Antioxidants and Intermittent Fasting – Good For Longevity?

Are blueberry antioxidants beneficial for intermittent fasting? (Photo by Simply Bike)

Is it possible to live longer by combining the benefits of intermittent fasting (IF) and plant polyphenols? A new paper claims that taking polyphenol antioxidants during dietary restriction increases the lifespan of mice more than dietary restriction alone. The antioxidants used in the study were blueberry, pomegranate and green tea extracts.

The subject of the paper – "Potentiation of dietary restriction-induced lifespan extension by polyphenols" – is certainly enough grab the attention of anyone interested in life extension. The abstract seems promising too (link). Here's a quote:

Dietary restriction (DR) extends lifespan across multiple species including mouse. Antioxidant plant extracts rich in polyphenols have also been shown to increase lifespan. We hypothesized that polyphenols might potentiate DR-induced lifespan extension. [––] Polyphenol compounds may potentiate IF-induced longevity by minimizing specific components of IF-induced cell stress.

Let's look at these claims in more detail. First off, it's not clear from the abstract what exactly the authors mean by "dietary restriction". The full paper, however, reveals that they use the term to describe pretty much any kind of diet where access to food is limited, including traditional calorie restriction and intermittent fasting.

The longevity confusion

The problem with that opening sentence is that dietary restriction extends lifespan across multiple species only when it equals calorie restriction. That is, you can make a mouse live longer by only feeding every other day, as long as it results in less calories consumed. This is an important distinction, because many people – including longevity scientists – keep propagating the myth that intermittent fasting has the same benefits as calorie restriction. It doesn't. The reason that IF prolongs lifespan in some species is because the animals fail to compensate for the missed calories on their feeding days.

The next sentence is just as problematic. Yes, plant antioxidants have been shown to increase lifespan, but the question is, compared to what? So far, no one has succeeded in exceeding the known maximum lifespan of mice by feeding them antioxidants. Instead, what we see in many studies is that the antioxidant group lives longer than the control group.

The problem is that almost always, neither group lives very long. Poor diets, poor animal husbandry, poor environment – all play a role in how long the animals live. So, in essence, the antioxidants merely make the unhealthy mice a bit healthier. But this is like making a human live 70 years instead of 60 years by giving them some veggies with his daily bread and then claiming that "vegetables extend human lifespan".

Comparing lifespans

That said, there are some interesting figures in the full paper. The graph below shows the survival rates of the three groups; one fed the control diet, the second fed the same diet but only every other day, and the third fed a diet supplemented with polyphenols every other day:

There's a big drop in the survival rate of the control group around 22 months. For the IF groups, the survival curves look a lot better. So how does this compare to the average lifespan of similar mice kept in good laboratory conditions? Here's a graph of age ranges and survivorship of C57BL7/6J mice (the same strain used in this study):

This survival curve is based on a cohort of 150 male and 150 female mice. As you can see, at 28 months half of the mice are still alive. That's about 850 days, which is a pretty normal figure for mean lifespan of this strain of mice in the literature.

Once again, in the antioxidant study the control group dies earlier than is normal. For some reason, half of the mice are dead at 22 months instead of 28 months. One possible reason is the use of a high-fat diet to "mimic the effects of a Western diet", as the authors put it. This seems like a strange idea to me, because a typical Western diet is no more a high-fat diet than it is a high-carbohydrate diet. Furthermore, plenty of humans (myself included) seem to do quite well on a high-fat diet, whereas with mice it's somewhat different.

The survival curve of the IF mice in the first graph is slightly better than that of the normal-fed mice in the second graph. But that is hardly a surprise, given that both the IF group and the IF + antioxidant group had lower body weights than the control group. In other words, the intermittent fasting once again made the mice eat less than the control group, which in turn resulted in a slightly longer lifespan. It's good to keep in mind, however, that with just 10% calorie restriction longer lifespans have been reported in other studies, so the result is not too impressive.

Conclusion

Perhaps the most interesting result is that the IF + antioxidant group lived slightly longer than the IF group. There's no concensus as to whether it's a good idea to combine CR or IF with antioxidants. It may be that plant polyphenols are essential for optimal nutrition and good for activating sirtuins (which play at least some role in longevity), but there is also some evidence suggests that taking antioxidants may interfere with hormesis and thus diminish the effects of CR.

In this study, the antioxidants had a beneficial effect. While the IF diet by itself activated pro-inflammatory pathways, adding plant polyphenols to the diet blocked this effect. The authors identified 20 gene sets that were down-regulated by the addition of polyphenols, most of them related to immune response, inflammation, cell differentation and tumorigenesis. 

This suggests that if you're doing intermittent fasting, adding some blueberries, pomegranates and green tea to your diet may not be such a bad idea. Note, however, than the mice did not have access to polyphenols during their fasting days, so this study tells us nothing about taking antioxidants during fasting. It also doesn't say much about how polyphenols affect regular calorie restriction without IF in humans.

For more information on intermittent fasting and longevity, see these posts:

Lithium in Drinking Water May Lead to Longer Life
Does Intermittent Fasting Increase Lifespan?
Alternate-Day Feeding and Weight Loss: Is It the Calories Or the Fasting?
Slowing Down Aging with Intermittent Protein Restriction

Read More......

Guest Post: Natural Alternatives for Arthritis Treatment

Glucosamine is also found in seashells. (Photo by DavidRPhoto)

Guest post by Emily Matthews

Glucosamine sulfate and chondroitin sulfate have long been used as supplements to ease the pain of arthritis. Both compounds are found naturally in animal cartilage and glucosamine can also be found in seashells. A person who wishes to increase the amount of glucosamine and chondroitin in their diet should take them together as supplements, but only from a reputable manufacturer of vitamins and supplements. Medical professionals are uncertain as to the dosage for the average person.

Chondroitin

Chondroitin is a more complex molecule than glucosamine. It's made up of intact or hydrolyzed glycosaminoglycans with attached sugar molecules. Studies from masters degree programs show that it’s not as effective as glucosamine in treating arthritis, as the body doesn’t absorb as much of it; chondroitin is such a large molecule that it's difficult to pass through the normal intestinal barrier. The benefit of chondroitin comes because at least some of it can be broken down into glucosamine in the digestive track.

Glucosamine

Glucosamine is a simple molecule made up of glucose and an amine, which is a building lock of protein. The main effect of glucosamine is to stimulate the creation of glycosaminoglycans, which helps cartilage remain spongelike and act as a cushion between joints. As some people age, their bodies lose the ability to manufacture glucosamine and so the cushioning effect of cartilage is lost. Some studies claim that glucosamine supplements are more effective than placebos or non-steroidal anti-inflammatory drugs in easing arthritis pain

GAIT Trials

In a recent study, the National Center for Complementary and Alternative Medicine conducted the Glucosamine Chondroitin Arthritis Intervention Trial, or GAIT to see if glucosamine and chondroitin sulfate gave any benefits in the treatment of arthritis of the knee. The study was conducted to see if the supplements, used alone or separately, eased the pain of 1583 sufferers of this form of arthritis.

In GAIT, the people who participated in the double blind trial took glucosamine alone, chondroitin sulfate alone, the two supplements together, the prescription drug celecoxib, or a placebo. The results of the trial were that celecoxib significantly reduced the pain of knee arthritis and that glucosamine and chondroitin, taken alone or separately, were no better than the placebo in reducing pain. However, there was a small group of participants with what they described as "moderate to severe pain" who found that the glucosamine and chondroitin sulfate combination reduced their pain significantly.

The efficacy of glucosamine and chondroitin in treating arthritis is uncertain. Glucosamine seems to provide some relief for some arthritis sufferers. Chondroitin is too large a molecule to be absorbed by the body in any appreciable amount. If the glucosamine and chondroitin combination works for some people, it’s probably because enough chondroitin is broken down to increase the effect of the glucosamine.

