Wednesday, April 29, 2009

Biotechnology and the Future of Aging

The will to be in control of evolution is an integral part of human nature.

It's always a pleasure to watch inspirational speakers, especially when the topic is my favourite one: the problem of aging.

This talk, given by biotech ethicist Gregory Stock, is actually several years old but was posted only recently in TED Talks. Since he makes some rather bold predictions about the future, it's interesting to compare the current situation with the one in the video.

For example, at one point, he says that we are eventually going to use existing embryo screening technology to choose the physical and psychological traits we want for our children – which essentially means making "designer babies", to use a term favored by the media. As it happens, Stock was right. Just a few months ago, there was a newspaper article about technology allowing parents to select things like hair color for their children before they're born.

Unsurprisingly, the whole idea of cheating nature through technology was written about in a fairly negative tone. The "ethical problems" were emphasized, and some of the doctors interviewed in the article vowed never to use their sacred technology to promote the pure evil that is trait selection. As Stock mentions in his presentation, people will object to these technologies and attempt to ban them, but eventually, they will happen anyway. I whole-heartedly agree with his conclusion that it's really not a matter of "if" but a matter of "when". Besides, banning technologies like this in one country just means that they will be available in another one, with the added negative effect of being affordable only by the rich.

One doesn't need to look very far to realize that other aspects of conquering aging are also happening as we speak. Using tissue engineering and stem cells to "speed up" evolution is something with which we are making real progress, and growing new body parts is not just science fiction anymore. At first, these innovations will probably be used to treat diseases and other existing conditions, but gradually, the emphasis will shift to preventative methods, and from there to self-improvement.

There is, of course, nothing wrong with such self-improvement. It's built into human nature. Ever since the first caveman developed a tool to aid him in hunting, we've been coming up with ways to deal with all the hazards nature keeps throwing at us. During the history of mankind, we've found solutions to many of the problems, but aging has remained an unsolved mystery.

And yet, it's not unrealistic to be somewhat optimistic about the future. If Gregory Stock is right, the victory over aging may not be so far away after all.

For more information on aging, see these posts:

How to Live Forever: My 5 Steps to Immortality
Anti-Aging in the Media: 60 Minutes on Resveratrol
Anti-Aging in the Media: The Globe and Mail on Telomerase
Anti-Aging in the Media: Rolling Stone on Ray Kurzweil

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Monday, April 27, 2009

Tea Tree Oil vs. Korean Red Ginseng – Hair Growth Battle Conclusion

Oil from the tea tree is often used as a hair growth tonic.
Oil from the tea tree is often used as a hair growth tonic. (Photo by J-Bot)

It's time to end one of the longest-running experiments ever seen on this blog. Yes, I'm talking about the hair growth battle between tea tree oil and Korean red ginseng. For those who haven't read how it all began, a recap before the results is in order.

Tea tree oil – is it anti-androgenic?

My hair growth experiment with tea tree oil began last summer, after having tried a tea tree oil toothpaste to treat mouth sores and to improve dental health. I'm still not sure it actually did anything; there was a period of sore-free chewing, but then again, I haven't had mouth sores in many months now, even though I'm using Colgate these days in my search for teeth-whitening toothpastes. I'm thinking it may be due to the 2,000 IU vitamin D3 I've been taking for several months.

Anyway, my interest in tea tree oil was aroused when I read a study that said tea tree oil may have an antiandrogenic effect. If true, it would make tea tree oil a potential treatment for hair loss. Of course, I had to try it on myself.

Adding a carrier oil and Korean red ginseng

At first, I mixed the tea tree oil with sesame seed oil and rubbed in on one side of my right leg. Then, after a month without any visible results, I changed the carrier oil to cocoa butter and added some Korean red ginseng (also known as Panax ginseng) into the mix. Korean red ginseng has actually been shown to have hair growth promoting activity.

After another month, I decided to split the experiment into two parts and apply the ginseng on one side of the leg and the tea tree oil on the other. This time, I got rid of the carrier oil and just applied the pure extract. Not mixing the ginseng and the tea tree oil seemed like a good idea, since their potential method of increasing hair growth was different – one is claimed to be antiandrogenic and the other a stimulant. Therefore, I expected hair growth to be reduced on the tea tree oil treated side and increased on the ginseng treated side.

Switching from tea tree oil to tea tree conditioner

That was almost ten months ago. For months, I applied the two compounds pretty meticulously on my leg. Granted, I missed a day here and another one there, but I did stick with the routine most of the time. At no time did I see any results. Some months ago, my tea tree oil ran out, and I began applying a tea tree oil hair conditioner instead. It absorbed very well, so I figured it could be a decent replacement. Still, no results.

In the past two months, I've been applying the tea tree oil and the ginseng on two of my toes as well. I've even tried the ginseng on one side of my face. And what happened? Yep, you guessed it – no results.

The conclusion

I have no doubt that tea tree oil can be useful as an antibacterial and an anti-inflammatory. However, for all the posts on various forums claiming it works for hair growth as well, I've yet to see even a shred of evidence that it does. My personal experience certainly suggests otherwise.

That said, it very likely won't do harm either, and in fact, I quite liked one tea tree conditioner I used for a week during a vacation. It made my scalp feel very clean. Unfortunately, I was unable to find another bottle to take back home with me. The one I currently have doesn't have the same effect (by the way, if you're buying a tea tree oil shampoo or conditioner, make sure tea tree oil (or the latin name Melaleuca) is mentioned fairly early on in the ingredient list; otherwise the concentration will probably be too low to have any effect).

So what is the conclusion? I cannot say for certain that neither tea tree oil or Panax ginseng are able to affect hair growth, but at least they did not do so in my case when applied on the leg. If others wish to try the same experiment, I wish them good luck, and hope they will report back with results.

For me, it's once again onto bigger and better things, because quite frankly, I'm tired of rubbing this stuff on my legs and toes!

For more information on hair growth, see these posts:

North African Plant Extract (Erica multiflora) Increases Hair Growth
Hyaluronic Acid for Skin & Hair – Experiment Conclusion
2% Nizoral Shampoo Increases Hair Growth More than 2% Minoxidil
Emu Oil and Hair Growth: A Critical Look at the Evidence

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Thursday, April 23, 2009

Does Ginkgo Biloba Improve Cognitive Performance?

Does Ginkgo Biloba Improve Cognitive Performance?
Ginkgo biloba extract is made from the leaves of the maidenhair tree. (Photo by inoc)

The leaves of the maidenhair tree, Ginkgo biloba, are used in traditional medicine to treat various disorders. In recent years, the extract made from the leaves has also gained reputation as a possible memory and learning booster, as well as a natural treatment for Alzheimer's disease. But does it really work?

Unlike some other traditional medicines, Ginkgo biloba has actually been studied quite a bit. However, the results regarding its effects on brain function are inconclusive, which is why in this post, we'll take a closer look at what the current understanding of the matter is.

Ginkgo biloba and brain aging

Possibly the most interesting property of Ginkgo is its suggested ability to prevent or slow down brain aging, especially Alzheimer's disease. Unfortunately, many of the studies show rather disappointing results. A standard dose (120 mg) of Ginkgo biloba given for 6 months had no effect on cognitive functioning in patients with early stage dementia (link). Furthermore, in a study with over 3,000 participants, the same dose given for 6 years did not reduce dementia progression and Alzheimer's disease (AD) incidence compared to placebo (link).

However, a recent analysis found that a dose of 240 mg per day increased cognitive test scores in patients with AD and probable vascular dementia (link), suggesting that higher doses may be needed to see results. The timing of administration may also be important. In rats, Ginkgo had a positive effect on spatial memory tasks when given before the task, but no effect on memory when given after the task (link).

