It’s amazing to think that 100 years ago, scientists were still debating whether oily skin causes acne. These days, sebum’s (oil) pore clogging powers are so established that we barely think about it anymore. However, there’s another possible rabbit hole to venture down: what about the ingredients of that oil?
As it pumps out of the sebaceous gland, before alteration by the environment, the average human oil sample consists of 12% squalene, 26% wax, 41% triglycerides and 16% free fatty acids. Could acne patients have a fatal deficiency in one ingredient? Back in the 1970s, it seemed to be a hot topic in the world of dermatology, before the experiments suddenly dried up, with a trickle restarting in the 2000s.
It wouldn’t be the first wrinkle of complexity added to an old acne topic. It would mirror p.acnes bacteria, which was always known to cause acne, but turned out to have particularly vicious substrains.
Before we start, this article will cover your skin’s oil as it is produced. We’re not discussing oil sitting on your face, with its antioxidant defences depleted by cigarette smoke and air pollution. That can happen to anybody, so this article is covering something deeper, more integral.
Difference #1 – vitamin E
This is the classic, the one we hammer home all over this website. It’s a classic difference which has a simple corrective solution, but has barely entered the mainstream.
Sure, vitamin E oils are all over amazon, but its sheer importance isn’t really understood by the masses. All newly manufactured oil is equipped with vitamin E, firstly to protect the fragile sebum ingredient squalene (see below).
Secondly, your skin lacks any vitamin E transporters within its tissues. A fountain of oil flowing over the skin is the only delivery method, diffusing into the layers of skin below, creating an antioxidant shield.
The importance for acne? Unprotected squalene easily mutates into squalene peroxide. This free radical rolls two acne dangers into one, sparking inflammation and clogging your skin pores at double the rate of normal oil.
Now consider an experiment referenced here. Juvenile acne patients had approximately 22% less alpha tocopherol, the most active form of vitamin E, in their sebum than clear-skinned people. Adult acne showed a smaller yet significant 10% difference. The vitamin E gap is pretty much accepted by scientists now.
The reasons? There could be obscure genetic factors, but the main cause is simply a dietary deficiency. However, even if you do eat plenty of almonds and olive oil, your vitamin E can be seriously diluted if you have mega oily skin.
The happy consequence is that this difference is easy to correct. After eating more vitamin E, it takes 14-21 days for levels to increase in sebum (study).
Of course you could also apply topical vitamin E in grapeseed oil or argan oil, but whether this is recycled and incorporated into newly manufactured sebum is unknown.
Given the lack of transporters, the smart guess is probably not. Therefore, topical vitamin E will definitely protect against wafting clouds of cigarette smoke, but you cannot ignore your diet.
This is the simplest, least controversial difference on our list.
Difference #2- linoleic acid
Also known as omega 6, linoleic acid is the evil twin of omega 3s, or linolenic acid from fish.
It’s important for the immune system, but the average American eats 5-20 times more than necessary. My advice for acne is to reduce your consumption by kicking vegetable oils to the curb…
…yet somehow, studies show reductions in acne-prone sebum.
ONE: back in 1976, when linoleic acid was still called octadeca-9,12-dienoic acid, 5 controls, 5 slight and 9 severe acne patients had the sebum on their scalp examined. The acne prone sebum contained much less linoleic acid. It made up 0.56%, 0.27%, and 0.19% of its total fats respectively, a “statistically significant” correlation (study).
TWO: this 1988 study tested acylceramides, part of the skin barrier. In 6 acne patients and 6 age and sex-matched controls, linoleic acid levels were much lower in acne-prone skin. For example, in the two 22 year old males, the acylceramides contained 18% linoleic acid versus 28% for the control. In the 24 year old females, it was 15% vs 27%. The key point is that sebum supplies the acylceramides with fats.
How this happens is a puzzle, because unlike vitamin E, your diet matters little. Bloodstream linoleic acid is used initially, but the moment oil production starts in the sebaceous glands, the gates slam shut (study). Therefore, this fixed quantity is diluted very easily.
There’s two causes of hyper oily skin. The number of seboyctes, sebum-producing cells, can multiply, or the amount of oil pumped out by individuals cells can increase. Only the latter leads to linoleic acid deficiency (study). Therefore, the reduced linoleic acid in acne patients could easily be from oily skin alone. Yet in study 1, there was no correlation to increased sebum production whatsoever. There’s mysteries everywhere.
What’s better understood is the connection to acne. Firstly, linoleic acid has antibacterial properties which can suppress p.acnes. Secondly, linoleic acid helps to construct lamellar granules, part of the skin barrier, which controls proper skin cell shedding. Linoleic acid can even decrease oil production by acting on PPAR receptors, the same ones that accutane stimulates, so essentially, your sebaceous glands produce the very substance which defeats them.
Finally, there’s ceramides, which need linoleic acid to do their work like bolstering the skin barrier. Malfunctioning ceramides are strongly linked to acne (study).
This difference is partially why I recommend the fantastic topical treatment grapeseed oil.
