Quick Study Analysis: Does Shampoo Cause Depression?
tl;dr: Maybe, but it's a fascinating demonstration of a link between a common chemical structure and brain activity.
Ubiquitous Industrial Contaminants: DEA
This morning I read this:
“Bacteria (and Their Metabolites) and Depression”
From the problematic Derek Lowe, last mentioned here:
He discusses a recent study that looks at a variant of cardiolipin, a favorite topic of mine.
This story, however, has nothing to do with seed oils, but it does concern a related topic; what happens when we introduce new substances into our food chain.
In this case the substance is diethanolamine (DEA).
It’s not food, in fact the FDA considers it to be a possible human carcinogen.
“The [National Toxicology Program] NTP completed a study in 1998 that found an association between the topical application of DEA and certain DEA-related ingredients and cancer in laboratory animals. For the DEA-related ingredients, the NTP study suggests that the carcinogenic response is linked to possible residual levels of DEA.”
So what’s the link to depression?
The study Lowe discusses (Bang, 2025, all quotes bold & italic) explains that:
“Recently, a particularly robust and intriguing study that employed genetic, diet, disease, and microbiota data from several thousand individuals identified a strong association between Morganella morganii and major depressive disorder (MDD). While the strongest association of M. morganii is with MDD, its abundance is also associated with inflammatory diseases, including type 2 diabetes (T2D)”
It turns out that these microbes, M. morganii, take DEA from their environment—your gut—and incorporate it into cardiolipin, replacing the glycerine that ought to combine the two sides of the molecule with DEA. They call these novel molecules MmDEACLs (M. morganii DEA cardiolipins).
Strictly speaking, these are not normal metabolites of bacteria.
“DEA does not occur naturally; it is produced on a large scale from the reaction of ethylene oxide and ammonia.”
DEA Induces Inflammation In Vitro
Once these Franken-cardiolipins are released into the gut, they can stimulate an immune response. This paper looks at interleukin-6 (IL-6), a commonly-utilized pro-inflammatory signalling molecule in the body, discussed at length in this post:
The authors used an in vitro model to establish that MmDEACLs produced an inflammatory response by increasing production of IL-6 via toll-receptor 2 (TLR2), a common inflammatory pathway.
They then confirmed this pathway using similar human cells.
Interestingly, they only saw the inflammatory response in unsaturated fats (MmDEACL-1 and -3 above), but the MmDEACLs only included the following fats:
Palmitic (16:0) SFA
Palmitoleic (16:1) MUFA
Oleic (18:1) MUFA
So no PUFA; as I said, this doesn’t have anything to do with seed oils.
They don’t, however, establish a clear mechanism between DEA and depression. Depression is commonly thought to be associated (linked) with inflammation, and they do show that in isolated cells these Franken-cardiolipins do induce inflammation. But this is different from feeding people DEA to see if they get depressed.
Due to the presumed carcinogenic properties of DEA, that study will never be done. They do, however, make a strong case that this connection is causal.
Altered Cardiolipin and Depression
This isn’t the first study to find a link between altered cardiolipin and depression, although it is the first looking at this DEA alteration.
Oxidized cardiolipin have been linked with depression in the literature. Antiphospholipid syndrome is a disease characterized by antibodies to oxidized cardiolipin, and it is commonly associated with depression along with a wide variety of other psychiatric and other signs and symptoms.
“This syndrome can affect all organ systems; therefore, it can present to any specialty.” (Rege, 2015)
Here we get back to the seed oil topic.
“For many years, there has been the assumption that antiphospholipid antibodies are directed against native, ‘self,’ phospholipids. From a heuristic point of view, we feel it useful to pursue the concept that many antiphospholipid antibodies are not generated against native phospholipid molecules, but are in fact directed against non-self modifications.” (Hörkkö, 1996)
The non-self modifications examined in this paper are to Ω-6 fats such as linoleic acid.