Degradation of amyloid precursor protein (APP) generates amyloid beta, which is the primary component of amyloid plaques found in the brains of Alzheimer's disease patients. In aged but not young mice, long-term treatment with high amounts of Ginkgo biloba extract have been shown to reduce APP levels in the cortex (link), which may partly explain the neuroprotective effect seen in some studies. In addition, Ginkgo seems to stimulate neurogenesis (link) and increase synaptic plasticity (link, link).

Combining Ginkgo with other compounds may increase its effectiveness. In one study, a composition of ginseng and Ginkgo extracts showed an improvement in hippocampal neurotransmitter status in APP transgenic mice (link). A combination of Ginkgo biloba, vitamin E, phosphatidylserine and pyridoxine had a long lasting positive effect on cognitive functioning in aged dogs (link).

Overall, the data on Ginkgo biloba's effect on brain aging is mixed. One review found that out of 34 placebo-controlled clinical trials, 21 showed significant benefits, 8 showed modest benefits, 4 showed a trend in favor of Ginkgo, and 2 found no advantage (link). Another recent review concluded that the evidence supporting the use of Ginkgo for dementia or cognitive impairment is inconsistent and unreliable (link).

Ginkgo biloba, stress and anxiety

Besides aging, cognitive impairment can also result from stress. In rats, Ginkgo biloba has been shown prevent learning and memory impairment and neuronal loss resulting from chronic stress (link, link) and to improve fear conditioning (link).

Though many studies have shown a cognitive benefit only in old animals, in one study, Ginkgo reduced anxiety also in younger human patients in a dose-dependent manner (link). Another one found a calming effect in healthy patients (link), which may be linked to Ginkgo's potential ability to reduce blood pressure during stress (link). In subjects between 50 and 65, depression, fatigue and anger were reduced with a daily dose of 240 mg (link).

On the other hand, a combination of Ginkgo biloba and Panax ginseng had no effect on mood, somatic anxiety, menopausal symptoms, sleepiness and cognition in post-menopausal women (link). Interestingly, however, one study found that both extracts had an effect on brain wave activity (link).

Ginkgo biloba in healthy people

Since Ginkgo is also sold as nootropic, a review of the studies on healthy people is in order. One study found an improvement from 120 mg Ginkgo in longer-term memory in old patients but no effect in young patients (link). An older study with middle-aged patients found that a dose of 240 mg resulted in increases in self-estimated mental health and quality of life and also an increase in motor performance compared to placebo (link).

A very large study including 3,500 volunteers aged between 35 and 80 years found no association between moderate doses of Ginkgo or ginseng and performance on learning and memory (link). A combination of Ginkgo and Bacopa monniera was also ineffective in healthy subjects (link). However, higher doses of Ginkgo (360 mg) and Panax ginseng (400 mg) may be needed to see cognitive benefits (link).

A reanalysis of three studies concluded that 120 mg of Ginkgo biloba modestly improves memory performance but may have a detrimental effect on the speed of attention task (link). However, a review of 15 randomized clinical trials suggests that several of the studies had methodological flaws, and that neither acute nor long-term administration has been shown to improve cognitive function in healthy young people (link).


Many studies have been done, but the evidence supporting Ginkgo biloba as a cognition enhancer remains inconclusive. Some studies have found a benefit while others show no effect. Based on the animal data, Ginkgo biloba has a neuroprotective effect and may help prevent cognitive decline resulting from aging and chronic stress. In humans, the case is less clear, especially when it comes to healthy, young people.

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

L-Carnitine, Acetyl-L-Carnitine and Cognitive Function in Humans
Increasing Intelligence by Playing a Memory Game – Experiment Update
Caloric Restriction Improves Memory in the Elderly
Intermittent Fasting Reduces Mitochondrial Damage and Lymphoma Incidence in Aged Mice

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Monday, April 20, 2009

L-Carnitine, Exercise Performance & Oxidative Stress

L-carnitine may reduce oxidative stress from exercise.
L-carnitine may reduce oxidative stress from exercise. (Photo by mikebaird)

The case for carnitine supplements in preserving brain function seems strong enough (especially in animals, but also in humans), but what about carnitine and exercise benefits? In this post, we'll look at the studies on the effects of carnitine in aerobic and anaerobic exercise.

In the studies on carnitine and cognition, the only forms of carnitine that were used were L-carnitine and acetyl-L-carnitine. In the studies below, glycine propionyl-L-carnitine and L-carnitine L-tartrate are mentioned as well. Glycine propionyl-L-carnitine (GPLC) is a propionyl ester of carnitine that includes an additional glycine component for better absorption. L-carnitine L-tartrate (LCLT) is a salt form of L-carnitine, which is used mostly because it's not as easily degraded.

Carnitine and exercise performance

Aging results in an atrophy of the muscle fibers, an increase in fat mass, and a decrease in skeletal muscle oxidative capacities. When Bernard et al. fed old rats with L-carnitine at 30 mg/kg body weight, the L-carnitine levels and oxidative activity of muscle cells was restored. A positive change in body composition was also seen: the carnitine-fed rats decreased their abdominal fat mass and increased muscle capabilities.

According to Panjwani et al., L-carnitine in a dose of 100 mg/kg body weight improved exercise endurance of rats both at sea level and high altitude conditions. The effect was more pronounced during the latter.

Thalassemia is an inherited blood disease that is associated with poor physical fitness. El-Beshlawy et al. report that when thalassemic patients were given L-carnitine at 50 mg/kg body weight or placebo for 6 months, oxygen consumption, cardiac output, and oxygen pulse at maximal exercise increased significantly in the carnitine group. The authors note that L-carnitine works better the younger the patients are.

Jacobs et al. looked at glycine propionyl-L-carnitine and its effect on high-intensity cycling performance in healthy, trained individuals. The authors conclude that short-term oral supplementation enhanced peak power production and decreased post-exercise blood lactate accumulation.

Spiering et al. gave healthy resistance-trained men 2 grams of LCLT or placebo for 23 days. In the participants receiving carnitine, forearm muscle oxygenation was reduced. At the same time, malondealdehyde levels decreased. The authors propose that this seemingly contradictory effect may have been due to enhanced oxygen consumption.

On the other hand, Eroğlu et al. saw no difference in the metabolic and blood lactate values of male and female badminton players after taking 2 grams of L-carnitine prior to exercise. Bloomer et al. studied the effects of 1-3 g GPLC on aerobic and anaerobic exercise performance in healthy men and women. No difference was seen between the treated and placebo groups.

Carnitine and oxidative stress from exercise

Later, Bloomer & Smith looked at how GPLC affects oxidative stress from aerobic and anaerobic exercise. Both forms of exercise increased oxidative stress even in those receiving the carnitine supplement. However, GPLC reduced resting levels of malondialdehyde, which is a marker for oxidative stress.

In a study by Broad et al., twenty active males were given either 2 grams of L-carnitine L-tartrate or placebo for two weeks. When comparing the results from a 90-minute exercise test before and after treatment, no change was seen in fat, carbohydrate and protein contribution to metabolism in either group. Plasma ammonia tended to decrease in the carnitine group, however, which may suggest a potential reduction of metabolic stress from exercise.

In a study by Volek et al., 2 grams of L-carnitine L-tartrate for three weeks resulted in a reduction of post-exercise levels of malondialdehyde. Muscle disruption, markers of purine catabolism and cytocosolic proteins were also attenuated, suggesting that carnitine is effective in assisting recovery from squatexercises.

Kraemer et al. looked at how LCLT supplementation and post-exercise feeding affect hormonal and androgen receptor responses. Before exercise, LCLT upregulated androgen receptor content. Resistance exercise increased androgen receptor content in the placebo group only, while post-exercise feeding increased it in both groups. The authors suggest the upregulation of androgen receptors by LCLT may promote recovery from resistance exercise (I suppose the androgen-related effect might also be of interest to those worried about hair loss).


