Wednesday, August 26, 2009

A Year of Intermittent Fasting: ADF, Condensed Eating Window, Weight Loss, And More

Even with intermittent fasting, you should watch what you eat.
Even with intermittent fasting, you should watch what you eat. (Photo by Bryan Bruchman)

I can't believe it's been a year since I started my intermittent fasting experiment. By now, I've gotten so used to it that most of the time it doesn't even feel like an experiment anymore. It's become more like an integral part of my diet.

Which is a good reason to spice things up a little. As I wrote two months ago, I made a temporary change to the experiment and switched from my usual 24-hour cycle of fasting and feeding to a condensed eating window of 6-8 hours just to see what happens.

I found the smaller eating window even easier than alternate-day fasting (ADF). In practice it meant that I skipped breakfast and lunch, and then had a big meal and some snacks when I got home. While at work, I only drank water, coffee and tea. During a 24-hour fast I usually get very hungry and slightly dizzy at one point close to the end of the fast, but skipping breakfast and lunch did not result in a similar feeling of hunger. Sure, I ate with good appetite once I got home, but my energy levels did not drop at all during the day.

I didn't measure my calorie intake, but based on the fact that I gained a kilo during this period, I assume I ate as least as much as I did before. So personally, cramming all of the daily calories into a window of 6 to 8 hours was not a problem. I was already used to eating huge meals, and the eating window was big enough to include lots of snacks or even another meal.

For someone considering intermittent fasting for weight loss, I would recommend either 24-hour fasts or using a shorter eating window than I did. A daily 20-hour fast with a 4-hour eating period improves insulin sensitivity and levels of circulating adiponectin, which are key factors in regulating fat storage and thus weight gain. Further, most of the studies showing benefits from intermittent fasting used an alternate-day feeding schedule.

The implication is that while an eating period of 6-8 hours is probably superior to the usual combination of breakfast, lunch, dinner, and snacks (which keeps your blood sugar constantly high), fasting between 20 to 24 is the choice with more positive studies behind it. This leads me to believe that the most important thing is not how small the eating window is, but rather how long the fasting period is. That is, while eating for 1 hour every 12 hours would technically constitute as a daily eating window of 2 hours, I suspect eating for 2 hours and fasting for 22 yields better results. Whether a 2-hour feeding window and a 22-hour fast is slightly better or worse than eating and fasting for 24 hours is unclear, but what is clear is that both work and that the latter is much easier in practice.

That said, I've been able to both lose and gain weight during my intermittent fasting experiment, depending on what and how much I eat. Anyone who claims that IF allows you to gorge on junk food while losing weight is plain wrong. Combining intermittent fasting with a low-carb diet is, in my opinion, the way to go if quick weight loss is your goal. This way you're getting the insulin benefits from fasting and the lowered insulin response from consuming few carbohydrates.

Another crucial factor would be total energy intake during the eating periods. Based on personal experience and what I've read from other people, there's a tendency to "load up" on calories just before the fast begins, whether you're hungry or not. This makes the fast much easier, because you'll be digesting the food for longer and the hunger won't begin until late the next day. For anyone who wants to get the health benefits of IF (such as reduced mitochondrial free radicals, one of the seven types of aging damage) but maintain their weight, this is probably a good idea, but for anyone else, it can easily render attempts at weight loss useless.

To counter this, my suggestion is to follow the intermittent fasting routine but to eat only when you feel hungry. If the fast is about to begin and you still feel bloated from your previous meal four hours ago, so be it. Don't try to stuff yourself with food as a pre-emptive strike if you don't feel like it. You'll probably feel the hunger pangs earlier the next day, but it'll pass after a few hours, and you'll feel more energetic afterwards.

The take-home message of the above is that despite what you may have heard, intermittent fasting by itself is no guarantee you'll lose weight. It can be used for weight loss, weight maintenance or even weight gain, depending on the implementation: the length of the fasts, the composition of the diet, and total energy intake. By optimizing those three factors, you can shift your weight into any direction you want. By disregarding them, it becomes a genetic gamble.

IF improves insulin sensitivity, which is a good thing, but the relationship between higher insulin sensitivity and weight is not as straightforward as it might seem (more on that later). The easiest way to lose weight for most people is still avoiding a high insulin response in the first place. Reading other people's experiences with intermittent fasting, it seems that most of them have the best results when they combine IF with diets that don't contain refined carbohydrates (including whole grain products), such as Atkins or paleolithic nutrition. When unrefined carbs are brought to the table, the disagremeent over the superior diet begins.

I'm now switching back to my old way of eating and fasting for 24 hours. Further evidence may prove me wrong, but at the moment, I feel that it's more beneficial for overall health than a condensed eating window of more than 4 hours. Squeezing the eating window just seems like too much of a hassle for me, though some people on IF manage to do just that.

I've also done a small experiment with dry fasting (meaning no food or water) and ketosis in my search for the optimal form of fasting, but I'll save that for another post. Meanwhile, I warmly welcome you to post your own experiences with intermittent fasting.

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

Green Tea, Black Tea & Oolong Tea Increase Insulin Activity by More than 1500%
A High-Protein Diet Is Better than a High-Carbohydrate Diet for Weight Loss
Green Tea Extract Enhances Abdominal Fat Loss from Exercise
Slowing Down Aging with Intermittent Protein Restriction

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Monday, August 24, 2009

The 7 Types of Aging Damage That End up Killing You

The 7 Types of Aging Damage That End up Killing You
The longer you live, the more time you have to explore the world. (Photo by iko)

If aging merely meant the passage of time, there'd be nothing wrong with it.

