The Forgotten Anti-Aging Classic: Retinoids Are the Skin's Best Friend

Before you whip out $150 for a Goji berry skin cream, how about giving retinoids a go? (Photo by km !)

When it comes to skin care, retinoids appear to be a true star. A star among useless junk floating around the space we call cosmetics.

What other compound has decades of research behind it and been shown to actually reduce wrinkles? I can't think of any. What I can think of is new products that promise the world and cost a fortune constantly being advertised in health magazines, in the hopes that middle-aged women with deep wallets and an insatiable thirst for looking younger would fall for their marketing claims.

And they do. These anti-aging, youth-restoring, skin-plumpening, illness-curing magical creams and gels in their tiny little jars sell like there's no tomorrow. The price tag is unimportant, as long as the wrinkles will be gone.

But of course, a hundred bucks later, the wrinkles will still be there, ready to absorb the next product with its new moleculer structure that will revolutionize the cosmetic industry. I shake my head in amusement and disbelief at this sight of desperate women grabbing stacks of hard-earned or divorce-obtained cash from their Louis Vuitton purses and throwing them at salespersons, demanding to be lulled into a false dream of a wrinkle-free tomorrow.

Okay, so maybe I'm exaggerating here (I've never seen them actually throw cash), but you get the point. Why is not everyone using retinoids if they wipe the table with everything else? Maybe they aren't that good after all. Maybe it's yet another marketing trick. Maybe they were lying about retinoids too!

To find out the truth, it's time to take the red pill and do a quick review of some of the studies on retinoids, before I once again plunge myself into the wonderful but scary world of skin care in the form of an experiment. Yes, I will be trying the stuff on myself.

What are retinoids?

Retinoids are derivatives of vitamin A – that is, they are chemical compounds related to vitamin A. We absorb retinoids from foods, mainly animal sources, in the form of retinyl esters, which are then hydrolized to yield free retinol. Retinol, along with retinal, tretinoin, isotretinoin and alitretinoin, form a class known as first-generation retinoids. Etretinate and acitretin form the second generation, while tazarotene, bexarotene and adapalene form the third.

Topical retinoids were originally approved by the FDA for treating acne, but it was quickly realized that retinoids improved the skin in other ways too. Currently, three prescription-strength retinoids are available and sold under various brands: tretinoin (Atralin, Avita, Retin-A, Retin-A Micro, Renova), tazarotene (Avage, Tazorac), and adapalene (Differin). Retinol creams are generally available without a prescription, but they are also less potent.

How do retinoids work?

One mechanism behind some of the beneficial effects of retinoid is an increase in the thickness of the skin. Even though retinoids actually thin the stratum corneum – the strong, flexible and dry outermost surface of the skin – they thicken the epidermis and the dermis underneath it (link). The end result is a thicker, more youthful looking skin.

Retinoids are also powerful exfoliators. They help peel off dead skin cells on the surface of the skin and increase the turnover of keratinocytes (link). Keratinocytes, the major cells in the epidermis, move from the basal layer to the epidermis, where they differentiate and then die. The cells are thus constantly exfoliated naturally as new keratinocytes form at the basal layer. Retinoids speeds this process up and gets rid of old cells to give room to younger, healthier cells.

Furthermore, retinoids increase the production of hyaluronic acid (link, link) and collagen (link). Together they give the skin a more hydrated and firmer appearance. Retinoids also stimulate dermal fibroblasts, which are cells that make the structural framework of animal tissues (link), and replaces disorganized collagen fibers with new, well-organized fibers (link). Angiogenesis, the formation of new blood vessels, improves blood flow to the skin and is the reason behind the healthy, rosy glow reported by tretinoin users (link).

What can retinoids do for my skin?