While the evidence for the effects of carnitine on exercise is inconclusive, carnitine may improve physical fitness in old or unhealthy people. Furthermore, the studies suggest carnitine reduces markers of exercise-related oxidative stress, especially malondialdehyde.

For more information on exercise and carnitine, see these posts:

L-Carnitine, Acetyl-L-Carnitine and Cognitive Function in Humans
L-Carnitine, Acetyl-L-Carnitine and Cognitive Function in Animals
Green Tea Extract Increases Insulin Sensitivity & Fat Burning during Exercise
Coenzyme Q10, Exercise and Oxidative Stress

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Sunday, April 19, 2009

Topical Vitamin C for Skin: Re-examining the Case

Vitamin C reduces wrinkles – but only when used topically. (Photo by √oхέƒx™)

Lately, I've been reading the Skin Aging Handbook by Nava Dayan in an attempt to educate myself on how skin aging happens and what can be done to prevent it.

A few months ago, I concluded my experiment with a product called SkinCeuticals CE Ferulic acid. As the name implies, it's a topical that contains vitamin C & E and ferulic acid. I was impressed by the studies behind the product, so I bought some sample bottles and applied it on my face for about half a year.

Unfortunately, I didn't see any visible results. I hypothesized that it might have been due to the ascorbic acid being oxidized, because in some bottles the liquid was a deep orange color instead of a light yellow. Since the product is quite expensive, I decided to move on to other things for the time being.

Reading the book, however, has re-sparked my interest. The evidence for the anti-aging benefits of topical vitamin C is much more positive than I had thought. Below is a compilation of the beneficial effects of ascorbic acid on the skin:

  • Increases the transcription rate of DNA in vitro
  • Increases fibroblast proliferation by a factor of four to six in vitro
  • Doubles collagen synthesis of fibroblasts in vitro
  • Has anti-inflammatory properties in vitro
  • Enhances collagen production (type I and III) in vivo
  • Protects from UV-induced photodamage and skin cancers in vivo
  • Reduces uneven pigmentation in vivo

In other words, topical vitamin C is able to both prevent and reverse photoaging, including wrinkles. Here's a picture taken from the book showing results after a year of using vitamin C:

Topical vitamin C serum and skin aging
Vitamin E, too, has photoprotective properties. Unlike vitamin C, vitamin E works both topically and orally, but the form of vitamin E is important. For topical use, d-alpha-tocopherol seems like the best option.

The reason why vitamin C serums should have vitamin E (and preferably ferulic acid) as well is because they work synergistically to provide antioxidant protection. In other words, the combination works better than the single ingredients alone. It's also more stabile.

I'm currently looking for cheaper alternatives for the SkinCeuticals product, but the options seem pretty limited at the moment. One option is to buy the ingredients separately and make your own serum. In any case, I decided to take a risk and purchased another set of sample bottles to see if there's a difference the quality.

Indeed, that seems to be the case: the color of the liquid in the first bottle I opened is much lighter ('champagne' describes it well) than in the previous batch. Thus, most if not all of the bottles I had the last time had clearly oxidized, which means they were useless (and possibly even harmful, though I'm not sure of this). A waste of money, but at least I learned something.

I'm storing the current batch in the fridge just in case. The last time I applied the serum on my entire face and both hands. However, now that I have several more experiments related to skin going on, I'm applying it on my entire face, but only on the left side of the neck and my left hand.

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

Examining Possible Causes for Slower Wound Healing
Lutein for Skin Elasticity, Hydration and Photo-Protection – Experiment Begins
Coconut Oil Is Better than Olive Oil for Atopic Dermatitis
Bioactive Form of Silicon (BioSil) Improves Skin, Hair & Nails in Photoaged Women

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Friday, April 17, 2009

How to Live Forever: My 5 Steps to Immortality

Would you get bored if you had the chance to live forever?
Would you get bored if you had the chance to live forever? (Photo by mandj98)

As the description of this blog says, the idea behind my human experiments is to help me (and others) live longer and healthier. Unlike some people, who seem to know they will eventually want to die of old age, I haven't specified any upper limit on how long I want to live. In fact, there is no upper limit, because I don't want to die at all. I want to live forever.

Sounds ridiculous, right? How on earth is something like intermittent fasting going to make me live forever? The answer is it's not, at least not by itself. The key to understanding the five-step plan is to see that a healthy lifestyle is all about avoiding the most common causes of death, while people more gifted than me work on postponing the evitable.

These rather simple steps lay down my current strategy for dealing with the all-consuming, world-destroying, meaning-shattering problem that is aging.

1. Eating a healthy diet

A lot of the posts on this blog are focused on diet. Many of the experiments I've tried are related to diet. For me, searching for clues on what might be the optimal diet is a continuous process, a neverending quest. It's challenging, but also immensely interesting and rewarding.

Some people think or at least secretly hope that if they just eat healthy, they'll somehow be excluded from the sphere of aging. As if making that extra effort would make Death spare his scythe, just this once. These are the same people who look at their friends indulge in unhealthy pleasures like smoking, drinking, fast foods, while quietly thinking to themselves that their abstinence will have some grand payoff in the end.

It might, but not in the way they think. I have no disillusions about a healthy diet making me live forever. Whether it's a raw food diet, low-carb diet, a paleolithic diet, caloric restriction or intermittent fasting, none of these things alone will make me or anyone else immortal. The only reason I'm constantly tweaking and seeking to improve my diet is to avoid the causes of death that result from eating poorly. In other words, the goal of eating healthy is to maximize my natural lifespan.

But what exactly is the maximum natural lifespan? It seems that 120 years is about as long as the human body can survive without any extreme rejuvenation therapies. Even then genes probably play at least some part; some people lead very healthy lifestyles and still die before the age 100.

Nonetheless, and this is the important point, if the life expectancy for a person eating an average diet is about 80 years, and the life expectancy for someone eating a very healthy diet is 100 years, that's a difference of 20 years. As we will see, those extra 20 years might prove to be extremely important.

2. Leading an active life

Some people think being sedentary is alright as long as you eat healthy. Others say you can eat anything you want as long as you exercise and stay fit. I tend to lean towards the former, which is why leading an active life is second on my list, and diet is first. Of course, by combining the two, I'm expecting better results than from either one alone.

Exercise, just like eating healthy, is a way of preventing that which is preventable. If I can reduce the risk of high blood pressure and osteoporosis by jogging, give me a pair of running shoes. If lifting weights will help keep the heart muscle healthy, show me the way to the gym. Again, there is no exercise out there that will make me live forever, whether it's high-intensity interval training or ancient Tibetan yoga, but a decent routine will probably give me a handful extra years I wouldn't otherwise have.

Note that an active life doesn't just mean an active life physically, but mentally as well. It's no secret that people who have a sense of purpose in life tend to live longer, and people who actively use their brain tend to have better cognitive function at old age. When it comes to the brain, it's use it or lose it. From what I've read and seen in other people, being passionate about something – be it science, arts, music, gardening, or whatever it is that interests you – is much better for longevity than leading a passive life.

3. Taking supplements

This step includes basically anything that can be taken in capsule form: nutritional supplements, drugs, herbal extracts, etc. I will just categorize them all under the term 'supplement' for simplicity. The distinction between a supplement and a drug is arbitrary anyway.

Since it's not currently practical (not to mention enjoyable) to eat only supplements, a healthy diet without supplements is a better choice than a poor diet with supplements. Therefore, supplements are after diet on the list. They're also after exercise, because at the moment, we have more data on the benefits of exercise than we do on the benefits of supplements. Again, by combining the three, I'm expecting better results than from using a single approach.