In fact, it'd be a good thing. The older you got, the more things you would know, the more skills you would've acquired, the more experiences you would've had, and the more people you would've met. All this while retaining the strength and vigour of youth. Doesn't sound too bad.

The problem is that what aging really means is the passage of time accompanied by a set of degenerative biological processes that harm the abilitity of our bodies to function and eventually cause us to die. What good is all that knowledge and all those experiences if you can't remember any of it? What good are all those skills when you're no longer able to use them?

We don't really know why we age. That's an interesting question in its own right, but it's beyond the scope of this post. The point of this post is to take a closer look at the biological processes that accompany the passage of time and together form the seven classes of aging damage.

It is because of this process of biological decay that we grow old. Not old the way vampires are "old" yet still magically look the same, but the way people and animals are old
fragile, weak and sick. To be clear, despite what most people tell themselves, there is nothing good about growing old, because all it really means is a cumulative and irreversible increase in fragility, weakness and sickness.

The good news is that despite decades of studying aging, we have identified only seven types of primary damage to our bodies from aging. The rest are secondary consequences of primary damage. If you prevent the primary damage from occurring, you will prevent the secondary consequences as a result, but not vice versa.

And why is it a good thing that there are seven causes of aging? Because it means that the aging process is not a complete mystery anymore. Or rather, the consequences of the aging process are not a complete mystery to us. Even though we don't have a clear explanation for why these seven types of damage occur in the first place (i.e. why are we not born biologically immortal?) we have a pretty good understanding of how they work.

And if we know all the things that are going wrong with our bodies as we age, we can begin to fix them.

The three approaches to the sinking boat problem

Imagine that the human body is a boat. For many years, the boat sails without a problem. But then, somewhere in the middle of the ocean, there's a problem: a hole has appeared in the bottom, and the boat is going to sink.

Now imagine that on that boat, there are three people: an architect, a mechanic, and a museum keeper. You go to them and ask each one in turn what could be done to fix the situation.

The architect has no experience in repairing boats. He is interested in understanding the nature of boats. He has heaps of drawings of boats and calculations for which kind of materials are suitable for a specific type of boat, but he doesn't actually build the boats. His suggestion is to study the boat carefully to understand the exact reasons that caused the hole to appear. If we understand the causes, he figures, we are better equipped to fix the problem.

You know there's no time for all that because the boat is sinking fast, so you go to the museum keeper. He runs a museum with old boats on display and has some experience on renovating worn down boats for museum use. He's not really interested in making them actually usable at sea; all they need to do is look good. His suggestion is to just let the boat sink, because sink it will, and then come back later to drag it from the bottom of the ocean and put it on display.

That doesn't feel like such a great idea either, so you turn to the mechanic. He has no idea where the hole came from, isn't familiar with the exact type of boat, and is in no hurry to visit the ocean floor. But he does have a plan: have two of you scoop the water back into the sea as fast as possible, while the other two find something to fill the hole with. There's no guarantee that another hole won't appear later on, but at the very least, his plan is going to buy you extra time.

At this point, extra time sounds pretty damn good, so you go with the mechanist's suggestion and grab the nearest bucket to start scooping.

Gerontology, engineering and geriatrics

There are three approaches to the study of aging: gerontology, engineering and geriatrics. In the boat metaphor above, the architect is the gerontologist, the mechanic is the engineer, and the museum keeper is the geriatricist.

Broadly defined, gerontology is the study of aging. It encompasses a wide range of subfields, but for the purposes of this post, biogerontology is the subcategory of interest. Biogerontologists seek to understand the biological processes that cause aging. A fascinating field of study, for sure, but as the boat example illustrates, when you're the one actively falling apart, perhaps a bit too theoretical.

Geriatrics, on the other hand, is a branch of medicine focused on the health care of the elderly. The emphasis is on treatment rather than prevention. One could even say it's about alleviating the symptoms rather than reversing the damage, much less fixing the cause. The problem is that the geriatricist has no interest in helping you unless your boat is already beyond repair.

The engineering approach to aging is to fix the damage as it occurs. The purpose is not to fully understand all the reasons that the damage happens in the first place, interesting as it may be; it's enough to know that it's there. Rather, the emphasis is on periodic repair and maintenance, so that even after years of use, the boat still looks, feels and sails like new. And if during those extra years of use maintenance buys us we learn something new about how to make boats more resistant to damage, all the better.

To me, the engineering approach is a matter of priorities. Yes, it would be fascinating to understand the complete workings of the human body, but it's much less fascinating to die trying now than it is to live significantly longer and find out later. Besides, the more years you have left, the more time you have for things like research and thus the more chance of succeeding in mapping out every possible metabolic pathway. Life should be our first priority in everything, because death cuts everything else short.

The seven deadly sins of aging

Without further ado, let's take a look at what the seven types of aging damage are and what we think can be done about them. Again, while identifying the different ways in which aging manifestates itself doesn't really explain why the damage happens, or even why there are exactly seven types of damage, it does provide us with clear goals for an engineering approach to life extension.