Okay, enough technical talk; how does all this translate into real life? While retinoids are succesfully used to treat conditions such as acne vulgaris and to improve wound healing, they also have several skin health benefits in normal persons with signs of skin aging. Here's a list of positive effects seen in retinoid users, as reported in the literature (e.g. link, link, link, link, link):

• Increased skin thickness and firmness
• Increased skin hydration
• Increased skin tolerance to external factors
• Reduced visible signs of sun damage
• Reduced fine wrinkles
• Restoration of even skin tone and reduced hyperpigmentation
• Reduction in dark circles under the eyes
• Reduced skin roughness
• Reduced irritation from shaving
• Less risk of skin cancer
• Reduced stretch marks
• A healthy, 'rosy glow'

In one self-assessment, 83% of the participants rated their skin as improved after 6 months of using 0.05% tretinoin. With continued use, fine lines and coarse wrinkles keep improving, and as mentioned before, the epidermis and dermis thicken significantly. The effects are not only cosmetic in nature, as is the case with products like moisturizers, but rather reflect the fact that underlying damage is being actively repaired.

How to use retinoids

Prescription retinoids come in varying strengths: 0.025%, 0.05% and 0.1%. Since retinoids can cause skin irritation, they may take some getting used to, especially with stronger creams and gels. Common symptoms are exfoliation, stinging, burning, redness and itching, but they generally start to subside within 2 to 6 weeks. Even the strongest concentration seems to be tolerated quite well after a while (link). No abnormalities in the skin have been reported even after years of continued use, making tretinoin safe for long-term use (link).

Many people start with 0.05% strength, and if they find it too irritating, switch to 0.025%. If your skin is very sensitive, consider starting with the 0.025% and gradually moving to higher concentrations. Or, alternatively, start by using the product only every other day or even twice a week and then switch to daily use once your skin is accustomed to it.

Many of the studies have used 0.05% tretinoin with good results, but stronger creams may be even more effective (link). Retinol causes little to no irritation but produces weaker results (link). One study suggests isotretinoin, which is commonly used orally but is also available as a topical gel, may be more effective than tretinoin (link). Retinoid gels in general appear to be stronger than creams, so a 0.05% gel may be more irritant (but also more effective) than a 0.05% cream.

It is recommended that retinoids are applied in the evening or at night rather than in the morning. Some people say the reason is because they increase susceptibility to photodamage, but I haven't found evidence to support this claim. Rather, a good reason not to apply it in the morning is that retinoids themselves are degraded by sun light. Before applying, it's also recommended to wait 15-20 minutes after washing your face, presumably to reduce absorption and thus irritation.

My retinoid experiment

To see if all the pro-retinoid hype is really true, I'm going to try retinoids on myself. But, instead of just applying it on my face and trying to remember what I looked like before I started using retinoids, I'm only going to apply the product on the left side of my face.

Or, to be precise, I have two products I'm going to be testing: tretinoin cream (0.05%) and tretinoin gel (0.05%). Both are generic versions from alldaychemist.com, which sells them without prescriptions (hooray for individual choice!). I'm starting off with the cream to see how well my skin can handle retinoids in the first place.

For more information on skin care, see these posts:

Topical Vitamin C for Skin: Re-examining the Case
Silica for Hair, Nails & Skin: BioSil vs. JarroSil
How I Accidentally Grew Hair on My Left Temple with Retinol – Experiment Conclusion
Coconut Oil Is Better than Olive Oil for Atopic Dermatitis

Sugar and AGEs: Fructose Is 10 Times Worse than Glucose

Beware – apples are high in fructose. (Photo by Simon Pais-Thomas)

The search for answers to the AGE mystery continues. So far, we've seen that even though cooked meat is high advanced glycation endproducts, people who eat meat still have lower levels of AGEs circulating in their body than vegetarians.

One suggested explanation for this is that AGEs produced inside the body (known as endogenous AGEs) are more important than AGEs formed during cooking (known as exogenous AGEs). Specifically, the literature points to fructose being worse than glucose when it comes to AGEs. That could explain how people eating lots of fruit and no meat can still have high levels of AGEs.

It seems to be common knowledge that fructose is ten times more prone to glycation than glucose once inside the body. But is this number correct? To find out, it's time to look at some studies that have actually compared glucose and fructose in terms of endogenous AGEs.