“Of particular note is the marked binding of MDA2 to the aged cardiolipin preparation. MDA2 is a previously cloned monoclonal antibody directed against the model epitope of OxLDL, MDA-lysine (12). Thus, the binding of MDA2 most likely indicates that malondialdehyde, generated from peroxidation of linoleic acid in cardiolipin, formed MDA-lysine adducts with BSA that was used to dilute the primary antibody (Pathway 1, Fig. 1).” (Hörkkö, 1996)
Similarly to the DEA cardiolipin, these antibodies are binding to the head of the molecule, not to the fats that are attached to the head (Hörkkö, 1996).
My physician, Joshua Durham, has been able to reduce anti-cardiolipin antibodies in his patients by prescribing a low–seed-oil diet.
Altered Cardiolipin Impairs Mitochondrial Function and Energy
“Cardiolipin is almost exclusively associated with membranes designed to produce ATP through the electrochemical gradient generated by the electron transport chain. Such membranes include the bacterial plasma membrane and the inner mitochondrial membrane. This ubiquitous and intimate association between CL and energy-transducing membranes suggests an important role for CL in mitochondrial bioenergetic processes.” (Paradies, 2014)
Mitochondrial ATP production is dependent on non-oxidized cardiolipin, and oxidized cardiolipin will cause mitophagy and autophagy, organized methods of cellular quality control (Paradies, 2002).
DEA also alters mitochondria function and shape, and the effect thought to be through its affect on phospholipids, likely cardiolipin (Barbee, 1979). This study fed DEA to rats and saw alterations in the shape of mitochondria. They’re not supposed to be round—structures labeled “M”.
No human is going to consume that much DEA, and it’s not nearly as as bad as what happened to the mitochondria of rodents fed seed oils at levels similar to human consumption.
How Did DEA Get In My Gut?
DEA is not a food item, but it is used in cosmetics, shampoos, and dish soaps. A study from China (Wu, 2022) found DEA in plasma of people with depression—one wonders if it’s used in food there…
Perhaps it’s left on dishes as a contaminant after they are washed? It’s unclear.
Here’s more from the FDA on what chemicals DEA might be found in.
Amusingly, they note:
“Based on information filed with FDA's Voluntary Cosmetic Registration Program, it appears that DEA and DEA-related ingredients are used much less frequently in cosmetic products than they were when the NTP completed its study.” (FDA, 2006)
So good on industry.
However, as (Bang, 2025) notes:
“DEA does not occur naturally; it is produced on a large scale from the reaction of ethylene oxide and ammonia…. It is used industrially, agriculturally, and in over 40 types of consumer products, and aggregated U.S. production in 2019 was more than 500 million pounds, most of which entered the environment.”
Lovely. Wikipedia sheds a bit more color on that:
“Diethanolamine is widely used in the preparation of diethanolamides and diethanolamine salts of long-chain fatty acids that are formulated into soaps and surfactants used in liquid laundry and dishwashing detergents, cosmetics, shampoos and hair conditioners.”
(Wikipedia has already updated the entry to include (Bang, 2025). Impressive.)
Yes, I did go check the ingredients of my shampoo.
“Water, Sodium Laureth Sulfate, Coco-Betaine, Glycerin, Sodium Chloride, Hexylene Glycol, Polyquaternium-10, Sodium Benzoate, Fragrance, Peg-60 Hydrogenated Castor Oil, Apple Fruit Extract, Salicylic Acid, Aloe Barbadensis Leaf Juice, Linalool, Niacinamide, Pyridoxine HCL, Hexyl Cinnamal, Citric Acid, Sugar Cane Extract, Sodium Acetate, Hydroxypropyltrimonium Lemon Protein, Isopropyl Alcohol, Tocopherol, Phenoxyethanol, Citrus, Lemon Peel Extract, Radish Root Ferment Filtrate, Camellia Sinensis Leaf Extract, Potassium Sorbate, Sodium Hydroxide.”
Good heavens. But it doesn’t obviously seem to include DEA. Unfortunately, my dishwasher soap doesn’t disclose their ingredients on the web, but the package doesn’t list it either.
