Tuesday, December 30, 2008

7 Human Experiments of 2008 – Year in Review

A lot of this year's experiments had to do with food. (Photo by ToUsMiC Place)

The year 2008 is drawing to an end, which means it's time to take a look at the experiments of the past twelve months.

1. High-fat diet experiment

The first experiment I ended this year was the high-fat diet (read the conclusion here). The idea was to eat a diet high in fat and see what happens in terms of cholesterol and weight gain. On the menu were all the fats and oils your doctor warned you about: butter, cream, coconut oil and even lard. Saturated and oh so tasty.

As I increased my fat and protein intake, I got rid of a lot of carbohydrates. In the beginning of the experiment I removed potatoes, bread and pasta from my diet but still ate rice occasionally. As time passed, I stopped eating rice as well. Meat, fat, fruit and some vegetables were the staples of the diet, which made it a kind of a mix between Atkins and the Paleo diet. The one grain product I didn't give up (and still haven't) was beer, which I, as you may have noticed, consider a divine invention. I was on the diet for about a year and a half in total.

So what happened? Well, for one thing I proved my hypothesis that eating lots of fat does not make you fat. In fact, I lost a few kilos on this diet and got my body fat to less than 8%. My blood pressure levels rose from very low levels into the normal range, which I attribute to all the fat in the diet.

My cholesterol levels were in a pretty good shape, which means that eating cholesterol and saturated fat does not necessarily clog your arteries; once again, I propose it's the amount of carbs you consume with them that makes a difference. And the matter is not as simple as saying that high cholesterol levels are bad in general (or even that HDL is all good and LDL is all bad).

While I did eat some carbs (in the form of fruit and vegetables), my carbohydrate intake was considerably lower than that of most people. On the other hand, my fat intake (especially saturated and animal fat) was considerably higher than what is normally considered healthy.

2. Vitamin B experiment

In this experiment, I took up to 5 times the Recommended Dietary Allowances (or RDA) of the vitamin B complex just to see what happens. I increased the size of the doses as the experiment went on, but didn't notice anything – not even a niacin flush (read the conclusion here).

Looking back, this was a fairly boring experiment with no exciting results to report. I guess the take home message is that taking lots of vitamin B won't kill you. Not after a few weeks, at least.

3. Caloric restriction experiment

This experiment was one of the more difficult ones for me. My caloric restriction lasted only for a week, during which I reduced my calorie intake to 1,750 kcal per day. I quickly learned that the days of enjoying cheese and wine would have to be swept into the past if I were to succeed in the experiment. Some sleepless nights were spent thinking about food and how great it is to eat stuff.

The trick was to choose foods with a high satiety index and a low energy index, which means eating nutrient-dense foods with little calories. Raw foods (including meat) and salads seemed a good way to go about it, and after a while the hunger seemed to diminish. Still, the fact that I couldn't drizzle my much-loved olive oil over everything made me rather depressed.

What made the week even more difficult was the fact that I was out on most nights drinking beer, which is pretty high in calories but makes you even hungrier. The thing I hated most, however, was having to count the amount of calories in each meal. Yes, there are some good tools to do that, but weighing everything and entering it into the software was a huge hassle for me.

The benefits of CR seem pretty good (mice and rats have been shown to live longer, and the calorie-restriced monkeys look much younger and healthier than their counterparts), so if you're serious about life extension, you might want to give it a go. Some willpower is definitely required.

4. Weight gain experiment

Nicknamed "Fat camp" by yours truly, this experiment was meant to help me gain back the weight I lost on the caloric restriction diet. This, of course, not only meant eating more in general, but eating the very carbohydrates I had so passionately rejected before.

Surprisingly, gaining weight proved to be somewhat difficult for me. My appetite was not as great as it had been before going on CR, so there were times I almost had to force myself to eat. Trying a combination of protein, fat and beer (but no other carbohydrates) and not gaining weight also lead me to formulate my beer gut theory.

Eventually (after 43 days, to be precise), I managed to gain a few kilos and, in the dead of night, I escaped from the fat camp and left behind me the walls I had helped to build.

5. Biotin experiment

In this one, I took 5 mg of biotin daily to see whether it would have an effect on hair and nail growth. No studies have proven the claims circulating the internet about biotin making hair grow stronger, so naturally I had to test it on myself.

After a month the bottle was finished, and no results were visible. I concluded that it was ineffective, and that the positive effects I had read about were either due to some people being biotin deficient, in which case biotin supplementation really might help, or simply imagined.

6. MSM + chondroitin + glucosamine experiment

By this time, the idea of affecting hair and nail growth with supplements had intrigued me so much that I decided to start another experiment. This time I took a powder with MSM, chondroitin and glucosamine, which are claimed to improve joint health, increase the speed of hair and nail growth as well as make them thicker.

After I'd ran out of the disgusting sulfur cocktail (having seen no results), I bought a powder that had only MSM in it, since MSM is supposedly the key ingredient in terms of hair and nail growth. This increased my dosage from 1,000 mg to 4,000 mg. Even this large dose failed to show any results, which drove me to go overboard and take 8,000 mg of the stuff daily. The disappointing conclusion was that MSM did absolutely nothing except taste very bad.

7. Coenzyme Q10 experiment

In this experiment, I took 200 mg of coenzyme Q10 to see if it would have an effect on general health and exercise performance. There have been some suggestions in the scientific literature that it might increase lifespan, which made me even more interested, as did the fact that it has been used to treat gum disease.

The studies on coenzyme Q10 seem to be inconclusive, and as I reported in the conclusion, three months of supplementation had no effect on me; not health-wise, not exercise-wise. Since it's one of the more expensive supplements, I stopped taking it after I had finished the two bottles I purchased. It does seem like a promising supplement, however, and if I was older I would probably continue using it.

Currently ongoing experiments

The above is of course an incomplete of all the experiments started during this year, since I have several experiments going on as I write. They are listed in the up right corner of the page under the title Ongoing experiments, right below Latest posts.

I will write more about them as they progress and as they're finished. Meanwhile, you can cast your vote to help me decide what I should experiment with next. The options are ginkgo biloba, melatonin, quercetin and hyaluronic acid. If you'd like to read more about one of these, choose your favourite one and click "Vote". Or if your choice is not on the list, just drop a comment.

Until then, happy New Year!

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Monday, December 29, 2008

Coenzyme Q10 for Exercise & Better Health – Experiment Conclusion

The effects of CoQ10 supplementation on exercise are still unclear. (Photo by ericmcgregor)

This post marks the end of my experiment with CoQ10. The idea was to see whether taking coenzyme Q10 would have an effect on general health and exercise performance.

I've been taking 200 mg of CoQ10 (the ubiquinone form – for an explanation of the differences between different forms see this post) somewhat irregularly since summer. I actually had supplements to last me only three months, but I've had a couple of longer breaks in between to see whether I would notice a difference.

As with many other supplement experiments, I didn't. I've tried taking a capsule before going to the gym to see if it boosts my performance, but I haven't seen any noticeable effects. No effects from taking a capsule later in the day, either. This is not really surprising, since the studies on CoQ10 and exercise, though many, are inconclusive (for a more detailed discussion of CoQ10, exercise and oxidative stress, see this post).

Any other health benefits are pretty hard to tell, but I think it's safe to say that it hasn't made me immune to all disease, because I've caught a few colds during this experiment.

Still, I must say that the data on CoQ10 and older people is quite promising. Since levels of coenzyme Q10 drop with age and supplementation (especially with ubiquinol) seems to be an effective way to raise them, anyone over the age of forty would be wise to consider reading up on the possible benefits – and the negative effects of too little CoQ10 in the body.