First, a bit of background. Glycosylation is the enzymatic process that links sugars with proteins in a controlled way. Glycation, on the other hand, is the nonenzymatic linking of sugar molecules with proteins in a random way. As the name implies, glycation is the bad boy behind the formation of AGEs.

It was already known in the 1980's that glucose was not the only sugar capable of combining with proteins. Studies had shown that fructose could react with proteins in aqueous solutions and form colored, fluorescent derivatives. What was not clear was whether fructose could react nonenzymatically in mammalian tissues to form random crosslinks the same way glucose does.

The authors of an early study showed that fructation does indeed happen (link). And not only that, but also that fructose can actually cause more crosslinking than glucose:


Graph A above shows fluorescence in bovine ribonuclease from fructose and glucose, while graph B shows crosslinking from fructose and glucose. Fluorescence, which appears to happen after crosslinking and is used as a marker of AGEs, can be readily detected in skin collagen as we age (link). Combined with reduced cell proliferation, it gives aged skin that thin and fragile look. The squares in the graphs show what happened when hexose was removed from the solution, and the triangles show what happened with hexose removed and D-penicillamine added.

Here, the formation of fluorescence is about three times as great for fructose than glucose, but covalent, non-disulfide crosslinking was induced 10 times more rapidly by fructose than by glucose. On the other hand, when the authors tested them in human serum albumin, it was glucose that reacted at 8 times the rate of fructose, for reasons that are not entirely clear.

A paper published one year later concluded that the rate of protein-bound fluorescence generation was 10 times greater with fructose than with glucose (link). The authors also state that fructation converts Amadori products, which are intermediate steps in the whole process, to AGEs faster than glycation. So not only does fructose form more AGEs than glucose, it forms then faster than glucose.

Some of the discrepancies between the results from different papers may have to do with the inaccuracy of methods of measurement. One paper points out that two common glycation assays, serum fructosamine and phenylboronate affinity, would accurately measure only glucose-derived Amadori products (link). These measurements would routinely and misleadingly show glucose to produce 4- to 20-fold more Amadori products than fructose. One reason for this is that Amadori products from glucose and fructose are chemically different; the former is a ketone and the latter is an aldehyde.

The second reason is that, as mentioned earlier, Amadori products from fructose form AGEs faster than those from glucose. Therefore, looking only at the Amadori product step of the process will give the wrong picture, because some of the glycation is still in the Amadori products when fructation has already moved on.

The authors then compared the effects of both fructose and glucose on fluorescence. The authors' analysis shows that fructose is indeed much more prone to glycation than fructose:


At day 8, the difference appears to be about 8-fold. At day 24, it's about 3-fold. As the authors note, this is certainly bad news for diabetics who substitute fructose for glucose, thinking fructose is safe just because it doesn't raise insulin like glucose does. As we've seen here, things are more complicated than what they seem.

Another paper looked at the effect of glucose and fructose on fluorescence and protein-bound carbonyl groups (link). The latter are intermediate products that are featured in the formation of all AGEs. Again, the results show fructose to be much more prone to glycation than glucose:


Note that not only is the fructose graph much higher than the glucose graph, the amount of fructose was only 25% of the amount of glucose used. Exact figures are not reported, but seeing as after ten days, carbonyl formation and fluorescence appear to be a little over twice as great with just one fourth the fructose, fructose would be 8-9 times more effective than glucose. This is consistent with the earlier results.

Another paper states that fructose forms carboxymethyllysine (CML), a type of non-crosslinking AGE, up to 17 times more effectively than glucose (link). CML is a handy marker for AGEs in general, as they can be formed through glycation, fructation or lipid peroxidation, making it possible to compare various sources of AGEs.

To summarize, the claim that the ability of fructose to form AGEs is 10-fold greater than that of glucose does not appear to be too far off. In the case of fluorescence, which happens after AGE formation, the figures in the literature are consistently in the range of 8 to 10. For crosslinking, the 10-fold increase seen with fructose vs. glucose supports this, while for CML, the reactivity of fructose may be even higher.

