Green Tea in Skincare

We use licochalcone, a Chinese licorice root extract, in Acne.org Moisturizer and Acne.org AHA+ (10% glycolic acid). This is what gives both products their characteristic yellow color. I chose licochalcone because it is powerfully calming to the skin and works especially well on irritated, acne-prone skin. It targets inflammation and has antioxidant properties and has proven its efficacy over the years that it has worked so well within the Acne.org line of products. However, it is extremely expensive ($6000 per kilogram), and some people don’t love the yellow color it imparts. Because it is such a specialized ingredient, we are also at the mercy of cyclical weather changes and potentially unreliable harvests in the few places where this particular species of licorice is grown.

For these reasons, I have kept my eye out for another comparable calming ingredient with research to back up its use on acne-prone skin. Green tea, or more particularly, the major polyphenol within green tea called EGCG, is one of the strong top contenders. I have been intrigued with green tea for several years now, but the more I look into it the more I’m liking what I’m seeing. Researchers performed two more studies within the last two years on EGCG and its effect on acne, both with promising results. The data is showing that EGCG not only produces anti-inflammatory effects, but may also help reduce skin oil (sebum) production.

Any change to Acne.org products takes lots of time to study, mock up, and ultimately implement, and I am still not 100% convinced that I can’t find anything even better than EGCG, but I’m intrigued to say the least.

References:

  • Im M, et al. “Epigallocatechin-3-gallate suppresses IGF-I-induced lipogenesis and cytokine expression in SZ95 sebocytes.” Journal of Investigative Dermatology. 2012; 132(12): 2700-8.
  • Yoon JY, et al. “Epigallocatechin-3-gallate improves acne in humans by modulating intracellular molecular targets and inhibiting P. acnes.” Journal of Investigative Dermatology. 2013; 133(2): 429-40.

…we still have no clue.

After scouring the research from the last several years regarding sebum (skin oil), acne bacteria, gene transcription, and a bunch of other super techie stuff, the answer to what causes acne is…um…we still have absolutely no idea. Most diseases are tricky things, and acne is no exception. Scientists are really only still scratching the surface when it comes to nailing down what actually happens that starts the acne ball rolling.

Let’s take acne bacteria for instance. Over the past few years, scientists have located more strains of P. Acnes, the bacteria present in human skin. We don’t know which strains might be harmful and which might actually be helpful. Furthermore, we don’t know which of the secretions of which of the bacteria strains cause problems and why. Additionally, we don’t know if it’s the secretions that cause a problem or if certain strains of bacteria interact with cells in some other way, such as interacting with cell RNA, toll-like receptors, or inflammation. And, um…if these bacteria do interact with skin cells in some way, we don’t know whether it’s dermal cells, oil cells, or immune/inflammatory cells.

The story is equally muddled when you look at the immune response of the skin, the inflammatory cascade, cell signaling, et cetera, et cetera.

Regardless, it’s not all bad news. Some directions of inquiry are starting to look more interesting than others. For instance, scientists are starting to frame acne as an inflammatory disease and are focusing in on how to mediate the body’s inflammatory response in the skin.

With time, we may be able to better specify what causes acne, which could theoretically lead to a cure. Rest assured that I’ll keep on top of the latest research. In the meantime, The Regimen should work well to keep acne under complete control, and in more severe cases, Accutane is an option as well.

The more I learn about antibiotic therapy for acne, the more wary and less enthused I become. Due to overuse and misuse over the past twenty years, antibiotic resistance has become widespread throughout the skin of the world population. This is evidenced by the increasing ineffectiveness of both oral and topical antibiotics in clinical studies. Antibiotics never worked very well for acne, and now they work even less well.