Some people are almost irrational in their faith in supplements. Like with eating a healthy diet, they think that if they just take enough of their favourite vitamin every day, maybe they'll be able to cheat death. Granted, this idea is appealing, because even now, there are several supplements available that can provide us with compounds in concentrations thousands of times stronger than what is found in nature. Resveratrol is one such example. Thus, some supplements do allow us to cheat nature. None of them allow us to cheat death, however.

It's worth noting that many people are also irrational in their position against supplements. They feel no supplement is worth taking, either because it hasn't been shown to extend lifespan in humans, which would require waiting on the sidelines for a hundred years, or precisely because the compounds in them don't exist in similar quantities in nature. The latter view is especially common among those who support the argument from naturality, which basically says that anything that is unnatural is bad. But death, of course, is entirely natural.

I view supplements as a third way of preventing various causes of death and promoting general health. There is no single magic pill that will instantly give me an extra ten years of life, but there are a lot of supplements with promising health benefits: acetyl-L-carnitine, vitamin D3, vitamin K2, resveratrol, and curcumin, just to name a few. Anything that can delay even some of the manifestations of the aging process, if not the actual process, is useful in my books. Preventing death is a battle that must be fought on all fronts.

4. Rejuvenation therapies

This is without a doubt the most important step on the road to immortality. Without radical life extension methods, immortality is never going to be possible. If diet, exercise and supplements are pistols in the war against aging, good for taking out single enemies but not enough to conquer an entire army, the coming of life extension technology is the point in battle when the tanks roll in.

This doesn't mean that we will have a single therapy that will bless us with another 100 years each time we use it. Rather, what will likely happen at first is that we will have an engineering approach to the problem of aging: identifying the things in the body that are susceptible to deterioration and fixing them one by one, with priority on the parts that break down first.

This is a useful strategy, in my opinion, because it means we don't have to come up with the ultimate solution for aging right away. Instead, we can do our best to replace parts as they break down, and use those extra years to discover more efficient solutions. The key here is that these engineering methods will do much more for lifespan extension than diet, exercise and supplements ever can. They are the only to way to truly beat nature at its own game.

Perhaps in the long run, after several iterations of mechanical problem-fixing, we may even find that one-size-fits-all cure for aging. Or we may have discovered a way to transplant our brain onto a more suitable vessel, one unburdened by biological deterioration. It's impossible to know what the future looks like, but I have no doubt that at some point, all this will be possible.

5. Cryonics

And then there's the caveat: even though I have no doubt all of the above will happen, I have many doubts about when it will happen. Anyone who argues that immortality can never happen is in my mind certainly wrong, assuming the world is not destroyed by a meteor or something. Furthermore, anyone who argues that immortality won't happen within the next 10,000 years is in my mind almost certainly wrong. On the other hand, someone who argues that immortality won't happen in my lifetime may well be correct.

That's a frightening argument, but one that must be considered carefully. If immortality is impossible at any point in the future, it becomes irrational to pursue it. However, if it's probable that immortality will be possible within the next 10,000 years, as I suggest it is, but impossible within the next 100 years, it becomes rational to pursue it. But if the first real rejuvenation therapies will be here in the year 2100, what can we who are alive today do?

The best solution at this point is cryonic suspension. In layman's terms, you put yourself in ice and wait for better times. We already know how to do the suspension part, and even though we don't know how to bring people back, I think it's only a matter of time before we do. Even if my chances of ever waking from the glacial slumber are small, it's still a more rational choice for me than being buried or cremated. For the skeptics who still think your cells would freeze and explode in cryonic suspension, see the FAQ at Alcor's website.

Cryonics is more efficient and more safe now than it was when the first people took the plunge to the long chill. The mainstream media hasn't caught up with cryonics as much as it has with anti-aging, but as the world's millionaires and forward-thinkers get older and more desperate to find ways to be around when the future arrives, I think cryonics will become more fashionable.

I realize cryonics is a last resort. I hope rejuvenation therapies will see the light of day before I'm too old, but if they don't, I'm definitely headed for the ice box, not the grave. Also, if I knew I was going to die of a terminal disease, I would make arrangements for cryonics. At the moment, it would mean having the funds and likely moving to the United States. In the coming years, I think we'll see companies offering cryonics services in the rest of the world too.


My plan for achieving immortality consists of two main parts and a backup plan. The goal of the first part is to maximize my natural lifespan by avoiding diseases and staying healthy for as long as possible. That means following three basic steps, in the order of importance: eating a healthy diet, leading an active life and taking supplements.

Hopefully, these three steps will able me to live to see step four, the coming of rejuvenation therapies and radical life extension technologies. This is the step that is needed for true immortality to be possible.

If it looks like step four is not going to happen in my lifetime, it's time for the the backup plan or step five, which is cryonic suspension. Hopefully future generations will discover a way to bring me back from my icy sleep so I can join the party.

For some people, doing all this just to increase the chances of living forever might be too much of a hassle. Those with little imagination will not even see the appeal in living forever. Passive people are sure they would eventually get bored with life. Naturalists argue it's unnatural to try to cheat death. Religious people claim we shouldn't play God. Pessimists say it's a nice idea, but it will never work.

For me, however, the prize is too great not to try my best.

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

End Aging to End Anxiety: Filmmaker Jason Silva Talks about Immortality
Anti-Aging in the Media: Vancouver Sun on Immortality
Anti-Aging in the Media: NOW Magazine on the International Anti-Aging Show
Anti-Aging in the Media: The Globe and Mail on Telomerase

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Thursday, April 16, 2009

North African Plant Extract (Erica multiflora) Increases Hair Growth

Erica multiflora grows in the dry heat of Tunisia.
Erica multiflora grows in the dry heat of Tunisia. (Photo by krc)

Since it's been a while since I've written about exotic substances and hair growth, it's once again time to baldly go where no man has gone before and post some more news from the hair loss front.

Kawano et al. recently published a study suggesting that a plant called Erica multiflora increases hair growth in vitro and in vivo in mice. The abstract has already made its way into several discussion forums, but what does the full paper say?

Like true pioneers of scalp health, the authors collected several different plants from Tunisia and tested their effect on hair growth. Among the plants was Erica multiflora, an aromatic plant used in North Africa to treat inflammation and hypertension, which has also been shown to reduce cholesterol and triglyceride levels. It was extracted by immersing 10 grams of dried plant in 100 ml of 70% ethanol for two weeks and then filtered to remove plant parts and sterilize the extract.

In vitro hair growth effects of Erica multiflora

For the in vitro experiment, human follicular dermal papilla cells were treated with the extract. Out of the six plant extracts tested, only Erica multiflora significantly increased the growth of human follicular dermal papilla cells. Some of the plants actually tended to decrease hair growth.

The growth promotion activity of Erica multiflora was clear only when a high concentration extract was used. 500 mcg of extract per ml increased hair growth by 9%, while a concentration of 5,000 mcg per ml increased it by 44%.

Treating the cells with the extract for 12 hours stimulated the cells, while longer treatments did not have a similar effect. According to the authors, Erica multiflora had the ability to stimulate dermal papilla cell mitosis but not to promote DNA synthesis.

In vivo hair growth effects of Erica multiflora

For the in vivo experiment, the extract was applied on the backs of shaved mice. Since the mice were of the same age, they were known to be in the telogen (resting) phase of hair growth. The mice were then injected with the 500 mcg/ml extract or phosphate-buffered saline.

Hair growth was seen after 3 weeks of injection of Erica multiflora. The authors note that the extract stimulated the normal hair cycle, inducing hair follicles at the next anagen and telogen stages. Vasodilation also occurred near the anagen-stimulated area. They conclude that since there was a delay between the injection and increased hair growth, the extract stimulated the shift from telogen to anagen phase indirectly.


