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

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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......

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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

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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?

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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......

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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......

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Friday, October 29, 2010

Aubrey de Grey Interview in Wired.com

Aubrey de Grey's life extension diet emphasizes the importance of beer.
Aubrey de Grey's life extension diet emphasizes the importance of beer.

One of my favourite people in the world, the British gerontologist Aubrey de Grey, recently did an interview with Wired Science (link). If you've read his interviews before, you pretty much know what to expect, but there were a couple of new things in there that I found interesting (he's swearing, for one thing).

The gist of Aubrey de Grey's work is keeping people healthy indefinitely. You can call this unlimited healthspans or radical life extension or rejuvenation therapies or whatever, but the idea remains the same: to cure the biological process of progressive deterioration known as aging. For most people, the word "immortality" still has something of a negative connotation. This has not gone unnoticed by de Grey:

I’ve been out there represented as an immortality merchant since forever. These days, I can afford to not just acquiesce and let journalists use phrases like “immortality,” or at least not in the title of the bloody ass thing.

The reason he doesn't like titles like "Aubrey de Grey is here to make you immortal" is because it makes biogerontology sound like science fiction; something that a handful of people are working on in their garage. The public is apparently not ready for immortality.

And yet there are a growing number of people in the world who are ready to live longer and healthier lives. To any reasonable person, the word "immortality" is a positive thing, as long as one understands what the concept of biological immortality means. What it doesn't mean is that you'll be hurling through space long after the earth has been destroyed in a nuclear war, unable to die. It also doesn't mean that you'll be able to survive getting hit by a truck (although if it did, that would be a positive thing too).

What biological immortality means is that the chronological progress of time no longer dictates when and how you die. Your health will no longer be a simple function of time. Your body will remain youthful and vigorous regardless of how old you are. You can still die – certainly so if you want to die for some reason – but it won't be because of your body deteriorating every year. How this is a bad thing to some people has been beyond me for quite some time now.

The first step in solving the problem of aging will be done in mice. From there on, says Aubrey de Grey, it'll be smooth sailing:

What’s going to happen is the curmudgeons — the card-carrying gerontologists who think it’s very dangerous to be over-optimistic — will eventually recognize the data available to us from mice is so solid we can go out publicly and say, “It’s only a matter of time.” That’s going to take a panel of interventions in mice that’s so comprehensive we actually add two whole years to the lifespan of mice that are already in middle age before we start.

That may be overcautious. We may be able to get gerontologists on board with a more modest result than that. However, at that point, game over. My job will be done. I can retire. Because that will be the point when Oprah will be all over it and the following day it will become impossible to get elected unless you have a manifesto commitment to have a war on aging.

I agree with de Grey. People like Oprah have such a big influence on public opinion that it's ridiculous. I can even imagine someone being very pro-aging before hearing someone like Oprah promoting it, and then changing their mind completely. Once you get the public behind the idea, you'll get the politicians as well. Not that I give a damn about influencing politicians – without all the bureacracy and regulations in the field of medicine, I bet we'd already made a much larger progress in rejuvenation therapies! I'd rather take care of my own health than put it in the hands of any government official.

Another crucial point about people like Oprah: they have a lot of money. And since people with lots of money tend to be interested in preserving their wealth, it makes sense that the same people are also interested in preserving their health. After all, what's the point of having billions of dollars if you're not going to be around to enjoy them?

One thing that de Grey has not really commented on before is how come he doesn't get massive donations from aging billionaires. Some of them have already made plans to cryopreserve themselves, but if you have the chance to stick around without spending five decades in an ice box, why not do that instead? The biggest reason seems to be that billionaires haven't taken the organizations seriously enough:

Wired.com: For most of the billionaire philanthropists that travel in the same circles you do, out of the three things, is it mainly that they just don’t like your organization?

de Grey: I think for a very large, a very sufficient proportion of such people, yes, it’s that third thing. Because I see these people a lot. I go to TED, and there’s no holding back when it comes to 1) the desirability of the goal, and 2) the demonstration of sufficient comprehension of what I’m talking about to understand they believe the plan is feasible. So yes, absolutely.