Emily Matthews is currently applying to masters degree programs across the U.S., and loves to read about new research into health care, gender issues, and literature. She lives and writes in Seattle, Washington.

For more information on glucosamine, chondroitin and arthritis, see these posts:

Green Tea Protects Cartilage from Arthritis in Vitro
Green Tea Protects from Arthritis in Rats
MSM + Chondroitin + Glucosamine for Hair & Nail Growth - Results after Seven Weeks
MSM + Chondroitin + Glucosamine: A Sulfur Cocktail for Hair and Nails

Read More......

Green Tea Polyphenol Heals Stomach Ulcers

Green tea is a good candidate for treating stomach ulcers. (Photo by toughkidcst)

Non-steroidal anti-inflammatory drugs (NSAID) are generally used for treating pain and reducing fever. The most common NSAIDs are aspirin and ibuprofen. While effective, these drugs have some pretty nasty side effects. For example, up to one in four regular users develop a chronic gastric ulcer at some point.

In addition to causing gastric, peptic and duodenal ulcers, NSAIDs also delay ulcer healing. In the United States, upper gastrointestinal problems from non-steroidal anti-inflammatory drug use result in 16,500 deaths every year. What's worse, almost half of the prescriptions for NSAIDs are estimated to be unnecessary. Anti-ulcer drugs, on the other hand, are expensive and do not prevent the ulcers from recurring.

In a recent Indian study, the effectiveness of the anti-ulcer drug omeprazole and one of green tea's polyphenols, epigallocatechin gallate (EGCG), was compared in mice (link). The mice were first given enough of a NSAID called indomethacin to cause stomach ulceration. After that they were split into three groups: the first group was given a standard effective dose of omeprazole (3 mg/kg), while the second group was given EGCG in various doses (0.5–5 mg/kg). The third group acted as the control group and was given no treatment.

After three days, the ulcers of the mice in the control group had not healed at all. The omeprazole-treated mice had healed ~75% of their stomach ulcers. The effectiveness of the green tea polyphenol was dose-dependent: with 3 mg/kg, the ulcers healed as effectively as with omeprazole, while the largest dose (5 mg/kg) resulted in ~82% healing.

Non-steroidal anti-inflammatory drugs cause gastric ulcers through a variety of mechanisms. They increase the production of reactive oxygen species (ROS), increase lipid peroxidation and cause an imbalance in cytokines which regulate the immune system. In this study, EGCG improved all three factors even more effectively than omeprazole.

Although both omeprazole and epigallocatechin gallate have antioxidant properties, the mechanisms through which they work differ from each other. The main reason omeprazole works is because it reduces the production of gastric acid, whereas green tea is said to increase gastric acid release. While more studies are probably needed, the authors of the paper consider EGCG a promising candidate for treating stomach ulcers because it has not been shown to have negative side effects even with large doses (although there are potential problems with high-dose green tea extracts).

For more information on green tea, see these posts:

Green Tea Protects from the Psychological Effects of Stress in Rats
Tea, Coffee and Cocoa: All Good for Your Teeth
Green Tea and Capsaicin Reduce Hunger and Calorie Intake
Green Tea Extract Increases Insulin Sensitivity & Fat Burning during Exercise

Read More......

Biotin Goes Back on the Menu

Is there evidence behind biotin and hair growth? (Photo by Martin Neuhof)

Long-time readers of the blog may remember that one of the earliest experiments I did was with biotin, also known as vitamin B7. The purpose was to see whether taking a biotin supplement would affect nail and hair strength.

I wrote back then that although a lot of people seemed to believe biotin is good for hair and nails, there were no studies showing it really did anything except in rare cases when the subject was biotin deficient. After two weeks, I posted a quick update. When I'd been taking 5 mg for a month, I concluded the experiment. As you might expect, I didn't see any results.

I've since learned that one month is way too short for any kind of results when it comes to hair growth experiments. In most cases, six months would be the minimum, otherwise you're just wasting money without really learning anything new.

A pubmed search on biotin and hair growth still doesn't come up with any interesting studies. The only thing biotin seems to be proven to do is help with uncombable hair syndrome (link):

We report a family affected to the fourth generation by uncombable hair syndrome. This syndrome is characterized by unruly, dry, blond hair with a tangled appearance. The family pedigree strongly supports the hypothesis of autosomal dominant inheritance; some members of the family had, apart from uncombable hair, minor signs of atopy and ectodermal dysplasia, such as abnormalities of the nails. The diagnosis was confirmed by means of extensive scanning electron microscopy. A trial with oral biotin 5 mg/day was started on two young patients with excellent results as regards the hair appearance, although scanning electron microscopy did not show structural changes in the hair. After a 2-year-period of follow-up, hair normality was maintained without biotin, while nail fragility still required biotin supplementation for control.

In this study, 5 mg biotin was taken daily. Even much smaller doses seem to be helpful for uncombable hair syndrome, however (link):

Three children are reported with uncombable hair syndrome, consisting of slow-growing, straw-colored scalp hair that could not be combed flat. The hairs appeared normal on light microscopy but on scanning electron microscopy were triangular in cross section, with canal-like longitudinal depressions. Oral biotin, 0.3 mg three times a day, produced significant improvement after 4 months in one patient, with increased growth rate and with strength and combability of the hair, although the triangular shape remained. The other two patients were unique in having associated ectodermal dysplasia. Their hair slowly improved in appearance and combability over 5 years without biotin therapy.

These studies confirm the fact that biotin does play a part in hair growth, and that it's possible to affect even the growth rate through biotin supplementation. Although the cause of uncombable hair syndrome is unknown, a biotin deficiency (perhaps due to genetic reasons) may play a part. On the other hand, the syndrome often improves by itself with age.

Studies like this do not really warrant supplementing with biotin if you're suffering from androgenic alopecia or just want to make your hair grow thicker and faster. And yet a lot of people seem to believe biotin will do the trick. They keep saying there's "a lot of evidence" for biotin and hair growth, but the references are missing. The actual studies are always about biotin deficiencies or like the ones I quoted above.

However, a while ago I came across one study from 1992 that actually looked at the effect of biotin supplements on hair loss. It's no wonder I didn't find it earlier, since it's not indexed in pubmed. Nor do I have access to the full paper, but here's the abstract:

An examination of the effect of biotin on alopecia and hair quality.

The effect of a daily oral dose of 2,5 mg biotin was studied in 93 patients with the symptoms hair-loss (mostly androgenetic alopecia) and reduced hair quality. The mean duration of treatment was 7,9 +/- 2,8 months. An obvious improvement of hair-loss was reported in 64%, and a slight improvement in 9%. Hair quality was clearly improved in 70% and slightly in 12%. Brittle finger nails as an additional complaint were improved in 80%. If alopecia, decreased hair quality and brittle finger nails occurred in combination, improvement was observed frequently collectively. The study allows - as already shown in a previous investigation concerning brittle finger nails - to suggest biotin as an effective and well tolerated therapy in cases of alopecia and decreased hair quality.

The majority of subjects had improvements in hair loss and hair quality from taking 2.5 mg biotin daily. Sounds good, right? Makes you wonder why nobody has attempted to repeat the experiment if the results are real. Another thing that strikes me as odd is the duration of the experiment. Why a mean duration of 7.9 months with standard deviation? Weren't all the subjects taking biotin for the same duration? Did they just quit whenever they felt like it? That just sounds like bad study design, which makes me somewhat skeptical of the results.

Still, it's intriguing enough to make me add biotin back on the supplement menu for the time being. Although a "it can't hurt and might help" mentality may be dangerous in some cases, I'm unaware of any negative side effects from taking 5 mg biotin daily. This time I'm aiming for at least six months instead of just one.