According to a “Global Alliance to Improve Outcomes in Acne” published in the Journal of the American Academy of Dermatology, antibiotics should be avoided as the sole treatment of acne. Researchers agree strongly that if antibiotic therapy is used, it should be combined with other therapies. When you look at the superior effectiveness of these other therapies the question arises as to why someone would want to include antibiotics at all. For example, when one takes into consideration the fact that benzoyl peroxide kills 99.9% of acne bacteria on its own and does not create resistant colonies of bacteria, one has to wonder why so many prescriptions for antibiotic acne therapy–over 11 million per year–are still written. According to an article published in the journal Expert Opinion on Pharmacotherapy, “…evidence demonstrates that [topical antibiotics] are no more effective against inflamed lesions than [benzoyl peroxide], and are less effective against non-inflamed lesions…To date, [benzoyl peroxide], as both mono- and combination therapy, is the most evidence-based approach.” Other acne treatments exist, and while they may not be as effective as benzoyl peroxide, they easily outpace antibiotics.

The misuse of antibiotics can also cause antibiotic resistance in other skin bacteria, especially the bacteria known to lead to impetigo and folliculitis. If all of this weren’t enough, when we look at how gene mutations work in bacteria, we see that genes which allow for resistance to antibiotics are easily transferred from acne bacteria to other bacteria in the skin, thus further promoting unwanted antibiotic resistance in other skin bacteria.

If your doctor has you on antibiotic therapy for acne and nothing else, it may be time to have a talk with her/him. The authors of the expert opinion review also note that topical antibiotics should be used for no longer than 3 months and oral antibiotics for no longer than 6 months. So, if you have been on antibiotic therapy for a long time, it may also be time for an appointment with your dermatologist. Since poor compliance with antibiotic regimens are one of the main causes of antibiotic resistance, just make sure you do not stop antibiotic therapy on your own without consulting with your physician first.

The last few days I have spent going through all clinical studies/trials regarding acne and Omega-3 fats, iodine, antioxidants, chocolate, calorie intake, fatty/oily food, digestion, and zinc. Adding to this what I have learned regarding dairy and glycemic load, I’m sorry to say that nothing stands out for me as a smoking gun when it comes to diet and acne. We simply don’t have enough research yet, and nothing feels super compelling to me at this point. However, at least researchers are looking into how diet may affect acne, so hopefully by the next time I review the literature, the evidence available to the scientific community will start taking shape. In the meantime, based on digesting everything the research community has to offer regarding diet and acne, here is what I am personally going to do as far as diet goes:

1.  Keep taking fish oil and eating wild delicious sushi :)  I take 4 fish oil pills per day to make up for my Western-style diet, which like almost everyone living in modern society, is overly rich in Omega-6 fats from vegetable oils, grains, etc. There is enough evidence to persuade me of the overall health benefits of Omega-3s and I feel good taking fish oil regardless of whether or not it may be helping with my skin. Also, when I go out to eat, I specifically ask whether the fish or sushi on the menu is wild. Farm raised seafood is far inferior in Omega-3s and other nutrition than wild seafood.

2.  Keep taking a zinc supplement. Having dived deeper into the role of zinc, I am still convinced that it is likely an important nutrient when it comes to combating inflammation and keeping bacteria in check. I’ll keep taking my 30mg per day.

3.  Not worry about iodine, chocolate, fatty/oily food. I’ll keep eating seaweed salad and seafood (contain iodine).  There exists no evidence showing that the amounts of iodine consumed in these foods is in any way detrimental for acne. Based on the available evidence, I’ll also continue eating a little dark chocolate every day without worrying about how my skin will react. I will also keep eating the occasional naughty greasy meal without fear.

4.  Try to be generally healthy. Antioxidants are important calming agents in the body, and eating antioxidant-rich colorful fruits and vegetables is fun and tasty anyway. When it comes to glycemic load, whether or not scientists know if it will help with acne yet, I’ll try to keep my meals balanced with carbs, fat, and protein to keep my energy and mood level and avoid crashes.

A full update to the diet and acne page of acne.org is on its way with much more information on each of the above mentioned topics. In the meantime, when you look at the evidence at hand, eating healthy and in moderation will suffice as a general wrap up for what we know regarding diet and acne at this point. Not exactly a Eureka moment.

If you eat a high glycemic diet with foods like white bread, sugary soda, white potatoes, and white rice, you will experience insulin spikes. This we know. What we don’t know (sorry Josh) is whether this sort of diet will directly affect acne.