However, at this point I don't see enough reason for me to continue taking it. The price is quite high, and the possible positive effects of CoQ10 on young, healthy people are mostly unknown.

I've saved the last remaining capsules to see whether rubbing the stuff on my gums does anything. The studies suggest that using CoQ10 both topically and orally promotes oral health, but during the months of eating the stuff I noticed no change in the small gingival pocket I have near one of my teeth.

Who knows, maybe topicals are the way to go here. Look out for an update in the coming weeks!

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Thursday, December 25, 2008

Green Tea, Black Tea & Oolong Tea Increase Insulin Activity by More than 1500%

If you like milk with your tea, I have bad news. (Photo by yoppy)

Increasing insulin activity is vital for those suffering from diabetes, but making sure one's insulin is working properly should be important to anyone interested in health.

Insulin is a hormone released by the pancreas when blood glucose levels rise. The purpose is to keep blood glucose in a normal range. It is insulin's job to tell the body's cells to take up glucose from the blood so that the levels return to normal.

In type 1 diabetes, the pancreas is no longer able to produce insulin. This causes higher blood glucose levels and eventually death, unless the missing insulin is replaced through injections or other methods.

In type 2 diabetes, the pancreas produces insulin, but normal insulin levels are inadequate to cause the cells to take up glucose from blood. This is known as insulin resistance, which can result in health problems ranging from coronary artery disease to blindness. One known cause of insulin resistance is obesity.

One way to keep insulin working properly is drinking tea. According to an in vitro study by Anderson & Polansky, black, green and oolong teas resulted in more than 15-fold increases in insulin activity.

The figure above shows that when added insulin was present, insulin activity was higher. However, when added insulin was absent, insulin potentiation was greatest. This means that when there was no added insulin, tea had the greatest effect on the activity of insulin.

As the strength of the tea increased, so did the insulin-enhancing activity, up to a point; the highest amount of tea leaves shows more activity than the lowest amount but less activity than the middle amounts.

The authors note that the most active components were epigallocatechin gallate (EGCg), followed by tannins, epicatechin gallate and theaflavins. EGCg was more than three times as effective as tannins and epicatechin gallate. Caffeine and catechin showed no activity.

When milk was added to the tea, insulin potentiation was decreased. One teaspoon (5 grams) of milk decreased activity by 33%, while 50 grams of milk decreased the activity by more than 90%. Both whole milk and skimmed milk had the same negative effect, as did nondairy creamers and soy milk. Lemon juice, on the other hand, had no effect.

Herbal teas, instant teas and iced teas showed no increases in insulin activity.

The authors mention that other studies have shown that when humans are given tea catechins prior to eating starch, the elevation of insulin is suppressed. So how can tea both increase insulin activity and suppress insulin levels? According to the authors, a possible explanation is that because tea increases the activity of insulin, less insulin is needed to get the same results as before. That is, when tea is present, the pancreas makes less insulin but the insulin does its job better.

So if you're drinking tea to keep your insulin levels and blood sugar in order, or to help with weight loss, drink your tea straight up or with lemon juice, but skip the milk. That's bad news for all the chai latte aficionados out there, but good news for those who get their camellia sinensis on old school style.

For more information on green tea and black tea see these posts:

Drinking 10 Cups of Green Tea Daily and Not Smoking Could Add 12 Years to Your Life
Black Tea is More Effective in Reducing Superoxide Dismutase than Green Tea
Green Tea Reduces the Formation of AGEs
Dental Health Effects of Green and Black Tea

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Tuesday, December 23, 2008

Intermittent Fasting Experiment – Update after 5 Months

During the fasting periods, there really is no spoon. (Photo by alicepopkorn)

It's now been over five months since I started my intermittent fasting experiment, which means it's time for an update.

To recap, when I started in August, I went straight for the 24/24 version of intermittent fasting. That means I eat for 24 hours and then fast for 24 hours. I usually either start or stop eating at 4 PM, so every other day I miss breakfast and lunch and every other day I miss dinner. On the other hand, I don't really think in terms of "three warm meals per day" anymore, so breakfast, lunch & dinner have sort of lost their meaning.

This kind of fasting is also known as alternate-day feeding (or ADF) in a lot of the mouse and rat studies. That's a fitting term for rodents, because they don't have the same sleep pattern that humans do; that is, they don't sleep 8 hours per night and then stay awake for 16 hours. Instead, they sleep short periods throughout the day and night and eat when they feel like it.

In humans true alternate-day feeding is difficult, because the fast would begin at 12 o'clock in the night and you'd have to go for an entire day without food. With intermittent fasting, where you can break or begin the fast in the middle of the day, you get to eat at least something each day. This makes it much more convenient for humans but still retains all the health benefits of ADF.

The obvious question in most people's minds is probably "What about the hunger?" Well, in the beginning hunger was certainly an issue. Even though caloric restriction had been much more difficult due to constantly being hungry and having to count everything, my first fasting periods were still somewhat hard to get through.

I then tried green tea and black tea, both of which were moderately effective at reducing the feeling of hunger. The best thing, however, was coffee, which not only reduced hunger but also improved my concentration and mood. I now start each morning with a cup of coffee, and it definitely has helped a great deal. I also drink green and black tea throughout the day, but it's mostly for other health benefits.

As much I love coffee and tea, the most important thing has been time. During the course of this experiment I've noticed less and less hunger during the fasting periods. I assume it takes a while for the body to get used to the new situation, where it suddenly isn't constantly provided with energy. Nowadays, I rarely feel extremely hungry even in the last few hours of the fast. Sure, I have a great appetite when it's time to eat again, but I feel very energetic during the fast. I've now even been able to hit the gym during a fast, which seemed quite difficult during the first two months.

At first I thought I felt less hungry because I was sleeping a lot (9-10 hours per night) and thus spending less energy. When I reduced my sleep to seven hours, I noticed I felt no more hungry, even though I spent more time awake (and got much more things done). In fact, I don't think I've ever felt so energetic during the dark winter months while sleeping this little.

So if you're considering giving intermittent fasting a go but have doubts about the hunger issue, rest assured that it will get easier with time. You could always start easy and fast for 12 hours, then 13, 14, etc. until you get to 24 hours.

One thing fasting unfortunately doesn't seem to have changed is the immune system; some people have said they haven't been sick since they started intermittent fasting or caloric restriction, but I'm currently fighting the flu virus unsuccesfully. Just in time for the holidays, too. Oh well, you can't have it all, can you?

Merry Christmas to everyone reading this blog!

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Wednesday, December 17, 2008

Getting Tocotrienols from Natural Food Sources: Is It Possible?

Barley is a decent source of tocotrienols. (Photo by nakae)

In my previous post about tocotrienols – a form of vitamin E – I mentioned I've begun taking a tocotrienol supplement to see whether it has an effect on hair growth.

If you're like me, you're probably wondering whether it's possible to skip the supplement and get tocotrienols from natural foods instead. In this post, I'm going to answer that question by looking at some of the studies.

Fruits and vegetables

A study by Chun et al. measured the tocotrienol content of tens of different fruits and vegetables sold in the United States. The results are a pretty depressing read: even the foods that scored the highest are still very low in their tocotrienol content. None of them are near the amounts found in the supplements currently available.

Among fruit, the winner was coconut, which had 0.79 mg of alpha-tocotrienols and 0.18 of gamma-tocotrienols per 100 grams. The second place went to cranberry with a gamma-tocotrienol content of 0.33 mg per 100 g. This means that to equal the amounts in Toco-Sorb and Toco-8, you'd have to consume about ten kilos of coconut or more than a hundred kilos of cranberry.