For more information on hair growth, see these posts:

Soy Isoflavones and Chili Pepper for Hair Growth – Experiment Update
Emu Oil vs. Hair Again® Topical Gel: Hair Growth Battle Conclusion
Do Flax Lignans Reduce Hair Loss from MPB?
2% Nizoral Shampoo Increases Hair Growth More than 2% Minoxidil

Read More......

Soy Isoflavones and Chili Pepper for Hair Growth – Experiment Update

Spicy peppers contain capsaicin, which should promote hair growth. (Photo by Jonathon W)

Several readers have been asking for an update on my hair growth experiment with soy isoflavones and capsaicin. I admit it's long overdue, so here goes!

First some background on the experiment. Why soy isoflavones? I know there are a lot of people who think soy is the ultimate poison, and while I'm not a big fan of soy as a food, the science behind isoflavones and hair growth is strong enough for me to give it a go. Soy isoflavones have been shown to increase IGF-1 in the skin, which in turn promotes hair growth. Although soy also reduces DHT in rats and in humans, the effects on IGF-1 seem to be the primary way through which isoflavones grow hair.

Capsaicin seems to have a similar effect on IGF-1, and in both mice and humans, the combination of soy isoflavones and capsaicin appears to be more effective than capsaicin alone. I have not seen a direct comparison of soy isoflavones and soy isoflavones + capsaicin, however, so it's unclear how important capsaicin really is. Nevertheless, I chose to take both for the experiment.

The participants in the study were given a capsaicin supplement, but I decided to take the natural route and just add cayenne pepper or chili powder into my food instead. It's difficult to determine just how much capsaicin I've been ingesting this way, since the capsaicin content depends on a lot of variables. As I wrote when the experiment began:

The only problem is that it's pretty difficult to estimate the amount of capsaicin; a tablespoon of ground chili will contain anywhere between 0.8 mg and 480 mg of capsaicin. In the study, 7 mg per day was consumed, so if I manage to eat a tablespoon, I should have decent odds of ingesting at least as much capsaicin.

The amount of isoflavones I've been eating, on the other hand, has been easy to measure. One capsule contains 60 mg of isoflavones, which is 15 mg less than in the study.

And what about the results? I've not taken any pictures, since unlike in the retinol experiment, there's not much visible going on. I haven't cut my hair in years, and the length of my hair is still the same as it was before (the maximum length of your hair is genetically determined), so it's safe to say that isoflavones and capsaicin haven't done anything in that department.

I also haven't seen any increase in the rate of hair growth, which is perhaps a bit surprising, since you might expect an increase in IGF-1 to increase the speed at which hairs grow. But then again, I have no reliable way of measuring my IGF-1 levels either. I've simply been looking at a few hairs and measuring how much they grow each month.

The one thing I noticed during this experiment is something of a shed in the beginning. There's no way to be sure it's the isoflavones and capsaicin working, but I haven't noticed anything similar with the other experiments. After a few months, I seemed to not only shed more hairs in general, but especially from the front of the scalp. Moreover, many of these hairs had not grown to their full length yet.

As most of you probably know, that can be a good or a bad sign. A lot hair growth drugs, including finasteride, cause an initial shed, after which the hairs grow back stronger and healthier. Then again, inflammation also causes hairs to shed earlier than they should, only they grow back weaker every time.

At this point, it's still too early to tell, since the new hairs are still growing. At least on the surface they look fine. What's funny is that there are some spots where several hairs are pretty much the exact same length. The two possible reasons is that those hairs were shed at the same time and now regrowing, or that the isoflavones and capsaicin increased the number of hair follicles. I suspect the former, but I can't be sure.

So what's the next step? I've already ordered a second bottle of isoflavone capsules, and since I like to use chili in my food anyway, I'll pretty much keep doing what I've been doing so far. If I see any dramatic changes, I will post about them, but if not, I will just consider the isoflavones and capsaicin thing a preventative measure and move on to more interesting experiments.

That's it for today. I hope you found this update useful, and if you have further questions or you've done a similar experiment of your own, please let us know in the comment section.

For more information on hair growth, see these posts:

Topical Retinoids Increase Hair Growth in Most People
BioSil, JarroSil & Beer – Silicon Experiment Conclusion
Zinc Pyrithione Reduces Shedding and Moderately Promotes Hair Growth
Eclipta Alba Extract Grows Hair Quicker than Minoxidil

Read More......

Vegetable vs. Animal Sources of Vitamin A: Why Eating Carrots Isn't Enough

Think you're getting enough vitamin A from carrots? Think again. (Photo by Ben Hussman)

In the comment section of my previous post on genes, diet and cavities, a couple of readers commented that vitamin A is necessary for proper dental health. I replied that I get plenty of beta-carotene (the vitamin A precursor found in vegetables and fruits) from red palm oil, which I use for most of my cooking these days.

Today, however, I came across a couple of papers looking at how well humans actually absorb beta-carotene and convert it to vitamin A (link, link). To my surprise, the conversion rate was much poorer than I'd previously thought. The first paper, which looked at beta-carotene absorption in 11 men, had this to say:

The vitamin A activity of ß-carotene is variable. The carotene in fruit, grains, and oils seems to be more effective as a source of vitamin A than that in dark-green leafy vegetables.

So, not all sources of beta-carotene are equally good in terms of absorption. The conversion rate also depends on the amount of beta-carotene (the higher the amount, the lower the rate) and whether fat is included or not.

Strikingly, only 6 of the 11 men included in the study absorbed and converted the beta-carotene they were given. The remaining 5 were classified as non-responders. The authors conclude that the vitamin A activity of beta-carotene can be "surprisingly low and variable". Even in those who did respond to supplementation, mean absorption was only ~4% and the conversion ratio was ~0.05.

In a similar study on 11 women, the same thing happened: only 6 of the women absorbed and converted beta-carotene enough to be measurable, while 5 women were non-responders. In those who did respond, mean absorption was ~6% and the conversion ratio ~0.1. This confirms earlier findings reporting that women absorb and convert beta-carotene more efficiently than men; the same also appears to be true in rats.

These figures suggest that the commonly accepted conversion rates of beta-carotene from plant sources may be too optimistic. Even red palm oil might not be up to par with animal sources. In one study, switching from green leafy vegetables to red palm oil did increase retinol levels, but only in subjects who were vitamin A deficient to begin with (link). And for many Westerners who don't eat palm oil or organ meats, the reality is even worse:

Also, it seems that the vitamin A activity of ß-carotene that is not dissolved in oil and emulsified is low and variable. Most ß-carotene in the American diet is not consumed in an emulsified form with fat. Our intent was to replicate a typical diet to develop better leads for how the body utilizes its given resources. The fat content of the meal that accompanied the doses in our study was the recommended amount, 30%. Many professionals recommend lower-fat diets.

Now there's something for the low-fat raw food vegetarians to chew on. On the other hand, the absorption of retinol, found in animal sources such as liver and eggs, appears to be much higher. Most of the estimates I've seen on various websites are between 60-90%, but even that may be too conservative, as the only actual study I could find showed that absorption was >99% (link).

Since my vitamin D levels are already good, and I take vitamin K2 supplements, the missing link in the trinity of dental health could indeed be vitamin A in my case. While I do eat eggs every now and then, their retinol content is only about 10% of that of liver. I guess it's time to put organs on the menu.

For more information dental health, see these posts:

Genes, Diet and Oral Health: Why Do Some People Get Cavities and Others Don't?
Tea, Coffee and Cocoa: All Good for Your Teeth
Dental Health Effects of Green and Black Tea
Preventing Mouth Ulcers with Tea Tree Oil Toothpaste - Results after Two Months

Read More......

Green Tea as a Pro-oxidant: Too Much of a Good Thing?