The extract of Erica multiflora stimulated human follicular dermal papilla cell growth by up to 44%. When injected onto the backs of shaved mice, the extract increased vasodilation and stimulated the change from the resting phase to the growth phase of hair.

For more information on hair growth, see these posts:

Bioactive Form of Silicon (BioSil) Improves Skin, Hair & Nails in Photoaged Women
2% Nizoral Shampoo Increases Hair Growth More than 2% Minoxidil
Lygodium japonicum Promotes Hair Growth by Inhibiting Testosterone to DHT Conversion
Chinese Hibiscus Leaf Extract Increases Hair Growth in Mice

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Wednesday, April 15, 2009

Examining Possible Causes for Slower Wound Healing

Blueberries reduce inflammation, but do they affect wound healing?
Blueberries reduce inflammation, but do they affect wound healing? (Photo by a2gemma)

I'm not sure why, but during the past few months, I've noticed my wounds healing slower than usual. Even fairly minor scratches take more than a week to heal fully, and bigger cuts seem to take at least three weeks. The bleeding stops normally and everything, but after that, the healing process just takes longer than it used to.

This has had me wondering what the cause might be. I've ruled out most of the supplements I've taken, because the experiments have only lasted for a couple of months and haven't really coincided with the slower wound healing. The supplements I've been taking for several months are vitamin C (500 mg), vitamin D (2,000 IU), and AOR Ortho-Core multivitamin (2 capsules). None of these should interfere with wound healing; on the contrary.

The first thing that comes to mind besides supplements is intermittent fasting, which I've been doing for about nine months now. As it happens, there is a paper (here.) that says caloric restriction and intermittent fasting reduces cell proliferation in epidermal tissue, which would likely have an effect on wound healing as well.

Another possible reason could be a low level of inflammation. Low inflammation is of course generally a good thing, but there is some evidence suggesting it might interfere with the wound healing process. Intermittent fasting apparently reduces inflammation markers quite a bit, and green tea protects from arthritis by reducing inflammation in vivo and in vitro. As you may know, I drink several cups daily.

Other staples of my diet with possible inflammation-reducing properties include dark chocolate and my morning smoothie with a hefty dose blueberries, blackcurrants, strawberries and raspberries – all high in antioxidants and polyphenols, which are said to lower inflammation. Avoiding processed carbohydrates and starchy foods probably plays a part as well.

It was also pointed out to me that low levels of zinc may contribute to slow wound healing, so I looked around for some more information. One paper (here) suggests low levels of zinc delay wound healing during hip replacement, and another one (here) mentions correcting a zinc deficiency resulting in improved wound healing.

A zinc deficiency is rare, however, and it's less clear whether increasing zinc intake from less than optimal levels will speed up wound healing. Also, one paper (here) suggests very high doses may in fact negatively affect wound healing, similarly to a zinc deficiency. Nevertheless, zinc supplementation apparently stimulates healing of bone fractures (abstract available here).

The RDA for zinc in adult males is 11 mg. According to CRON-O-Meter, my typical daily menu contains only ~5 mg of zinc. My multivitamin gives me another ~4 mg, bringing me to 9 mg. On the days I replace the fish in my warm meal with meat, my zinc intake is higher, so I probably average pretty close to the RDA.

I'm not entirely convinced the RDA is the same as thing optimal (it certainly isn't for vitamin D), so as an experiment, I'll be taking 15 mg zinc as a supplement to see if it speeds wound healing. Meanwhile, I'll keep an eye out on other possible causes. And if you have a theory or personal experiences, feel free to drop a comment.

For more information on diets and health, see these posts:

Intermittent Fasting Improves Insulin Sensitivity Even without Weight Loss
Low-Carb vs. Low-Fat: Effects on Weight Loss and Cholesterol in Overweight Men
The Effects of a High-Fat Diet on Health and Weight - Experiment Conclusion
How the Accumulation of Minerals Might Cause Aging in Humans

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Tuesday, April 14, 2009

Green Tea and Capsaicin Reduce Hunger and Calorie Intake

Add cayenne pepper to your green tea and reduce your appetite?
Add cayenne pepper to your green tea and reduce your appetite? (Photo by loxosceles)

In my own experience, drinking green tea can moderately help with hunger during a fast. But what about the effect of green tea on appetite in general? Does it help you lose weight by making you want to eat less?

In a brand new study, Reinbach et al. put subjects on two different diets: one resulted in a positive energy balance (meaning they ate more calories than they spent) and the other in a negative energy balance (meaning they ate less than their normal calorie intake). During the three weeks on each diet, the subjects were also given green tea, capsaicin, sweet pepper, a combination of capsaicin and green tea, or a placebo, to see how the supplements affected their appetite.

The diets

During the negative energy balance diet, the subjects ate 10% of their normal calorie intake for breakfast and 15% for lunch. On the positive energy balance diet, the calorie intakes were 20% for breakfast and 40% for lunch. At dinner, the subjects were allowed to eat as much as they wanted. The amount eaten at the ad libitum dinner was measured for each treatment group.

The treatments were given to the participants with each of the three meals consumed daily. Those in the green tea group received 3.5 dl of green tea drink, containing ~600 mg catechins and ~75 mg caffeine. The capsaicin capsules contained 510 mg of cayenne pepper. The CH-19 sweet pepper (Capsicum annuum L) capsules contained 2.3 mg capsiate.


Despite eating more at dinner during the negative than the positive energy balance diet, the subjects lost weight on the negative energy balance diet and gained weight on the positive energy balance diet, suggesting that total energy intake was indeed lower during negative energy balance.

All treatments reduced energy intake at dinner during positive energy balance. The most effective treatment was the combination of green tea and capsaicin, followed by green tea alone. Although there was a slight decrease in calorie intake from all treatments even during negative energy balance, the effects were more noticeable during positive energy balance. Energy intakes are shown in the figure below.

Green tea, capsaicin and sweet pepper: effect on calorie intake
The participants taking green tea and capsaicin reported the least hunger and most satiety on both diets. The combination of green tea and capsaicin also significantly reduced liking over meals. Green tea or capsaicin alone didn't have the same effect. Furthermore, green tea and capsaicin, together or separately, reduced the desire to eat fatty, salty and hot foods.


Green tea, capsaicin, sweet pepper, and a combination of capsaicin and green tea all reduced calorie intake during positive energy balance. A similar but less significant effect was seen during negative energy balance. Green tea with capsaicin (yielding ~1,800 mg catechins and 1,530 mg cayenne pepper daily) was the most effective treatment in reducing calorie intake and appetite.

Based on these results, supplementing with green tea, capsaicin or sweet pepper may be more helpful for controlling excessive eating than for staving off hunger during a low-calorie diet or a fast.

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

Green Tea Increases Weight Loss during Caloric Restriction in Rats
Green Tea Extract Increases Insulin Sensitivity & Fat Burning during Exercise
Green Tea Extract Enhances Abdominal Fat Loss from Exercise
A High-Protein Diet Is Better than a High-Carbohydrate Diet for Weight Loss

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Monday, April 13, 2009

L-Carnitine, Acetyl-L-Carnitine and Cognitive Function in Humans

Afraid of age-related mental decline? Carnitine supplements may help.
Afraid of age-related mental decline? Carnitine supplements may help. (Photo by qmnonic)

In the previous post, we looked at the animal studies on carnitine and its effect on cognition. The results were generally positive: both L-carnitine and acetyl-L-carnitine protect the brains of rodents from the effects of aging and stress.

Since, however, we're more interested in whether carnitine is useful as an anti-aging brain supplement in humans, it's time to look at human studies. All the relevant papers related to humans and cognition I could find from the past three decades are briefly discussed below.