In other words, there's a lack of professionalism, not necessarily in what the organizations actually do but in how people view them. The Methuselah Foundation is a case in point:

In the beginning, the only thing the Methuselah Foundation did was the longevity prizes for mice. Then, we started funding research directly. We thought it was a really cool idea to have one organization with two very complementary approaches to the same mission. But in fact, it didn’t really work, especially not in terms of messaging.

The foundation has now been split into two, one for prizes and one for funding research. Hopefully this will attract more investors. Besides business and funding, Aubrey talks about some personal things as well. And his love of beer, of course:

I drink exactly the right amount of beer evidently. [laughs] It’s ridiculous, really. Yet, I have to show I’m enjoying my life. It’s public knowledge I am polyamorous as well. That’s something that goes down not so well with some of my more politically sensitive friends and colleagues. But it goes quite well with some other people. [laughs]

Polyamorous, huh? He even goes to say that the whole monogamy thing is "archaic" and will probably be a thing of the past some time in the future. I didn't know de Grey was against monogamy, but I happen to agree. I think the whole concept of jealousy is an unnecessary biological impulse that was useful in the past but will no longer be needed in the future. It certainly isn't a product of the rational side of the brain.

I guess contrarians tend to have a lot in common. When you start to question the official truth in one area, you begin to wonder about other obvious truths as well. I'm sure you've noticed the disproportionate amount of libertarians among the paleo crowd, for example. In many cases it boils down to questioning whether government really knows best.

For some reason, the paleo community is still mostly stuck in the "aging is good" dogma, however. They're determinately against diabetes, obesity, cancer, cardiovascular disease, and every other modern plague, and yet they are unwilling to strike the problem at the root.

Basically, they want to live healthy for 80 years and drop dead. To me that's nonsensical. What's your opinion?

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

Russian Scientist Claims to Have Found Cure for Aging
How Do People Feel about Life Extension?
Aubrey de Grey in Helsinki, Finland
Why Aging Is a Global Disaster That Needs to Be Solved

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Wednesday, September 15, 2010

Russian Scientist Claims to Have Found Cure for Aging

Could there really be one pill that keeps you young indefinitely?

This news recently hit the media (link), and the headlines so far have been pretty wild. Catchphrases like "forever young" and "secret to eternal life" will surely spark interest even among the non-immortalist crowd, but how much of it is just hype?

So what is this news all about? The drug in question is the work of professor Vladimir Skulachev, who has dedicated his life to study (and solve) aging. Now he's finally found an antioxidant with anti-aging properties and plans to start selling it in just a few years.

Despite what supplement salesmen will tell you, antioxidants by themselves are not worth much in terms of extending lifespan. In fact, the whole "free radical theory of aging" was put to rest a long time ago. Yes,  antioxidants extend the lifespan of simple organisms, but they've repeatedly failed in mice and rats, and there's no evidence that antioxidants would make humans live longer.

There's a pretty simple reason for that, too: normal antioxidants don't reach the mitochondria where most of the free radical damage occurs. No matter how much vitamin C pills you pop or how many acai berry shots you down, you won't be making any difference in the rate of mitochondrial damage.

It appears that Skulachev has synthesized a mitochondrially targeted antioxidant. There's no detailed information in the article, but based on the papers Skulachev's group has published in the past, it looks like the compound in question is SkQ1, an antioxidant attached to a positively charged ion. Experiments have shown that SkQ1 prolongs the lifespan of a variety of species, including mice (link, link).

Clinical trials on humans are underway, and if everything goes smoothly, the drug will be out in a few years. After successful results from animal studies using eye drops, Skulachev tried it on his own cataract. After six months, his cataract was gone.

So what's the catch here? Well, looking at the lifespan data from mice, they're not talking about an increase in maximum lifespan but in median lifespan. The oldest mice receiving the drug did not live longer than the oldest mice in the control group, they just had a squared mortality curve. In other words, the mice that got SkQ1 made it to old age more often than the control mice.