This approach of focusing on rejuvenation rather than slowing down aging itself is referred to as SENS, or Strategies for Engineered Negligible Senescence, a term originally coined by Aubrey de Grey in his book The Mitochondrial Free Radical Theory of Aging. Each of the SENS strategies targets one of the seven types of damage, listed below.

1. Cell loss and shrinking tissue

Worn out cells in the body are usually replaced by cell division. However, as we age, some of the cells we lose can no longer be replaced or they are replaced very slowly, which means that cells are being lost faster than they are produced.

In skeletal muscle, cell loss means shrinking tissue and weaker muscles. In the heart muscle, it means a more fragile heart. In the brain, it means a loss of neurons and causes a host of mental problems. Currently, one of the best approaches to cell loss is exercise, but its effects are nevertheless very limited.

The solution: stimulating cell division or introducing new cells (repleniSENS)

2. Mutations in the cell nucleus

Two types of changes in our chromosomes occur as we age: mutations and epimutations. The former are changes to the DNA itself, while the latter are changes to the propensity of the DNA to be decoded into proteins.

In some cases, changes to the DNA can lead to the formation of cancer. Non-cancerous mutations and epimutations do not in most cases contribute to the aging process, and in the rare cases that they do pose a problem, they are taken care of by other strategies (repleniSENS and apoptoSENS), so we don't have to worry about them at this point. Cancer, however, is definitely a problem, as anyone who's looked at mortality statistics in the Western world can testify .

The solution: removing the genes needed for telomerase (OncoSENS)

3. Mutations in the mitochondria

Mitochondria are known as the "power plants" of cells, because they play a key role in energy production. They also control cell growth and the cell cycle. Mitochondria contain their own mitochrondrial DNA (mtDNA), which encodes a small but important part of the proteins in the mitochondrion.

The problem is that the mitochrondrial environment is highly oxidative, and the repair mechanisms are much less sophisticated than those in the cell nucleus, which contains most of the DNA. The result is that mitochondria are very vulnerable to the accumulation of mutations, which is thought to accelerate aging. Therefore, preventing the accumulation of mitochondrial mutations requires a strategy of its own.

The solution: moving the DNA into the cell nucleus for better protection (MitoSENS)

4. Cells that refuse to die

Sometimes cells can acquire a state in which they are no longer able to divide but refuse to die, causing damage to neighboring cells. There are three classes of cells that can go into this harmful state: visceral fat cells, senescent cells and immune system cells. The problems that the accumulation of these cells cause are insulin resistance, tissue degradation, and vulnerability to infection.

Normally, the body is able to get rid of such harmful cells through apoptosis, a signal for the cell to kill itself. When the cells stop responding to these signals, other methods are needed to destroy them. While surgery can be used to remove visceral fat, the main alternatives to destroying senescent and immune system cells are injecting something to force apoptosis or stimulating the immune system to kill the cells.

The solution: forcing cell suicide or using the immune system to kill target cells (ApoptoSENS)

5. Tissue stiffening from crosslinks

The body is much better at keeping the insides of cells clean than it is maintaining proper functioning outside the cells. Inside the cells, proteins are regularly destroyed and rebuilt to keep things running smoothly, but outside, some proteins are recycled very slowly or never. With time, these long-lived proteins can run into problems.

Chemical reactions can sometimes cause two proteins to form a chemical bond known as a crosslink, which hinders their ability to slide across or along each other. Advanced glycation endproducts (AGEs) are probably the most famous example of crosslinks. When too many crosslinks occur, tissues lose their elasticity and problems arise. In artery walls, for example, tissue stiffening causes an increase in blood pressure. Breaking these crosslinks is needed to maintain a youthful state.

The solution: using specific enzymes or proteins to break crosslinks (GlycoSENS)

6. Junk outside the cells

This is another form of junk outside the cells that accumulates with aging, but it differs from crosslinks in that it has no useful function whatsoever. This junk should be cleared out of the body, but as in the case of death-resistant cells, the body is not able to digest or remove the material.

An example of junk outside the cells are the amyloid plaques in the brains of Alzheimer's patients. This web-like material accumulates in everyone's brains with age, but problems become visible only after a certain threshold has been reached. In supercentenarians, extracellular junk is one of the biggest killers.

The solution: stimulating the immune system to clear out the junk (AmyloSENS)

7. Junk inside the cells

As mentioned earlier, the body is fairly good at breaking break down proteins and other molecules in the cell which are no longer useful. However, sometimes these molecules have gone through chemical changes that makes the cell unable to digest them any longer. They then end up in the lysosome, which is the most powerful place to degrade molecules. If the lysosome is unable to get rid of them, they end up as intracellular junk and stay there practically forever.

In dividing cells this is not too big of a problem, because each division dilutes the junk, and the threshold where problems occur is not reached. But in non-dividing cells, the accumulation of this junk eventually causes the cells to stop functioning correctly. The result is problems such as atherosclerosis, blindness, liver spots, and a host of neurogenerative diseases.

The solution: making the lysosome more powerful to degrade the junk (LysoSENS)


There you have it, the seven types of aging damage that need to be fixed in order for true rejuvenation engineering to happen. And how do we know the list ends here? Isn't it possible there are other causes we just don't know of yet? Theoretically, yes, but it seems highly unlikely. Here's an explanation taken from the SENS Foundation website:

We can be confident that this list is complete, first and foremost because of the fact that scientists have not discovered any new kinds of aging damage in nearly a generation, despite the facts that research into aging has been slowly accelerating and that we have had ever-increasingly powerful tools with which to investigate the aging body.