Carnitine and age-related cognitive decline

Cipolli & Chiari studied the effects of acetyl-L-carnitine on mildly impaired elderly people. The subjects were given 1.5 g of ALCAR for two periods of 45 days. They report that ALCAR was effective in improving memory function and constructional thinking, while its effect on relational behavior was less consistent.

Long-term oral treatment with acetyl-L-carnitine seems to slow the progression of Alzheimer's disease as well. Spagnoli et al. report that while both the control group and the ALCAR-treated group had worsened after one year, the subjects receiving ALCAR showed a slower rate of cognitive deterioration in all measures, including verbal critical abilities and long-term verbal memory.

Thal et al. note that patients with Alzheimer's disease treated with 3 g of ALCAR per day declined at the same rate as the control group on all measures. A closer look revealed that early-onset patients on ALCAR declined more slowly than those on placebo, while late-onset patients responded poorly. The authors suggest that acetyl-L-carnitine may help AD patients aged 65 or younger but not older patients.

Later, however, Thal et al. treated early-onset AD patients (45 to 65 years old) with 1 g of ALCAR daily for one year and found little to no improvement in cognitive ability compared to the control group. Only the Mini Mental State Estimation (MMSE) showed a decrease in deterioration.

On the other hand, Passeri et al. report that mildly demented patients aged over 65 years showed significant improvement in behavioural scales, memory tests, attention barrage test and verbal fluency test. The treated group received 2 g of ALCAR daily for two months. Thus, perhaps the severity of the dementia is also a factor when determining the effectiveness of ALCAR.

In a really long-term study by Rai et al., patients with Alzheimer's disease were given either 2 g of ALCAR or placebo for two years. The differences between groups were small; the authors suspect this was due to the small sample size (only 20 patients). Still, there was a trend for less deterioration in the treated group, especially in short-term memory tasks.

L-carnitine may even work in those who have had their 100th birthday. Malaguarnera et al. report that 2 grams of L-carnitine resulted in significant improvements in mental fatique and MMSE compared to the control group. They also reduced their fat mass, increased their muscle mass, and had less physical fatique.

Carnitine and depression

In an old study, Bella et al. gave sixty senile subjects (aged 60-80 years) suffering from depressive symptoms either 3 g of acetyl-L-carnitine or placebo daily. After two months of treatment, the severity of depressive symptoms and quality of life as measured by a questionnaire had improved significantly compared to the control group.

Similar results are reported by Tempesta et al. who treated patients suffering from depressive syndrome with ALCAR for a month. ALCAR treatment was highly effective in reducing depressive tendencies. General somatic symptoms and anxiety, asthenia and sleep disturbances were largely unaffected, however. Unfortunately, the dose used by the authors is not mentioned in the abstract, and the full paper is so old that I'm unable to access it.

Carnitine and other neuropsychological problems

Cirrhosis patients often have disturbances in mental state and neuromuscular function. Malaguernerna et al. studied the effects of ALCAR on cirrhosis patients by giving them either acetyl-L-carnitine or placebo. After 90 days, the ALCAR group showed improvements in neuropsychological functioning and greater reductions in serum ammonia levels.

Persons with Down syndrome are at a greater risk to develop Alzheimer's disease. Pueschel studied the effects of acetyl-L-carnitine on neurological, intellectual and social functions in adults with Down syndrome. In this case, ALCAR administration did not improve central nervous system functions.

Carnitine in young, healthy people

All of the studies so far have been dealing with old or otherwise impaired people. The results suggest carnitine has a protective role in brain functioning, but what about healthy people? Unfortunately, the data is very lacking. In fact, I could find only one study that looked at the cognition-boosting effects of carnitine in young, healthy participants.

In an unpublished research paper, Rohde describes an experiment where college students were given either 1 g of ALCAR in two 500 mg doses or placebo daily for two weeks. Their cognitive ability was then tested on a computer software. The ALCAR group out-performed the controls on 83% of the measures, which suggests acetyl-L-carnitine may indeed be helpful for those still have all their mental capacity.

However, since this is an unpublished study, and there are no other studies available, I would be fairly cautious about the results. Also, there's at least one study that showed carnitine had no effect in young rats. Nonetheless, some people without cognitive problems report increased physical and mental energy from taking ALCAR, so perhaps there's something to it. A human experiment may be in order to find out for myself.


Most of the studies on acetyl-L-carnitine show a benefit in treating mental decline and Alzheimer's disease, although a few studies reported no effects. It is unclear whether ALCAR works better in younger AD patients. L-carnitine was shown to reduce mental and physical fatique even in those aged over 100 years, however.

ALCAR also seems to relieve symptoms and improve quality of life in patients suffering from depression. The data for neuropsychological problems resulting from other diseases is mixed. One unpublished paper suggests ALCAR in two 500 mg doses may improve cognition in healthy, young people.

Taken together with the animal studies, the results suggest acetyl-L-carnitine and L-carnitine can reverse some of the effects of aging and possibly causes as well.

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

L-Carnitine, Acetyl-L-Carnitine and Cognitive Function in Animals
Increasing Intelligence by Playing a Memory Game – Experiment Update
Caloric Restriction Improves Memory in the Elderly
Moderate and Severe Caloric Restriction Alter Behavior Differently in Rats

Read More......

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Thursday, April 9, 2009

L-Carnitine, Acetyl-L-Carnitine and Cognitive Function in Animals

L-Carnitine, Acetyl-L-Carnitine and Cognitive Function in Animals
A 3.5 oz serving of beef steak will give you 95 mg of carnitine. (Photo by

Carnitine is required in the mitochondria for the generation of metabolic energy. It is biosynthesized from lysine and methionine primarily in the liver and kidneys.

Carnitine concentrations in the cells decrease with age, which is why carnitine is also marketed as an anti-aging supplement. Supplementary carnitine is sold as L-carnitine, which is the bioactive form of carnitine, or acetyl-L-carnitine (ALCAR), which is the acetylated form of L-carnitine.

But what is the evidence behind the claimed anti-aging effect? Fortunately, several studies have been done. In this post, we'll look at the currently available animal data on the effects of both forms of carnitine on cognition. I'll save the human studies for next time.

Carnitine and age-related cognitive decline

In one of the earliest studies, Bossoni & Carpi showed that acetyl-L-carnitine supplementation improved the learning ability and memory processes of rats and mice, both with oral treatment and injections. The doses ranged from 0.3 mg/kg to 100 mg/kg body weight. ALCAR also antagonized amnesia, when electroconvulsive shocks were given to the mice during one of the learning tests.

A few years later, Ghirardi et al. reported that 8 months of ALCAR supplementation protected rats from age-related deterioration in spatial learning. Similarly, Valerio et al. showed that aged rats performed better in active and passive avoidance tests when given ALCAR. These tests are used as models of learning and memory capacity. The doses are not mentioned in the abstracts, and the studies are so old that I'm unable to access the full papers.

Recently, Freddi et al. gave 15-month-old male rats 60 mg/kg acetyl-L-carnitine per day orally for six months and tested their spatial memory with a maze-water task. The ALCAR-fed rats found their way through the maze significantly faster than the control rats. The control rats also showed age-related degenerative morphological changes in their basal forebrain regions while the treated rats did not.

Old rats have higher rates of lipid peroxidation than young rats in many brain regions. Lipid peroxidation means the process where free radicals steal electrons from the lipids in cell membranes, which results in cell damage. Rani & Panneerselvam report that when old rats were injected with 300 mg/kg L-carnitine for 21 days, lipid peroxidation decreased in many areas of the brain. Superoxide dismutase activity was restored to youthful levels, which suggests the neuroprotective effect of L-carnitine is in part due to its ability to increase antioxidant levels. L-carnitine had no effect on young rats, however.