For more information on AGEs and aging, see these posts:

AGE Content of Foods
Eating Meat or Going Vegan? Comparing AGE Levels in Vegetarians and Omnivores
The 7 Types of Aging Damage That End up Killing You
Yerba Mate Inhibits AGE Formation

Emu Oil vs. Hair Again® Topical Gel: Hair Growth Battle Conclusion

We put a man on the moon, so why can't we grow hair? (Photo by Zach_MancesterUK)

This post marks the conclusion of the hair growth battle between emu oil and Hair Again®. The idea was to see whether either product would promote hair growth as advertised.

For the past eight months, I've been applying Hair Again® topical gel on my left temple and emu oil on my right temple. Given that the rather small can of gel has lasted me this long, it's obvious there have been occasions when I've forgotten or just decided not to use it. In particular, I've skipped applying the gel and the oil when I've washed my hair, because they tend to make my hair look greasy.

Nonetheless, I believe this is a long enough time to see results. And, since I've only applied the gel to a small area, it's not too surprising it has lasted so long. I should note that at first, I only used it on my temple, but about halfway through the experiment, I started applying it on my left eyebrow as well. In addition, I've used it on the small gap in my hairline which seems to run in the family. I occasionally but rather inconsistently applied the emu oil to my right eyebrow.

So what about the results? Well, the first observation is that nothing positive has happened on the right temple. I know emu oil is touted as some kind of ancient remedy of the Aboriginees, claimed to improve wound healing, skin wrinkling and hair growth, but I saw no such effects. It's supposed to permeate the scalp skin easily, but I found it to leave a very greasy feeling for a long time, especially if I used it on my face. Granted, the skin on the temples and on the scalp may be different, and perhaps it really does feel good on the scalp, but used in the way I used it, I can't say I liked the product.

In fact, on more than one occassion, I noticed an itching feeling and small red bumps from irritation on my right temple after applying the emu oil. That didn't happen when I put it on my face, where it just left a greasy residue. There was no change in skin smoothness and no increase in eyebrow growth.

With Hair Again®, things were a little more interesting. As you may know, I managed to grow a couple of new hairs on my left temple using a retinol cream from the same company. Those hairs are still there, and while I'm not sure whether I'd classify them as vellus or terminal hairs, they have grown to over 2 cm in length. Since the gel I used for this experiment also contains retinol, I was expecting results at least as good as with the ordinary retinol cream.

The full ingredient list is pretty impressive: coenzyme Q10, superoxide dismutase, retinol, vitamins E & D3, glutathione, beta glucan, beta carotene, beta-sitosterol, quercetin, progesterone, and melatonin. Most of these have studies behind them showing that they have the ability to grow hair in vitro, and getting all of them in one product is not a bad deal at all. But as everyone who has been tried hair growth products on themselves knows, in vitro studies rarely translate into hair growth in vivo.

And such was the case here as well. Unlike emu oil, the gel is absorbed quite nicely, and despite its yellowish color, doesn't leave your skin yellow. However, after months of use, it's still uncertain whether the product actually does anything. If I look really closely, I think I can see some vellus hair growing on the temple that weren't previously there, but the effect has definitely been more modest than with the retinol cream. Furthermore, my eyebrows have not thickened, and nothing has happened with the small gap in the hairline.

It could, of course, be that these ingredients only work on the scalp where hair is already growing. Maybe there is a crucial difference between the temples and the hairline and say, the crown. Certainly, many people report that they have more success with hair loss treatments in filling in crowns than temples and receding hairlines.

However, since it clearly is possible to grow new hairs on the temples – an area affected by androgen receptors just like the rest of the scalp – using retinol, one of two explanations come to mind: either the amount of retinol is too small, or the rest of the ingredients cancel the effect. To my knowledge, all the ingredients in the gel work by reducing androgen receptors or DHT (again, in vitro) and not by promoting hair growth per se, like minoxidil does. The fact that I saw no thickening of the eyebrows supports this view.

