Tuesday, December 21, 2010

Hibiscus Tea Increases HDL, Lowers LDL and Triglycerides

Hibiscus tea is often served cold with sugar 
Hibiscus tea is often served cold with sugar. (Photo by molossoidea)

When it comes to health benefits and drinks, green tea gets most of the publicity. And with good reason – from what we know, it seems to have the widest range of positive effects out of all beverages. But that's not to say that there aren't other less known drinks out there that have health benefits of their own.

One such beverage is hibiscus tea, a herbal infusion made from the calyces of the Hibiscus sabdariffa flower. Hibiscus is also known as sorrel, roselle, karkadé and flor de Jamaica, depending on the region. Earlier this year, I wrote about two studies showing that hibiscus tea reduces blood pressure. In the second study, hibiscus tea was compared with black tea, and guess what – hibiscus tea wone hands down.

In fact, the group that drank black tea saw an increase in blood pressure. That was black tea – as far as I know, there have been no direct comparisons between green tea and hibiscus tea, but even green tea's effects on blood pressure seem to be small or nonexistent. So green and black tea, while very healthy, may not be enough if you want to cover all bases.

I wrote in the earlier posts that to my knowledge, there had been no studies on hibiscus tea and cholesterol, even though the drink is traditionally used to lower cholesterol. Today, however, I found a paper that shows hibiscus tea is good for cholesterol too (link). Granted, the paper appeared in the Journal of alternative and complementary medicine, which has published some papers that seem to be of questionable quality, but this one seems pretty legit.

For the experiment, 60 patients with type II diabetes were randomly assigned into two groups. One group got black tea and the other got hibiscus tea (which the authors refer to as "sour tea"). The participants were told to drink one glass (1 tea bag in boiling water, steeped for 20-30 minutes) twice a day for a month.

The subjects that drank black tea did not show improvement in any of the parameters measured. None of the changes in total cholesterol, LDL, HDL, triglycerides and lipoprotein (a) were statistically signifcant.

Those who drank hibiscus tea, on the other hand, saw several improvements in their cholesterol levels. Total cholesterol went from 236.2 to 218.6 mg/dL. HDL increased from 48.2 to 56.1 mg/dL, while LDL decreased from 137.5 to 128 mg/dL. Triglycerides went down rather dramatically, from 246.1 to 209.2 mg/dL. Lipoprotein (a) was unchanged.

The authors also reference several other papers showing similar results in humans and animals. For example, one study showed a reduction in cholesterol levels in healthy men and women taking a hibiscus extract (link). This would suggest that the beneficial effects of hibiscus are not only limited to diabetic patients.

I'm not sure why I didn't find these papers the last time I did a pubmed search, but I'm glad I came across them now. I guess it's time to put hibiscus tea back on the menu, next to green tea and rooibos tea.

My favourite way to drink it is to make a big glass of hibiscus tea the normal way, then after 15 minutes of steeping pour the tea through a sieve into a larger container, add twice as much cold water and put it in the fridge. It's ready to drink in about an hour. It's especially good in the summer, best enjoyed with ice and a little sugar for taste.

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

The Many Health Benefits of Rooibos Tea
Black Tea Is More Effective in Activating Superoxide Dismutase (SOD) than Green Tea
Refined vs Red Palm Oil and Cholesterol
Anthocyanins from Berries Increase HDL and Lower LDL

Read More......

Digg Technorati del.icio.us Stumbleupon Reddit Blinklist Furl Yahoo

Sunday, December 19, 2010

World's Oldest Woman and Oldest Man: 1986–2010

World's Oldest Woman and Oldest Man: 1986–2010
I came across this graph while browsing through the latest issue of Rejuvenation Research. The black line shows the age of the oldest living woman; the grey line shows the age of the oldest living man. The data spans from 1986 to 2010.

A couple of things pop out from this graph. First, during the last 24 years, the oldest person in the world has always been a woman. Not a big surprise there, since women live longer in general. Quite a few men have gotten past 112 years, but reaching 116 seems impossible. For female supercentenarians, reaching 114 is relatively common, and a few have even reached 116.

The second thing that catches the eye is the highest point on the graph: that's Jeanne Calment, who died in 1997 at the age of 122, making her the longest-living person ever in the world. No one else has reached even 121. Shigechiyo Izumi is missing from the graph – he was claimed to have died at the age of 120, but according to the authors, he was in fact 15 years younger.

Looks like there's a slight trend towards longer-living supercentenarians, but I'm not sure it's significant. Certainly we haven't seen anyone like Jeanne Calment in over a decade. What this graph doesn't tell us, of course, is whether the percentage of people who reach 110 years of age has changed significantly during the same time period.

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

Jumping Head First into the Fountain of Youth
Aubrey de Grey Interview in Wired.com
Russian Scientist Claims to Have Found Cure for Aging
The 7 Types of Aging Damage That End up Killing You

Read More......

Digg Technorati del.icio.us Stumbleupon Reddit Blinklist Furl Yahoo

Tuesday, November 30, 2010

Jumping Head First into the Fountain of Youth

Jumping Head First into the Fountain of Youth
Go on, it'll knock 50 years right off your age. (Photo by JB London)

I don't know if you noticed, but yesterday a study on telomeres and aging hit the news big time. Various media bought into the hype, claiming that aging had been reversed in mice. Daily Mail, for example, published a story that begins as follows (link):

Have they found the elixir of eternal youth? Scientists reverse the ageing process in landmark trial

The secret of eternal youth has been unlocked by scientists in remarkable research that paves the way for a ‘forever young’ drug. Lives could be longer and healthier, free from illnesses such as Alzheimer’s and heart disease, with skin and hair retaining its youthful lustre. Such a drug might allow men and women to have children naturally until they are a ripe old age.