Difference #3 – squalene
The signature compound of sebum, which is barely found elsewhere in the human body. Squalene probably has the single most studies studying its differences in acne. For example:
ONE: two German studies (link, link), both from 1972, are unfortunately locked behind a wall of language translation. But in both, squalene was significantly elevated in acne-prone sebum. They also agreed that free fatty acids were lower while triglycerides were higher. Seeing as they were both German, and conducted only months apart, they might have used the same measuring techniques too, adding to the reliability.
TWO: a much bigger study, also from 1972. In 217 human beings, squalene was much higher in the controls, in both male and female sebum. This was much more consistent than free fatty acids, which were decreased in males only, and triglycerides, increased in males only.
THREE: more recently, 9 males aged 15-20 were gathered. Those with acne averaged at 34% more squalene in their sebum. The overall squalene proportions were higher too – at 20% versus 15% for controls (2009 study).
That’s only a sample. The evidence for increased squalene is strong, and the connection to acne is pretty clear too. We’ve already discussed how when your oil production is flowing like a fountain, the protective vitamin E inside will inevitably get diluted. Vitamin E deficiencies have always been our main focus, but now, unusually high squalene may be just as important. The deadly squalene peroxide could have two opportunities to form.
Could squalene cause acne in other ways? It’s possible, but if anything, it would be protective. Nowadays, more and more skincare formulas use squalene as a special ingredient, and its natural functions include UV protection and skin lubrication. It’s in your sebum for a reason.
As for how squalene gets elevated, we barely know anything.
In sebum, some squalene gets transformed into cholesterol, so scientists theorise that either 1) the enzymes that control this conversion are decreased, or 2) that the “squalene synthase” enzymes which make squalene itself are increased. However, this is pure guesswork; there’s no actual evidence. For all we know, deficiencies in zinc could increase squalene. It could be wacky estrogen levels, or eating too few omega 3s.
Difference #4 – sebaleic acid
This is the wildcard, a substance which few dermatologists let alone acne patients have ever heard of. Elevated levels were actually discovered in sebum before scientists knew what it was. Sebaleic acid is totally unique to sebum, occurring nowhere else in the body.
The story started in 1972. Scientists discovered that out of 59 fatty acids, only 1 was elevated in 12 male acne patients compared to 8 controls (study). Within the triglyceride portion of sebum, the mysterious fat made up 1.68% and 0.60% of fatty acids respectively. 1 year later, a study triumphantly declared it to be 5Z,8Z-octadecadienoic acid, since renamed sebaleic acid.
45 years later, and sebaleic acid is now almost forgotten. For example, sebaceous glands manufacture sebocytes, individual cells which slowly swell with oil. We know that sebaleic acid partially forms the phospholipid layer which ultimately bursts to releases this oil, but its full roles in human skin are mysterious.
By an amazing stroke of luck though, one of the few studies we do have fits with acne like a jigsaw puzzle.
You might remember neutrophils, the immune system agent which unleashes free radicals against damaged flesh to break it down, ready for replacement. In normal human skin cells, leukotrenes use arachidonic acid, a relative of linoleic acid, as the raw materials to manufacture neutrophils.
In this study, it was observed that in sebum, sebaleic acid acted as that raw material instead. Overpresent sebaleic acid increased 4 different free radicals, including 5-HODE and 5-oxo-ODE. The conclusion said it all: the conversion “could be involved in neutrophil infiltration in inflammatory skin diseases“.
As for why it gets elevated, the theory is that your sebaceous glands are capable of stockpiling sebaleic acid at a much later stage. If the linoleic acid stream is closed off but your oil production then goes into overdrive, possibly stimulated by hormones, sebaleic acid might act as a replacement. This 1986 study observed that the two fatty acids changed in direct, inverse correlation with each other. But it’s still possible that your linoleic acid can sometimes be normal, while your sebaleic acid is sky high.
Sebaleic acid is the most obscure, but interesting difference in acne patients’ oil.
Real world analysis – do the differences matter?
So here we have four clear differences in acne-prone oil. But is there actually anything you can do with it? Or is it pure intellectual discussion, mildly interesting yet ultimately a pointless distraction?
Firstly, we know how to manipulate 3 of these to our advantage, which is good. Vitamin E is obvious; we’ve been doing it for years, increasing the quantity in our diet. Meanwhile, with linoleic acid and squalene, we have no idea how to change the natural born composition. There may be an answer floating around at the back of a frustrated scientist’s mind somewhere, eluding his grasp, but right now we’re clueless. What we do have are strategies to mitigate the damage. There’s topical oils like grapeseed oil for linoleic acid, and for squalene, your strategies are identical to vitamin E.
It’s with sebaleic acid that we slip up. We have nowhere to start. It might exist in an inverse correlation to linoleic acid, but topical linoleic acid won’t achieve anything, because it doesn’t alter sebum as it is created.