Therefore, my suspicion is that no matter where you apply the product, it will have a weak cosmetic effect at best. You might grow some vellus hairs, which could be useful, but I doubt it will reverse your hair loss. And if you just want to grow some vellus hairs, you might want to go with pure retinol instead. Or retinoids, if you're willing to risk some skin irritation in the beginning.

Anyway, I'm glad that the experiment is finally over, and I can move on to new and more exciting experiments. I already have a couple of good ones planned. I'll keep you posted.

For more information on hair growth, see these posts:

Eclipta Alba Extract Grows Hair Quicker than Minoxidil
Tea Tree Oil vs. Korean Red Ginseng – Hair Growth Battle Conclusion
Silica for Hair, Nails & Skin: BioSil vs. JarroSil
2% Nizoral Shampoo Increases Hair Growth More than 2% Minoxidil

Should Saturated Fat Be Avoided in Low-Carb Diets?

Butter fat is about 12% myristic acid, which increases both LDL and HDL. (Photo by No. Meds)

Browsing through older issues of Nutrition & Metabolism, I came across an interesting article on saturated fats. It's a commentary to another article, titled "The case for low carbohydrate diets in diabetes management" (link). In the original paper, the authors argue that low-carb diets are better than traditional low-fat, high-carbohydrate diets for weight loss, blood pressure, metabolic syndrome and dyslipidemia. They also note that low-carb diets reduce triglycerides and increase HDL.

However, the authors are skeptical of the popular Atkins diet, because of its potentially high saturated fat content. Their recommendation is to limit saturated fat consumption and to use monounsaturated and polyunsaturated fats instead. So, while they succesfully dispel common myths about low-carb diets, they still propagate the myths about saturated fat being detrimental to health.

The authors behind the commentary, Volek and Forsythe, go over several myths about saturated fat and cholesterol (link). While they commend the authors of the first paper on their observations on low-carb diets in general, they note that restricting saturated fat is unnecessary.

The reason is that much of the bad reputation of saturated fat comes from overgeneralizations and misinterpretations of the data. To make a statement like "saturated fat is bad for you" doesn't really tell us much. Even if we narrow it down to saturated fat being bad for cholesterol, it still just leaves us with more questions.

Is all saturated fat bad or just some? Does the amount of saturated fat matter? Do combinations of different saturated fats behave differently than single saturated fats? And importantly, what does "bad for cholesterol" mean exactly – does it increase total cholesterol, increase LDL, decrease HDL, or something else entirely?

While the commentary doesn't answer every possible question on saturated fat and cholesterol, it does shed light on some of these questions. Since I was so inspired by this article, I've also referenced quite a few related studies not mentioned in the commentary.

First, there are different types of saturated fat. One way of categorizing fats is according to their carbon chain length, and this factor plays a part in how fats affect cholesterol levels. For example, stearic acid, which has an 18-carbon-chain (C18) and is found especially in meat and cocoa butter, does not raise cholesterol levels (link). Palmitic acid (C16) and myristic acid (C14) seems to raise cholesterol the most (link, link). Depending on the study, the cholesterol-raising effect of lauric acid (C12) is either slightly lower (link) or higher than that of palmitic acid (link). Clearly, saying that all saturated fats behave the same way is an oversimplification.

Second, the dietary context in which saturated fat is consumed plays a crucial part. Nobody eats only saturated fat. The lipid profile will depend not only on the amount of saturated fat, but also on the ratio of protein, fat and carbohydrates. Replacing carbohydrates with any fat will lower fasting triglycerides, and replacing carbs with saturated fat also raises both HDL and LDL (link). When total fat intake is relatively low, increased saturated fat intake is associated with less progression of atherosclerosis (link). Interestingly, the same study also showed that when replacing carbohydrates or protein, polyunsaturated fats were not associated with progression of atherosclerosis, but when they replaced other fats, they were.