The secret of eternal youth, huh? And just in case you missed what that would be like, the writer states:

The experiments mirror the plot of the film The Curious Case of Benjamin Button, where the lead character played by Brad Pitt ages in reverse.

Except, of course, that Brad Pitt was born as an old man and eventually turned into a fetus and died, which is not exactly the kind of eternal youth I'm looking for. As you might guess, the paper and its authors are slightly less modest about the results – but only slightly. Professor Ronald DePinho, who did the mouse experiments, says:

In human terms, it would be like having a 40-year-old person who looked 80-plus and reversing the effects to the levels of a 50-year-old.

Reporters obviously love statements like this, but the truth behind the hype is somewhat different. First, mice are not humans, so drawing conclusions about what results from mice would mean "in human terms" without actually replicating the experiments in humans can be misleading.

Second, and more importantly, the mice were not normal mice: they were genetically modified to have no telomerase – which, in simple terms, lengthens telomeres – resulting in prematurely short telomeres and thus premature aging. The authors then gave the mice a drug that kickstarted telomerase, and lo and behold, many of the signs of premature aging began to reverse.

Thus, this is very far from giving the same drug to a healthy person and making them live forever. The rejuvenation in this case applies to the damage caused by having artificially short telomeres, not to all the other kinds of damage that comes with aging. This is precisely why the mice given the drug "become normal", so to speak, but were not rejuvenated in the sense that the whole "fountain of youth" metaphor might suggest.

If this were truly a fountain of youth, the mouse would have lived exceptionally long – but they didn't. They lived as long as normal mice.

While I'm glad that the attitude of the media towards life extension seems to be positive and even optimistic these days, the people writing these articles don't seem to have much grasp of reality when it comes to anti-aging science. I don't claim to be an expert, but even a quick glance at the abstract of the paper (link) would have shown that this is not only "ten years away from being available for sale", it's simply not directly applicable to healthy people.

What I found encouraging, however, was that the mice given the drug not only stopped accumulating more damage, but that their organs did indeed begin to rejuvenate. I say encouraging because it shows that aging damage can be repaired and not only slowed down – which is a crucial difference, because for most of us alive today to make it past 120, it will have to be repaired and not just halted.

Another positive thing about the study is that the mice whose telomerase was reactivated did not get cancer. Since one of the purposes of telomere shortening is said to prevent harmful mutations from spreading, many people worry that boosting telomerase may increase the risk of cancer. It would be interesting to see what the same drug does to normal mice.

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

Aubrey de Grey Interview in Wired.com
Russian Scientist Claims to Have Found Cure for Aging
How Do People Feel about Life Extension?
Anti-Aging in the Media: The Independent on Immortality

Read More......

Digg Technorati del.icio.us Stumbleupon Reddit Blinklist Furl Yahoo

Tuesday, November 23, 2010

Ashwagandha as a Nootropic – Experiment Update

The search for nootropic herbs continues.
The search for nootropic herbs continues. (Photo by Jim Brekke)

It's time for an update on my self-experiment with Ashwagandha, which began earlier this year in February. The herb in question, also known as Withania somnifera, is one of the many used in Ayurvedic medicine. Since many people use it as a nootropic, being a fan of cognitive boosting I figured I had to try it myself.

While Ashwagandha is commonly used for its relaxing properties, a review of the literature shows that it has a range of benefits. I've gone through the nootropic effects of Ashwagandha in detail in my previous post, so I'll only list them briefly here:

  • Activates the GABA receptor
  • Inhibits acetylcholinesterase (AChE)
  • Reduces alcohol and morphine addiction
  • Decreases stress
  • Improves sperm count and motility
  • Increases testosterone and reduces prolactin levels
  • Improves memory function in mice
  • Regenerates nerve fibers and dendrites
  • Little or no risk of toxicity
  • Negative effects on libido at very high doses

An impressive list, as you can see – but note that some of the results are from rodent studies or studies on humans suffering from high stress. The fact that Ashwagandha has been shown to bring things back to normal, so to speak, doesn't necessarily mean that it'll improve things beyond baseline in healthy people. Indeed, Ashwagandha is considered an adaptogen, which refers to herbs that supposedly normalize the body's functions.

For the purposes of my experiment, I bought a bottle of NOW Foods' Ashwagandha extract, which contains 450 mg of the root extract (standardized to a minimum of 4.5 mg withanolides) per capsule. My evaluation was based on subjective effects on mood, libido and stress.

The bottle is now finished, and I'm somewhat disappointed to conclude that I didn't notice much effects from the product. I tried various approaches: taking a capsule in the morning, during the day, or in the evening, but none of them resulted in anything clearly noticeable. The only possible effect I saw was more vivid dreams when I took Ashwagandha before going to sleep, but even then the results were inconsistent. All I can say is that the combination of magnesium and Ashwagandha before bed seemed to give me a good night's sleep.

As for boosts in mood or cognition, I didn't see any. Neither did I notice a difference in my libido or stress levels. I did try taking two or three capsules at once to see if a larger dose would help, but as far as I can tell, it made no difference. At least there were no negative effects either.

To be clear, I'm not saying that Ashwagandha is useless, just that this particular product at these doses didn't do anything for me. NOW Foods has very reasonably priced products, but there are probably several ways of making a herbal extract and a wide range of effectiveness between brands, so I'm tempted to try a couple of different brands before concluding the experiment.