Scientists hypothesize that a high glycemic diet and its resulting insulin reaction will result in higher levels of hormones (IGF-1 and androgens) which may contribute to clogged pores and increased skin oil production.

When it comes to high glycemic diets in particular, scientists also postulate that eating this way may lower the amount of beneficial proteins (IGFBP-3) and natural retinoids, which help keep skin cell growth in check and pores from becoming clogged.

However, as is becoming customary in my research on diet and acne, we do not have enough research to make any strong correlations. The only 2 studies which have been done on glycemic load and acne have been performed by the same group of Australian researchers, led by Robin Smith, and while acne lesion counts appear to reduce on low glycemic diets, results are inconclusive. What stands out most sharply is the lingering question of whether glycemic load leads to decreased acne symptoms or whether it is the weight loss that tends to go hand in hand with this sort of diet that causes the reduction in acne. To answer this question, we need data on whether a reduction in acne symptoms is sustained after weight loss has leveled off. Until then, I’m happy that the scientific community is at least starting to investigate.

Thanks for voting for what you guys wanted me to concentrate my acne research on. The last I looked at the poll results diet and acne was winning. Now I see that scars have a few more votes. Well, scars will be next. But first, let’s delve into diet and acne. In fact, let’s get deep and dirty and nitty gritty with it shall we? Yes? Great, then we shall :) I’ve read every published trial and review of literature since 2008 regarding diet and acne there is good news and bad news.

Good news: Scientists are all over it! No longer is diet and acne relegated to a back seat. According to the Journal of the American Academy of Dermatology (2010), “…it is evident that dermatologists can no longer dismiss the association between diet and acne…In light of the last decade of research investigating the relationship between diet and acne, it is no longer dermatologic dogma to state that any association between diet and acne is mere myth.” In other words, researchers are conducting studies and we’re getting interesting data.

Bad news: The data is still spotty and almost all of the recent studies come with serious “design limitations” as they call them. An example of a design limitation is researchers relying on subjects’ personal recollection of their diet habits instead of actually watching what they eat. Another example of a design limitation is trusting subjects to define for themselves whether they have “acne” instead of employing a professional to count lesions across a study cohort. In other words, we can’t trust the data that’s coming out yet. We need more trials, and better trials, before we make conclusions.

Um, a little more bad news: Because pharmaceutical companies do not make money from educating the public on diet, funding for diet and acne studies is sparse. But hey, even without the pharmaceutical companies, we’re seeing a resurgence of interest in the topic of diet and acne.

My gut feeling on the subject: Regardless of whether some hunter/gatherer tribes do not have acne, it is literally impossible for us to go back to a hunter/gatherer way of living, and for real concrete answers to acne, we’ll have to include diet as only one piece of a much larger puzzle. As much as I would love for it to happen, I don’t think we’re going to find a magic bullet. I don’t think we’ll find a super bad food or food group which we’re all eating which is causing acne. I also don’t think educating people to “eat right” and “low glycemic” will clear people up to the degree any of us want.

I’ll keep updating the blog with specifics regarding some diet and acne subtopics like dairy, glycemic load, iodine, etc. for the next few updates. Hopefully with all of us wading deep into the muck of the latest research we can pool our minds and get food working for us as much as possible.

I’m diving headfirst into acne trials and medical journal articles, starting with Accutane. What do you want me to research after that?

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An article released this month in the British Journal of Dermatology took a look at the evidence scientists have boldly gathered from 1950 through 2010 regarding when and where acne bacteria tends to exist and in what amounts. The patterns they found are intriguing and seem to suggest that acne bacteria, known as P. Acnes, may not cause clogged pores.

Over the past 60 years, various researchers have taken biopsies of “normal” skin, acne prone skin, and inflamed and noninflamed acne lesions, and then counted the bacteria they found. It turns out that across the vast majority of the 14 studies of this nature, acne bacteria is not always present, even in active acne lesions. A small but compelling percentage of acne lesions are “sterile” and contain no bacteria whatsoever.