In addition, it might makes a difference which other fatty acids are consumed with saturated fats. For example, when palmitic acid is consumed with linoleic acid (an unsaturated omega-6 fatty acid), it ceases to increase cholesterol levels (link). When dietary olive oil is replaced with palm oil, which is high in palmitic acid, no change in cholesterol is seen (link), possibly because other fatty acids are also present in the average diet.

The form in which the saturated fatty acid comes is also important. In a synthetic form, myristic acid raises total cholesterol less than palmitic acid (link). However, when compared to palm oil, myristic acid raises total cholesterol more (link). All this goes to show that it's surprisingly difficult to draw conclusions about how saturated fat from natural sources affects cholesterol levels based on studies using single fatty acids.

The third and final point is that the effect of saturated fat on total cholesterol levels is not very interesting, since total cholesterol is a poor predictor of disease. Rather, it's the effect on triglycerides, the LDL/HDL ratio, and the size of lipoprotein particles that we're mostly interested in. And, unfortunately for those who are scared of saturated fat, reducing saturated fat intake decreases HDL, especially large HDL (link). On the other hand, increasing saturated fat intake decreases triglycerides, increases HDL size (link) and increases LDL size during low-carb diets (link). High HDL combined with large LDL and HDL particle size is common among people who are long-lived (link).

As for how individual saturated fatty acids affect these factors, different studies report different findings. Most reviews on the subject agree that all saturated fatty acids except stearic acid increase LDL (link). Lauric acid has been shown to increase especially HDL (link), while stearic acid was shown to improve the ratio of total cholesterol to HDL more than palmitic or myristic acid (link). In fact, palmitic acid doesn't seem to change HDL one way or the other, whereas myristic acid increases it, albeit less than it increases LDL (link).

So, to wrap things up, the take home messages of the above are:

1. The effect on cholesterol depends on the length of the carbon chain: in general, stearic acid is neutral, while palmitic acid, myristic acid and lauric seem to increase total cholesterol.
   
   
2. Saturated fats don't exist in a vacuum: all the other stuff in the diet will also make a difference in how cholesterol levels are affected by saturated fat.
   
   
3. Make sure you know what you're trying to achieve: if avoiding saturated fat, care should be taken to minimize reductions in HDL levels and lipoprotein particle size.

Of course, looking at individual fatty acids doesn't really tell us much about how saturated fats from food sources like meat, coconut, palm fruit, and butter affect cholesterol levels, but as I'm running out of time and space here, that'll have to be a subject for another post.

For more information on fat and cholesterol, see these posts:

SAs, MUFAs vs. PUFAs: Fat Storage Depends on Type of Fatty Acid in Rabbits
Blood Test Analysis: The Cholesterol and Saturated Fat Issue Revisited
Low-Carb vs. Low-Fat: Effects on Weight Loss and Cholesterol in Overweight Men
Anthocyanins from Berries Increase HDL and Lower LDL

Capsaicin and Soy Isoflavones Promote Hair Growth

A teaspoon of dried chili pepper has enough capsaicin to increase IGF-1. (Photo by Giuliagas)

This is the third post in a series about the effect of soy on hair growth. So far, we've seen that soy protein reduces DHT in men, and that soy isoflavones reduce DHT but increase testosterone in mice. While this seems like a good thing from a hair loss perspective, it doesn't guarantee that eating soy will actually prevent balding. So, time for some more studies.

The paper we'll look at today suggests that a combination of isoflavones and capsaicin grows hair in mice and in humans (link). The mice received capsaicin via injection and isoflavones through their diet, while the human participants took both orally as supplements.

Study method

For the mouse study, the mice were divided into three groups: one received capsaicin only, the second received capsaicin and isoflavones, and the third was a control group. Though the full paper doesn't explicitly state soy isoflavones anywhere and just talks about isoflavones in general, the "Fujiflavone P40" product they used in the diet is extracted from soy beans, so we can assume that the results apply to soy isoflavones.