In humans, this would translate to something like being relatively healthy at 90 years old but still dying around 100 years of age. There's no evidence that you could live to be 150 by taking SkQ1. Thus, claiming that "the cure for aging" has been found or that the "fountain of youth" is finally here is just plain wrong.

Aside from the reality check, this is still very good news. Even squaring the curve would be a fantastic thing in humans – if it works in humans. That would mean that a lot of the diseases associated with aging would be postponed significantly and old people would enjoy a better quality of life.

And, for those of us trying to stay as healthy as possible while waiting on true rejuvenation therapies, drugs like this would be warmly welcome.

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

Selegiline and Lifespan Extension
Does Intermittent Fasting Increase Lifespan?
The Curious Case of Human Hibernation
How Do People Feel about Life Extension?

Read More......

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Saturday, August 21, 2010

Refined vs Red Palm Oil and Cholesterol

Palm oil, palm kernel oil, palm olein and palm stearin are all different products of the palm tree.

Palm oil is extracted from the pulp of the fruit of the oil palm. Palm kernel oil, on the other hand, is extracted from the seed of the oil palm. While red palm oil (also known as crude palm oil) is easily distinguishable by its deep orange to red color, refined palm oil and palm kernel oil can be hard to tell apart. Both are white to yellowish in color and solid at room temperature.

Palm oil contains about 45 g saturated, 40 g monounsaturated, and 8 g polyunsaturated fatty acids per 100 g. Though not as saturated as coconut oil, palm oil is still at the top of the list when it comes to saturation. Palm kernel oil is even more saturated, containing more than 80% saturated fatty acids.

It's no surprise that palm oil has been labeled an unhealthy fat by most health experts. Obviously, this much saturated fat must send cholesterol levels through the roof and, as a result, cause heart disease. Right?

Well, not quite. After going through pubmed for all the abstracts (and a couple of full papers) on palm oil and cholesterol, it's clear that the case is everything but clear. The heart disease part deserves it's own post, but for now let's concentrate on how palm oil really affects cholesterol levels.

Palm oil and cholesterol in animals

In one study, partially refined, bleached and deodorized (RBD) palm oil was fed to rats on different diets (link). All groups that were given palm oil as part of their diet had significantly lower total cholesterol (TC) levels than the control group. In addition, when normal and hyperlipidemic rats were given palm oil, they had higher HDL levels than hyperlipidemic rats that were not fed palm oil. Similar results were seen in another study where rats given palm oil had a higher ratio of HDL to total cholesterol and lower triglycerides than the control rats (link).

An earlier study that fed rats with various fats for a year came to a different conclusion (link). TC was higher in rats fed palm oil than in rats fed with other fats such as sunflower oil or butter. Triglycerides were higher in palm oil and butter groups than in sunflower oil groups. And, to make things even more confusing, rats fed palm oil for four weeks showed a tendency for slightly lower triglycerides and HDL, whereas sunflower oil tended to increase triglycerides and HDL (link).

Basically what the above studies show is that the results vary greatly. Sometimes palm oil improves TC/HDL ratio, sometimes it worsens it. Sometimes triglycerides decrease, sometimes they increase. What's more, these two don't even have to go hand in hand, which makes it hard to decide whether the overall effect is good or bad.

One question that raises at this point is whether refining the oil makes a difference. One study that compared unrefined (that is, red/crude) and refined palm oil found that rats fed unrefined palm oil had lower total cholesterol, LDL, VLDL and higher HDL than those fed refined palm oil (link). Perhaps the tocotrienols in red palm oil play a role? Maybe so, but there is also one study that did not see a difference in cholesterol levels between rats fed red palm oil and refined palm oil for three months (link).

There are also other variables that might affect the end results. For example, I found one rat study that directly compared the effects of fresh and once or repeatedly heated palm oil (link). The rats that were given either fresh or once-heated palm oil did not have any deleterious effect, whereas palm oil heated five times increased total cholesterol and thiobarbituric acid reactive substances (TBARS) levels. This means that even though palm oil tolerates heat much better than most oils, using the same oil many times may not be a good idea.