Is too much green tea harmful for you? (Photo by tornado_twister)

I was browsing through the latest studies on green tea and came across a paper saying EGCG, one of the green tea polyphenols, increases protein cross-linking (link). I was intrigued, because this was the first time I'd heard of such an effect. The abstract also mentions that there's increasing evidence EGCG can generate reactive oxygen species and break DNA strands in biological systems. In effect, it says that the antioxidant is actually a pro-oxidant.

I looked up some of the references and indeed, even green tea's polyphenols (at least EGCG, possibly some others) have oxidative effects under certain in vitro conditions. For example, in human whole blood lymphocytes, EGCG either suppresses or induces DNA strand breakage, depending on the concentration.

In concentrations between 0.01-10 μM (micromoles/L), strand breakage decreases, but once the concetration gets higher than 1000 μM, it increases instead. In purified blood lymphocytes, concentrations of 1-100 μM induce and concentrations of 0.01-0.1 μM suppress DNA strand breakage.

Sounds an awfully lot like hormesis, doesn't it? As with everything, the dose makes the poison. The interesting part, of course, is whether drinking green tea can cause similar harmful effects in real life.

Luckily, one study looked at the effect of green tea on DNA strand breaks in rats (link). The smaller dose (which according to the authors is equivalent to one desiliter of green tea in humans) had no effect, but the larger dose (equivalent to half a liter) significantly reduced strand breaks.

Half a liter of green tea, equal to about three cups, increase total plasma antioxidant capacity only moderately. When only EGCG is taken into account, the results vary somewhat from study to study, but concentrations rarely exceed 1 μM (link). Also, plasma antioxidant activity has a plateau, which suggests that the absorption mechanism of green tea polyphenols becomes saturated after a certain point:

To make the tea used in the study, 500 ml of boiling water was poured on 20 grams of green tea leaves (8-10 tea bags), and the tea was then allowed to infuse for 10 minutes. That makes for a very strong tea, much stronger than the ones used in the other studies. The volunteers drank 300-400 ml of the tea, after which blood samples were collected at different time intervals

In this study, there was no difference between those who drank 300 and 400 ml of the tea. Even then, the increase in antioxidant activity was only 4% at the peak. Thus, it seems unlikely that harmful levels could be reached by simply drinking plenty of green tea. In one Asian population, 10 cups of green tea daily reduced total mortality compared to those who drank less green tea and/or smoked.

Theoretically at least, extracts and supplements could be a different matter, because they often contain a higher percentage of EGCG than green tea and come with things that increase absorption. For example, piperine increases plasma levels of EGCG.

One green tea extract containing 40% EGCG resulted in a peak  of 0.8 μg/mL in human subjects; when the same extract was complexed with phospholipids, the peak was 1.9 μg/mL. If my calculations are correct (which they often aren't; please correct me if I'm wrong), then these would be ~1.75 μM and ~4.14 μM, respectively. Again, in whole blood lymphocytes concentrations between 0.01-10 μM, strand breakage was decreased, and it took concentrations higher than 1000 μM to increase strand breakage.

All in all, it appears that green tea in reasonable quantities (at least up to 10 cups) does not cause it to act as an oxidant in vivo. It's unknown what a much higher amount would do, assuming you could somehow bring yourself to drink 50 cups. I haven't seen any human studies on such amounts. But if the plateau effect is indeed true, then you might not be able to reach high plasma levels of EGCG no matter how much you drink.

With supplements, the situation is different. Piperine and phospholipids make reaching higher plasma values possible, which can be a good thing or a bad thing, depending on what you're using the supplements for. Some conditions require higher doses than others, so you'll have to judge the proper approach on a case by case basis. However, since EGCG does have the potential of being a pro-oxidant in vitro and is toxic to the liver in very high amounts, be careful not to overdo it with green tea supplements.

For more information on green tea and health, see these posts:

Green Tea Protects from the Psychological Effects of Stress in Rats
Tea, Coffee and Cocoa: All Good for Your Teeth
Green Tea and Capsaicin Reduce Hunger and Calorie Intake
Green Tea Catechin Reverses the Effect of DHT in Prostate Cancer Cells

Read More......

Nootropics, Longevity and More: The Year 2010 in Review

Comments or suggestions for the year 2011? Drop a comment! (Photo by Altus)

Happy New Year everyone! I hope your holidays went well and you're ready to make 2011 even better than last year. But before we do that, let's take a look at some of the best bits and pieces from 2010.

In January, I finally got a chance to see Aubrey de Grey for the first time. His presentation in Helsinki, Finland was mostly familiar to me already, but I enjoyed it nonetheless. Perhaps the most interesting part was when the audience got to ask questions; I thought Aubrey's answers were good, especially given that some of the comments were pretty frustrating (apparently some people think going through their entire family history somehow qualifies as a question). If you want to check out the presentation, the video is still available online through the link above. And in case you want to know more about Aubrey himself, he was also interviewed in Wired.com a while ago.

Nootropics are gaining more and more attention these days. Even 60 minutes ran a segment on students boosting brain power to do better in their studies. Amphetamine derivatives are still the most popular choice – but whoever comes up with an "organic herbal formula" that actually works as well as Adderrall is going to be rich. I also did an experiment with Ashwagandha to see whether it had a nootropic effect. It didn't, at least not the brand I was using.

And then there was the experiment with BioSil, the stuff that is supposed to make your hair and nails stronger. The science seems solid, but as I wrote in my conclusion, the price of the liquid supplement doesn't seem worth it, since orthosilicic acid, the active ingredient, is also present in my favourite beverage.

Speaking of hair, a lot of people have asked for an update on the soy isoflavones + capsaicin experiment, another one of my attempts at finding a magical hair growth formula that will make me filthy rich. The experiment has been going on for six months now, which is longer than the five months that the original study lasted, so perhaps a proper update is indeed due. So far I haven't seen much visible changes, however. I'm now adding various kinds of chili powders and pastes to almost all my foods, but I'm thinking of ordering capsaicin supplements to be sure I'm getting enough to match the study. And I also need another bottle of soy isoflavones.

I've tried a lot of useless supplements and topicals, but last year I came across something that really, actually works: retinoids. I've now been using them for over a year and I can really see the difference. My advice to anyone looking for real results is to forget about all the overpriced skin creams that are really nothing but moisturizers and go for tretinoin instead. Of course, since it actually works it's prescription stuff, so you can't just buy it from the store, you'll have to order it online and hope your package doesn't get confiscated by the customs officers who surely know better what you need than you do. Thank god for regulations!

Probably the longest and most throrough post of last year was about human hibernation and how it might relate to longevity. In addition to a look at the current state of hibernation science, there's also the odd legend of lotska, the art of hibernation allegedly practiced by poor Russian peasants:

At the first fall of snow the whole family gathers round the stove, lies down, ceases to wrestle with the problems of human existence, and quietly goes to sleep. Once a day every one wakes up to eat a piece of hard bread, of which an amount sufficient to last six months has providently been baked in the previous autumn. When the bread has been washed down with a draught of water, everyone goes to sleep again. The members of the family take it in turn to watch and keep the fire alight.

And of course, no post on slowing down metabolism would be complete without Indian fakirs and frozen mountain climbers. Check it out if you have the time, it's fascinating stuff.

While the Russian peasants may have spent most of their winter sleeping to avoid starving, there are also those who can eat as much as they like and still avoid getting fat. Even without any exercise. I'll let other bloggers fight it out over the details of the energy equation and whether a calorie truly is a calorie, but take a look at the BBC documentary in the link to see what I mean. Also check out the comment section, some interesting anecdotes in there.

How is the life extension movement doing these days? Well, the same old (and false) arguments against longer lifespans are still there, but the overall mood is pretty optimistic. Personally, I've noticed that younger people tend to be more open to the possibility of life extension than middle-aged people. Go figure. Meanwhile, the Russians have apparently found the cure for aging, although I haven't heard anything new on SkQ1 since September. But that's okay, because the next fountain of youth is already here.