Faced with this kind of consistent evidence, the authors hypothesize that acne bacteria does not initiate acne. How could it, they seem to ask us to ponder, if it doesn’t exist in all acne lesions?

However, the authors go on to state that after a pore has become clogged, acne bacteria can make the situation worse through a number of means, including increasing the skin’s cell production, causing stickiness inside the pore, and kicking inflammation into higher gear, amongst others.

So what causes acne? Is it our body’s immune response? Inflammation? Genetics? Vitamin/Mineral deficiency? The search continues…but as we move forward, let’s keep this evidence regarding bacteria in mind.

Are any of you wondering why it seems like your moisturizer isn’t working as well as it used to? You’re not alone. Every year around this time people come to me complaining that their moisturizer just doesn’t seem to be as powerful as it used to be. “Aha!,” I’ve exclaimed, in the nicest way possible of course, “It is not your moisturizer! It’s just winter.” It’s true that people experience increased dry skin in the winter. But this year I decided to do a little more digging to find out exactly why. As it turns out, there is startlingly little scientifically sound explanation to be found, and myths abound.  As is often the case, it falls to us to sift through the nonsense and make some sense of this issue.

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First, let’s dispell the myths:

When weather gets cold, it gets dry. This is claimed so often and by so many “reputable sources” that I almost took it at face value myself. But when I decided to double check this pervasive claim, it completely fell apart. I looked at historical charts of humidity levels across the United States throughout the seasons.* It turns out that humidity levels show no particular trend from summer to winter. In fact, in many cities, even Northern cities, humidity levels are higher in the freeze of winter than in the bask of summer.

The winter is blustery and wind dries out the skin. Many of us can recall experiencing our share of cold, windy winter days, and could swear that we experience “windburn”, characterized by dryness, redness, and irritation after being outside on these blustery days. But a look at the evidence forces us to consider other possible causes. The only experiment I could find was performed all the way back to 1937, and was published in Popular Science. Scientists founds through using a wind tunnel that wind alone does not create “reddening or chapping” of the skin. Furthermore, upon browsing through historical wind speed charts, I found that that much like humidity levels, wind speeds show no yearly trend. There is no evidence of higher winds in the winter months. Regardless of all this evidence against the wind creating redness, dryness, and irritation, many sources not only talk about the existence of windburn, but will even explain why it occurs. The most widely used explanation is that wind removes surface lipids (oils) from the skin. Exactly how the wind performs this feat is conspicuously absent from all of these articles. Furthermore, if wind is just as strong in the summer, why don’t people seem to experience windburn as much in the summer? Another common explanation that attempts to explain windburn, which is the current explanation on Wikipedia, is that windburn is actually just sunburn caused by the wind removing surface lipids (oils) which help protect us from UV rays (another claim I am yet to find evidence to support). While the wind can remove some of these surface lipids year round, they say, the removal of the surface lipids in the winter coincides with a season when we do not protect our skin as valiantly from the sun. Thus the redness and irritation people experience is simply a sunburn. This explanation is incomplete at best, and completely misinformed at worst. Yet another explanation, albeit less frequently posited, claims that wind removes sweat, which normally helps filter UV rays. Again, how sweat helps filter UV rays is conspicuously absent.

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Whew. So, now that we have gone through the myths, the fact remains that many people experience dryer skin in the winter. Why? After looking at all of the available evidence, I have a hunch it can be attributed almost entirely to:

Artificial heat: Mother nature can heat up or cool down the great outdoors while keeping humidity levels steady, but when we heat indoor areas, this lowers humidity. When you look at the science of relative humidity (I won’t bore you), this is how it works. For an everyday example, notice how when you heat your bathroom while taking a shower there is less steam in the air. Since most of us live and work in artificially heated indoor environments in the winter, it’s likely we experience long-term exposure to lower humidity environments during the winter months. This dries out the skin, causing many of us to wonder why our moisturizer isn’t working as well as it used to. Back to my original point, “It’s not your moisturizer!” And introducing my new, improved answer, “You’re living in lower humidity indoor environments in the winter!”