Similarly, comparing fresh and oxidized (either through heating or prolonged exposure to air) palm oil shows that while both increase total cholesterol compared to rats eating a normal diet, oxidized palm oil increases it even more, and that this is due to an increase in LDL, not HDL (link). Further, oxidized palm oil increased the mean arterial blood pressure of the rats, while fresh palm oil did not.

Unlike humans, hamsters fed oil and dietary cholesterol quickly develop hyperlipidemia. Hamsters that were given various palm oils had dramatically lower levels of total cholesterol, LDL and VLDL than hamsters given coconut oil (link). The three forms of palm oil were red palm oil, refined palm oil and refined palm oil with red palm oil extract. In the hamsters that were fed red palm oil or refined palm oil with red palm oil extract, HDL levels were significantly higher and triglycerides significantly lower than in hamsters fed coconut oil.

The best one of the three was unrefined red palm oil, but as you can see, even refined palm oil had favourable effects. Note also that adding an extract of red palm oil into the refined palm oil improved things, which supports the idea that the carotenoids, tocotrienols and tocopherols play a role in the health effects of red palm oil.

In another study, hamsters given palm oil had higher levels of total cholesterol, HDL and triglycerides than those given olive oil or maize oil (link). The title of the paper suggests that the amount saturated fat is directly responsible for HDL levels in hamsters: when they eat little saturated fat, HDL is low, and vice versa. However, in the previous study HDL increased after switching from coconut oil to red palm oil, even though coconut oil is higher in saturated fat.

In vervet monkeys, palm olein oil reduced the risk the risk for developing early atherosclerotic lesions while not significantly affecting cholesterol levels compared to monkeys given lard or sunflower oil (link). Note, however, that palm olein oil is not the same as palm oil. Although it has a high palmitic acid content like palm oil, palm olein oil is the refined, liquid fraction of palm oil. The solid fraction is palm stearin. Palm olein is about 45% saturated and 55% unsaturated, while palm stearin is 60% saturated and 40% unsaturated. While they may have different effects, at least in rats palm stearin, palm olein and palm oil all increased HDL in one study (link).

Palm oil and cholesterol in humans

While animal studies may give us an idea of what to expect, we are not rats, hamsters or monkeys. Humans are adapted to a different kind of diet through evolution, and cholesterol studies in animals can be pretty misleading when applied to humans.

First, let's take a look at what happens when you give palm oil to people with what doctors would call hypercholesterolemia or high cholesterol. In women with high cholesterol, soybean oil, rice bran oil and palm oil all reduced LDL and TC, despite their differing fatty acid composition (link). Thus, saturated fat does not necessarily increase LDL.

In this study, only soybean oil reduced HDL. Soybean oil also reduced small dense LDL (sd-LDL), while palm oil consumption increased it. That same LDL was more susceptible to oxidation in those who consumed soybean oil, however. Since oxidized LDL appears to be the best predictor of atherosclerosis, perhaps an increased number of small LDL particles with less oxidation is better than increased oxidation with less particles.

When older women with high cholesterol were given sunflower oil (which is very high in PUFA) or palm olein, the latter increased TC and LDL, especially in women with high TC to begin with (link). Contrast this with the previous study where the palm oil normalized cholesterol levels. Still, no difference was seen in TC/HDL ratio. HDL increased only in those with normal cholesterol levels. Again, palm olein also decreased LDL oxidation, especially in those with high cholesterol.

There's also a study that compared sunflower oil and palm olein in older women but with normal cholesterol. This time, the diet containing palm olein increased TC and HDL compared to a sunflower oil diet (link). Another study found palm oil and sunflower oil to cause no difference in HDL, whereas palm oil increased TC and LDL (link). A third comparison of the two oils found the same (link).

Perhaps palm oil and palm olein have different effects on cholesterol? That sounds plausible, but one study found no difference between palm oil, palm olein, palm stearin and soybean oil in terms of LDL, HDL and triglycerides (link). Then again, not all palm oleins are equal. When red palm olein and palm olein was compared with sunflower oil in patients with excessive fibrinogen (a blood clotting factor) in their blood, red palm olein came out on top (link). Palm olein increased TC more than red palm olein and sunflower oil. LDL increased in the palm olein group compared to the sunflower oil group.