Challenging as fixing this damage may be, the fact that we know what we need to do should still leave you with a fairly optimistic view of things. As I've said before, solving these problems is really a question of "when", not "if". And the sooner it is, the better – for all of us.

Even if you're not studying or working in the field, there are a couple of very practical ways to help make these rejuvenation therapies come true in your lifetime. The SENS website has a pretty good list of things with something for everyone, but I'll mention two important ones here.

Money is always needed, so one good option is to donate to the Methuselah Foundation or to the SENS Foundation to support research (and if you're sceptical of donations actually doing anything, here's some good news: a recent target of $16,000 was succesfully reached and exceeded earlier this month for research on using lasers to remove intracellular junk).

Another important thing is to talk to people and spread the word: many people don't have any idea that life extension is not just science fiction anymore. Significantly longer and healthier lifespans are the future, and just how far away this future is depends entirely on us.

For more information on preventing aging, see these posts:

How to Live Forever: My 5 Steps to Immortality
Slowing Down Aging with Intermittent Protein Restriction
Who Wants to Live Forever? Results from a Global Survey
Anti-Aging in the Media: New York Times on Caloric Restriction and Resveratrol

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Monday, August 17, 2009

Silica for Hair, Nails & Skin: BioSil vs. JarroSil

Silica has been shown to increase nail thickness. (Photo by James Jordan)

It's time for another update on my experiment with orthosilicic acid, the bioavailable form of silica.

For the past four and a half months I've been taking BioSil, a supplement that contains silica in a more absorbarble form known as choline-stabilized orthosilicic acid (ch-OSA). In one study, this form of silica improved skin, hair and nail quality in women after 20 weeks, so I decided to see whether it would affect my nail and hair growth too.

During the first two and a half months, I took 5 mg of BioSil daily to see whether a lower dose would be effective. I concluded that it might have increased nail thickness slightly, but that the rate of growth was unchanged. I also saw no increase in hair growth speed or thickness.

As the study on women used 10 mg instead of 5 mg daily, I doubled my dose after the 10 week mark. For the past two months, I've been on the 10 mg dose. The total time of my experiment is therefore very close to the duration of the study on women. The difference is that until about halfway through, I was taking half a dose.

To evaluate the effectiveness of BioSil, I've been cutting my nails every 14 days and trying to measure the speed of my nail growth. I've also looked at variation in the thickness of roots and tips of shed hairs. Based on my subjective evaluation, there's been no significant change. My nails are thicker than they were some years ago, but I suspect the change is due to a healthier lifestyle in general rather than supplementing with silica. During these past months, I've seen no further improvement.

I also took a two-week break from BioSil to see if my nail growth speed would come to a decline. Again, based on subjective evaluation, there's been no change. Nevertheless, I'm continuing the experiment at least until I've taken 10 mg of orthosilicic acid daily for 20 weeks. That way comparisons between my own experiment and the published study are more comparable.

However, from this point on, I'm switching from BioSil to JarroSil. Both are silica supplements that contain orthosilicic acid in a stabilized form, but the method of stabilization is different: JarroSil uses PEG and a boron compound, while BioSil uses choline.

If you've used BioSil before, then you might be aware that Jarrow used to sell BioSil. Currently, the Belgian supplier of BioSil has sold the rights to Natrol, so Jarrow decided to make their own form of stabilized orthosilicic acid and give it a different name.

What about price? Well, one 1 oz (30 ml) bottle of Natrol's BioSil costs $23.99 at iHerb and contains 120 servings of 5 mg orthosilicic acid. A 2 oz (60 ml) bottle of Jarrow's JarroSil costs $17.99 and contains 120 servings of 4 mg of orthosilicic acid. So a month of daily 10 mg doses will cost you $12 with BioSil and $11.25 with JarroSil. Not much of a difference.

Jarrow claims that their product is 2.5 more bioavailable than other formulations, but as of yet, there are no studies showing that this is true. Also, quite a few of the studies have used the (ch-OSA found in BioSil, while other formulations have been studied less. At this point, we just don't know which one is better. Maybe this experiment will shed more light on the issue.

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

Topical Vitamin C for Skin: Re-examining the Case
Lutein for Skin Elasticity, Hydration and Photo-Protection – Experiment Begins
Do Flax Lignans Reduce Hair Loss from MPB?
Coconut Oil Is Better than Olive Oil for Atopic Dermatitis

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Thursday, August 13, 2009

Protein, Vitamins and Wound Healing

A vitamin deficiency will impair the healing of wounds.
A vitamin deficiency will impair the healing of wounds. (Photo by marie b.)

I wrote a while ago that my wound healing has slowed down for some reason. It's nothing too dramatic, but small cuts and scratches don't seem to heal as fast as they used to.

In the previous post, I mentioned low zinc levels as a possible cause and decided to take 15 mg of zinc daily in addition to the 9 mg I get from my diet and multivitamin. Since I didn't see much of a difference with or without extra zinc, and because I'm not convinced that supplementing with zinc is necessarily a good idea, I stopped after a few weeks.

While I haven't injured myself lately to see if there's been a change, I've been doing some reading to know more about what effects wound healing. Recently, I found an old paper from 1955 titled Nutrition and Wound Healing (link). I know science moves on and everything, but since there's that certain something about old studies that I like, I decided to write a blog post about the paper.

