#AAN2018 – Diet Rich in Essential Omega-3 Fatty Acid Linked to Lower ALS Risk in Study

#AAN2018 – Diet Rich in Essential Omega-3 Fatty Acid Linked to Lower ALS Risk in Study

A diet that includes foods rich in omega-3 polyunsaturated fatty acids like alpha-linolenic acid — an essential plant-derived fatty acid found in flaxseed, canola, and other oils — is linked to a lower risk of developing amyotrophic lateral sclerosis (ALS), researchers report.

But their work also found that diets rich in arachidonic acid — another polyunsaturated fatty acid found in meats like chicken and beef, and in eggs — was associated with a higher ALS risk.

These results were in the presentation, “Pre-diagnostic Plasma Polyunsaturated Fatty Acids and the Risk of Amyotrophic Lateral Sclerosis,” given at the 2018 Annual Meeting of the American Academy of Neurology on April 22. The AAN conference runs in Los Angeles through April 27.

The presence of polyunsaturated fatty acids (PUFAs) in the human brain is known to modulate several “triggers” for ALS, such as oxidative stress, over-excitation of neurons (a condition called excitotoxicity), and inflammation.

Diets rich in omega-3 PUFAs were previously reported to be linked to a lower ALS risk. However, research has also shown that high consumption of omega-3 PUFAs accelerated disease progression in a mouse model.

For this reason, researchers examined whether PUFAs levels in the blood  — prior to an ALS diagnosis — were linked to a greater or lesser risk of developing the disease.

They compared 275 people who went on to develop ALS while part of five U.S. study groups to two control groups (no ALS). Participants were matched for age, sex and race.

Results showed that individuals with higher blood levels of alpha-linolenic acid had a lower risk of ALS.

Alpha-linolenic acid is an essential omega-3 fatty acid that can only be obtained from diet, as we are not able to synthesize (produce) it. This essential omega-3 fatty acid is found in high amounts in flaxseeds and flaxseed oil, and in canola, soy and walnut oils (although in low amounts).

“Adjustment for BMI [body mass index, a measure of body fat based on height and weight], smoking, education attained, plasma urate [also called uric acid] and other n−3 polyunsaturated fatty acids [omega-3 PUFAs], did not materially change the findings,” the researchers wrote.

But people with higher blood levels of arachidonic acid — part of the omega-6 PUFA family, and found in foods like meats, eggs and dairy products — had a higher risk of ALS.

Overall, these results suggest that,“polyunsaturated fatty acid profile may modulate the risk of ALS. Consumption of foods high in alpha-linolenic acid may help prevent or delay the onset of ALS,” the study concluded.


  1. Charlie says:

    All ALS-afflicted families will know the statistics of possibly developing this awful disease. They will also likely know that ALS incidence is statistically and significantly greater than the average in the case of military veterans.
    Anyone who saw the documentary yesterday about the US Army’s toxic Fire-Pits in Iraq and Afghanistan and the explosion of neurological illnesses experienced by veterans, might usefully ponder how these soldiers show so much vulnerability to ALS-and-similarly horrendous neurological illnesses.
    Now extrapolate, not unreasonably, into the general population with neuro-toxic agents found in common foods and you have a reasonable cause for investigation of this toxicity.

    Instead of looking for yet the next gene affected in the ALS patient profile (and discovering even more SYMPTOMS) it might be useful to explore whether a CAUSE of ALS exists in neuro-toxins in the military and non-military duties/diet.

  2. Angeline Pacy says:

    This study was long-overdue…and not even because the 2013 mouse study went wrong and shockingly has no correlation to the positive 2014 Omega-3 study or this 2018 Omega-3 study within humans. These studies should have been done years ago and more (to include lipid ratios and other therapeutic targets beyond the blood). Now that this topic is off the plate, I would like to move on to many more important items on the plate…

    1.) The positive Omega-3 surveil in ALS patients (published in 2014) doesn’t just cite the benefits of ALA but marine-sourced Omega-3 fatty acids (EPA and DHA) that lowered ALS risk: “Consumption of both α-linolenic acid (RR = 0.73; 95% CI: 0.59 to 0.89; P trend=0.003) and marine n-3 PUFAs (RR=0.84; 95% CI: 0.65–1.08, P trend=0.03) contributed to this inverse association.”

    2.) Researchers found that higher ALA reduced ALS risk in this newly published 2018 Omega-3 study (above). Yes, that is significant but not necessarily well-interpreted. Why not the the EPA and DHA too?

    3.) I am concerned about the interpretation of this study. ALA is a well-recognized fatty acid but due to its differences in human lipids, the body takes extra time to convert them properly. This stands in contrast to EPA and DHA in which the body metabolizes more quickly (requiring significantly fewer conversions). Fewer conversions (or steps required to metabolize) means that they will be elevated in the serum longer than their anti-inflammatory counterparts, EPA and DHA (also building blocks of myelin) that are converted faster.

    4.) In this instance and in so many more, dietary recommendations are being made without considering that the blood is not necessarily the therapeutic target. In the case of ALS, what should be the therapeutic target? Membranes, for starters. Where else? I will leave this to your imagination.

    5.) The observation of elevated arachidonic acid is fantastic but also is not cut-and-dry. In inflamed Alzheimer’s brains, we see a reduction of CNS Arachidonic Acid (AA). But, systemic elevation (and serum elevation of AA, as is the case in the ALS study) of AA is a notoriously pro-inflammatory (especially in comparison to it’s ratios to EPA and DHA and Omega 6). Both doctors Ski Chilton and Barry Sears are wonderful references in assessing true lipid health (measuring fatty acid ratios in comparison to one another, greater reflections of health). Perhaps, low levels of AA in the brain correlates to disease in ALS patients, like the Alzheimer’s brains? I don’t know but we need to know.

    6.) The only substance I know that can modulate Arachidonic Acid in Alzheimer’s brains (improving low levels) and has a demonstrated ability to lower elevated AA in the body is R-lipoic Acid (the enantiomer of the Lipoic Acid compound to which all of it’s therapapeutic benefits are attributed). I use the BioEnhanced R-Lipoic Acid and the Liquid K-RLA (both stabilized, purified industry standards) in a therapeutic dose. Here is a wonderful list of applicable citations: https://www.facebook.com/angeline.pacy/posts/10155841097037296

    7.) Has this study been published in the literature yet (beyond conference proceedings)? I would love to see the data and methods.

    Follow-Up: while I enjoy the wonderful benefits of ALA in the form of flax seeds and more, it does not have the versatility of EPA and DHA. I am concerned that the ALS community will miss the subtleties in study interpretations. What is more, dietary consumption of Arachidonic Acid is not the only way in which this conditionally pro-inflammatory substance increases in the body. The body can produce Arachidonic Acid, especially within pathological states. This is an important target for this community.

  3. Angeline Pacy says:

    Oops. Correction to point number 3. It should have said, “More conversions (or steps required to metabolize) means that they (ALA) will be elevated in the serum longer than their anti-inflammatory counterparts, EPA and DHA (also building blocks of myelin) that are converted (and therefore metabolized) faster.”

    The point here is that ALA may be elevated in comparison to DHA and EPA because it takes longer to metabolize. What is more, the blood isn’t necessarily the best therapeutic target.

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