The active ingredients in Ashwagandha are supposedly the withanolides, so in theory, any product that contains a sufficient amount of them should give similar results. Nonetheless, based on other people's experiences, some brands may be more effective than others. If you have personal experiences (positive or negative) with Ashwagandha, please share them in the comment section. Specifically, if you can recommend a brand that worked for you – preferably one that is available at iHerb – I will consider trying that product next.

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

60 Minutes on Boosting Brain Power
Nootropic Battle Conclusion: Acetyl-L-Carnitine vs. Ginkgo Biloba vs. Taurine
Green Tea Protects from the Psychological Effects of Stress in Rats
Does Ginkgo Biloba Improve Cognitive Performance?

Read More......

Digg Technorati del.icio.us Stumbleupon Reddit Blinklist Furl Yahoo

Thursday, November 11, 2010

The Twinkie Diet: Thoughts on Weight Loss and Cholesterol

You can lose weight on any diet, but is it healthy?
You can lose weight on any diet, but is it healthy? (Photo by OkayCityNate)

A few days ago, CNN reported on a nutrition professor who lost 27 pounds in ten weeks eating mostly Twinkies (link). Not only that, but health markers improved too – LDL went down and HDL went up.

Some people seem to think the results resolve the old question of whether calories are all that matter in weight loss. After all, if you can lose weight by eating Twinkies, Doritos and Oreos, what else could it be than calories? Surely that's just about the worse diet you can have.

While I'm obviously a big fan of self-experimentation, I think the results have been misrepresented in some cases. What do I mean by that? Let's look at the experiment and the results a bit more closely. Here's a quote from the article:

For a class project, Haub limited himself to less than 1,800 calories a day. A man of Haub's pre-dieting size usually consumes about 2,600 calories daily. So he followed a basic principle of weight loss: He consumed significantly fewer calories than he burned.

If we take the 2,600 calories daily as the correct figure, then for the ten weeks, Haub was running an 800 calorie deficit. It's hardly surprising that he lost weight. When you cut back enough on your energy intake, you start losing weight – in this sense, a calorie is a calorie.

But since this is an experiment with only one participant, it's impossible to say whether more or less weight would have been lost if the diet had been different. Did all the sugar he was eating prevent him from losing the maximum amount of body fat? There's no way to tell.

There are some hints, however, that it's not all about calories. The amount of calories consumed may be the primary factor in how much weight or fat is lost, but that doesn't rule out other factors. In rats, for example, green tea increases weight loss during calorie restriction. The rats consuming green tea burned more of their body fat and absorbed less fat from the diet, despite eating the same amount of calories.

In real life settings, the argument that a calorie is a calorie is difficult to examine, because the number of calories we burn is not constant – it depends on many variables. We now know, for instance, that genetics play a role. Some people have a hard time putting on weight, because the more they eat, the more calories they burn. They may get an urge to exercise more, for example. And anyone who's tried different diets knows that some foods make you more energetic than others, despite having a similar number of calories.

But that's not all. Some people don't put on weight even when exercise is forbidden. Their bodies just start using all that excess energy in other ways: increasing metabolic rate, heat production, etc. Is a calorie really a calorie in this case?

Then there's the question of how to count the absorption of calories from different macronutrients. If you divide people into two groups and feed both the same amount of calories, but have one group eating more protein and the other group eating more carbohydrates, their weights will be different. In general, high-protein diets result in more weight loss than high-carbohydrate diets.

As you can see, the question is hardly as simple as some people make it out to be. And there are more similar things that complicate the issue. Stephan from Whole Health Source has a good post on the Twinkie diet and how it relates to hormones and fat mass regulation, and I'm sure there are other health bloggers who have picked up on the same article.

Putting the calorie issue aside, perhaps the thing that aroused the most interest was the part about improved biomarkers. Sure, you can lose weight eating a terrible diet, as long as your eating very little, but shouldn't that wreck your health in other ways? Apparently not:

Haub's "bad" cholesterol, or LDL, dropped 20 percent and his "good" cholesterol, or HDL, increased by 20 percent. He reduced the level of triglycerides, which are a form of fat, by 39 percent.

But that's not really big news. You see similar things happening in many studies where the participants are put on weight loss diets, regardless of what the diets are like. Even in the studies where overweight people are put on the conventional low-fat, high-carb diet – which is not really a good approach for improving cholesterol levels, glucose and insulin – these health markers improve while they're losing weight. As a spokeswoman for the American Dietetic Association says in the article:

"When you lose weight, regardless of how you're doing it -- even if it's with packaged foods, generally you will see these markers improve when weight loss has improved," she said. 

However, as in the case of the amount of weight lost, there's really no way to tell based on this experiment whether his health markers would have changed differently on another diet with the same calories. Low-carb and low-fat diets have very different effects on cholesterol during a calorie deficit, for example (note also how the subjects lost more weight during the low-carb diet despite eating more).

Since the study only lasted for ten weeks, the fact that his LDL and triglycerides decreased while HDL increased doesn't say much about the long-term effects. I wonder what his cholesterol levels would have been after a year of following the Twinkie diet.

Also, there's more to cholesterol than just LDL, HDL and triglycerides. In the case of lipoprotein particles, size matters. A diet consisting mostly of sugary snacks is probably not going to do a whole lot of good for LDL particle sizes in the long run. And even when HDL and LDL levels look good on the surface, there's oxidized LDL and lipoprotein (a) to worry about.