It's probably no surprise that nutrition does have an effect on wound healing in humans and animals. The authors write:

It was shown in 1922 by Ebeling that a 10 per cent rise in the temperature of a cold-blooded animal would double the rate of wound healing. This indicates that wound healing is a chemical reaction. Thus, if the local factors discussed previously are kept at an optimum, the most important variable is the supply of the components for the chemical reaction. To accomplish this in the human being nutrition must be adequate.

By local factors, they mean things like bacteria, the amount of dead tissue and the vascularity of tissue to be repaired, which are not dependent on nutrition.

Wound healing and protein

So what is important when it comes to nutrition? Obviously, protein must play a role in the generation of new tissue. It seems like a reasonable assumption that a diet low in protein slows down wound healing. Conversely, a diet high in protein might be expected to speed up the wound healing process.

The authors mention a study from 1919 showing that animals on a high-protein diet had shorter healing times of surface wounds than animals on a high-fat, low-protein diet. Another study from 1935 showed that hypoproteinemia, a condition in which there's an abnormally low level of protein in the blood, resulted in poorly healing wounds in dogs. The reason was delayed formation of fibrous tissue and the accumulation of fluid beneath the skin. When proteins were reintroduced, the wounds healed normally. The same applies to humans:

Levenson and associates have presented numerous cases of healing burns in humans with a marked delay in healing being manifested in the hypoproteinemic patient.

It should be noted that protein intake by itself doesn't help much if some of the requisite amino acids are not present and protein synthesis cannot occur. Hence, there's a difference between consuming 100 grams of protein from eggs and consuming 100 grams of protein from beans.

There's no indication, however, that increasing protein intake above normal levels would further speed up wound healing. Since I eat either meat or fish daily as part of my semi-paleolithic diet, I don't think low protein levels are the issue in my case.

Wound healing and vitamins

What about vitamins? We know that vitamin D and vitamin A play a role in bone growth, so perhaps they are involved in the healing of wounds as well. According to the authors, the case is not clear cut:

In general, it appears that large doses of either vitamins A or D inhibit the healing of soft wounds in experimental animals. There is conflict as to whether small dosages are helpful. Bush and Lam feel that vitamin A will hasten the healing in vitamin A-deficient animals.

The same pattern rises again: fixing a deficiency will improve things, but increasing intake further won't do much good (and may even be harmful). The B-complex group of vitamin seems to fit into this category too, with rats deficient in pyridoxine (vitamin B6) and riboflavin (vitamin B2) showing impaired wound healing. Vitamin B12 has also been suggested to increase the strength of wounds in rats during the early healing period.

While vitamin C is necessary for building collagen and capillaries in healing wounds, it's not entirely clear how much vitamin C is optimal. Low levels of vitamin C are common among patients with wound disruption, and long-term depletion of vitamin C can halve the tensile strength of healing wounds. Yet, it takes more than a month of ascorbic acid depletion to see an effect. As the authors state, the data on vitamin C and wound healing is somewhat contradictory:

A similar interpretation might be made from the work of Carney, who observed no difference in the healing of war wounds of soldiers in the Italian campaign on vitamin C-deficient diets and low serum levels, compared to those on adequate diets and high serum levels. On the other hand, most surgeons have the feeling that wound healing is impaired proportionately to the degree of ascorbic acid deficiency.

There are no clinical reports on wound healing and disruption in patients alternately treated with large vitamin doses presently in vogue, compared to control to whom no additional vitamins were administered.

There are a couple of newer studies showing that ascorbid acid may improve wound healing when administered via injection, but studies on dietary vitamin C and wound healing are more scarce. One study on guinea pigs did suggest that increases in dietary ascorbic acid improved wound integrity (link).

Wound healing and other factors

An interesting point the authors mention is that the pH of wounds may play a role in wound healing. In lower organisms, the pH varies markedly from the regressive phase to the regenerative phase. Furthermore, animals on an acid diet were shown to have shortened wound healing times.

In my previous post, I wrote that intermittent fasting may be one reason for slower wound healing:

There is a paper (here) that says caloric restriction and intermittent fasting reduces cell proliferation in epidermal tissue, which would likely have an effect on wound healing as well.

In contrast, the authors quote studies on salamanders and rats showing that fasting accelerates wound healing, as long as they're not starved. Despite how fasting is defined here, it does seem to fly in the face of the study that says both CR and IF reduce cell proliferation in mice. Perhaps the severity of the wound is also important here.


A deficiency in protein or vitamins results in impaired wound healing, but increasing dietary protein or vitamin intake above normal levels does not necessary speed up wound healing. There are conflicting results as to whether fasting increases or decreases the speed of wound healing.

For more information on nutrition, protein and vitamins, see these posts:

Slowing Down Aging with Intermittent Protein Restriction
A High-Protein Diet Is Better than a High-Carbohydrate Diet for Weight Loss
Dietary Vitamin K2 May Reduce Prostate Cancer
Fish Oil Decreases Inflammatory and Atherogenic Gene Expression

Read More......

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Wednesday, August 12, 2009

Dietary Vitamin K2 May Reduce Prostate Cancer

Edam cheese has more vitamin K2 than other cheeses. (Photo by Sifu Renka)

Vitamin K2 hasn't really made it into the mainstream yet, but a lot health blogs have caught up on its importance.