Carnitine and stress-related cognitive decline

ALCAR also seems to protect the brain from hypobaric hypoxia, a condition in which the body is deprived of adequate oxygen due to a high altitude. It can cause oxidative stress, neurodegeneration and memory impairment. When Barhwal et al. exposed rats to hypobaric hypoxia for two weeks, their condition improved when they were supplemented with ALCAR. There was a decrease in free radical production, lipid peroxidation and protein oxidation, and a decrease in the levels of glutathione.

The stimulant drug ecstacy (MDMA) is known to increase mitochondrial oxidative stress in the brain. When Alves et al. gave injected rats with acetyl-L-carnitine (100 mg/kg body weight) prior to ecstacy, the oxidative damage from the drug decreased significantly. ALCAR reduced carbonyl formation, decreased mitochondrial DNA deletion, improved the expression of respiratory chain components and prevented the decrease of 5-HT levels in many regions of the brain.

Excessive doses of insulin can also cause mitochondrial swelling and neuronal death in the brain of patients with diabetes mellitus. Hino et al. induced hypoglycemia in rats that were given L-carnitine in their drinking water. Although the mortality rate remained the same as in the control group, the rats that did survive the high insulin dose had improvements in cognitive function. L-carnitine effectively inhibited mitochondrial dysfunction and prevented neuronal injury.

Sezen et al. induced brain damage to rats with radiation and found out that vitamin E (40 mg/kg) and L-carnitine (200 mg/kg) separately reduced the severity of brain damage. Both supplements increased the activity of superoxide dismutase and catalase enzymes, again suggesting that L-carnitine has an antioxidant role. Combining vitamin E and L-carnitine didn't yield additional benefits, however.

Similarly, Túnez et al. compared the effects of vitamin E (20 mg/kg), L-carnitine (100 mg/kg) and melatonin (3 mg/kg) on rat brain and liver damage from a single dose of thioacetamide, which increases lipid peroxidation. All three protected the rats from oxidative stress, with melatonin offering the best protection.


Acetyl-L-carnitine (ALCAR) has been shown to improve learning ability and memory processes in aged rats. L-carnitine was shown to reduce lipid peroxidation and increase superoxide dismutase activity in the brains of old rats but not young rats.

Both ALCAR and L-carnitine also protected rats from artificially induced oxidative stress in the brain. The protective effect was again associated with decreased lipid peroxidation and increased superoxide dismutase activity in the brain.

Taken together, these results suggest that L-carnitine and acetyl-L-carnitine protect the brain from both age-related and stress-related damage in rodents. The protection may be due to carnitine's ability to increase antioxidant levels.

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

Increasing Intelligence by Playing a Memory Game – Experiment Update
Caloric Restriction Improves Memory in the Elderly
Moderate and Severe Caloric Restriction Alter Behavior Differently in Rats
Intermittent Fasting Reduces Mitochondrial Damage and Lymphoma Incidence in Aged Mice

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Tuesday, April 7, 2009

Green Tea Increases Weight Loss during Caloric Restriction in Rats

The catechins in green tea are not the only healthy polyphenols of tea.
The catechins in green tea are not the only healthy polyphenols of tea. (Photo by Augapfel)

It's time for some more green tea news from the weight loss frontier. If you're planning on doing calorie restriction to lose weight, you might want to consider adding green tea to your daily menu.

In a recent study, Sogawa et al. compared the anti-obesity effects of two types of tea, green tea and Awa tea, on male rats. The rats were first put on a weight-gain phase, where they were fed good old lard along with their standard diet. Then, they were put on a 50% calorie restriction (CR) diet to induce weight loss. During the CR diet, the experimental groups were supplemented with 3% green tea extract or 3% Awa extract, while the control group was given no supplements.

Awa tea is a traditional tea from the Tokushima prefect in Japan. It is made by fermenting tea leaves with lactic acid bacteria. Interestingly, this results in a tea with less catechins than green tea but with a similar polyphenol content, which means that catechins are just one type of polyphenols in tea.


During the calorie restriction period, all three groups lost a significant amount of body weight. The green tea and Awa tea groups lost ~25% more weight than the control group, with no difference between the two types of tea.

Body fat ratio remained the same in the control group but decreased by ~10% in both tea groups. Green tea and Awa tea supplementation also reduced visceral fat accumulation compared to the control diet.

Plasma insulin levels were slightly lower in the tea groups, but the difference was not statistically significant. This is interesting, since green tea has been shown to increase insulin sensitivity both in vitro and in healthy humans during exercise. On the other hand, plasma leptin, which is also associated with body weight and fat ratio in humans, was significantly lower in both tea-supplemented groups.


Calorie-restricted rats supplemented with green tea and Awa tea lost more weight and fat mass than non-supplemented rats. Green tea and Awa tea also decreased plasma leptin concentrations. No significant differences were seen between the two types of tea, suggesting that other polyphenols than catechins (which are mainly found in green tea) also have health benefits.

Although fat intake was similar in all three groups, rats supplemented with tea had larger amounts of fecal lipids, which suggests that green tea and Awa tea effectively inhibited the fat absorption rate.

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

Green Tea Extract Enhances Abdominal Fat Loss from Exercise
Drinking 3 Cups of Green Tea Increases Plasma Antioxidant Activity in Humans by 12%
Green Tea Extract Increases Insulin Sensitivity & Fat Burning during Exercise
Green Tea Protects from Bone Loss in Female Rats

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Monday, April 6, 2009

A High-Protein Diet Is Better than a High-Carbohydrate Diet for Weight Loss

A High-Protein Diet Is Better than a High-Carbohydrate Diet for Weight Loss
Casein is the main protein in cheese made from cow milk. (Photo by cwbuecheler)

The war over weight loss is usually fought between the low-carb and the low-fat folks, both of whom are absolutely convinced they're right and the other side is wrong. If you've read diet forums, you know what I'm talking about (and if you've read my blog, you know that it's really the low-fat people who are wrong).

Protein, the third macronutrient, is often forgotten in the heat of battle. Putting the question of fat intake aside for a moment, which is better for weight loss, carbohydrates or protein? That is the question Claessens et al. set out to answer in their recent study. They first put obese people on a low-calorie diet to induce weight loss and then divided them into two groups: the high-carbohydrate group and the high-protein group. The idea was to see whether they would gain back the weight they lost during their calorie restriction diet.

Composition of diets

During the first 5 weeks of the study, all of the subjects consumed a liquid diet providing 500 kcal per day. In addition, they were allowed to eat an unrestricted amount of vegetables, except for pulses. All participants lost weight during this period.

During the next 12 weeks, the subjects were told to eat as much as they like but maintain a fat intake of about 30%. The high-carbohydrate (HC) group was told to consume at least 55% of their energy intake as carbs, while the high-protein group was told to eat a diet with at least 25% protein. The HC group was also given a 25 g maltodextrin supplement twice per day.

To compare the effects of so-called slow and fast proteins, the high-protein was further split into a whey protein group and a casein protein group. The distinction between slow and fast proteins is made based on their absorption pattern. Whey protein is quickly absorbed and thus a fast protein, while casein is slowly absorbed and therefore a slow protein. The subjects in the high-protein group were given either 25 mg casein (HPC group) or 25 mg whey (HPW group) twice per day.

At the end of the study, the HC group consumed 63% carbs, 16% protein and 21% fat. Mean total energy intake was 1868 kcal. Both HP groups reported consuming 42% carbs, 35% protein and 23% fat. According to urinary nitrogen excretion, however, the protein intakes of the HP groups were between 27-28%, which means that the difference in protein intake between the groups was probably not as big as one might hope, though it's still significant. Mean total energy intakes were 1848 and 1812 in the HPC and HPW groups, respectively.