The winner of the vegetable category was frozen & blanched corn, which had 0.38 mg of alpha-tocotrienols and 1.02 mg of gamma-tocotrienols per 100 g. Canned corn kernels fared pretty well, too, with 0.12 mg of alpha-tocotrienols and 1.30 mg of gamma-tocotrienols. Still, you'd have to consume ridiculous amounts of these as well to get tocotrienols in any meaningful doses.

The study didn't mention beta-tocotrienols and delta-tocotrienols at all, but it's probably safe to say that their amounts were not that significant either.

Animal products

Compared to the dishearteningly low tocotrienol levels of fruits and vegetables, animal products don't seem to be much better. Ye et al. report:

Samples included raw and cooked bacon, all beef hot dogs, raw and braised pork loins, raw and pan fried pork liver, raw chicken, chicken hot dogs, chicken nuggets, patties and tenders, frozen, glazed chicken wings, and raw and baked Orange Roughy and Tilapia fillets, canned chunk light tuna and fish sticks. The data represents analysis of 130 samples collected through USDA sampling protocols.

Alpha- and gamma-tocotrienols were measurable in some chicken, processed chicken, bacon and pork loin but at levels usually less than 0.1 mg/100g. Frozen chicken patties (cooked and uncooked) contained more than 0.4 mg/100g alpha- and gamma-tocotrienol.

So most meat has just as little tocotrienols as fruits and vegetables. Who's ready for ten kilos of uncooked chicken patties?

Oils and fats

According to Chiew et al., crude palm oil contains 21.2 mg of alpha-tocotrienol, 30.8 mg of beta-tocotrienol, 63.0 mg of delta-tocotrienol and 8.3 mg of gamma-tocotrienol per 100 grams. During the refining process the amounts are reduced, but even refined palm oil beats fresh fruits, fresh vegetables and animal products.

I was unable to find actual studies on the tocotrienol content of other oils, but looking at the helpful figure over at tocotrienol.org, palm oil is clearly the best one in the fat group. Coconut oil the second best, but it's still miles away from palm oil and doesn't contain any delta-tocotrienols.

The rest of the oils, including my favourite, the ubiquitous olive oil, are absolutely useless in this regard.

Grains and seeds

The tocotrienol content of some grains and seeds, on the other hand, looks somewhat better.

A study by Frega et al. mentions that annatto seeds contain a respectable 140-147 mg of delta-tocotrienols per 100 g. Toco-Sorb and Toco-8 only contain about 15 mg of delta-tocotrienols, so a mere 10 grams of annatto seeds would be enough to get an equal amount.

However, the authors mention that most of the tocotrienols were of the delta form, so it might not compare to the supplements in other areas. Looking at annatto supplements this seems to be the case: usually 90% of tocotrienols in annatto seeds are delta-tocotrienols, while 10% are alpha-tocopherols.

According to tocotrienol.org, rice bran has 23.6 mg of alpha-tocotrienols and 34.9 mg of gamma-tocotrienols per 100 g. Barley has 67 mg of alpha-tocotrienols and 12.0 mg of both beta- and gamma-tocotrienols. These are much higher amounts than fruits, vegetables and meats have, but neither contain delta-tocotrienols. They're also not a particularly good choice if you're on any kind of low-carb diet, like me.


As you can see, getting tocotrienols from food sources is problematic. Fresh fruits and vegetables contain so little tocotrienols that we can just forget about them. Animal products don't seem to be of much help either.

The first thing that shows any promise is palm oil. This is hardly surprising, since Toco-Sorb and Toco-8 are both made from palm fruit extract. Still, you'd have to eat about 200 grams (about one cup) of palm oil to match the extracts used in the supplements. This would be almost 1,900 kcal in energy, so unless your diet consists of only palm oil (okay, you could throw in a few chicken patties as well), this is an unfeasible choice.

The next possible option are annatto seeds, which have 15 mg of delta-tocotrienol (the amount used in the supplements) per 15 grams. That's only 1-2 tablespoons. The problem with annatto is that it only has delta-tocotrienol and a small amount of alpha-tocotrienol.

Barley is also a decent choice, with 100 grams providing 67 mg of alpha-tocotrienol and a bit of beta- and gamma-tocotrienol. As you may know if you've read my blog, I'm not a big fan of eating grains and cereals, but if you wished to go this route, combining barley and annatto seeds looks like a viable option.

For now, I'm sticking with the supplements.

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Tuesday, December 16, 2008

Mixture of 5-Aminolevulinic Acid and Iron Increases Hair Growth in Mice

5-ALA is also used in photodynamic therapy to treat skin cancers. (Photo by Hamed Saber)

5-aminolevulinic acid (5-ALA) is a substance found in most organisms. It is used for plant growth as well as photodynamic therapy, since it increases sensitivity to light irradiation.

According to some studies, it might also help with hair growth. In a study reported in this month's issue of Journal of Dermatology, Morokuma et al. report:

Methods: The effect of a 5-ALA and iron ion admixture on hair growth and cell proliferation in mice was examined. The dorsal hair of 8-week-old male CeH/HeN mice was clipped, and a 5-ALA and iron ion admixture was applied to the dorsal skin once daily for 21 days in a room supplied with common room lights. Hair growth was later examined by calculating the ratio of the area showing hair growth to the total clipped area. For the cell proliferation assay, a 5-ALA and iron ion admixture at several different concentrations was added to a culture medium containing keratinocytes or fibroblasts, and the cell numbers were counted.

Results: Mice treated with an admixture of 5-ALA and iron ion showed significant hair growth, as revealed by the Tukey–Kramer test. The stimulatory effect of the mixture was almost identical to that of 5% minoxidil. No proliferation of keratinocytes or fibroblasts was observed, however, when an admixture of 5-ALA and iron ion was added to the medium.

Conclusions: The results suggest that an admixture of 5-ALA and iron ion stimulates murine hair growth in vivo independent of epithelial and mesenchymal cells, although the precise mechanism is still uncertain. This mixture has the potential to become a beneficial new treatment for alopecia.

Granted, this study was done on mice, but significant hair growth after only two weeks is still a promising result. Unlike other hair growth remedies like Asiasari radix (read about it here) and green tea (read about it here), 5-ALA does not seem to increase skin cell proliferation, which means it must work through some other mechanism.

Also, this study used a mixture of 5-ALA and iron ions, so some of the effect might be due to the iron ions. Unfortunately, I don't have access to the full study yet, so I can't say what kind of a mixture they used. Iron ions by themselves apparently did nothing, however.

There is also a rather vague abstract available of an article that appeared in Fragrance Journal in 2005. Author Tanaka reports:

It has been known that high-concentration dose of ALA easily metabolize into and are stored as protoporphyrin IX (PPIX), increasing sensitivity of light irradiation (use of photosensitizer for PDT). On the other hand, ALA with minerals such as iron increases activity of animals. We found remarkable hair growth stimulation effects in combination ALA and iron (Fe-ALA). We assume that Cytochrome induced from ALA and iron in mitochondria activates hair growth. We hope Fe-ALA will be new and effective hair growth promoter.

Cytochromes are a type of hemoprotein that carry out electron transport. The author suggests that 5-ALA and iron together increase cytochrome activity, which results in hair growth. I'm guessing the study was done on mice or rats, though the abstract doesn't mention anything about this. Judging by the mention of mitochondria and high-concentration doses, I assume they used 5-ALA orally instead of topically, unlike in the first study I mentioned.

Apparently the absorption of 5-aminolevulinic acid through the skin is quite low. There are, however, ways of improving the absorption. Tokuoka et al. suggest using l-menthol:

Enhancing effect of l-menthol and its derivatives, l-menthyl formate, l-menthyl acetate, and l-menthyl propionate, on skin permeation of 5-aminolevulinic acid (ALA) through Yucatan micropig full-thickness skin was investigated using a Franz-type diffusion cell. ALA solutions were prepared using ethanol-water mixed solvents with l-menthol or the derivative. Skin permeation coefficients (Kp) of ALA with more than 3.0 wt% of l-menthol was significantly larger than that without l-menthol. In addition, Kp of ALA with the derivative increased as follows: l-menthol ≍ l-menthyl propionate <>. These results suggest that l-menthol and the derivative are effective to enhance ALA skin permeation.