What we can say with some certainty is that regardless of how you do it, returning to a normal weight seems healthier than being obese. In the maintenance phase, which lasts much longer, more things should probably be taken into consideration. Haub himself seems to have mixed feelings about his experiment:

"I wish I could say the outcomes are unhealthy. I wish I could say it's healthy. I'm not confident enough in doing that. That frustrates a lot of people. One side says it's irresponsible. It is unhealthy, but the data doesn't say that."

While the health markers are interesting, it would have been interesting to hear more about his experience in general. How did he feel before, during and after the diet? Was he feeling energetic or tired? How was his mood? Did he have any problems, digestion, bad skin, etc?

Before you kickstart your own Twinkie diet, note that professor Haub also had a multivitamin and a protein shake daily, which may have influenced the results somewhat. And if you've already tried a strange diet and managed to lose weight, drop a comment and tell us how it went.

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

Alternate-Day Feeding and Weight Loss: Is It the Calories Or the Fasting?
A Year of Intermittent Fasting: ADF, Condensed Eating Window, Weight Loss, And More
Green Tea and Capsaicin Reduce Hunger and Calorie Intake
Green Tea Extract Increases Insulin Sensitivity & Fat Burning during Exercise

Read More......

Digg Technorati del.icio.us Stumbleupon Reddit Blinklist Furl Yahoo

Monday, November 8, 2010

Tretinoin Results After a Year – Experiment Update

Retinoids – one of the better ways of looking young.
Retinoids – one of the better ways of looking young. (Photo by eisenbahner)

Some of you have been asking for an update on my experiment with retinoids. Now that I've gone through my first tube of tretinoin, it's time to review the results.

As I mentioned in my review of the anti-aging benefits of retinoids, I have both tretinoin cream (0.05%) and tretinoin gel (0.05%). I decided to go with the cream first, applying it only on the left side of my face. The right side has therefore acted as the control side.

Looking back at the first post on this experiment, it seems it's been over a year since my order arrived. Given that I've used the cream regularly and actually stuck with the experiment more strictly than with some other experiments of mine, it strikes me as odd that I only finished the 20 gram tube a few weeks ago. Granted, I have applied only a small amount and only on one half of the face, and I've had some breaks, but still, a little really seems to go a long way in this case.

I use the cream either nightly or every other night after washing my face and before going to bed. This seems to be the most common way to use retinoids. However, contrary to what is recommended, I often apply the tretinoin after a shower. The reason why this is not recommended is because after a hot shower, the pores of the skin will be open, and the peeling and redness that sometimes result from retinoids may be worse.

For me, this is a positive thing and a good a reason to use retinoids after a shower, since the absorption of the retinoids will be increased. I don't get much redness or peeling with the 0.05% strength anyway, unless I apply it to very sensitive areas. For example, I've tried it below the eyebrows, close to the eyelids, where the skin is very thin, and it was a rather painful experience. Applying tretinoin under the eyes is not problematic, though.

In my first post on retinoids I included a list of benefits that I'd seen mentioned in the literature. Here's the list again, along with a comment on whether the claim has been true so far in my case:

  • Increased skin thickness and firmness – YES
  • Increased skin hydration – NO
  • Increased skin tolerance to external factors – NOT SURE
  • Reduced visible signs of sun damage – NOT APPLICABLE
  • Reduced fine wrinkles – NOT SURE
  • Restoration of even skin tone and reduced hyperpigmentation – YES
  • Reduction in dark circles under the eyes – NOT APPLICABLE
  • Reduced skin roughness – YES
  • Reduced irritation from shaving – NOT APPLICABLE
  • Less risk of skin cancer – NOT APPLICABLE
  • Reduced stretch marks – NOT APPLICABLE
  • A healthy, 'rosy glow' – NOT SURE

As for skin thickness, I can't really be sure, as it would have to be measured with professional equipment. Skin firmness is one of those things that I notice after applying tretinoin and even in the morning. My face just feels kind of tighter on the side where I've applied it. The feeling tends to go away after a few days of not using the cream, though.

Skin hydration is another thing I don't really know how to estimate properly. One thing I do notice is that the left side of my face is quite often dry the next morning, which is a result of the peeling effect. It's not painful, however, and putting on some moisturizer gets rid of the problem.

I assume that by "external factors", things such as pollution and maybe UV rays are meant. Since I haven't burnt in the sun lately, and there's not much pollution here, I can't really say whether there has been an effect or not. I also don't have visible signs of sun damage (although I'm sure some internal, non-visible damage does exist), so I can't comment on that. I would expect this to be one of the areas where tretinoin is most effective, however.

The reduction of fine wrinkles is a tricky one. I've been trying to observe changes in three things during the experiment: fine forehead wrinkles, crow's feet (the wrinkles next to the eyes), and nasolabial folds. The fine lines on my forehead have not changed either way. I have to look pretty close to see them, but they are the same on both sides of the face.

The crow's feet, on the other hand, have gone through various changes. They too are visible only if I look very closely, but on the left side of the face they've gone from good to worse to better. At first, it seemed like they got deeper with the peeling, but now the skin looks somehow different compared to the other side, and I'm inclined to say the fine lines are less visible. A similar thing is happening with a few fine lines on my lower eyelid, very close to the eye, where I've applied the cream only randomly. It does indeed seem worse now than the right side. I think this is consistent with how retinoids work – they thin the dry outermost layer of the skin but eventually thicken the dermis and epidermis. This, along with the exfoliation, can make things look worse in the beginning.