Effects on body weight & body fat

During the 12 weeks of ad libitum eating, subjects in the HC group gained weight, while those in the HP groups kept losing weight. Fat mass and waist circumference also increased in the HC group, but decreased in the HP groups. The graphs for body weight and body weight change are shown below (the upward lines are the high-carb group and the downward lines are the high-protein groups).

High-protein vs. high-carbohydrate diet and body weight
Thus, despite similar energy intakes, those who ate more carbohydrates gained weight, while those who ate more protein lost weight. Furthermore, despite losing weight, the HP group actually gained fat-free mass.

Effects on blood pressure & cholesterol

Systolic and diastolic blood pressure increased slightly in the HC group, but the increase was not statistically significant. In the HP groups, however, a modest but significant decrease in blood pressure was seen.

Both groups modestly increased their HDL and LDL levels during the 12 weeks. No significant differences were seen between the groups. Triglycerides increased in the HC group but remained constant in the HP group.

Effects on insulin and glucose

Fasting insulin increased in the high-carbohydrate diet group and decreased in the high-protein diet group, but the changes were not statistically significant. Fasting blood glucose increased in both groups, with the increase reaching significance only in the HP groups. With glucagon, the situation was the opposite: the increase reached significance only in the HC group.

It's not entirely clear why the high-protein diet increased fasting blood glucose more than the high-carbohydrate diet. The authors comment:

This may be related to the gluconeogenesis-stimulating and/or glucagon-stimulating effect of high protein intake, which both will lead to increased hepatic glucose output.
-- Although impaired fasting glucose is a risk factor for the development of impaired glucose tolerance and type 2 diabetes in a high-risk population, there is no evidence that elevations of fasting plasma glucose within the normal range, as in the majority of our subject population, are associated with increased risk. Furthermore, no adverse effect of the high-protein diet on HbA1c was found in our subjects.

So, while this is an interesting result that deserves a closer look, I wouldn't be too worried at this point about high-protein diets and glucose levels it as long as your insulin levels are fine.


After a 5-week low-calorie diet, a high-protein ad libitum diet resulted in further weight loss compared to a high-carbohydrate ad libitum diet, which resulted in weight gain. Despite a decrease in body weight, body fat percentage and fat mass, fat-free mass increased in the high-protein groups. Energy intakes were similar in all groups.

Cholesterol levels increased similarly in both groups, but triglycerides increased only in the HC group. Fasting blood glucose increased in both groups, with a larger increase seen in the HP groups. Blood pressure decreased slightly in the high-protein groups.

No significant differences were seen between those eating a casein (slow) protein or a whey (fast) protein supplement.

For more information on carbohydrates, protein and fat in diets, see these posts:

Low-Carb vs. Low-Fat: Effects on Weight Loss and Cholesterol in Overweight Men
A Typical Paleolithic High-Fat, Low-Carb Meal of an Intermittent Faster
The Effects of a High-Fat Diet on Health and Weight - Experiment Conclusion
Caloric Restriction Improves Memory in the Elderly

Read More......

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Sunday, April 5, 2009

Anti-Aging in the Media: NOW Magazine on the International Anti-Aging Show

Some say our fascination with eternal youth is worse than death.
Some say our fascination with eternal youth is worse than death. (Photo by Eric Vondy)

So far all of the newspaper articles on anti-aging I've written about have been either positive or neutral. Most have been hopeful but cautious. None, however, have been clearly negative towards the idea of life extension.

Susan Cole from NOW Magazine is here to put an end to the madness of anti-aging. In a provocative piece titled 'Anti-Anti-Aging: Why I Find the Anti-Aging Movement Despicable', she takes on the International Anti-Aging Show – a road show with seminars on various aspects of longevity and health, and apparently the root of all evil.

A quick look at the seminars reveals that a lot of the stuff is pretty light-weight and even bordering on nonsense, with topics ranging from weight loss to natural healing. But they also have seminars on more serious-sounding topics, such as cosmetic surgery and hormone replacement.

Now, I can certainly see why the author of the article is angry at the dubious claims made by some of the speakers. Consider, for example, Dr. Nick Delgado, the sexual healer who will tell you "how the frequency of intimacy can increase ones longevity by 50%". The fact that there are no 150-year-olds around should raise some questions. As Mrs. Cole puts it:

These exhibitions have nothing to do with health and everything to do with profit. If health were the priority, organizers might consider the immense stress that the term anti-aging puts on people who are – and this can't be helped – aging.

I can also understand why she's angry at skin creams and cosmetic treatments being marketed under the banner of 'anti-aging' – all these products can do is treat or mask the effects of aging. Most of them don't even do that.

What I don't understand is that she's angry at the very idea of anti-aging. Here's a quote that describes her radically negative position:

I loathe the term anti-aging. It makes my skin crawl and my blood boil.

And why does she hate the term so much? Let her explain:

I consider anti-aging shows to be part of an ideological war against older people. North Americans already live in a youth-obssessed culture that dismisses elders as dispensable, useless pieces of human flesh. Wisdom has no value, while doing everything you can to look like you have none does.

Here's where we begin to see where she's coming from. Anti-aging is to be hated, because it's a direct attack on old people. With our ever-growing obsession with looking younger, feeling younger and being younger, we're making it clear that old age is something bad, something to be avoided. Therefore, old people, by virtue of being the opposite of what we ourselves want to be, are to be avoided, too.

This is of course a big fallacy. The idea of anti-aging is not to spit on the elderly and treat them as "useless pieces of human flesh" (I can almost hear the blood gushing in her veins when she wrote that) – it's to prevent all the bad things that come with old age and that make life less enjoyable. Who in their right mind could be against preventing human suffering?

Rather than specifying each age-related problem and saying "I'm anti-cancer, anti-arthritis, anti-diabetes, anti-Alzheimer's, anti-Parkinson's" etc. it makes more sense to be anti-aging, because what those problems have in common is that they all more or less stem from the biological process of aging.

Thus, if we could prevent aging, we could prevent all of the aforementioned problems too. Anti-aging, as a term and a concept, is a strike at the root.

So why would anyone who is, for example, anti-cancer (and I have to assume even Mrs. Cole isn't enraged by the idea of cancer treatments) be against anti-aging? The answer is fear and lack of knowledge. People are unaware that we have an actual chance at slowing down aging and eventually bringing it to a complete halt. And because they're unaware of that chance, they attempt to rationalize aging as something that is naturally good.

This is the pro-aging trance; the strange and terrible mindset where bad things become good only because they are unavoidable, and which makes people utter the most irrational sentences:

Personally, I'm not against aging. Because I'm nowhere near ready for the alternative.

As you can see, the most problematic side of the pro-aging trance is that its proponents will also force their love of aging on other people. It's not enough for them to grow old and die; aging must be enjoyed by all. Death has to be shoved down the throats of everybody, whether they like it or not.

Of course, not even the most hardcore deathist can resist cheating just a little in the game of aging, when given the chance:

Speaking as someone who etches a little powder onto my rapidly balding eyebrows every day, I'm not so totally opposed to a bit of make-up to help the eyes pop out and to give the cheeks a little lustre.

So you see, it's okay to use make-up to appear more youthful, exercise to stay fit, eat properly to stay thin, and treat disease to stay healthy. Nobody is against that. However, it's not okay to stop the process that makes all those increasingly difficult with time. That's where the deathist draws the line.

In case you don't get the logic, don't worry: there is none. The deathist will have nothing to do with it. Using logic would be an attack on crazy people.

For more information on anti-aging, see these posts:

Caloric Restriction Improves Memory in the Elderly
Anti-Aging in the Media: National Post on Caloric Restriction
Anti-Aging in the Media: Vancouver Sun on Immortality
Anti-Aging in the Media: Rolling Stone on Ray Kurzweil

Read More......

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