Adding l-menthol or one of its derivatives thus increased the absorption. The most effective form was l-menthyl acetate (which you can online, by the way). Another way of improving the skin delivery is reported by Pierre et al.:

PURPOSE: To optimize 5-ALA-PDT via improving the highly hydrophilic 5-ALA limited penetration into the skin, we propose the use of the known skin penetration enhancer, oleic acid (OA).

RESULTS: The flux and in vitro retention of 5-ALA in viable epidermis increased in the presence of 10.0% (w/w) OA. The amounts of PpIX, evaluated both by chemical tissue extractions and in vivo measurements by an optical fiber probe, increased after applying 5-ALA formulations containing 5.0 or 10.0% OA. Moreover, in vivo kinetic studies showed an increase in skin PpIX accumulation when formulations containing 10% OA were used; PpIX accumulation was also maintained longer compared to controls.

CONCLUSIONS: Both in vitro and in vivo results show the OA potential as an optimizer of 5-ALA skin delivery.

Oleic acid, which is what this study used, is a monounsaturated fatty acid found mainly in olive oil and grape seed oil. The results suggest either one might be effective as a carrier oil for the 5-ALA.

As far as I know, there are no hair growth products on the market that contain 5-ALA as one of the ingredients. However 5-ALA, though on the expensive side, is available for purchase from several manufacturers.

For more information on hair growth, see these posts:

Asiasari Radix Extract Grows Hair in Mice and in Human Skin Cells
Vitamin E Tocotrienols May Grow Hair in Humans
3 Quick Ways to Find Out Whether Your Hair Growth Product is Working
Green Tea Extract Grows Hair in Vitro, May Work in Vivo

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Asiasari Radix Extract Grows Hair in Mice and in Human Skin Cells

"Seek and ye shall find" is the hair loss researcher's motto. (Photo by Psymeg&Chooch)

There are probably hundreds of yet undiscovered plants that may aid in hair loss. The problem is, most of the time we don't even know where to look.

Fortunately, there are some scientists who are dedicated to collecting the strangest looking plants nature has to offer and making hair growth potions out of them. One of the less known plants that shows promise in treating hair loss is Asiasari radix, which is the root of the Asiasarum plant (known as Saishin in Japanese).

In a 2005 study from the Journal of Dermatological Science, Rho et al. report:


We examined the effects of 45 plant extracts that have been traditionally used for treating hair loss in oriental medicine in order to identify potential stimulants of hair growth.


Six-week-old female C57BL/6 and C3H mice were used for evaluating the hair growth-promoting effects of the plant extracts. Topical application onto the backs of the C57BL/6 and C3H mice was performed daily for 30 days and 45 days, respectively. Protein synthesis was measured by the cysteine uptake assay, using cultured murine vibrissae follicles. Proliferation of the immortalized human keratinocyte cell line (HaCaT) and human dermal papilla (DP) cells was evaluated by the MTT and thymidine incorporation assays. The mRNA levels of several growth factors that have been implicated in hair growth control were measured by reverse transcription-polymerase chain reaction (RT-PCR).


Among the tested plant extracts, the extract of Asiasari radix showed the most potent hair growth stimulation in C57BL/6 and C3H mice experiments. In addition, this extract markedly increased the protein synthesis in vibrissae follicle cultures and the proliferation of both HaCaT and human DP cells in vitro. Moreover, the A. radix extract induced the expression of VEGF in human DP cells that were cultured in vitro.


These results suggest that the A. radix extract has hair growth-promoting potential, and that this effect may be due to its regulatory effects on both cell growth and growth factor gene expression.

The authors first rubbed a 1% solution of Asiasari radix extract mixed in 40% ethanol on the backs of mice. According to the paper, the extract induced earlier telogen-to-anagen conversion, which means that the resting phase of the hair got shorter. It also increased the depth and size of the hair follicles.

One possible explanation for the observed hair growth is that the extract increased the uptake of cysteine, an amino acid, in mouse hair follicles cultured in vitro by 129%. Cysteine uptake has been shown to correlate with hair follicle growth.

The authors also tested the effect of Asiasari radix on human kerotinocyte cells and cultures of human hair dermal papilla cells. The proliferation of the cells increased by 106.5% and 115%, respectively. In layman's terms this means that the extract increased the number of cells that are involved in producing hair.

Vascular endothelial growth factor (or VEGF) expression was also increased by the application of the extract. VEGF plays an important role in angiogenesis, the growth of new blood vessels from pre-existing vessels. VEGF expression is typically higher during the anagen (growth) phase and lower during the catagen (shedding) and telogen (resting) phases of hair. It is not certain whether VEGF directly affects hair growth, but it has been suggested that one of the ways that Minoxidil works is by regulating the expression of VEGF.

Interestingly, Asiasari radix did not inhibit type II 5-alpha-reductase, which is the enzyme that converts testosterone to DHT. DHT, in turn, is the hormone that causes hair loss in those individuals who are genetically susceptible. This means that Asiasari radix grows hair through other mechanisms than reducing DHT.

As far as I know, there is currently no product on the market that has Asiasari radix in it, so for now you'll have to scout the Japanese woods and make your own Saishin potion.

For more information on hair growth, see these posts:

Vitamin E Tocotrienols May Grow Hair in Humans
3 Quick Ways to Find Out Whether Your Hair Growth Product is Working
Green Tea Extract Grows Hair in Vitro, May Work in Vivo
Mixture of 5-Aminolevulinic Acid and Iron Increases Hair Growth in Mice

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Friday, December 12, 2008

Vitamin E Tocotrienols May Grow Hair in Humans

This is what palm fruit looks like. (Photo by sarcozona)

How does vitamin E affect hair loss? Currently, very little information exists on the subject.

The reason is that no official studies have really been done. There is only one study, which is related to a recently granted patent by Carotech. The product related to this patent, Toco-8 is a palm fruit extract that contains both tocopherols and tocotrienols.

These forms of vitamin E are said to be more efficient than alpha-tocopherol, which is the most common (and potentially harmful, if recent studies are to be believed) ingredient in most vitamin E supplements.

Let's take a look at the patent. Ho et al. report:

Eleven volunteers were randomized to receive the tocotrienol formulation supplementation while 8 volunteers were in the placebo group. All volunteers were randomized to receive one capsule comprising either (i) a mixture of tocotrienols and alpha-tocopheral, or (ii) a placebo, twice daily after food over a period of at least 5 months. They were seen for an efficacy evaluation every month throughout the study. The control was a placebo capsule containing 600 mg of soya bean oil, and the tocotrienol formulation consisted of capsules containing a mixture of about 50 mg of tocotrienols and about 23 i.u. alpha-tocopherol.

At the end of the supplementation period, all volunteers in the tocotrienol formulation group had positive results, recording an increase in the number of hairs in the evaluation area. Seven volunteers (64%) showed regrowth of between 10-35% while 3 volunteers (27%) had 50% or greater regrowth. One volunteer had regrowth of more than 100%. The mean percentage of increase in the number of hairs is 42.4.+-.40.9% (mean.+-.SD). The increase is statistically significant (p<0.05)>0.05) in the number of hairs was detected between baseline and post-supplementation, thus indicating that the placebo effect did not occur during this study.