As for nasolabial folds, they are not very deep but nonetheless visible. I haven't seen much change there, unfortunately, and sometimes I feel like the left side looks better, while other times I see no difference. I know there are many people who wonder whether retinoids can help with nasolabial folds (and many who believe they can't), but more time will have to pass before I can make a proper evaluation.

I don't have skin cancer, stretch marks or even irritation from shaving, so I can't really comment on those. The dark circles under my eyes have changed more drastically as a result of other lifestyle changes such as diet, so it's hard to see much difference there either.

The biggest difference for me has been in skin tone and skin roughness. It may not be visible to other people without me pointing it out, but I immediately see the difference in the mirror. I never even thought about skin tone and hyperpigmentation before, but I see now that the left side of my face has a much more even tone and looks smoother than the right side. There is indeed a slight "rosy glow" on the skin over the cheek bone, but otherwise there is no redness – unlike on the right side, where the tone is less even and slightly red. The pores of the skin also seem smaller on the left side, including the nose. In general, it just looks healthier and better.

So there you have it, my experience with retinoids so far. I've tried a lot of different stuff and written about it here, but this is the clear winner. For once, the results are actually visible. I'm now going to start applying tretinoin on both sides of the face, probably trying the gel version next. Since my left side already has a head start, it'll be interesting to see how fast the right side can "catch up".

Oh, and for the Scandinavians out there looking for where to buy retinoids: I can't help you there. I ordered six tubes from alldaychemist.com over a year ago, but due to repeated problems with customs, they no longer ship to any Scandinavian countries. The same is true for other online drugstores I've tried. No luck.

That's a real shame, because their stuff was dirt cheap and of a high quality. What can I say, this is a perfect example of the long-term effects of the Scandinavian socialist mindset – no one is responsible of their own actions, the government takes care of everyone, the bureacurat knows better than you.

EDIT: I almost forgot; I've also applied tretinoin to my left temple, and it looks like there are a couple of new hairs growing. This is the same temple that had some new hair growth with retinol, the milder version of retinoids. Those hairs are still there, but they don't grow very long – not exactly like vellus hairs but not terminal either. And I think my left eyebrow has some more hairs than the right one, although the difference is slight.

For more information on skin care, see these posts:

Topical Retinoids Increase Hair Growth in Most People
BioSil, JarroSil & Beer – Silicon Experiment Conclusion
Topical Vitamin C for Skin: Re-examining the Case
Lutein for Skin Elasticity, Hydration and Photo-Protection – Experiment Begins

Read More......

Digg Technorati del.icio.us Stumbleupon Reddit Blinklist Furl Yahoo

Friday, July 30, 2010

What a "Heart-Healthy" Diet Does to Your Cholesterol Levels

What a Heart-Healthy Diet Does to Your Cholesterol Levels
It's the butter that is bad for you, not the bread... right? (Photo from flickr.com)

What happens when you follow the American Heart Association's dietary recommendations? You know, a diet high in whole grain, vegetables, fruit and berries, but low in animal protein and fat, especially that nasty artery-clogging saturated fat.

According to conventional wisdom, you will be healthier in general. In particular, your cholesterol levels are supposed to improve – though it's never quite clear what "improvement" here means. Is it lower total cholesterol? Or perhaps lower LDL and higher HDL? And what about triglycerides and oxidized LDL?

Fortunately, a few years ago the Journal of the American Heart Association published a study that looked at what happens to cholesterol levels while on the officially heart-healthy diet (link). In contrast to many other studies, the participants in this one were healthy and had normal cholesterol levels to begin with. The idea was to see whether adopting an optimal diet would make them even healthier.

Study design and composition of diets

The study included 37 healthy women and consisted of two phases. During the first phase, the women followed a low-fat, low-vegetable diet for five weeks. After that, there was a three week washout period, followed by the second experimental diet. This second diet was the "optimal" diet, which was also low-fat but this time included lots of vegetables, fruit and berries. To make sure that the dietary guidelines were followed, the meals were supervised.

Both diets included 8 portions of grain products, 3-4 portions of low-fat or fat-free dairy products, and 2 portions of lean meat, chicken or fish. In the first phase, the subjects were given 2 portions of fruit and vegetables per day. In the second phase, the amount of fruit and vegetables was increased to 4-5 and 5-6 portions, respectively.

Dietary fats were replaced vegetable oils and spreads which contained minimal amounts of trans fats. The amount of total fat and saturated fat decreased, whereas the amount of polyunsaturated fats increased. To replace the lost calories, the subjects ate more carbohydrates and protein. Fiber intake also increased; in the second phase, it was nearly twice as much as at baseline.

Thus, both diets were very close to official recommendations: they included only moderate amounts of fat and animal protein, the fat was mostly from vegetable oils high in polyunsaturated fatty acids, dairy products were low in fat or fat-free, and grain products high in fiber were included. In addition, the second phase was high in veggies, fruits and berries.

HDL, LDL and triglycerides

After the low-fat, low-vegetable phase, total cholesterol was unchanged. On the other hand, triglycerides and HDL decreased, while LDL levels increased. The increase in LDL was apparently not statistically significant, which is probably due to the small sample size.

When the amount of vegetables, fruit and berries was increased, total cholesterol decreased. Triglycerides remained the same, but both HDL and LDL decreased:

The effect of a low-fat diet on cholesterol

Thus, reducing the amount of fat in the diet and replacing animal fats with vegetable oils did not change total cholesterol but did change the cholesterol profile: HDL and triglycerides decreased, while LDL increased. From the "good cholesterol, bad cholesterol" standpoint, adopting a low-fat diet actually changed things for the worse.