Long-time readers of this blog probably remember that I did intermittent fasting for over a year. Part of the reason was that I wanted to see if 24-hour fasts could be done – I wanted to be the master of my hunger, so to speak. However, the most important reason were the studies showing positive effects from intermittent fasting without restricting total calories. You know, the whole "cleaning cells from junk through autophagy" thing.

But alas, after going through the studies more carefully, I was disappointed to find out that whenever intermittent fasting increased lifespan in mice, total calories had also been restricted. In effect, intermittent fasting extends lifespan only in conjuction with caloric restriction. Some of the other benefits of fasting may still be valid, to a degree at least, but without potential gains in lifespan, I don't see the point in doing a strict 24/24-hour cycle of fasting and feasting anymore. Besides, I now think that even full-blown calorie restriction would only give me a few extra years. Why? Because humans just can't do CR the same way rodents can. More on this later. Meanwhile, see my updated health regimen.

Of course, there were also several other posts which I didn't mention here; see the archives section in case you missed them. And just so you don't miss anything interesting in the future, remember to subscribe to my feed and to follow me on Twitter, which I use to post stuff (life extension, health, science) I don't have time to blog about in depth. Oh yeah, and tell your friends to do so too!

For summaries of previous years, see these posts:

10 Human Experiments of 2009 – Year in Review
7 Human Experiments of 2008 – Year in Review

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Soy Isoflavones and Chili Pepper for Hair Growth – Experiment Begins

The hotter the pepper, the more capsaicin it contains. (Photo by Andreas Adermark)

I've written so many posts on soy isoflavones and hair growth that I figured it's time to start another experiment to see for myself whether the claims are true.

Even though it looks like soy isoflavones alone are sufficient to increase dermal levels of IGF-1 and thus promote hair growth, the most effective combination seems to be isoflavones and capsaicin. If you haven't seen the pictures from that paper for some reason, I recommend taking a look at the latter link. This combination is the one I will be testing.

The soy isoflavones supplement I have is by NOW Foods. It contains 60 mg of isoflavones (genistein, daidzein and glycitein) per capsule. This is slightly less than the 75 mg used in the human study, but since I don't want to take 120 mg per day, it'll have to do.

As for capsaicin, I'm going with the natural route and adding chili pepper to my foods during the experiment. There are capsaicin supplements too, but since I like spicy foods anyway, I don't think supplements are worth the extra money in this case.

The only problem is that it's pretty difficult to estimate the amount of capsaicin; a tablespoon of ground chili will contain anywhere between 0.8 mg and 480 mg of capsaicin. In the study, 7 mg per day was consumed, so if I manage to eat a tablespoon, I should have decent odds of ingesting at least as much capsaicin.

As you can see, this is not an exact replica of the human study, but I think my own experiment will be very close to what other people might try at home. The study lasted for 5 months, which is how long you should give any treatment before realistically expecting results. I will post an update after I run out of capsules and we'll see what happens then.

Keep in mind that this is not the only thing I have going on at the moment that might affect hair growth. Though not technically experiments, I've been using ketoconazole and piroctone olamine shampoos regularly, because the science behind them looks pretty good. I'm also consuming some ground flax seeds every now and then, which could be beneficial for hair.

Since I started to use these three things, I've noticed a slight decrease in the number of hairs lost daily. Whereas I counted 60-80 before, I now seem to lose about 40-50 hairs daily. Both of these figures are within the normal range, so these additions to my health regiment are mostly about preventing (or at least delaying) any future hair loss. Still, if the hair growth promoting effect of isoflavones and capsaicin is as strong as the rodent and human studies show, I would expect some visible changes even in people without androgenic alopecia.

Lastly, my experiments with retinoids and an Ayurvedic topical called Nutrich oil are still running. I'm applying both of them on my temples, one on the left and the other on the right, to see if they increase hair growth. So far I have not noticed any dramatic changes, so I don't think they will obfuscate the results of this experiment too much.

I'll keep you updated on how things go. Meanwhile, if you've tried soy isoflavones or capsaicin, drop a comment and share your experiences!

For more information on hair growth, see these posts:

BioSil, JarroSil & Beer – Silicon Experiment Conclusion
Emu Oil vs. Hair Again® Topical Gel: Hair Growth Battle Conclusion
Eclipta Alba Extract Grows Hair Quicker than Minoxidil
Do Flax Lignans Reduce Hair Loss from MPB?

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My Current Health Regimen v2.0

One of the changes has been an increased intake of fruit and vegetables. (Photo by YimHafiz)

This is my updated health regimen, aimed at adding a significant number of healthy years to my expected lifespan. As it's subject to change, I will keep this post updated accordingly. Major revisions (such as v2.0) will appear once a year or so; minor changes (such as v2.1) will be made as needed. With every major revision, I will move the post from the archives to the front page.

Since a long, healthy life is preferable to a short life by most people, following the regimen would make sense even without considering technological innovations. The true goal of my regimen, however, is to stay alive long enough to see rejuvenation therapies become a reality. In the long run, each year that I'm able to add to my expected lifespan now through things like dietary changes, exercise, and supplements, may grant me several extra years in the future.

Therefore, even those lifestyle changes that require considerable effort and resources while offering a seemingly limited benefit, make sense if one looks at the big picture. For a chance to see the world in 2090, I'm willing to skip the cheeseburger today.

My health regimen consists of four categories: diet, supplements, physical exercise, and brain health. All of the items under each category have some kind of scientific basis, and in contrast to my ongoing experiments, will remain a part of the regimen for the time being. Therefore, my current experiments are not a part of my long-term health regimen – unless they prove to be beneficial, in which case they'll be moved from ongoing experiments to the regimen.

Main changes from v1.0: none.

Avoiding harmful foods

The most important part of my diet is avoiding unhealthy things; increasing the intake of healthy things only comes in second. This is because preventing damage from happening in the first place is easier than repairing it later on.

I consider the worst culprit of modern diets to be an emphasis on grain products, fructose, and polyunsaturated fatty acids. There's considerable evidence to suggest that most people would do much better without them. Hence, things like pasta, rice, bread, candy, fruit juices, and most vegetable oils are off the daily menu. I only eat them rarely, and then simply because they taste good. For the past few months, I've allowed myself to eat whatever I want once a week (usually foods like pizza or fresh bread), which seems to be working well.

I originally cut back on my fruit intake, which used to be quite high some years ago, because I learned that fructose increases triglycerides especially in men, and fructose is not handled very well by the body in general. I later learned that fructose also forms AGEs much more rapidly than glucose, which kept me from reintroducing most fruits to my diet and eat berries instead, since they contain more nutrients per fructose calorie. However, I've now increased even my fruit intake a little, having read more about the AGE-inhibiting effects of phytonutrients found in fruit. I will expand on this later, but for an example of what I'm talking about, see my post about carotenoids inhibiting lipid peroxidation.

While much of this fits well with paleo dieting, I also diverge from the paleo diet these days. You may or may not remember that I used to be a potato hater back in the day, both because they could not be eaten raw (making them anti-paleolithic) and because of their high carb content. Basically, potatoes are just empty calories. But once you have your insulin sensitivity and blood glucose under control, I don't think a few potatoes now and then is much of a concern. At least they're low in fructose.

As you may recall, I followed a low-carb diet for the past year with an emphasis on paleo foods. I got on the low-carb, high-fat wagon in the first place to prove that eating a diet high in fat does not make you fat – and it didn't. However, this diet combined with my year-long intermittent fasting experiment resulted in a moderate-to-high intake of protein, the longevity effect of which I'm now questioning. To lower my protein intake slightly means eating either more fat or more carbohydrates, and since my fat intake is already very high, I've reintroduced some carbs into my diet. That is, I now occasionally eat potatoes not because I think they are necessary for health, but because they are low in protein. More on protein and longevity in future posts.