However, in terms of the weight of the hair, no statistically significant difference (p>0.05) between pre- and post-supplementation was detected for both groups of volunteers (tocotrienol and placebo). The mean percentage of weight increment was 16.4.+-.42.5% in the tocotrienol formulation group while that of the placebo group had an increase of 5.7.+-.40.1%. (Table 2).

The above-mentioned studies therefore indicate that supplementation with a formulation comprising a mixture of tocotrienol, alpha-tocopherol and pharmaceutically acceptable excipient appears to promote hair growth and increase the number of hair in persons experiencing hair loss.

According to the patent, all subjects in the tocotrienol group experienced hair growth, measured by the number of hairs on the scalp. The minimum increase was 10% and the highest increase was 100%. Average increase was 42%.

What is unclear to me is whether the "50 mg of tocotrienols" mentioned in the study means 50 mg of each tocotrienol or 50 mg total. In any case, the product they formulated based on this study contains the following amounts of tocotrienols:

30 mg d-alpha-tocotrienol
4 mg d-beta-tocotrienol
52 mg d-gamma-tocotrienol
14 mg d-delta-tocotrienol

It also has 30 mg (200% RDA) of d-alpha-tocopherol, which seems kind of high. It might be, though, that the dangers of d-alpha-tocopherol are present only when the other tocopherols and tocotrienols are not present. I'll look into this later.

Since this is a new product and not many know whether it actually works, I figured this is the perfect chance for me to conduct yet another experiment in the strange world of hair growth. Instead of Toco-8, I'm going to be taking a similar product by Jarrow Formulas called Toco-Sorb, which has the following amounts:

17.3 mg d-alpha-tocotrienol
2.6 mg d-beta-tocotrienol
31.5 mg d-gamma-tocotrienol
8.6 mg d-delta-tocotrienol

Looking at these numbers, I'll need to take two servings of Toco-Sorb to get the same amount of tocotrienols as with Toco-8. There's not much price difference between the two products: 60 servings of Toco-8 costs $29.95, while 120 servings of Toco-Sorb costs $30.74.

Toco-Sorb also promises 2-3 times better bioavailability through their "specialized lipid mixture". I have no idea whether this is true or not, but I'm guessing it can't hurt.

Go to next post on this experiment

For more information on hair growth, see these posts:

Asiasari Radix Extract Grows Hair in Mice and in Human Skin Cells
3 Quick Ways to Find Out Whether Your Hair Growth Product is Working
Green Tea Extract Grows Hair in Vitro, May Work in Vivo
Mixture of 5-Aminolevulinic Acid and Iron Increases Hair Growth in Mice

Read More......

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Wednesday, December 10, 2008

3 Quick Ways to Find Out Whether Your Hair Growth Product Is Working

If you wake up with this on your pillow, the product is not working. (Photo by How can I recycle this)

If you're slick bald, deciding whether or not a hair growth product is working is simple. Hair growing where it didn't? Product works. Scalp still a human solar panel? Product doesn't work.

However, in those who suffer (or think they might suffer) from general thinning, the matter is more complicated. To be able to judge the results of using a product just by looking in the mirror takes at least 6 months, more likely a year. That's because the hair cycle is so long. It takes patience.

A lot of people will try a product for a few months and stop using the product because they think the results aren't there. Most likely they'll then try another remedy – again for a few months – and just keep switching from one product to another. This, of course, tells them nothing about whether the products actually work or not. They might be effective but grow hair only after a year or so, or they may simply stop hair loss in its tracks (or just slow it down, but that would be very hard to objectively detect and isn't much help anyway).

The following tips are not perfect – far from it. They're not a match for the virtue of patience. Unless you notice an increase in hair loss, you should give any product at least six months before making the decision to quit using it.

They are, however, simple and helpful indicators of whether the product is working its magic or not. They should also give you some idea of the cause of your hair loss – genetics, inflammation or something else. Depending on how long your hair usually grows and how effective the product is, you might see changes in these indicators (or hair-o-markers as I like to call them) earlier or later.

So, let's take a look at what the three ways of measurement are.

1. Count the number of hairs you shed.

Before you embark on a great journey of hair growth, you should try to count as meticulously as possible the average number of hairs you normally lose each day. Why? Because this number will serve as a reference to which you will compare the number of hairs lost after having used the hair growth product for a while. Remember that anything up to a hundred hairs is considered normal.

Of course, noticing and counting every single hair you lose during the day is very difficult (unless you wear one of those hair nets to the office and count them at home). Instead, you could count the average number of hairs you lose in the shower, or the number hairs on your pillow in the morning. It's impossible to say what the "normal range" is in this case, but the important thing is to have an estimate of how much hair you lost before you started eating Rogaine with your cereal.

One of the things that happens with androgenic alopecia (and some other forms of hair loss) is that the anagen (growth) phase gets progressively shorter. So when a single hair used to grow for 5 years, the next generation hair from the same follicle grows only for 4 years, and then the next one for 3, etc.

And what does this have to do with the effectiveness of the product? If the hair growth product really is making the anagen phase longer, as they often are supposed to do, you should see a reduction in the number of hairs lost.

To see why this is so, imagine that the average anagen phase lasts only one day, after which the hair immediately falls off (this'd be the telogen phase). Now, if you have about 100,000 hair follicles, you'd see 100,000 hairs being shed each day. Let's say that the product doubles the length of the anagen phase, making it two days. You'd now see only 50,000 hairs on average being shed each day. You'd still need a nuclear bomb to clean your shower drain, but at least you'd have an indicator that the hair product is doing something.

2. Look at the thickness of the hairs you shed.

Another thing that happens with genetic hair loss is that the thickness of individual hairs produced by a hair follicle is progressively reduced. This process is known as miniaturization. It happens to most people as they age, whether or not they have androgenic alopecia or not – including women.

Since most hair loss remedies and growth products claim to increase the size of the hair follicle, you should see an increase in the thickness of the hairs. This can be difficult to detect just by looking at your head in the mirror, since how it looks will depend on things like lighting, the length of your hair, the dryness/wetness level of your hair, and the ridiculousness of the face you're making when you're doing it.

A much easier way is to look at the thickness of the hairs you shed. If you have photographic memory, great, but you could also save some of the hairs you shed before you start the experiment, so that you can compare their thickness to the ones you shed while you're rubbing raspberry ketones and fermented dog saliva on your scalp. You could even track the progression of your experiment by saving a couple of samples from different parts of the head every month. It's all about the scientific method, see?

3. Look at the length of the hairs you shed.

This kind of ties in with the first tip, but it's still a bit different. The length of the hairs you shed not only tells you how long the anagen phase of the hair was, it also gives you an indication of possible scalp inflammation. Whereas with androgenic alopecia the anagen phase gets slightly shorter with each hair cycle, with inflammation you might shed hairs before they reach the end of their natural growth phase. That is, hairs are being lost earlier than they normally would.

You could of course argue that inflammation merely shortens the anagen phase even further, and I wouldn't argue back, I would merely call you names for trying to be clever. The important thing is that if you notice you're losing a lot of hairs that are much shorter than they should be (i.e. shorter than the rest of the hair on your head), you might have a problem with inflammation. Some of the follicles are probably more resistant to inflammation than others, so you'd have some hairs being shed due to reaching the telogen phase and others being shed much earlier due to inflammation.

Of course, this tip really only makes sense if you keep your hair long enough to notice the difference. Otherwise even the hair that has been growing for years is still going to be short. In that case, looking at the thickness would make more sense, as inflammation can also cause the hair to grow thinner.


So there we have them, the three simple and time-efficient ways to keep track of whether you're growing hair or thinning further. Not exactly rocket science, but certainly an improvement over staring at your hair in the mirror in a semi-hypnotic trance.

As I've mentioned many times in my blog posts, subjective evaluations can be notoriously misleading (see, for example, this post). Hopefully these tips will balance things slightly towards objectivism.