So far, we've looked at palm oil vs. PUFA-rich oils, but what about other fats? Lard has a pretty similar fatty acid profile as palm oil. It has plenty of MUFAs and SFAs but only little PUFAs. Comparing palm oil with soybean oil, peanut oil and lard in Chinese adults showed that palm oil reduced TC and LDL, while lard increased both (link). Peanut oil had no effect. Palm oil also improved the TC/HDL ratio.

A study that fed palm oil, lard or puff-pastry margarine to obese women found no difference in cholesterol levels (link). It did find that obese women had lower HDL levels and higher fasting leptin (four times as high!) than normal-weight women, however. So, compared to lard, palm oil either reduces LDL or does nothing.

Peanut oil is 49% MUFA, 33% PUFA and only 18% SFA. The MUFA content is similar to palm oil but its PUFA content is much higher. One study found no difference between palm olein from red palm oil and peanut oil (link). Olive oil is even higher than peanut oil in MUFA, containing about 70% of its fatty acids in the monounsaturated form. One study found no difference between palm olein containing tocotrienols and olive oil in terms of cholesterol (link).

Coconut oil is much higher in saturated fat than palm oil. Unsurprisingly, it tends to raise cholesterol in most animal studies more than other fats. In humans, small amounts may not make a big difference. Enriching the diets of healthy, young women with palm oil or coconut oil did not result in differences in total cholesterol compared to consuming the same amount of energy MUFAs (link). In larger amounts the difference start to become clearer. Compared to coconut oil, palm oil generally results in lower total cholesterol, LDL and HDL (link).

Still, even high amounts of red palm oil doesn't necessarily increase cholesterol. In Chinese men, a diet containing 28% fat with red palm oil accounting for 60% of that, no change was seen in total cholesterol, triglycerides, or HDL after 42 days (link). Plasma concentrations of carotenoids and vitamin E increased, however.

Hydrogenation, which turns liquid fats solid, may also play a role. Compared to saturated fatty acids such as palmitic acid, hydrogenated fats containing trans fatty acids tend to increase total cholesterol and LDL while lowering HDL levels (link, link). One paper compared the effects of palm oil with partially hydrogenated fat and oils high in MUFAs or PUFAs (link). Partially hydrogenated soybean oil and palm oil resulted in higher LDL than regular soybean oil. There was no significant difference in TC/HDL between the oils, but HDL3 was higher after palm oil.

In another study, three different margarines were given to 27 young women (link). One of the margarines was based on palm oil, one on partially hydrogenated soybean oil and one was made with a high content of PUFAs. The PUFA margarine lowered total cholesterol and LDL compared to the other two, while soybean margarine lowered HDL compared to the other two. One study compared the effects of partially hydrogenated soybean oil, high oleic palm olein and unhydrogenated palm stearin (link). Both soybean oil and palm stearin increased TC/HDL compared to palm olein, with palm stearin having a lesser effect than soybean oil. 

Looking at the question from the opposite angle gives similar answers. The saturated fat in a typical Dutch diet comes mainly from animal fats and hydrogenated oils. Replacing them with palm oil resulted in an 11% increase in HDL and a 8% decrease in the LDL/HDL ratio (link). Triglycerides were also reduced.

In many of the studies, the subjects are either given supplements or they just basically scoop up the fat with a spoon. This is not how most people actually use these oils, however – they cook with them. When you put different oils into a frying pan and then eat them is when you start to see different results.

For example, using palm oil or soybean oil for cooking does not seem to change serum cholesterol levels much in the short term (link). However, cooking in soybean oil resulted in a 47% increase in triglycerides compared to palm oil, which goes to show that oils high in PUFAs are not very suitable for cooking. Also, some of the effects may only become visible after a longer period of time. There aren't many long-term studies in humans, but Mauritius is an exception. In 1987, the government changed the formula of the commonly used cooking oil from palm oil to soybean oil. As a result, total cholesterol levels dropped by about 0.8 mmol/L in the course of five years (link). There's no mention of triglycerides, unfortunately.