I still don't make nuts a dietary staple, because of their poor omega-3/omega-6 ratio and because I like to keep my PUFA intake low. That is, I aim not only for a good ratio of omega-3 and omega-6 fatty acids, I try not to eat too much of them in general. Omega-3 is particularly prone to undergo lipid peroxidation, and while nuts probably have micronutrients that protect them from oxidation to some degree, I'm playing it safe until I learn more.

Main changes from v1.0: slightly increased carb intake, slightly decreased protein intake, slightly decreased polyunsaturated fatty acid intake.

Eating healthy foods

Despite eating some more carbs these days, my diet is still fairly low in carbohydrates. My daily intake used to be around 100 grams; I have not measured my current intake, but I suspect it's around 100-150 grams these days. My main protein sources used to be meat, fish and eggs, but during the past year I've cut back on eating eggs because of their high methionine content. I'm still figuring out whether methionine restriction makes sense in humans, but in the meantime I limit my egg intake to 3-4 eggs a week.

Sources of fat, in the order of importance, are olive oil, palm oil, butter, cocoa butter, coconut milk, ghee, coconut oil, and sesame oil. Olive oil tops the list because I love the taste and because it's high in MUFAs but low in PUFAs and consistently does well in just about every health study. There may not be anything magical about MUFAs per se, but even if it's the polyphenols in olive oil that are behind all the positive health effects, olive oil still seems like a good choice. Palm oil is there because it's rich in tocotrienols (at least compared to other natural foods), low in PUFAs and high in SAs (making it suitable for heating), and because I've grown to like the taste.

Lard is off the menu for now because I ran out. Heavy cream has been replaced by coconut milk, partly because of dairy products increasing IGF-1, which may be bad for longevity (more on that in future posts). I don't eat cocoa butter raw (although I could, it's delicious), but I get plenty from all the dark chocolate I eat. Somebody asked me in the comment section why I eat sesame oil since it contains quite a bit of PUFAs, and noticing this was indeed so, I was going to remove it from my diet altogether. However, doing some reading I found that sesame oil seems to reduce markers of lipid peroxidation, so I kept it on the menu. I just use it for taste, however, so my intake of sesame oil is very low anyway.

Depending on my daily menu, anywhere between 50 to 70% of my total calorie intake is from fat. My daily menu has changed a bit, but percentage of fat is still the same. Most of this is saturated fat, which has been given a bad rep for reasons I believe are incorrect. I began reducing grain products and increasing my saturated fat intake years ago, and it hasn't killed me yet. In fact, my HDL has increased and my LDL has decreased on this diet. Triglycerides are not bad but could be better – a testament to my main vices, beer and wine.

There is one cereal grain I regularly eat, however: rolled oats. They're a convenient source of beta-glucan, which appears to be good for cholesterol and avoiding heart disease, and they don't contain gluten. Oats also contain quite a bit of quality protein. I used to eat them with milk and berries, but then switched to a combination of heavy cream and water to reduce my consumption of lactose and galactose (which easily form advanced glycation endproducts, AGEs). Now, I've stopped adding even heavy cream, because milk protein seems to interfact with the polyphenols in berries. So it's a mixture of coconut milk and water nowadays – not as good as cold milk, but still pretty good.

As for red meat, despite how it's portrayed in the media these days, I'm not convinced that meat consumption is harmful. Indeed, a recent review supports the hypothesis that processed meat, not meat in itself, may be harmful. The biggest problem I used to see with meat is the generation of AGEs. Though there is disagreement just how harmful consuming AGEs with food are, I tried to minimize the potential damage by avoiding overcooking and taking supplements. I no longer think AGEs in meat are a huge problem, however – more on this later. The reason I don't eat huge portions of meat like I used to is because of the high protein content.

And finally, the beverage department. I still love my daily coffee, which I drink 1-2 cups per day. Coffee has some nice health benefits too. Green tea is obviously staying on the menu; the studies showing positive health effects just keep on piling up. All in all, beer doesn't really belong to the "eating healthy foods" category, but even beer does contain some good stuff.

As you may recall, I used to drink yerba mate with meals to reduce the formation of AGEs. It's since come to my attention that yerba mate is carcinogenic at higher doses, so I now drink it only rarely. Green tea or black tea are safer bets, despite somewhat contradictory results in reducing AGEs and ALEs.

Main changes from v1.0: decreased egg intake, changes in the use of fats and oils, reduced yerba mate consumption, avoidance of lipid peroxidation.

A note on diet tweaking

It's much easier to point out things that are wrong in various foods than it is to prove something is healthy. These days, I'm more wary of advertising my diet as the best choice for everyone than I was before. Part of the reason is that the more I read and learn about nutrition, the more complicated everything becomes.

Case in point: I used to tell people vegetables are bad because, as an evolutionary strategy, they produce toxins to protect them from being eaten (which is true). Now, having learned of the importance of hormesis, I think vegetables are good because of those same toxins! I was also a huge fan of eating fruit (especially organic fruit) at one point, because it seemed to make sense from an evolutionary point of view. The, I got a little skeptical towards them because of their fructose content. Now, I think the benefits may outweigh the negatives.

All this, however, doesn't stop me from wanting to find the optimal diet for longevity. On the contrary, it's a healthy reminder not to get too emotionally attached to my health regimen, and to be ready to admit mistakes and make alterations as I learn more.

Going without food

The third key component of my diet used to be intermittent fasting. I stated in the first version of this post that "I may change my mind in the future, but for now I expect periodic food deprivation to remain in the regimen." That is still true to some degree: I no longer do a 24/24 hour cycle of fasting and eating, but I don't make it a point to eat three meals with snacks a day either. I often skip breakfast and lunch and eat only dinner.

The thing that lured me to try intermittent fasting was that there are studies suggesting that all or most of the benefits of chronic calorie reduction can be had by alternating zero calories with double the normal calories every 24 hours. While I no longer believe that IF is equivalent to CR, I do think that fasting in general is beneficial. An improved insulin sensitivity is a known result of intermittent fasting. Insulin sensitivity is associated with longevity, and among supercentenarians, insulin sensitivity is common.

Perhaps a more interesting thing about fasting is that it increases autophagy, a process in which the cell consumes a part of itself for energy. This can happen during ordinary cell maintenance, or when the body is deprived of nutrients. Since improved autophagy is at least in part why caloric restriction works, this makes other, less demanding forms of nutrient deprivation attractive options.

The reason I stopped doing strict IF is because I don't think there is much evidence that fasting for 24 hours and then eating for 24 hours is somehow optimal in itself. Most importantly, IF does not extend lifespan in most studies. Why IF is not equivalent to CR is not clear, but recent studies suggest protein may have a lot to do with it. My intermittent fasting diet resulted in huge meals with lots of protein, and I now suspect that this may have diminished much of the potential benefits.

Main changes from v1.0: no more 24/24 intermittent fasting, no more huge protein-heavy meals.

Supplements

The most important supplement in my regimen is vitamin D3. Most people are deficient in vitamin D, and the health benefits are so overwhelming that if there's one supplement I would recommend spending money on, it's vitamin D3. I usually take 5,000 IU of vitamin D3 daily, and at last check, my levels were at 45 ng/mL, which is in the optimal range. Now that it's summer, I'm taking 2,500 IU daily. I know some people take the same amount all year round, but since I do spend some time in the sun, I don't want to overdo it.

One of the supplements that has remained in the regimen since last time is vitamin K2, which is sort of a newcomer in the supplement scene but nonetheless has some impressive studies behind it. I'll write more about it in the future, but here's one study of interest for men: dietary vitamin K2 may reduce prostate cancer. Since fermented dairy products, which I'm not sure are the best choice for health otherwise, are the best dietary source of vitamin K2, I'm taking supplements instead. At the moment, I take 90 mcg of MK-7 (Jarrow MK-7) and 5 mg of MK-4 (Carlson Labs Vitamin K2) every third day in an attempt to find a balance between affordability and the long serum half-life of vitamin K2.