That’s 3 out of 4 then, but the vitamin E and squalene differences, fascinating though they are, don’t add much to your acne gameplan. Why? Because it’s a strategy I recommend for all acne patients anyway. Plus, you will automatically fix the problem by decreasing your overall oil production, because there will be less stress on your vitamin E reserves.
Linoleic acid and sebaleic acid are where things get interesting. These differences would wreak havoc even when your oil production is perfectly normal. Sebaleic acid would still provide the raw materials for inflammatory neutrophils, and a reduced flow of linoleic acid into ceramides would get even worse. Of course, it’s also nearly impossible to tell which deficiency affects you. Even in a laboratory, scientists have huge problems analysing sebum composition. But for the future, these two have potential as unique acne strategies.
Now we reach the real question: given the massive world of acne-clearing foods, vitamins and deadly villains like sugar, would these strategies even make a dent? Or would they be a drop in the ocean?
My guess is that your sebum composition is fairly important. Chronic inflammation is the root cause of acne, and rampaging neutrophils is right in the thick of it. Too little linoleic acid could even explain stubborn cases of acne that refuse to heal. Sebum is a direct part of the skin, not a malfunctioning protein in a faraway location like the gut.
For example, we recently discussed staphylococcus epidermidis, a friendly bacteria, another example of a promising obscure skin player. I would guess that your sebum composition is a notch above this in importance, ignoring the really integral angle of vitamin E.
It will never be your main focus, it will never beat a zinc supplement. I doubt that any acne patient alive needs this strategy, but altering your oil could be fairly significant one day.
Other possible players
WAXES – makes up 25% of sebum, yet the results are all over the place. The two German studies from 1972 tested it, one finding decreased levels in acne and another finding normal. Two years earlier, a 1970 study also found reduced levels. No obvious theories spring to mind either.
SAPIENIC ACID – like sebaleic acid, this is unique to human sebum, and the two are structurally related. Its name comes from our species, homo sapiens. It’s slightly better understood than sebaleic acid, as strong antimicrobial properties have been identified, against s. aureas, and maybe even p.acnes.
Like its cousin, could sapienic acid be connected with acne? In this study, there was no difference in sebum whatsoever.
THEORY 1 – antimicrobial peptides: this is completely made up, but human sebum is surprisingly unresearched for such a pivotal substance in acne. Human skin cells naturally manufacture antibiotics called human beta defensins, to ward off deadly infectious microorganisms. Even bees make them, like bee-defensin1, found in honey, which is partially why it’s a promising topical treatment.
I wouldn’t be surprised if human sebum contained natural antibacterial peptides too, maybe “sebumsin”. After all, it accumulates in skin pores (forming whiteheads) where bacteria naturally congregate. Many bacteria species consume sebum for fuel, and maybe this peptide evolved in response. If true, its quantities could vary from person to person.
THEORY 2 – antioxidants: it’s strange that squalene protection is so heavily dependent on vitamin E. Vitamin A is barely involved; the only other antioxidant identified in sebum is CoQ10, which the body can manufacture itself. Then there’s more obscure dietary carotenoids like lutein. If these antioxidants are secretly important, then they could vary just like vitamin E.
Also, if sebum is so specific about using vitamin E, then obviously its chosen antioxidant needs a narrow band of characteristics. Maybe, somewhere in fruits and vegetables, there’s a handful of unidentified antioxidants that possess these qualities and would massively strengthen your sebum when eaten, where most fail to make the cut. Maybe it’s punicalgin from pomegranates, or maybe it’s astaxanthin from salmon. This is a completely random theory.
THEORY 3 – the bacteria connection: one of the signature characteristics of p.acnes, the hardest acne bacteria on the block, is that it manufactures lipase enzymes which break down fatty acids in sebum. This creates glycerol, a fuel source that p,acnes greedily consumes. What if certain fats or waxes are much easier for p.acnes to break down than others? A certain sebum composition would make it far easier for p.acnes to take over. In my view, this is an extremely likely theory.
Conclusion
Of course, the final, disturbing possibility is none of these differences mean anything. They might be a mere correlation, not a causative relationship, two branches of the same tree which never interact.
For example, maybe a sebaleic acid increase is caused by zinc deficiency, just like red and inflamed pimples. The studies could be a pure smokescreen, but personally, I doubt it.
Like so many obscure nooks and crannies of the acneverse, this is topic we should keep a close eye on. We’ve been saying that a lot lately, but the patience always pays off: burdock root and fenugreek finally received acne studies recently after many years of waiting.
What should you do right now? Keep focusing on vitamin E and its squalene protecting powers. It doesn’t matter whether your levels are altered, and there’s no way to tell anyway! As for the other two, you still can’t tell, so topical treatments containing linoleic acid (grapeseed oil, sesame seed oil) are an excellent experiment to try. Actually, grapeseed oil is packed with vitamin E as well, making it the best sebum-correcting elixir we have right now. For sebaleic acid, our goal is to play the waiting game.
Never get distracted and forget the basics of reducing the oil, by correcting your vitamin A levels and insulin.
Thanks for reading!