One explanation is that vitamin K2 fits poorly into the conventional view of what is healthy, and everything that the conventional view disapproves of, contrarian health bloggers embrace. The irony of vitamin K is that contrary to what one might expect, vitamin K1 just doesn't seem to have the same punch as vitamin K2.

And the interesting difference between the two? The main dietary source of vitamin K1 (phylloquinone) in the Western world is green leafy vegetables, while the main sources of vitamin K2 (menaquinones) are meat and cheese.

For some people, advocating meat and cheese over green leafy vegetables is pure blasphemy, but when it comes to prostate cancer, it may not be such a bad idea. In this post, we'll take a look at a large study that found a reduced risk of prostate cancer in men who ate more vitamin K2 in their diet.

The EPIC study and dietary vitamin K intake

The European Prospective Investigation into Cancer and Nutrition (EPIC) is the largest study of diet and disease to be undertaken. It has more than half a million participants, most of whom are 35-70 years old. The study begun many years ago and is still ongoing, with results being published every now and then.

One of the papers from last years looked at the incidence of prostate cancer in the Heidelberg cohort of the EPIC study (link). The Heidelberg cohort included almost 12,000 men aged 40-65 years from Heidelberg, Germany. Their dietary intake of phylloquinone and menaquinones was assessed by using a food-frequency questionnaire and a list of the vitamin K content of ~2000 commonly consumed foods.

The median daily intakes of phylloquinone and menaquinones were 93.6 micrograms and 34.7 micrograms, respectively. Menaquinone-4 (MK-4) accounted for 14.4 mcg of total menaquinones, while menaquinone-7 (MK-7) accounted for only 0.8 mcg. The main dietary menaquinones in terms of quantity appear to be MK-4 and MK-9.

Vegetables, especially green leafy vegetables, were the main source of vitamin K1. In the case of vitamin K2, meat products were the main source of MK-4 and dairy products the main source of higher menaquinones. Since fermented dairy products contain only a very small amount of MK-7, and the only food that has a lot of it is natto, it's not surprising MK-7 intake was so low among participants. Nonetheless, even small amounts may be enough to see benefits.

Perhaps unsurprisingly, those who consumed more vitamin K appeared to be healthier in general:

Subjects in the upper quartiles of phylloquinone and menaquinones had a lower body mass index, were more likely to have a university degree, and were more likely to practice vigorous physical activity >2 h/wk than were subjects in the lower intake quartiles.

This was despite the fact that as the intake of vitamin K increased, so did energy intake. Smoking status, however, was not significantly different between quartiles of vitamin K intake. These factors, along with things like calcium intake and family history of prostate cancer were adjusted for in the multivariate analysis.

Dietary intake of vitamin K1 & K2 and prostate cancer

The analysis showed that dietary intake of phylloquinone was not associated with the incidence of prostate cancer. In other words, those who ate more vitamin K1 had just as much prostate cancer as the ones who ate less vitamin K1.

Menaquinone intake, on the other hand, was inversely related to the risk of prostate cancer after excluding cases who were diagnosed within the first two years of follow-up. When the authors looked at only advanced cases of prostate cancer, the inverse relationship was even clearer. Thus, in contrast to vitamin K1, those who ate more vitamin K2 had less incidences of advanced prostate cancer.

The food source of vitamin K2 was also important. Only menaquinones from dairy products were associated with a significantly lower risk of advanced prostate cancer, while those from meat products were not. Accordingly, the risk of advanced prostate cancer was lower in those who consumed more MK-5–9 but not in those who consumed more MK-4. In contrast, menaquinone intake from meat products were associated with a lower risk of all cases of prostate cancer, but this difference was not statistically significant.

If one were to interpret these numbers literally, then, it would seem that an increased intake of MK-4 (from meat sources) may reduce the risk of prostate cancer in general, while an increased intake of higher menaquinones (from dairy sources) reduces the risk of advanced prostate cancer.

So why would vitamin K2 reduce advanced prostate cancer but not total prostate cancer? The authors offers a possible explanation:

Our findings of stronger associations of vitamin K intake with advanced than with total prostate cancer could be a hint that menaquinones play a role in tumor promotion and progression rather than in tumor initiation.

In other words, vitamin K2 may not decrease your odds of getting prostate cancer, but if you do get it, menaquinones decrease the odds of the cancer reaching an advanced stage. This makes sense, given that menaquinones have been shown to have an antiproliferative effect on several cancer lines in vitro.


An increased intake of menaquinones (vitamin K2) but not phylloquinone (vitamin K1) is associated with a reduced risk of advanced prostate cancer. Based on this study, the main sources of vitamin K2 in the Western diet are meat and dairy products.

When comparing different food sources of vitamin K2, dairy products were more strongly associated with a reduced risk of advanced prostate cancer than meat products. Accordingly, higher menaquinones (MK-5–9), which are found mostly in dairy products, were more strongly inversely associated with prostate cancer than MK-4, which is found mainly in meat.

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

Red Meat and Mortality: A Closer Look at the Evidence
Green Tea Catechin Reverses the Effect of DHT in Prostate Cancer Cells
Intermittent Fasting Reduces Mitochondrial Damage and Lymphoma Incidence in Aged Mice
Slowing Down Aging with Intermittent Protein Restriction

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Monday, August 10, 2009

Fish Oil Decreases Inflammatory and Atherogenic Gene Expression

Salmon contains more than 2 grams of omega-3 fatty acids per 100 grams.
Salmon contains more than 2 grams of omega-3 fatty acids per 100 grams. (Photo by Marco Veringa)

While the argument over polyunsaturated fats in general continues, most people consider omega-3 fatty acids to be very beneficial.