Things were not much better when vegetables, fruit and berries were added to the low-fat diet. Total cholesterol was clearly reduced, which by some standards is admittedly a positive change. Importantly, however, this change was not achieved through a decrease in "harmful" LDL but in "healthy" HDL.

The amount of triglycerides did decrease compared to baseline, but the reason is unclear. Generally, replacing fats with carbohydrates seems to increase triglycerides. Also, triglycerides decreased after the first phase, when the diet was low in vegetables, and did not decrease further after the second phase, so dietary antioxidants don't seem to be the explanation either. One thing that comes to mind is alcohol intake, which is not reported in the study. Perhaps the subjects reduced their alcohol intake while on the experimental diets? That would show up as a lower triglyceride score, but we can't know for sure.

Oxidized LDL and lipoprotein (a)

Both oxidized LDL and lipoprotein (a) are independently associated with a higher risk of atherosclerosis – more so than total cholesterol or LDL. In fact, oxidized LDL (ox-LDL) is believed to cause clogging of arteries and inflammation. Lipoprotein (a), also called Lp(a), is a known risk factor in many cardiovascular diseases, although its function is not entirely understood.

The most interesting result of the study is that the number of oxidized LDL particles and Lp(a) increased significantly as a result of following the low-fat diets. Oxidized LDL increased by a whopping 27% in the first phase. Even after vegetables, fruits and berries were added to the diet, ox-LDL levels were still 19% higher than at baseline. Similarly, Lipoprotein (a) was 7% higher after the first phase and 9% higher after the second phase compared to baseline.

What this means is that two important risk factors of atherosclerosis worsened markedly after following the very dietary recommendations that are supposed to reduce risk of atherosclerosis. Although plasma antioxidant capacity correlated with the intake of fruit, vegetables and berries, the antioxidants in them were clearly not enough to protect from these harmful changes.

The changes in total cholesterol, HDL, LDL and triglycerides were relatively small, which may be partly due to the short duration of the study. However, the 27% increase in ox-LDL demonstrates that diet can have a dramatic even in a short period of time.


The authors describe the results as "unexpected". According to them, a decreased intake of fat – especially saturated fat – should have led to a decrease in risk factors. They quote a number of studies where replacing saturated fatty acids with polyunsaturated fatty acids led to a "beneficial" decrease in total cholesterol. So why did the risk factors of atherosclerosis not see a similar "beneficial" change?

It is true that fats and oils high in polyunsaturated fatty acids generally tend to lower cholesterol (although the relationship between different fatty acids and cholesterol is more complicated than that). A completely different question is whether total cholesterol even matters, however. Even official recommendations acknowledge that the ratio of LDL to HDL is a better predictor of CVD than total cholesterol.

As was to be expected, the low-fat diets in this study did reduce total cholesterol. But if that decrease happens by reducing HDL and not changing or even increasing LDL, is the change really for the better? Most importantly, if the drop in total cholesterol comes with a marked increase in Lp(a) and oxidized LDL, can the results really be seen as beneficial?

Since the results of the study are incompatible with the cholesterol hypothesis and dietary recommendations, the authors came up with an alternative explanation. According to their hypothesis, high Lp(a) and ox-LDL may in fact be a sign of existing artherial damage being fixed and therefore a positive thing – but of course only in the case of low-fat diets. Right.

For anybody who has been keeping up with the gradual destruction of the cholesterol hypothesis, these results are not all that surprising. For example, we already know that polyunsaturated fatty acids oxidize much more easily than monounsaturated or saturated fats. It seems logical that LDL would be oxidized also.

What is somewhat surprising, however, is that the study was published in a journal that promotes the official dietary recommendations as heart-healthy.

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

Which Oils and Fats Are Best for Cooking?
Carotenoids and Lipid Peroxidation: Can Vegetables & Fruit Reduce ALEs?
Sugar and AGEs: Fructose Is 10 Times Worse than Glucose
Anthocyanins from Berries Increase HDL and Lower LDL

Read More......

Digg Technorati del.icio.us Stumbleupon Reddit Blinklist Furl Yahoo

Friday, July 16, 2010

Why Are Thin People Not Fat?

How do some people manage to stay thin despite eating a lot?

You probably know at least a couple of people who just don't seem to get fat no matter how much they eat. Some of them don't even do much exercise. But is it really true that some of us gain weight more easily than others, or do thin people just eat less calories?

Most of the studies on obesity and weight loss have been done on subjects who are overweight to begin with. A BBC Horizon documentary titled Why are thin people not fat? looked at the obesity problem from a different angle. They chose subjects who were naturally thin and stuffed them with excess calories. None of the participants had watched their food intake before, but their weight had remained roughly the same for years.

The subjects were told to eat at least double their usual calories and to avoid exercise for four weeks. The target energy intake for men was 5,000 kcal and somewhat less for women. The purpose was to find out whether naturally thin people would start gaining weight, given a sufficiently large amount of calories. It was no exercise in healthy eating either: the menu included processed, calorie-dense foods such as cakes and milkshakes. Precisely the kind of thing that should make one fat.

The documentary begins by mentioning a similar experiment done on Vermont prison inmates in 1967. The inmates were grossly overfed with the purpose of studying the hormonal changes that happen when a person becomes obese. The prisoners who signed up were promised an earlier release.