I used to take a tablespoon of fish liver oil daily, because it has lots of omega-3 fatty acids in bioavailable form (EPA and DHA) and almost no omega-6 fatty acids. A higher dietary ratio of omega-3 to omega-6 seems to be very beneficial in general, and fish oil has been shown to decrease inflammation. A commonly quoted optimal ratio is between 1:1 and 1:4, which seems to be close to how our paleolithic ancestors ate. As part of my plan to avoid excess PUFAs, I've dropped fish liver oil from the menu. I'm currently in the process of weighing the pros and the cons; it may be that a tablespoon per day will prove to be worth it in the end.

I also used to take resveratrol with quercetin during fasts to increase autophagy. I would still continue to take them, but unfortunately I can't afford all the supplements I might like to take (including AOR Ortho-Core, which is off the list for the time being), so I take resveratrol only occasionally. Meanwhile, I'm on the lookout for other things that increase autophagy. Curcumin is a cheap alternative, and it has other health benefits too, which is why I add turmeric to most of my foods.

Since my damn blender keeps leaking from the bottom, I'm no longer making smoothies every day like I used to. So these days I just add some ground flax seeds to my rolled oats for the flax lignans. Flax lignans may prevent hair loss, among other health benefits. Some people prefer to take them in supplement form, but flaxmeal is a cheaper and equally effective way to consume flax lignans. For best effects, they should be consumed twice a day with ~12 hours in between. Other things I do to prevent hair loss is use shampoos with ketoconazole and piroctone olamine.

Main changes from v1.0: no more fish liver oil, some supplement cutbacks due to costs, increased curcumin intake.

Exercise

My exercise routine is probably the weakest part of my regimen, compared to how much effort I put into diet and supplements. In the summer, I run for 30-45 minutes once a week to get some aerobic exercise (I should start again, since summer is here!) The goal is to keep the heart and lungs healthy, reduce blood pressure, and improve mood. In the winter, when it gets too cold for running outside, I go to the gym for strength training instead. Strength training reduces the risk of injury, prevents osteoporosis, supports joint health, and prevents muscle loss resulting from aging.

I also practice martial arts, which combines aerobic and strength training, to a degree. The main reason for me, however, is that it provides me with a basic set of self-defense skills and improves coordination. With aging, there is usually an increased fear of falling and hurting oneself – something children naturally don't have. Getting thrown around every week is a way to maintain a healthier attitude towards my body and prevent an irrational fear of getting hurt. I want my mind to rule over my body, not the other way around.

Main changes from v1.0: none.

Brain training

Any anti-aging regime should also take into account the importance of maintaining mental health. It doesn't take a genius to see that people who use their brains actively retain their cognitive abilities far longer than those who are passive.

One of the ways I keep the rational side of my brain fit is reading scientific papers and writing about them on this blog. I like logical problems in general, and I think practicing problem-solving skills are important for everyone, whether it's through work or hobbies. To train the creative side, I do things like play instruments, compose music, and read and write fiction.

My biggest problem is and always has been rather poor short-term memory. I don't know whether it's because my mind is always occupied with a zillion things, but it's more than once that I've gone to the grocery store to buy something I need and come back with something else entirely. This kind of absent-mindedness seems to run in the family. I believe it can be improved through training, however. The memory game experiment intends to increase IQ, but it improves short-term memory as well (I've pretty much forgotten about this experiment lately, by the way – I'll have to start playing again!)

Main changes from v1.0: none.

Quick summary of the health regimen

As a part of my diet, I regularly eat the following foods:

- Meat, fish
- Olive oil, palm oil
- Butter
- Vegetables, berries, fruit, oats, dark chocolate, coconut milk
- Coffee, tea, wine, beer

I limit or avoid eating the following foods:

- Grain products like pasta, bread, and rice
- Fruit juices, candy
- Vegetable oils high in PUFAs

In general, my diet is high in fat and lowish in carbohydrates. I consume saturated fat and monounsaturated fat liberally but limit polyunsaturated fats.

My supplement regime consists of the following:

- Vitamin D3: 2,500-5,000 IU daily
- Vitamin K2: 90 mcg of MK-7 and 5 mg of MK-4 every third day
- Varying amounts of green tea daily
- Flax lignans: 1-2 tablespoons of ground flax seeds daily

My physical health regime consists of martial arts, running (in the summer), and strength training (in the winter). For mental health, I do things that train the creative and logical sides of the brain.

For more information on anti-aging methods and living longer, see these posts:

Anti-Aging in the Media: New York Times on Caloric Restriction and Resveratrol
How to Live Forever: My 5 Steps to Immortality
L-Carnitine, Acetyl-L-Carnitine and Cognitive Function in Humans
Caloric Restriction Improves Memory in the Elderly

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BioSil, JarroSil & Beer – Silicon Experiment Conclusion

Beer – it's not just the alcohol that goes to your head. (Photo by Fabrice ROSE)

This post is the long overdue conclusion to my silicon experiment. The idea was to replicate a study that found improved skin quality, nail thickness and hair growth using a bioavailable form of silicon known as choline-stabilized orthosilicic acid (ch-OSA).

For two and a half months, I mixed five drops of Natrol's BioSil product with juice. This was equal to 5 mg of ch-OSA, which is only half the dose used in the original study. In an update post, I wrote that there might have been a slight increase in the thickness of my nails. I did not see an increase in the speed of growth, however. Hair growth and skin quality were also unchanged.

I then increased the dose to 10 mg for the next two months. To make the experiment more scientific, I began cutting my nails every 14 days to see if there was any change in how quickly they grew. Again, there was no significant change in skin, nail or hair quality.

After the bottle of BioSil was finished, I continued the experiment with Jarrow's JarroSil product while keeping the amount of orthosilicic acid at 10 mg. There's not much difference in price between the two products, but one thing Jarrow definitely has over Natrol's orthosilicic acid is the taste: BioSil tastes pretty horrible, while JarroSil doesn't really taste much of anything.

I now have several months of experimentation behind me with JarroSil. After a month or so of taking 10 mg daily, I began a routine where I take the product for two weeks and then have two weeks off, all the while keeping an eye on hair and nail growth and skin quality.

Even though I had pretty high expectations from ch-OSA, given that it had the science behind it and people seemed to have good experiences with it in general, I can't say I noticed any improvements. Hair thickness has not increased, at least not visibly, and my skin looks the same regardless of whether I'm using the product or not. On some weeks I think my nails grow faster than on others, but this seems to be independent of silicon.

One reason for not seeing any positive results may be that the original study was done on middle-aged women. Perhaps the benefits of orthosilicic acid supplementation come with age. Another possible explanation is that dietary intake of orthosilicic acid also plays a role. The European Food Safety Authority has estimated that the typical dietary intake of silicon is 20-50 mg. Maybe I already get enough bioavailable silicon from my diet, and the extra 10 mg did not yield any additional benefits.

Speaking of bioavailable silicon, did you know that the best dietary source is beer? According to one study, beer contains a little less than 20 mg of silicon per liter on average, regardless of the type or geographic origin of the beer (link). The actual amount varies between 9 and 39 mg per liter.

About 80% of the silicon is in the form of orthosilicic acid, which is the bioavailable form. The absorption of silicon from beer is 55%. This means that a can of beer (330 mL) contains, on average, about 7 mg of silicon. Of this, about 5.6 mg is orthosilicic acid, about 3.5 mg of which is absorbed.