Finally, men and women seem to respond differently to dietary fats. When a small amount of red palm oil was given to healthy subjects for two weeks, all lipid fractions decreased, with a statistically significant decrease seen in LDL and triglycerides (link). A closer look revealed that there was a difference between men and women, however: in men, LDL actually increased mildly.

One study looked at the effects of palm oil in the context of high and low dietary cholesterol (link). Diets high in palm oil slightly increased total cholesterol and LDL with no significant changes in HDL or triglycerides. Interestingly, diets low or moderate in palm oil increased total cholesterol and LDL much more than the diets high in palm oil, even when the high-palm oil group consumed more eggs.

Tocotrienols are generally considered to have a cholesterol-lowering effect (link). The effects of tocotrienol supplements on cholesterol are not conistent, however (link, link). A possible explanation is that alpha-tocopherol might attenuate some of the cholesterol-lowering effect of tocotrienols (link).

Medium-chain triacylglycerods (MCTs) are usually thought to have a neutral effect on cholesterol, but a comparison of MCTs with palm oil and high oleic acid sunflower oil showed that MCT and palm oil had a similar effect (link). Sunflower oil resulted in lower total cholesterol. The authors conclude that "this study suggests that medium-chain fatty acids have one-half the potency that palmitic acid has at raising total and LDL-cholesterol concentrations."


So what do we make of all this? As I'm sure you noticed, there's a lot of different kinds of studies and a lot of conflicting data out there when it comes to palm oil and cholesterol. Some common themes appear in the results, however:

  • Compared to PUFA-rich oils, palm oil increases TC in most human studies
  • Compared to MUFA-rich oils, palm oil behaves neutrally in most human studies
  • Compared to SFA-rich oils, palm oil reduces TC in most human studies
  • In animals, palm oil tends to increase HDL and lower triglycerides
  • In humans, palm oil tends to increase LDL, at least in men
  • Palm oil makes LDL less susceptible to oxidation
  • Small amounts of palm oil don't make much of a difference either way
  • Palm oil tolerates cooking well, but don't use the same oil more than once
  • Red palm oil seems to have a more neutral effect than refined palm oil

Just from a cholesterol perspective, palm oil doesn't look all that bad – and we haven't even looked at how palm oil consumption affects cardiac risk! Although some conflicting evidence exists, in most of the studies the effect on cholesterol is closely related to the fatty acid composition of the oil.

Thus, when you compare palm oil with sunflower oil, you're most likely going to see an increase in total cholesterol, since polyunsaturated fatty acids tend to lower cholesterol compared to saturated fatty acids. Monounsaturated seem neutral in most cases. Still, keep in mind that individual fatty acids behave slightly differently. The high palmitic acid content of palm oil may explain why HDL levels are unchanged in many human studies.

One thing to remember is that if you use the oils straight from the bottle (e.g. on top of a salad), the difference between sunflower oil and palm oil may not be that great. However, if you use them for cooking, picking an oil high in PUFAs is asking for trouble. Saturated fats such as palm oil are less susceptible to oxidation and also make (the possibly increased) LDL less susceptible to oxidation.

Finally, while refined palm oil is most likely a better choice for cooking than less saturated fats, go for red palm oil whenever you can. Not all studies have shown a significant difference in cholesterol levels between red palm oil and refined palm oil, but some have, and tocotrienols have plenty of other health benefits as well.

What a "Heart-Healthy" Diet Does to Your Cholesterol Levels
5 Reasons Why Dark Chocolate Is Better than Milk Chocolate
Should Saturated Fat Be Avoided in Low-Carb Diets?
Coconut Lowers LDL, VLDL and Triglycerides, Raises HDL

Read More......

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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......

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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

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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?

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Tuesday, June 29, 2010

Soy Isoflavones Grow Hair by Increasing IGF-1 in the Skin

Food sources of isoflavones include tofu and miso soup.
Food sources of isoflavones include tofu and miso soup. (Photo by sokole oko)

Many of you have probably heard that soy isoflavones may be good for hair loss. How exactly dietary isoflavones work to promote hair growth is less clear, however.