Have other tips? Share them!

For more information on hair growth, see these posts:

Asiasari Radix Extract Grows Hair in Mice and in Human Skin Cells
Vitamin E Tocotrienols May Grow Hair in Humans
Green Tea Extract Grows Hair in Vitro, May Work in Vivo
Signaling Protein Ephrin-A3 Grows New Hair Follicles and Thicker Hair

Read More......

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Tuesday, December 9, 2008

1,000–8,000 mg of MSM Has No Effect on Hair & Nail Growth – Experiment Conclusion

Onions are a much tastier source of sulfur than MSM. (Photo by tanakawho)

This is the conclusion of my MSM experiment.

I've now been taking MSM powder for about four months. The idea was to see whether it has an effect on the growth of hair and nails, as it is claimed to do by some people.

Unfortunately, it doesn't.

I began the experiment by taking a powder that had 1,000 mg of MSM, 600 mg of glucosamine and 400 mg of chondroitin per portion (read about it here). I later started taking it with vitamin C (read about it here), which is sometimes suggested to increase absorption. After seven weeks, I hadn't noticed any effects (read about it here) on either hair or nail growth.

I then switched brands and bought a jar of pure MSM powder to increase the dosage. For three weeks, I took 4,000 mg of MSM, which was more than the amount given to the subjects in the study discussed below. I first took it all in one dose, and then tried separating it into two doses of 2,000 mg each (read about it here). Again, nothing happened.

Now, for the past three weeks, I've been taking a whopping 8,000 mg of MSM each day, which is more than I've seen or heard anyone else take. I've divided it into two doses of 4,000 mg, one taken in the morning and one later in the day.

No matter what the dose, I have seen absolutely no results from this foul-tasting powder during these four long months.

The rate of my hair growth has not increased; the rate of my nail growth has not increased; the thickness and brilliance of the hair has not increased; and the thickness and appearance of nails has not increased.

The study, which, as far as I know, is the only one studying the effects of MSM on hair and nails, doesn't seem to be peer-reviewed and is not available via pubmed. In the hair part of the study Lawrence reports:

INTRODUCTION: A total of 21 patients were studied for 6 weeks for the hair study component. The subjects were randomly assigned to either Group A (placebo) or Group B (LIGNISULMSM).

Sixteen of the subjects were men and 5 were women. Dosage was 3,000 mg/day in both Groups A & B.

The study participants were studied for hair length, brilliance, and diameter of the individual hair fibers using industry standard measurement scales at the beginning of the study period (t=0) and after 6 weeks (t=6 weeks).

RESULTS & DISCUSSION: Those subjects supplemented with LIGNISULMSM showed significant improvement in hair health, while those on placebo showed either no change, or only slight changes after 6 weeks. The most marked changes were measured in hair length and hair brilliance. The women showed the better results in hair growth, brilliance, and thickness of hair fibers.

All subjects supplemented with LIGNISULMSM were duly impressed with the changes in the health and appearance of their hair. The cosmetologists literally could differentiate which participants were on LIGNISULMSM by the appearance of the hair alone after 6 weeks.

It is expected that if the study were continued for 8 to 16 weeks, the results would have been even better for those on LIGNISULMSM as has been our past experience.

CONCLUSION: This pilot double blind, random study proves that oral supplementation with LIGNISULMSM is a valuable addition to hair care. Hair health was significantly improved in a short term of 6 weeks.

And then the nail part:

INTRODUCTION: A total of 11 patients were studied for 6 weeks for the nail study component. The subjects were randomly assigned to either Group A (placebo) or Group B (LIGNISULMSM). Dosage was 3,000 mg/day in both Groups A & B.

The study participants’ nails were measured for length, thickness, luster and general appearance using industry standard measurement scales at the beginning of the study period (t=0) and after 6 weeks (t=6 weeks).

RESULTS & DISCUSSION: Those subjects supplemented with LIGNISULMSM showed significant improvement in nail strength, thickness and appearance. Results would be better at periods of over 8 weeks from our clinical experience, but it was felt to be too difficult to keep clients enrolled in the study if it lasted longer than 6 weeks. This way we had no dropouts. Overall improvement rate was 80% even in this short study. All subjects supplemented with LIGNISULMSM stated they would continue to use LIGNISULMSM on an ongoing basis based on the improvement in nail health and appearance that was observed.

CONCLUSION: This pilot double blind, random study proves that oral supplementation with LIGNISULMSM is a valuable addition to nail care. Nail health was significantly improved by 80% overall in a short term of 6 weeks.

So according to the study, not only was MSM effective, it was effective in all participants receiving MSM. This bold statement by itself should make one very sceptical. Could it really have been that effective? How many other hair loss remedies have you heard of that claim to be 100% effective? That's right, none.

Both parts of the study mention using "industry standard measurement scales", but what exactly these measurement scales are is unclear. I assume they actually did measure things like hair thickness instead of just providing the subjects with a questionnaire. A subjective evaluation is almost meaningless when trying to estimate things like hair growth speed, since people are notoriously bad at making such evaluations themselves. Heck, a lot of people still think cutting their hair makes hair grow faster!

Still, even with assumed objective measurements we are left with some questions. How did they measure hair growth if the study only lasted for 6 weeks? How did they rule out seasonal variation? How does one measure "hair brilliance"? What does "nail luster" really mean?

So, based on the fact that only one study exists (and that the study may very well be flawed), and the fact that it had no effect on me, my conclusion is: it doesn't work. Certainly not in everyone, as the study suggests.

My first suggestion to anyone considering buying MSM is not to waste your money. Try something else instead, if you want to experiment (like green tea, for example).

My second suggestion is to take anecdotal evidence about MSM with a grain of salt. A lot of people who are experimenting with hair growth are taking all kinds of supplements, so even if they do see effects, there's no way of knowing whether it's the MSM or something else that's working. Besides, usually even the positive evidence is quite conservative ("I think my hair is growing faster, but I'm not sure"), which suggests people may just be imagining things.

Personally, I'm sort of disappointed it didn't have any effect on me. On the other hand, I'm glad I'm finally rid of it.

Having said that, if you've had positive effects from taking MSM, be sure to leave a comment and share your experience.

For more information on hair growth, see these posts:

Vitamin E Tocotrienols May Grow Hair in Humans
3 Quick Ways to Find Out Whether Your Hair Growth Product is Working
Green Tea Extract Grows Hair in Vitro, May Work in Vivo
Mixture of 5-Aminolevulinic Acid and Iron Increases Hair Growth in Mice

Read More......

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Monday, December 8, 2008

Green Tea Extract Grows Hair in Vitro, Might Work in Vivo

Green Tea Extract Grows Hair in Vitro, Might Work in Vivo
Rub this on your head and grow hair? (Photo by AMagill)

We've all heard about how Asians drink lots of green tea and usually have full heads of hair. Does this mean green tea improves hair growth?

Despite all the positive news about the health benefits of green tea, in my opinion the jury is still out on this one. Surprisingly, not a lot of studies have been done on green tea and hair growth in humans, especially when the green tea is topically applied.

In a recent study about green tea and human hair follicles, Kwon et al. report:

Green tea is a popular worldwide beverage, and its potential beneficial effects such as anti-cancer and anti-oxidant properties are believed to be mediated by epigallocatechin-3-gallate (EGCG), a major constituent of polyphenols.

Recently, it was reported that EGCG might be useful in the prevention or treatment of androgenetic alopecia by selectively inhibiting 5alpha-reductase activity. However, no report has been issued to date on the effect of EGCG on human hair growth. This study was undertaken to measure the effect of EGCG on hair growth in vitro and to investigate its effect on human dermal papilla cells (DPCs) in vivo and in vitro.