There is no data directly comparing the bioavailability of ch-OSA and orthosilicic acid from beer, but since the urinary excretion rates of the two appear to be similar, we can assume their absorption is also similar. Thus, two cans of beer would give roughly the same amount of orthosilicic acid as used in the study.

Jarrow and Natrol mention only that silicon is poorly absorbed from many food sources and that orthosilicic acid is easily polymerized, which dramatically reduces its bioavailability (the choline is added to prevent the polymerization). This is indeed true, but they neglect to mention that not all dietary sources of silicon are poor. Beer seems to be the best one, but even water and mineral water contain 2-5 mg of orthosilicic acid per liter (link).

Since beer is one of my vices, I think I get enough orthosilicic acid in my diet anyway, so I won't be investing into supplemental forms anymore. However, if your dietary intake is low and you're looking for ways to increase hair or nail thickness, supplementing with JarroSil or BioSil may be worth a shot.

Even though my conclusion to the experiment is that I did not notice any visible results, I'm not disregarding orthosilicic acid as worthless. In fact, a new study confirms some of the findings of the study on photoaged women (link):

Forty-eight women with fine hair were given 10 mg Si/day in the form of ch-OSA beadlets (n = 24) or a placebo (n = 24), orally for 9 months. Oral intake of ch-OSA had a positive effect on tensile strength including elasticity and break load and resulted in thicker hair.

It may be that some of the effects are more preventative rather than visible improvements. In the above study, for example, the increased thickness was in comparison to the placebo group, not the beginning of the experiment. Both groups saw decreases in hair strength; the supplemented group simply experienced a smaller decrease.

The next time someone argues that drinking is bad for the skin, you can counter them with the high silicon content of beer.

For more information on hair and skin, see these posts:

The Forgotten Anti-Aging Classic: Retinoids Are the Skin's Best Friend
Topical Vitamin C for Skin: Re-examining the Case
Lutein for Skin Elasticity, Hydration and Photo-Protection – Experiment Begins
Coconut Oil Is Better than Olive Oil for Atopic Dermatitis

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Dietary Supplement Increases Lifespan by 11% in Healthy Mice

When will they start serving anti-aging cocktails in bars? (Photo by fanfan2145)

Declining physical activity with aging is seen in almost all species – just think of how much more active kids are than elderly people. This decline contributes to things like metabolic syndrome and frailty in old age. More importantly, life is less enjoyable in general when you're physically unable to do the things you could when you were younger.

To some degree, this process can be slowed down by physical activity itself. People who exercise tend to be more physically fit than people who don't. Nevertheless, no matter how active you are, the decline can only be postponed, not completely prevented. To retain our youthful vigor indefinitely, scientific breakthroughs in regenerative medicine are needed.

And yet, anything that is postponing the inevitable at this point might just prove to have been postponing what is evitable in the future. Stay healthy and stick around long enough and you might just see those breakthroughs happen in your lifetime. That's why anything that gives us even a few extra years of healthspan should be warmly welcomed.

Many people who are proponents of exercise are skeptical of using dietary supplements to increase healthspan, and rightly so: there is little if any evidence to show that popping a generic multivitamin will do any good. But what about a supplement that has a more scientific basis to it? A new study shows that a dietary supplement containing readily available ingredients ameliorates locomotor, neurotransmitter and mitochondrial aging in mice (link). It also modestly extends their lifespan.

Study design

The dietary supplement was developed with five factors related to aging in mind: oxidative stress, inflammation, mitochondrial function, insulin resistance and membrane integrity. A slurry of the supplement was soaked onto pieces of bagel and then given to normal mice and transgenic growth hormone mice (which show accelerated aging compared to normal mice). Here's the ingredient list:

Ingredient	Mg
Bioflavonoids	7.93
Vitamin A (beta-carotene)	0.22
Vitamin B1	0.31
Vitamin B3	0.31
Vitamin B6	0.61
Vitamin B9	0.006
Vitamin B12	0.02
Vitamin C	3.51
Vitamin D	.0002
Vitamin E	3.27
Rutin	3.05
Chromium picolinate	0.003
Magnesium	0.46
Manganese	0.19
Potassium	0.18
Selenium	0.0005
Acetyl L-carnitine	1.47
Alpha-lipoic acid	1.83
Aspirin	1.32
Coenzyme Q10	0.61
Cod liver oil	12.20
Flax seed oil	12.20
Garlic	0.04
Ginger root extract	6.00
Ginkgo biloba	0.18
Ginseng	6.31
Green tea extract	4.88
L-Glutathione	0.31
Melatonin	0.007
N-acetyl cysteine	3.05

The amounts of ingredients in the original data are given in "mg/day/100 mice"; presumably all the treated mice were allowed to eat from the same food lot, which would mean that the amount of ingredients eaten varied between mice. I've divided the numbers by a 100 here to show the average amount for each mouse. You can get the original data from the link to the study if you need it.

Effect on activity levels

According to the authors, when the untreated normal mice reached 24 months of age, their physical activity levels had dropped by more than half. The untreated normal mice are represented by the second line from the top (and I may be missing something here, but it doesn't seem like the decrease is over 50% in the graph – still, a significant drop). Normal mice given the supplement, on the other hand, were almost as active in old age as in young ages.


As you can see, the transgenic mice (represented by the two bottom lines) showed much lower activity in general than the normal mice, which is to be expected. In the untreated transgenic mouse group (the first line from the bottom), activity was pretty uniformly low with not much further decline from aging. In younger transgenic mice (the second line from the bottom), the supplement clearly increased activity, but by the time they reached 13 months, they were as inactive as the untreated group.

According to the authors, exercise duration generally declined with age, but remained higher in supplemented normal mice across all ages. Bouts of intense activity decreased with age even in these mice, but this was offset by increases in moderate activity.

Effect on protein carbonyls

Protein carbonyls, a marker of oxidative damage, correlate negatively with cognitive skills and activity levels. Protein carbonyl levels were lower in the brains of supplemented mice than in untreated mice. Although this kind of damage tends to correlate well with aging (link), the number of protein carbonyls in the brain did not increase with age in either group of normal mice. In transgenic mice, supplementation resulted in a non-significant trend for reduced carbonylation.

Mitochondrial protein carbonyls increased with aging in normal mice. Young normal mice had only 34% of the mitochondrial carbonyls seen in old normal mice, and supplemented normal mice had only 64% of the carbonyls seen in untreated normal mice. In untreated transgenic mice, protein carbonyl levels were the highest, while in supplemented transgenic mice they were the lowest of all four groups. For some reason there appears to be U-curve in the level of protein carbonyls in transgenic mice, with young and old mice showing higher levels than middle-aged mice.

The fact that the dietary supplement reduced protein carbonyls in the brain and mitochondria means that it was able to cross the blood-brain barrier and mitochondria. These are considered key goals of aging interventions. Indeed, supplemented normal mice had an 11% increase in lifespan. The authors think of this as a modest increase and suggest that the increases in physical and mitochondrial activity are the reason the mice didn't live even longer. I'm not sure the "higher metabolic rate = pro-aging" theory they hint at is correct, but nevermind: the fact that normal, healthy mice showed increased maximum lifespan is what's important.

Conclusion

A dietary supplement containing non-prescription ingredients ameliorated the age-related decline in physical activity in both normal and senescence-accelerated mice. The supplemented mice retained their physical activity more than non-supplemented mice and had lower levels of protein carbonyls, an age-related marker of oxidative damage. Importantly, an lifespan increase of 11% was seen in normal mice, showing that an "anti-aging cocktail" based on dietary supplements is feasible at least in mice.

For more information on aging and lifespan extension, see these posts:

Aubrey de Grey in Helsinki, Finland
Giving Heat Shocks to Roundworms Extends Lifespan by Almost 40%
How to Live Forever: My 5 Steps to Immortality
Drinking 10 Cups of Green Tea Daily and Not Smoking Could Add 12 Years to Your Life

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