Each inmate was supposed to increase their body weight by 25 percent. However, as the experiment progressed, it turned out that no matter how high the energy intake got, some of the inmates could not reach their targets. Despite eating and eating, they just didn't gain enough weight. One of them could not increase his body weight more than 18%, even though his daily calorie intake reached a whopping 10,000 kcal.

For years, experts argued over the results of the Vermont prison study. According to the classical model of calories in, calories out, such high intakes should have led to a dramatic weight gain, especially since exercise was forbidden during the experiment. So how did some of the inmates stay thin?

This is the question that the BBC experiment tries to answer. I recommend watching the whole documentary, but here's a summary of the results:

  • All participants had trouble reaching their energy intake goals
  • Energy-dense foods such as chocolate made reaching the goals easier
  • Some of the subjects gained more weight than others
  • One of the subjects gained almost no weight but increased his muscle mass
  • All subjects returned to their normal weights after the experiment

These results confirm the observations from the Vermont prison study: despite very high calorie intakes, some people have a harder time gaining weight than others. The documentary also explains how naturally thin people are able to stay thin:

  • Appetite has a genetic basis
  • Age, weight, and diet of the mother during pregancy influence the child's weight
  • Eating habits learned during childhood carry on until adulthood
  • Naturally thin people avoid excess calories instinctively
  • People have a certain "natural weight" towards which the body aims
  • Basal metabolic rate plays a strong role in energy expenditure
  • The feeling of hunger is related to the number of fat cells
  • The number of fat cells can grow but never diminish

There's a lot of debate these days over the importance of basal metabolic rate (BMR) in the calories in, calories out model. It's interesting to note that nobody eats the exact same amount of calories per day, and yet weight remains in a very narrow range (at least in healthy, thin subjects). The one subject who stuck to his 5,000 kcal intake but gained almost no weight supports the idea that there is a kind of setpoint that the body tries to maintain regardless of calorie intake.

It also looks like in some people, the mechanisms to preserve the natural weight setpoint are stronger than in others. Increased heat production is obviously one way to maintain weight during increased energy intake. Some people (Michal Eades comes to mind) have also argued that as the number of calories eaten increases, the body starts to burn them by increasing small, almost involuntary movements such as tapping your fingers, moving your legs, etc. – physical activity which is not considered exercise but still uses up extra energy. I think this theory makes sense.

The last two points of the list are especially interesting. There are two key attributes to fat tissue: the size and number of fat cells. The number of fat cells in your body is typically pretty much determined during adolescence. Thus, eating affects first and foremost the size of your fat cells. As you store and burn energy, the fat cells in your body grow and shrink accordingly.

That's not all there is to it, however. If you keep eating even after the fat cells have grown to their maximum size, at some point the body will begin to produce new fat cells to store all that extra energy. The tendency to produce more fat cells probably depends on the individual.

The problem is that according to our current understanding, the number of fat cells can only be increased, never decreased. This means that any new fat cells produced as a result of (prolonged) overeating will always stay with you. What's worse, as the purpose of fat cells is precisely to store energy, the body will now send more signals of hunger to your brain to keep those fat cells filled up. Obviously this makes following diets that rely only on cutting back on calories very difficult.

The overall message of the documentary is that being naturally thin is a combination of many factors, some of which are genetically determined and some a result of the environment. Of course, individual choice also plays a role, but the studies on small children given unlimited candy show that even before we have the capability to think rationally about our food choices (kids will eat as much candy as they desire), there are differences among people.

For those who have to struggle to maintain or lose weight, things are more difficult – though not impossible by any means. It just means paying attention to your diet, venturing beyond governmental recommendations, and trying on yourself what works. I've had many overweight people tell me how difficult it is to lose weight, and then when I ask them if they've tried for example a basic low-carb diet, they've either tried it for a few weeks and quit, or they've deemed it "unhealthy", because all they can picture is Atkins on his deathbed and slices of bacon clogging their arteries.

Are you a naturally thin person who can eat and eat without gaining weight? Are you the exact opposite? Share your experiences in the comment section!

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

Alternate-Day Feeding and Weight Loss: Is It the Calories Or the Fasting?
Green Tea and Capsaicin Reduce Hunger and Calorie Intake
A High-Protein Diet Is Better than a High-Carbohydrate Diet for Weight Loss
Low-Carb vs. Low-Fat: Effects on Weight Loss and Cholesterol in Overweight Men

Read More......

Digg Technorati del.icio.us Stumbleupon Reddit Blinklist Furl Yahoo

Monday, July 12, 2010

Soy Isoflavones and Chili Pepper for Hair Growth – Experiment Begins

The hotter the pepper, the more capsaicin it contains.
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?

Read More......

Digg Technorati del.icio.us Stumbleupon Reddit Blinklist Furl Yahoo

Thursday, May 27, 2010

Does Intermittent Fasting Increase Lifespan?

Some say intermittent fasting makes you live longer.
Some say feasting and fasting will keep you younger. (Photo by bowtoo)

I often hear or read that intermittent fasting has all of the same benefits of calorie restriction. The idea is that by not eating every now and then while keeping total calories the same you would enjoy the same health effects as you'd get from simply eating less. Including living longer.

This mantra is repeated even in scientific papers, but is it correct? It's certainly easy to see the appeal: since actual calorie restriction means you're counting every calorie and going hungry for most of the time, intermittent fasting seems like a fantastic choice. Besides, the concept does make sense on the surface. Deprive your body of energy for a while, let autophagy do its work, and live longer. It seems to work for fruit flies and worms, after all, so why not humans?