EGCG promoted hair growth in hair follicles ex vivo culture and the proliferation of cultured DPCs. The growth stimulation of DPCs by EGCG in vitro may be mediated through the upregulations of phosphorylated Erk and Akt and by an increase in the ratio of Bcl-2/Bax ratio. Similar results were also obtained in in vivo dermal papillae of human scalps. Thus, we suggest that EGCG stimulates human hair growth through these dual proliferative and anti-apoptotic effects on DPCs.

In this study, one of the main green tea catechins, epigallocatechin-3-gallate (or ECGC) was used topically in cultured hair follicles, cultured dermal papilla cells, and the scalps of human volunteers.

In cultured hair follicles, the application of a 95% green tea extract more than doubled the length of hair follicles. Hair growth almost tripled. In the cultured skin cells, the extract increased the growth of new cells in a dose-dependent manner.

The authors report that EGCG affects the expressions of Erk, Akt, Bcl-2 and Bax, and suggest that this effect may be the reason behind the results seen in follicle and skin cell cultures.

To see whether similar effects happen in vivo, the authors mixed 10% EGCG in ethanol and applied it directly onto human scalps. Again, significant changes in the expressions were seen, which means that if their theory about these expressions being the cause of hair growth, ECGC works both in vitro and in vivo. The authors conclude that ECGC stimulates hair growth through its proliferative and anti-apoptotic effects, and that ECGC may prolong the anagen stage.

So can you do the same thing at home? It seems so.

To make your own inhuman experiment, you'd need to buy a green tea extract with as much catechins as possible (95% ECGC was used in the study) and mix it with ethanol. All you need to do then is rub it on your head and wait for results.

If you decide to try it, let me know what happens.

For more information on green tea, see these posts:

Drinking 10 Cups of Green Tea Daily and Not Smoking Could Add 12 Years to Your Life
Black Tea is More Effective in Reducing Superoxide Dismutase than Green Tea
Green Tea Reduces the Formation of AGEs
Dental Health Effects of Green and Black Tea

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Saturday, December 6, 2008

How the Accumulation of Minerals Might Cause Aging in Humans

Is "overmineralization" the reason behind aging?

This 8-minute documentary film postulates the theory that human aging is due to "overmineralization" – the accumulation of minerals such as iron and calcium.

The excess iron theory has been suggested before as an explanation to why women live about 5 to 8 years longer than men. Because women lose iron through menstruation, their iron levels are constantly lower than men's. The theory says that there is not only a correlation but a causation between age and iron levels. Keeping iron levels low should thus slow down aging in men as well.

The most interesting point in the documentary is that during childhood years, when minerals are used by the growth process, biological aging has not really begun. Only when growth has stopped do minerals begin to accumulate in the body and begin to cause aging. The document further suggests that in later life the rate of aging actually declines, because mineral levels reach a certain point above which they don't accumulate further.

Keep in mind, though, that the video is also an ad for a product called Longevinex®, which is said to help with this overmineralization. The objectiveness of the film can be debated, but the theory itself is quite interesting.

For information on anti-aging and longevity, see these posts:

End Aging to End Anxiety: Filmmaker Jason Silva Talks about Immortality
Growing New Body Parts: Breakthroughs in Regenerative Medicine
Drinking 10 Cups of Green Tea Daily and Not Smoking Could Add 12 Years to Your Life
Green Tea Reduces the Formation of AGEs

Read More......

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Thursday, December 4, 2008

Black Tea Is More Effective in Activating Superoxide Dismutase (SOD) than Green Tea

Once you go green, you could always go black. (Photo by mckaysavage)

Green tea is all the rage these days, but there are some areas where black tea simply performs better.

One such area has to do with superoxide dismutase (SOD), an enzyme that repairs cells. Superoxide dismutase reduces the damage done to cells by superoxide, which is the most common free radical in the body. In addition to this antioxidant effect, SOD acts as an anti-inflammatory and is also involved in the production of skin cells.

In short, superoxide dismutase is a good thing. Even better is that tea, especially black tea, seems to increase its activity.

A study on rats by Zeyuan et al. reports:

During a 75 day feeding experiment of rats consuming diets with addinged green tea (GT), black tea (BT), and their water extracts (GTWE, BTWE), blood glucose was significantly decreased in all experimental groups, by averages of 23.9% in GT and GTWE and by 22.8% in BT and BTWE; the blood triglycerides were significantly reduced, by 33.3% in GT and GTWE and by 25.0% in BT and BTWE.

The activity of superoxide dismutase was significantly increased, by averages of 117.0% in BT and BTWE and 90.8% in GT and GTWE. However, malondialdehyde was significantly decreased, by averages of 34.6% in BT and BTWE and 25.4% in GT and GTWE.

This indicated that the ability of green tea to reduce blood glucose and blook triglycerides was higher than that of black tea in the aged rats but that the antioxidative ability of black tea was better than that of green tea in the aged rats.

What the above means is that while green tea was very effective in increasing SOD activity (almost a 100% increase), black tea was even more effective. Clearly, while the fermentation process removes some of the catechins in tea, it has some beneficial consequences as well.

Note that green and black tea also had positive effects on blood glucose levels, triglycerides and malondialdehyde.

For diabetics or those thinking of adding tea to their diet to help with weight loss, these results look quite promising. Reduced triglycerides from tea consumption is also good news. Here green tea wins, but black tea performed pretty impressively too; one third reduction for green tea and one fourth reduction for black tea. Nothing to sneer at. Malondialdehyde, which is a product of lipid peroxidation that is mutagenic and carcinogenic, was reduced more by black tea than green tea, although both showed significant reductions.

One thing to keep in mind is that the amounts used in this study were higher than the average tea consumption. The average tea drinker consumes about 6 grams of tea per day, which is equal to 3 tea bags.

The rats in the study, on the other hand, consumed 5, 10 and 20 times the human dose. SOD activity increased with the dosage in both green tea and black tea groups. However, even with the lowest dose of brewed black tea, which was only 5 times more than the average human consumption, SOD activity almost doubled; the larger doses did increase it even further, but not as significantly. When black tea leaves were mixed in the rat chow instead of feeding them brewed black tea, the effects were similar.

Green tea behaved somewhat differently. With brewed green tea, the lowest dose increased SOD only slightly, but the middle dose was more than twice as effective as the lowest dose. The highest dose didn't improve SOD further than the middle dose. When green tea leaves were consumed with the feed, the middle and high doses more than doubled SOD activity, but the lowest dose had only a slight effect.

Applying these findings to humans means that in order to get optimal results, you'd have to consume 60 grams of green or black tea (i.e. the middle dose), which is equal to a respectable 30 cups of tea per day. Unfortunately increases in bladder size were not studied.

Still, the results are impressive, and drinking 2-10 cups of tea (or taking a tea extract supplement) will very likely have at least some beneficial effect.

And if Earl Grey is more your cup of tea than Japanese sencha, these results are something you can relate to all your trendy friends who are hating on old-fashioned black tea for no good reason.

Read More......

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Wednesday, December 3, 2008

Signaling Protein Ephrin-A3 Grows New Hair Follicles and Thicker Hair

Could Ephrin-A3 help you grow your very own fur coat? (Photo by Stephen Barnett)

For those interested in the latest studies regarding hair loss, here's an interesting paper by Yamada et al. from this month's issue of the Journal of Dermatological Science:

Ephrin-A3 not only increases the density of hair follicles but also accelerates anagen development in neonatal mice

BACKGROUND: Ephrins are cell-membrane-bound ligands for Eph receptor tyrosine kinases (Eph). Although ephrins are known to regulate a variety of developmental processes, little is known of their role in hair development. Previously, we studied the gene expression of dermal papilla cells from androgenetic alopecia and found that ephrin-A3 was significantly down-regulated.