And what about the cold? Strangely, none of the authors or reporters writing about winter and dry skin mention the effect cold air itself has on the skin. However, I have a hunch extreme temperatures may figure into a complete explanation of why some people experience dry skin in the winter. When we expose our skin to freezing temperatures, the skin reacts through natural protective methods, most prominently by withdrawing blood from the surface of the skin to protect core temperature. This is the first step which ultimately leads to the skin freezing which causes frost bite and cell death. My hunch is that perhaps even during shorter duration exposure to freezing temperatures which people sometimes experience on cold days, the skin still reacts through a more mild form of cell death. This mild cell death, while not as apparent as the blisters caused by frostbite, is evidenced by flakiness or dryness as the dead cells flake off. The redness experienced by many people after exposure to winter weather, while it would require further research for me to be more definitive, could be the result of cell death or simply the body returning blood to areas where it has been withdrawn.

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So, what can we do about it?

1.  Humidify your home/workplace. Install a humidifying system into your central heat. Alternately, if you use wood burning stoves or kerosene heaters, you can place pots of water on top and let the water evaporate, then repeat. You can always boil a large pot of  water on the stovetop as well, being careful to keep a close eye on it of course. There are commercially available electric stand-alone humidifiers as well. 60% humidity is a good general goal to shoot for. You can measure humidity with widely available humidity measuring devices which are available at most hardware stores, or you can be more relaxed about it and just notice how you–and your skin–feel. When the humidity reaches a comfortable level you will feel less dry and generally more comfortable. You should also notice less static electricity, less shocks, and less frizz to your hair. An easy way to tell if you’ve gone too far and over-humidified your space is if your windows start to pool water at their bases.

Perk: Adequately humidified air feels warmer than dry air at the same temperature. In other words, you can get away with heating to a lower temperature.

2.  Use more moisturizer: An extra pump or two of moisturizer each time you apply should help.

3.  Add jojoba oil: Since jojoba oil does not evaporate, 5-6 drops of jojoba oil added into your moisturizer each time you apply it will provide a boost of all-day moisture support.

*Yes, I know. There is more to the world than the United States, but…well, okay fine, I have no excuse. I’ll make a note to look outside the U.S. for my next research-related blog. :-)

keratinocytes: human skin cells

Thanks to modern medical science, we know that for some reason, acne follicles tend to overproduce cells, which in turn stick together and cause a clogged pore and ensuing zit. But why does this happen? Scientists have performed very few studies in an attempt to figure this out.

I just got through reading what was only the second study to ever attempt to scientifically understand what happens inside acne follicles vs. control follicles. Researchers from the University of Leeds in England performed the study back in 1994. Unfortunately, I think this control follicles were poorly selected. The researchers took biopsies of acne follicles from the upper back of patients who were an average age of 22. The control follicles were taken from the chest of people who were an average age of 41 during open heart surgery. In my opinion, the vast difference in age and location of biopsy between the acne follicles and control follicles largely discounts this study. Regardless, the researchers did make a couple of interesting points when discussing what might cause acne-prone skin to overproduce cells.

1) When sebum production increases, as it often does in acne-prone individuals, the sebum, as it leaves the follicle, takes with it too many of the cells lining the follicle wall. The follicle then reacts by overproducing cells to counteract this loss.

2) Linoleate (a.k.a. linoleic acid, an essential fatty acid) deficiency in sebum: Researchers have discovered that sebum in acne-prone skin contains less linoleate than normal. One hypothesis is that when sebum increases, linoleate content is diluted, and this decrease in linoleate signals overproduction of cells.

But in reality if you asked these researchers to tell you what cases acne, I think if they’d honestly reply, “well heck, who knows…”

The more you read about the potential cause of skin cell overproduction and clogged pore formation, the more complex it becomes. We have the hormone system to look at, sebum overproduction, the skin’s inflammatory response, systemic vitamin and mineral deficiency, bacteria over-proliferation, or a combination thereof…the possibilites are endless and the list goes on and on.

So, if and when science does finally figure it out, will we uncover a silver bullet? Or is the cause of acne a combination of factors? I’ll keep reading and let you know what I find. Please do the same if you can and let me know what you find out.