Because humans are more complex. While simple species like roundworms can be very useful for screening life extension therapies, they are no guarantee that the same therapies work in humans. There are a million ways to extend lifespan in roundworms and fruit flies, but much less in rodents, and even less in humans.

Unfortunately, it looks like intermittent fasting (IF) is one of these cases. For obvious reasons, we don't have lifespan studies on IF in humans, but what we do have is studies on rats and mice. And, despite what the popular belief is, the data is much less promising than one might hope. The rather disappointing conclusion of the studies seems to be that intermittent fasting without caloric restriction does not extend lifespan. When it is accompanied by caloric restriction (CR), it does extend lifespan – and it looks like the degree of life extension is highly dependent on the degree of CR.

The reason you see studies showing increased longevity from IF in the first place is because most rodents eat less when they fast every other day. While humans generally compensate for a fast by eating twice as much the next day, mice and rats generally don't. They do eat more, but not twice as much – which means they are calorie restricted.

Don't believe me? Let's take a look at all the studies on intermittent fasting and longevity in mammals. Note that I've skipped all the alternate-day feeding studies that have not looked at lifespans. There are a lot of papers showing other kinds of health benefits from fasting (some of which are also a result of CR!) , and I'm not saying fasting is not healthy in general, just that it does not seem to extend life.

A critical look at the studies

The first paper I could find on the subject is from 1945 (link), not too long after the positive effect of calorie restriction on lifespan was discovered. This paper briefly mentions an even earlier study from 1934, in which mice fasted for two days in a row each week. The average lifespan of the fasted mice was slightly longer than those of controls, but the difference was not statistically significant. There is no mention of weight and food intake.

In the 1945 study, male and female Wistar rats were put on various versions of intermittent fasting. The rats fasted either one day in four, one day in three, or every other day. Fasting was begun at the age of 42 days and was continued until the rats died.

With the exception of females fasted once every four days, the average lifespans of all fasted rats exceeded that of the controls. The increase in lifespan was slightly greater in males than in females, although females still outlived males in general. In male rats, the most effective method was fasting every other day, while in females fasting once every three days gave the best results on average. However, both the male and female rat that lived the longest (1057 and 1073 days, respectively) were fasted every other day.

Food intake was not measured, but since the intermittently fasted rats weighed less than the control rats, we can assume that they also ate less. No drastic retardation of growth was seen, however. So, the first available study on intermittent fasting shows that when rats are intermittently fasted, they don't compensate for all the missed calories on the ad libitum days, and thus are CR'd, and therefore live longer. No big surprise there.

After this study, there was a gap of four decades before similar experiments were done again. During the 80's and 90's, three papers on intermittent fasting and lifespan were published by the same team. In the first one, male Wistar rats were fed either ad libitum or every other day since weaning (link). The mean lifespan of the fasted rats was 83% greater than that of the control group. And, just like in the 1945 study, fasting resulted in a lower body weight. The abstract doesn't mention the exact weights, but since the fasted rats took 75% longer to become fully grown, it looks like they ended up eating significantly less.

In the second paper, male Wistar rats were again fed ad libitum or every other day since weaning (link). This time they were also allowed voluntary exercise. The fasted rats exercised less in their youth but more when they were older. They also lived longer and weighed less than the control rats. However, in contrast to the first study, their growth duration was the same while growth rate decreased. That is, it looks like in the first study both groups eventually grew to the same size, while in the second study the IF rats remained smaller.

The third paper looked at the longevity effect of intermittent fasting (every other day) on three strains of mice, beginning at various ages (link). In two of the strains, mean and maximum lifespan increased and body weight decreased. The A/J strain, on the other hand, showed different results. When intermittent fasting was begun at 1.5 months, the mice lived longer despite not weighing less. When it was begun at 10 months, they again weighed the same as controls but actually died earlier. The rats that began fasting at 6 months weighed less than controls at some ages but showed no difference in lifespan.


In summary, it looks like intermittent fasting extends lifespan in rats and mice only when it is accompanied by calorie restriction. It does not mean that the animals are also put on CR; rather, they just naturally end up eating less (unlike humans, who tend to be very flexible and good at compensating for calories). And, in the rare cases that the animals actually do eat twice as much the next day, their lifespans are not increased.

For those who are doing IF for other reasons than life extension – such as improving insulin sensitivity or ">weight loss – this is not necessarily a concern. While some of the other health benefits reported in the studies are probably a result of calorie restriction, just like lifespan increases, I suspect IF even without CR still has some benefits in humans. It's just that based on the rodent studies, those benefits won't be enough to make us live longer.

For more information on diet and longevity, see these posts:

Dietary Supplement Increases Lifespan by 11% in Healthy Mice
Slowing Down Aging with Intermittent Protein Restriction
How to Live Forever: My 5 Steps to Immortality
Intermittent Fasting Reduces Mitochondrial Damage and Lymphoma Incidence in Aged Mice

Read More......

Digg Technorati del.icio.us Stumbleupon Reddit Blinklist Furl Yahoo

Wednesday, May 19, 2010

My Current Health Regimen v2.0

One of the changes has been an increase in fruit and vegetable intake.
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.


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.


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

Read More......

Digg Technorati del.icio.us Stumbleupon Reddit Blinklist Furl Yahoo

Sunday, May 2, 2010

BioSil, JarroSil & Beer – Silicon Experiment Conclusion

Beer – it's not just the alcohol that goes to your head.
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

Read More......

Digg Technorati del.icio.us Stumbleupon Reddit Blinklist Furl Yahoo

  © Blogger template 'Perfection' by Ourblogtemplates.com 2008

Back to TOP