OBJECTIVE: To characterize the expression of ephrin-A3 in the hair cycle and evaluate the effect of ephrin-A3 on hair growth.

METHODS: We investigated gene expression and protein expression of each ephrin-As and EphAs in the skin of neonatal mice through the first and second hair cycle using quantitative PCR and immunohistochemical analysis, respectively. We also injected ephrin-A3 protein into the skin of neonatal mice and demonstrated the effect of ephrin-A3 on hair follicle development.

RESULTS: Expression of ephrin-A3 revealed a rapid increase at the beginning of the anagen phase, a peak during the mid-anagen, and a rapid fading during the telogen phase. In addition, we found ephrin-A3 protein was expressed in the developing hair follicles with a characteristic spatiotemporal localization. Furthermore, injection of ephrin-A3 into the skin of neonatal mice markedly accelerated the differentiation process of hair follicles. In addition, injection of ephrin-A3 unexpectedly increased the number of hair follicles.

CONCLUSION: These findings demonstrated that ephrin-A3 not only accelerates anagen development but also increases the density of hair follicles, and also suggested that an ephrin-A-EphA signal pathway is closely involved in hair follicle development.

What the study says is that ephrin-A3 – a signaling protein – is expressed more when the hair follicle is in its growing (anagen) phase and less in its resting (telogen) phase. When this protein is injected into the skin, three things happen: new hair follicles are formed, the hair follicles grow deeper, and hair grows thicker.

The results look promising, but how and when these results can be applied to humans remains yet to be seen.

For more information on hair growth, see these posts:

Asiasari Radix Extract Grows Hair in Mice and in Human Skin Cells
Vitamin E Tocotrienols May Grow Hair in Humans
Green Tea Extract Grows Hair in Vitro, May Work in Vivo
1,000-8,000 mg of MSM Has No Effect on Hair & Nail Growth - Experiment Conclusion

Read More......

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Tuesday, December 2, 2008

Coconut Lowers LDL, VLDL and Triglycerides, Raises HDL

All coconut products seem to be beneficial for cholesterol. (Photo by yimhafiz)

There is some confusion over whether coconut products like coconut oil, coconut water and coconut flakes raise or lower cholesterol levels. The traditional wisdom is that all saturated fats raise cholesterol, and as coconut is high in saturated fat, most people expect it to raise cholesterol.

However, in recent years, this theory has been criticized as more and more studies have shown beneficial effects from saturated fats and negative effects from polyunsaturated fats. Coconut especially seems to have positive effects on cholesterol and triglyceride levels. Trinidad et al. report:

This study investigated the effect of coconut flakes on serum cholesterol levels of humans with moderately raised serum cholesterol in 21 subjects. The test foods were as follows: corn flakes as the control food, oat bran flakes as the reference food, and corn flakes with 15% and 25% dietary fiber from coconut flakes (made from coconut flour production).

Results showed a significant percent reduction in serum total and low-density lipoprotein (LDL) cholesterol (in mg/dL) for all test foods, except for corn flakes, as follows: oat bran flakes, 8.4 ± 1.4 and 8.8 ± 6.0, respectively; 15% coconut flakes, 6.9 ± 1.1 and 11.0 ± 4.0, respectively; and 25% coconut flakes, 10.8 ± 1.3 and 9.2 ± 5.4, respectively. Serum triglycerides were significantly reduced for all test foods: corn flakes, 14.5 ± 6.3%; oat bran flakes, 22.7 ± 2.9%; 15% coconut flakes, 19.3 ± 5.7%; and 25% coconut flakes, 21.8 ± 6.0%.

In conclusion, both 15% and 25% coconut flakes reduced serum total and LDL cholesterol and serum triglycerides of humans with moderately raised serum cholesterol levels. Coconut flour is a good source of both soluble and insoluble dietary fiber, and both types of fiber may have significant role in the reduction of the above lipid biomarker.

What this study shows is that oat bran flakes and coconut flakes reduced LDL and triglycerides. Coconut was the most effective in reducing LDL, while oat bran was most most effective in reducing triglycerides. Looking at the full paper, HDL levels were slightly reduced in all subjects, but the authors conclude that this change was insignificant. Corn flakes reduced triglycerides but did not have a lowering effect on LDL (in fact, there was a statistically insignificant increase).

Coconut water seems to have a similar effect, at least in rats. Sandhya & Rajamohan report:

The purpose of this study was to determine the effect of coconut water feeding in cholesterol-fed rats. Male albino rats were fed tender coconut water and mature coconut water at a dose level of 4 mL/100 g of body weight.

Cholesterol feeding caused a marked increase in total cholesterol, very low-density lipoprotein (VLDL) + low-density lipoprotein (LDL) cholesterol, and triglycerides in serum. Administration of coconut water counteracts the increase in total cholesterol, VLDL + LDL cholesterol, and triglycerides, while high-density lipoprotein cholesterol was higher. Lipid levels in the tissues viz. liver, heart, kidney, and aorta were markedly decreased in cholesterol-fed rats supplemented with coconut water.

An increased rate of cholesterol conversion to bile acid and an increased excretion of bile acids and neutral sterols were observed in rats fed coconut water. Histopathological studies of liver and aorta revealed much less fatty accumulation in these tissues in cholesterol-fed rats supplemented with coconut water. Feeding coconut water resulted in increased plasma L-arginine content, urinary nitrite level, and nitric oxide synthase activity. These results indicate that both tender and mature coconut water has beneficial effects on serum and tissue lipid parameters in rats fed cholesterol-containing diet.

Again, LDL and triglyceride levels were reduced. Especially important is that the harmful form of LDL, very low-density lipoprotein (VLDL) was lowered when coconut water was present in the diet. Unlike the previous study, this one also showed an increase in HDL levels.

Cox et al. compared the effects of butter, coconut fat and safflower oil on cholesterol:

Objective: The aim of this present study was to determine plasma levels of lathosterol, lipids, lipoproteins and apolipoproteins during diets rich in butter, coconut fat and safflower oil.

Design: The study consisted of sequential six week periods of diets rich in butter, coconut fat then safflower oil and measurements were made at baseline and at week 4 in each diet period.

Subjects: Forty-one healthy Pacific island polynesians living in New Zealand participated in the trial.

Results: Plasma lathosterol concentration (P<0.001), p="0.04),"> Plasma total cholesterol, HDL cholesterol and apoA-levels were also significantly (P£ 0.001) different among the diets and were not significantly different between butter and coconut diets.

Conclusions: These data suggest that cholesterol synthesis is lower during diets rich in coconut fat and safflower oil compared with diets rich in butter and might be associated with lower production rates of apoB-containing lipoproteins.

The figures in the full paper show that total cholesterol and LDL levels were highest during the butter diet and lowest during the safflower oil diet. On the other hand, VLDL levels were highest during the safflower oil diet and lowest during the butter diet; so even though butter seems to raise LDL, it doesn't raise VLDL, which is the one harmful form of LDL. Coconut oil values were somewhere in the middle between butter and safflower oil values.

As for HDL and triglycerides, coconut oil takes the cake. HDL levels were highest during the coconut oil diet, and lowest during the safflower diet, while triglyceride levels were highest during the butter diet and lowest during the coconut diet.

So what should we make of all this? Based on these studies it seems pretty clear that coconut – regardless of whether it's coconut water, coconut oil or coconut flakes – reduces LDL, VLDL and triglycerides and slightly raises HDL. This is exactly what you'd want to happen with your cholesterol levels.

These results certainly suggest that coconut is good for cholesterol and at the same time cast doubt on the claims about saturated fat always being harmful.

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