As long-time readers may remember, I've written before about the effects of dietary isoflavones on humans and animals. For example, in male rats even a relatively low amount of soy isoflavones reduces DHT and increases testosterone. This alone would probably be enough to explain hair growth in rodents.

Of course, humans are a more difficult case. Most of the things that show promise in mice or rats don't work for humans with androgenic alopecia in the end. The good news is that soy isoflavones reduce DHT even in humans. The bad news is that the reduction may not be great enough. About 60 mg of isoflavones daily reduced serum DHT in healthy young men by only 15%.

Even this moderate drop would suggest a reduction in 5-alpha-reductase, which converts testosterone to DHT. However, the markers of 5-alpha-reductase looked at in the study did not show a difference between the treated and the control group.

And yet, a combination of capsaicin and soy isoflavones grows hair in both animals and humans. In this study, capsaicin injected into the skin was enough to grow hair in animals, although the combination was more effective. In humans, orally administered isoflavones and capsaicin resulted in hair growth in 88% of the participants with androgenic alopecia, which is a remarkable result for a supplement that reduces DHT by so little.

The authors speculated that capsaicin and soy isoflavones promote hair growth by increasing dermal levels of insulin-like growth factor (IGF-1). They suggested that a key factor was calcitonin gene-related peptide (CGRP), which acts as a vasodilator, among other things. It also increases IGF-1 in various tissues, including the skin.

This theory is supported by the fact that subcutaneous capsaicin increased CGRP release and IGF-1 expression in hair follicle cells in normal mice but not in CGRP-knockout mice. Soy isoflavones increased the production of CGRP, which explains why the combination was more effective than capsaicin alone.

Based on these studies, it was still unclear whether dietary isoflavones alone promote hair growth. Now, the same authors have investigated their idea further. In their new study, they fed isoflavones to mice whose backs were shaved and measured their hair growth (link). Again, both wild-type mice and CGRP-knockout were used.

The isoflavone supplement used was Fujiflavone P40, which contains 43.5% isoflavones. 5 g of the product was mixed per each kg of standard chow. On average, the mice ate 4.6 grams of food daily, which means that their daily intake of isoflavones was 0.0046 * 0.005 * 0.435 = ~10 mg (correct me if my calculation is wrong).

After three weeks of isoflavone administration, dermal CGRP and IGF-1 levels in wild-type mice increased significantly compared to the control group. In the knockout mice, no difference was seen between mice given isoflavones and the control group.

Hair follicle number also increased in wild-type mice given isoflavones. Compared to the control group, they had about 40% more hair follicles. The knockout mice had less hair follicles to begin with, and when they were given isoflavones, no improvement was seen. Thus, it seems that isoflavones grow new hairs through increasing dermal levels of CGRP and IGF-1.

Compared to the mice given isoflavones, the control mice seemed to take a longer time growing their existing hair back. Even the knockout mice that saw no increase in IGF-1 grew their hair back quicker when they were given isoflavones. This might be due to other effects of isoflavones, such as reducing DHT levels. Based on the pictures in the full paper, the wild-type mice grew their hair back even quicker, however. Wild-type mice given isoflavones also had a more pronounced darkening of hair than their control group.

So what is the take home message? Based on all these studies, it looks like soy isoflavones show very good potential for promoting hair growth. A part of their effectiveness may come from the fact that they reduce serum DHT and increase testosterone, but based on the rodent data, the real kick is from the increase in skin levels of IGF-1.

At the moment, there is no data comparing the effectiveness of soy isoflavones vs. capsaicin in humans. However, we do know that the combination is superior in increasing dermal IGF-1 in animals, and that the combination of both taken orally grows hair in humans with androgenic alopecia.

For more information on hair growth, see these posts:

Topical Retinoids Increase Hair Growth in Most People
BioSil, JarroSil & Beer – Silicon Experiment Conclusion
Zinc Pyrithione Reduces Shedding and Moderately Promotes Hair Growth
Hair Growth with Ayurveda – The Nutrich Oil Experiment

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