The human study included 48 volunteers, 25 men and 23 women. 34 suffered from androgenetic alopecia (AGA), 13 from alopecia totalis (AT), and one from alopecia areata (AA). The participants were randomly divided into two groups: the first one received 6 mg capsaicin and 75 mg isoflavone daily, and the second received placebo only.

Capsaicin and IGF-1

Insulin-like growth-factor 1 (IGF-1) is involved in promoting hair growth in humans and animals. Indeed, mice that have been genetically modified to overexpress IGF-1 develop hair follicles earlier than controls, and humans with an IGF-1 deficiency have sparse hair growth. One explanation is that IGF-1 produced by dermal papilla cells might promote hair growth through stimulation of keratinocyte proliferation in hair follicles.

When the mice in this study were administered capsaicin, their dermal levels of insulin-like growth-factor 1 (IGF-1) increased significantly. On the other hand, CGRP-knockout mice did not show increased IGF-1. The authors suggest that increased CGRP, or calcitonin-gene related peptide, production leads to increased IGF-1, which in turn leads to hair growth.

In mice, the combination of capsaicin and isoflavone increased IGF-1 more than capsaicin alone. This makes sense, since isoflavone increases CGRP production. In humans, IGF-1 levels were increased after 5 months in the participants taking capsaicin and isoflavone orally, while they were not increased in those receiving placebo.

Capsaicin, isoflavone and hair growth

After four weeks of treatment, the rats receiving either capsaicin or capsaicin and isoflavone had grown more hair then the control rats. Consistent with the observed increases in IGF-1, the combination of isoflavone and capsaicin was more effective than capsaicin alone.


The leftmost image above shows three of the control rats after 4 weeks. The center image is of the capsaicin group, and the rightmost image is of the capsaicin + isoflavone group.

After 5 months, hair growth was significantly increased in 64.5% of human volunteers administered with capsaicin and isoflavone, compared with 11.8% in the placebo group. Furthermore, 88% of the participants suffering from androgenic alopecia saw a promotion of hair growth when given capsaicin and isoflavone. This suggests that the treatment might be more effective for male-pattern baldness than other types of hair loss. Below are some samples of the humans treated with oral capsaicin and isoflavones.


The upper left picture (a) is of a 54-year-old male with androgenic alopecia. That's a pretty significant result right there. The picture in the upper right corner (b) is of a 29-year-old male with alopecia totalis. Some hair growth is evident, but not a full recovery. The lower left corner (c) is of a 39-year-old female with androgenic alopecia, showing some thickening of the crown area. The lower right corner (d) is of a 40-year-old female with alopecia areata.

Conclusion

A combination of soy isoflavones and capsaicin increases dermal levels of IGF-1 and promotes hair growth in humans and mice. While some in vitro studies have suggested IGF-1 to be deleterious to hair growth, this study shows that the result may be different in vivo.

The amounts used in the study are quite reasonable. Chilli, cayenne pepper and red pepper contain between 0.1 mg to 60 mg capsaicin per gram (link, link, link, link). Given that a tablespoon of ground spice weighs about 8 grams, one tablespoon of ground chili pepper would contain anywhere between 0.8 mg and 480 mg of capsaicin. The hotter the pepper, the more capsaicin it contains.

As for soy, the best source of isoflavones are soy beans, which contain about 200 mg isoflavones per 100 grams (link). Tofu contains ~35 mg per 100 grams, while soy milk contains only ~9 mg. Thus, to get the 75 mg used in the study, you would either need to eat about 40 grams of soy beans (dry weight), a little over 200 grams of tofu, or a little less than a liter of soy milk.

Both capsaicin and soy isoflavones (mainly daidzein and genistein) are also commonly available as supplements.

For more information on soy, cayenne and hair growth, see these posts:

Do Flax Lignans Reduce Hair Loss from MPB?
Soy Protein Isolate Reduces DHT in Healthy Young Men
Green Tea and Capsaicin Reduce Hunger and Calorie Intake
Emu Oil and Hair Growth: A Critical Look at the Evidence