The most important omega-3 fatty acids are alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). EPA and DHA are often marketed as good for heart health, and indeed there is a lot of evidence to support this claim. ALA, on the other hand, is much less effective, because it first needs to be converted to EPA and DHA by the body to be usable, and only a very small amount gets converted (link).

One of the best and easiest sources of EPA and DHA is fatty fish such as salmon. Another good option is fish oil or fish liver oil, which contain high amounts of EPA and DHA. While several studies have shown beneficial effects from consuming these omega-3 fatty acids, the mechanism of action has not been clear.

To shed light what EPA and DHA actually do in the human body, a new study looked at changes in gene expression after consuming fish oil (link). In healthy subjects, daily ingestion of fish oil changed the gene expression profile to a more anti-inflammatory and antiatherogenic status.

Study method

The study included 111 healthy elderly subjects (at least 65 years old) who did not take fish oil supplements and ate fish no more than four times a week. They were randomized to receive either fish oil with a low or high omega-3 content or sunflower oil.

The high-dose fish oil contained on average 1,093 mg of EPA and 847 mg of DHA, while the low-dose fish oil provided 226 mg of EPA and 176 mg of DHA. The total amounts omega-3 polyunsaturated fatty acids were 1.94 grams and 0.4 grams, respectively. According to the authors, the higher dose is about the same as eating 10 portions of fatty fish weekly, and the lower dose equals 2 portions weekly.


Consuming the high-dose fish oil resulted in gene expression changes of 1040 genes, whereas sunflower oil changed the expression of 298 genes. Out of these, 140 genes were overlapping, meaning that the combination of EPA+DHA uniquely changed 900 genes. Except for one gene, the direction of change was the same in both groups.

Supplementation with a high dose of EPA+DHA for six months significantly decreased the expression of genes involved in the inflammatory pathways, including eicosanoid synthesis, interleukin signaling, and MAP kinase signaling.

Moreover, a similar effect was seen in processes involved in the formation of atherosclerosis. Decreased gene expression was observed in pathways related to cell adhesion, scavenger receptor activity, and adipogenesis. Participants taking the high-dose fish oil also showed a reduction in oxidative stress. You can find the full figures from the paper here and here.

In the low-dose fish oil group, only a small sample of the genes were measured for changes in expression. The results showed that the lower dose of EPA+DHA also resulted in a down-regulation of genes and that this change was somewhere in between those seen from high dose EPA+DHA and sunflower oil.


Supplementing with 1.9 grams of EPA and DHA (~1.1 g EPA and ~0.8 g DHA) daily resulted in favourable changes in gene expression related to inflammation and atherosclerosis in elderly subjects. Among the genes whose expression was decreased were NF-kappa-beta targets, proinflammatory cytokines, and genes involved eicosanoid synthesis.

These results are in agreement with earlier ex vivo studies and support the idea that EPA and DHA, two omega-3 polyunsaturated fatty acids found in fish, are beneficial in reducing inflammation and preventing atherosclerosis.

For more information on inflammation and fish oil, see these posts:

Swine Flu and Avoiding the Cytokine Storm: What to Eat and What Not to Eat?
Examining Possible Causes for Slower Wound Healing
Green Tea Protects from Arthritis in Rats
Intermittent Fasting with a Condensed Eating Window – Part III: Fasting Blood Glucose, Cortisol & Conclusion

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Thursday, August 6, 2009

Anthocyanins from Berries Increase HDL and Lower LDL

Black currants are even higher in anthocyanins than blueberries.
Black currants are even higher in anthocyanins than blueberries. (Photo by Marylise Doctrinal)

You've probably heard a million times that berries are good for you, but how many of us know how they really benefit health?

Here's one good example: they improve cholesterol levels. Or, to be more specific, it's the anthocyanins in berries that do. A new study found that daily anthocyanin supplementation significantly increased HDL while decreasing LDL (link). In this post, we'll take a closer look at the paper.

Study method

The study included 120 subjects aged 40-65 years with dyslipidemia. Dyslipidemia generally refers to a poor lipid profile and can mean either high LDL, high triglycerides, low HDL, or a combination of these. A high total cholesterol alone does not necessarily count as dyslipidemia.

At the beginning of the study, the participants had total cholesterol levels around 225 mg/dL, LDL around 159 mg/dL, HDL around 46 mg/dL, and triglycerides around 200 mg/dL.

The subjects were given 320 mg anthocyanins or placebo daily for 12 weeks. The supplements contained 17 different anthocyanins extracted from bilberry and black currant. The participants were instructed to take the supplements twice per day (2 x 160 mg) 30 minutes after breakfast and supper and to maintain their usual diet and lifestyle.


Serum HDL cholesterol increased significantly more in the anthocyanin group (13.7%) than in the placebo group (2.8%) after 12 weeks of treatment. Serum LDL cholesterol decreased by 13.6% in those who consumed anthocyanins and increased by 0.6% in those who received placebo. No significant differences were seen in total cholesterol and triglyceride levels.

