultimately, this study determined that those with ALS have a level of AA that is about
2.5 times higher than those without the disease. And, according to the lead author of the study, this evidence might offer new approaches to therapy for those with ALS, however, “we don’t know yet why ocular and spinal neurons differ in lipid metabolism or what percentage of ALS patients have alterations in the arachidonic acid pathway”.
Now let’s look at how we can acquire caffeic acid.
The most common source of caffeic acid in the human diet is from drinking coffee, and the amounts are similar in both caffeinated and decaffeinated coffee. It is also found in certain vegetables, fruits, and herbs, the highest amounts being found in asparagus, barley, cabbage, olives, olive oil, spinach, tea, tomatoes, white grapes, white wine, and echinacea purpurea. (More dietary sources can be found here.)
And, while caffeic acid is both an antioxidant and an anti-inflammatory, and will suppress the AA pathway, the scientists warned that people with ALS should not try treating themselves with a caffeic acid supplement. They believe that it is an unregulated dietary supplement, and studies have not yet determined what a safe level of caffeic acid is, when used in supplemental form. And, in this case, I would agree: CA is not commonly available as a supplement, and thus there is very little research or feedback on its use as a synthetic isolate, and “not enough scientific information to determine an appropriate range of doses for caffeic acid”.
Since it appears to be debatable to use a caffeic acid supplement, a study I found while researching this newsletter seems appropriate to mention here.
This study found that “fatty acids resulting from the digestion of edible oils may improve the absorption of polyphenolic antioxidants”. And, lucky for us, the polyphenol they chose to study was caffeic acid.
Researchers explored the effect of three oils on the intestinal absorption of caffeic acid: coconut oil, olive oil, and soybean oil. In the study, rats were fed with a mixture of oil and caffeic acid, dissolved in distilled water; then their blood was analyzed. And the winner was coconut oil.
“Highest absorption of caffeic acid was observed in animals fed with coconut oil. In vitro transport percentages of caffeic acid in 2.5 mmol/L solutions of fatty acids were 22.01±0.12 (lauric), 15.30 ± 0.25 (myristic acid), 13.59 ± 0.35 (linoleic acid), 3.70 ± 0.09 (oleic acid) and 0.10–2.0 (all other fatty acids). Lauric acid and myristic acid are the two major fatty acids present in coconut oil. Therefore, these fatty acids may contribute to the higher absorption of caffeic acid in the presence of coconut oil.” (Study)
So, it might be a good idea to include some coconut oil when we are consuming any of the aforementioned foods high in caffeic acid, however, my research indicates that MCT oil would not be as valuable. MCT oil (a liquid fraction of coconut oil) does contain some lauric acid, but it does not contain myristic acid, and so would be an inferior option, for this purpose.
Given that foods containing CA can protect us from neurological/neuromuscular diseases, along with providing protection against the damage caused by EMF exposure, it seems like a good idea for us to regularly consume those foods high in this exemplary nutrient. Even more so since “test tube studies show that it might decrease the growth of cancer cells and viruses”. (Source)