Conclusion
This is really a nice example of epidemiology done right. It combines a number of fields I generally don’t have much faith in, epidemiology, microbiome, ‘pollution’, and food contamination, to produce a result that may plausibly play a role in a variety of different human disease processes, while shedding some further light on one of my favorite topics.
If DEA-induced mitochondrial disfunction and inflammation can impact disease, then seed oils, which are a many-orders-of-magnitude higher factor in human diet, should be taken even more seriously.
However, while I will certainly make an effort not to include DEA in my diet; if I’m not consuming it, I wouldn’t be too concerned about the finding of this paper.
Don’t eat novel chemicals.
References
Bang, S., Shin, Y.-H., Park, S.-M., Deng, L., Williamson, R. T., Graham, D. B., Xavier, R. J., & Clardy, J. (2025). Unusual Phospholipids from Morganella morganii Linked to Depression. Journal of the American Chemical Society, 147(4), 2998–3002. https://doi.org/10.1021/jacs.4c15158
Barbee, S. J., & Hartung, R. (1979). Diethanolamine-Induced Alteration of Hepatic Mitochondrial Function and Structure. Toxicology and Applied Pharmacology, 47(3), 431–440. https://doi.org/10.1016/0041-008X(79)90512-X
Food & Drug Administration. (2006, October 27). Diethanolamine. U.S. Food and Drug Administration; FDA. https://www.fda.gov/cosmetics/cosmetic-ingredients/diethanolamine
Hörkkö, S., Miller, E., Dudl, E., Reaven, P., Curtiss, L. K., Zvaifler, N. J., Terkeltaub, R., Pierangeli, S. S., Branch, D. W., Palinski, W., & Witztum, J. L. (1996). Antiphospholipid Antibodies Are Directed Against Epitopes of Oxidized Phospholipids. Recognition of Cardiolipin by Monoclonal Antibodies to Epitopes of Oxidized Low Density Lipoprotein. The Journal of Clinical Investigation, 98(3), 815–825. https://doi.org/10.1172/JCI118854
Lowe, D. (2025, January 28). Bacteria (and Their Metabolites) and Depression [Blog]. Science: In The Pipeline. https://www.science.org/content/blog-post/bacteria-and-their-metabolites-and-depression
Rege, S., & Mackworth-Young, C. (2015). Antiphospholipid Antibodies as Biomarkers in Psychiatry: Review of Psychiatric Manifestations in Antiphospholipid Syndrome. Translational Developmental Psychiatry, 3(1), 25452. https://doi.org/10.3402/tdp.v3.25452
Paradies, G., Petrosillo, G., Pistolese, M., & Ruggiero, F. M. (2002). Reactive Oxygen Species Affect Mitochondrial Electron Transport Complex I Activity Through Oxidative Cardiolipin Damage. Gene, 286(1), 135–141. https://doi.org/10.1016/S0378-1119(01)00814-9
Paradies, G., Paradies, V., De Benedictis, V., Ruggiero, F. M., & Petrosillo, G. (2014). Functional Role of Cardiolipin in Mitochondrial Bioenergetics. Biochimica et Biophysica Acta (BBA) - Bioenergetics, 1837(4), 408–417. https://doi.org/10.1016/j.bbabio.2013.10.006
Wu, Z., Yu, H., Tian, Y., Wang, Y., He, Y., Lan, T., Li, Y., Bai, M., Chen, X., Chen, Z., Ji, P., Zhang, H., Jin, X., Song, J., Cheng, K., & Xie, P. (2022). Non-targeted Metabolomics Profiling of Plasma Samples From Patients With Major Depressive Disorder. Frontiers in Psychiatry, 12. https://doi.org/10.3389/fpsyt.2021.810302
I think a big problem is the massive and varied amount of synthetic substances we are bombarded with. If it were only one or two here and there, I don’t think it would be so bad. We have to remain ever vigilant. The combinations seem to be far worse than individual chemicals.
Garnier Fructis shampoo?