In other words, while total cholesterol levels were similar between the groups, the lipid profile of those who ate anthocyanins was much better. Their HDL levels increased and LDL levels fell significantly, while in the placebo group only a slight improvement in HDL was seen. Here's a quote from the authors:

The 13.6% decrease in LDL and 13.7% increase in HDL observed in the present study would result in a nearly 27.3% reduction in coronary heart disease risk, which is meaningful and greatly promising.

No changes were observed in weight, BMI, waist/hip circumference, and blood pressure between the groups. Furthermore, anthocyanin consumption had no effect on red and white blood cell counts and hemoglobin.

Anthocyanins from berries or supplements?

So what about eating berries instead of taking supplements? According to one source, black currants contain 476 mg anthocyanin per 100 grams on average, while blueberries contain 386 mg (link). A second source says black currants contain 254-434 mg (link), while another source reports an anthocyanin concentration between 84-114 mg in blueberries (link), and yet another 62 mg for blueberries and 300 mg for bilberries (link).

According to the USDA database (link), raw blueberries contain about 160 mg anthocyanins and frozen blueberries about 90 mg. Wild raw blueberries take the blueberry cake with 320 mg, but raw bilberries are even better with 430 mg anthocyanins per 100 grams. Raspberries and strawberries contain a measly 20-40 mg, depending on whether they're frozen or fresh.

To make some sense out of this, it seems that blackcurrants and bilberries have the most anthocyanins, followed by blueberries. A cup of any of these berries per day would come pretty close to the amounts used in the study. Strawberries and raspberries are a distant third.

Keep in mind that these figures are not carved in stone, as it's impossible to give an exact calculation of how much anthocyanins a cup of berries will give you. The variation in anthocyanin content is very high, and the actual amount depends on the cultivar and also when and where the berries are picked. It's useful to know, however, that the concentration of anthocyanin actually increases with ripening, and that while freezing does destroy some of the anthocyanins, most of them survive the process (link).


Anthocyanins increased HDL and decreased LDL by more than 13% in subjects with dyslipidemia. The anthocyanins were extracted from bilberry and black currant and given in supplement form, 160 mg taken twice daily after breakfast and supper for a total of 320 mg.

A cup of black currants, blueberries or bilberries (frozen or fresh) would give roughly the same amount of anthocyanins as the supplements used in the study.

For more information on cholesterol, see these posts:

Niacin Raises HDL, Lowers LDL, VLDL & Triglycerides
Blood Test Analysis: The Cholesterol and Saturated Fat Issue Revisited
Coconut Lowers LDL, VLDL and Triglycerides, Raises HDL
Low-Carb vs. Low-Fat: Effects on Weight Loss and Cholesterol in Overweight Men

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Tuesday, August 4, 2009

Want to Help Practical Anti-Aging Research? Here's Your Chance

In the future, we won't need Photoshop.
In the future, we won't need Photoshop. (Photo by Tucia)

If you support the anti-aging movement but are unsure how to help in practice, here's a good chance to do just that without even leaving your computer.

The Immortality Institute has announced a matching grant for anti-aging research. The Institute will match every contribution for the study of laser ablation of lipofuscin up to $8,000. For every dollar you donate, they will donate one too, with the goal of reaching a total of $16,000 in donations.

And what exactly is lipofuscin and why is it important? Here's a quote from the Laser Research Grant website:

Lipofuscin is a byproduct of metabolism - a type of indigestible junk that slowly builds up within (and outside) human cells throughout life. It is most commonly recognized as the "stuff" that gives age spots their color.

As I've discussed on this blog before, the accumulation of waste seems to be a key factor in age-related disease and, ultimately, death from old age. Any technological innovations that target this problem should be warmly welcomed by anyone who is not looking forward to spending their retirement years in poor health.

The technology proposed here is using laser pulses to destroy lipofuscin, also known as Selective Photothermolysis. The use of lasers, LEDs, and infrared light is nothing new in cosmetics, but in this case, the goal is more about reversing damage rather than just covering it up. The research will be conducted by Nason Schooler at the SENS Foundation Research Center in Tempe Arizona. Here's a quote about the study itself:

The current proposed research will use various pulsed laser treatments to investigate the effects on worm lifespan. Human cell culture models will also be used to investigate the dynamics of lipofuscin destruction microscopically in actual human cells.

For more details on how the study will be done, see this video presentation by Mr. Schooler. If you want to further discuss the research – or anything related to increasing lifespans – I highly recommend paying a visit to the discussion forums (you can find me there as well, under the name JLL).

The matching grant is open until 17th August, so if you want to donate and get an extra bang for your buck, you have about two weeks (you can donate here). Currently, we're a few hundred short of $3,000, which does not include the matching sum from the Immortality Institute.

If you don't have hundreds of dollars to spend, that's okay – every bit helps. Also, the research will be conducted even if the goal is not reached (just on a lower budget), so donations will definitely not go to waste.

UPDATE: We gathered a whopping $10,077.80 in donations, which will be matched by $8,000 from the Immortality Institute and
by $9,038.9 from private investor Peter Thiel for a grand total of $27,116.70. This means that the goal was more than reached, and the research will take place as intended. Big thanks to everyone who donated!

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

How to Live Forever: My 5 Steps to Immortality
Who Wants to Live Forever? Results from a Global Survey
Anti-Aging in the Media: New York Times on Caloric Restriction and Resveratrol
Biotechnology and the Future of Aging

Read More......

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