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:

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.

Conclusion

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......

My Current Health Regimen v2.0

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

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

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

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

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

Main changes from v1.0: none.

Avoiding harmful foods

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

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

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

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

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

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

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

Eating healthy foods

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

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

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

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

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

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

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

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

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

A note on diet tweaking

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

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

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

Going without food

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

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

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

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

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

Supplements

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

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

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

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

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

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

Exercise

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

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

Main changes from v1.0: none.

Brain training

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

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

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

Main changes from v1.0: none.

Quick summary of the health regimen

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

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

I limit or avoid eating the following foods:

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

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

My supplement regime consists of the following:

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

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

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

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

Read More......

Fish Oil Decreases Inflammatory and Atherogenic Gene Expression

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.

Results

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.

Conclusion

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

Read More......

Swine Flu and Avoiding the Cytokine Storm: What to Eat and What Not to Eat?

Pomegranate juice is an ACE inhibitor. (Photo by JOE M500)

The scary connection between the 1918 flu pandemic (Spanish flu), the avian influenza (bird flu) and the swine influenza (pig flu) is that they all strike hardest those with healthy immune systems.

Usually, when people die of influenza, it's because they're old or their immune systems are compromised in other ways. Not so with the swine flu. As with the other two pandemics, death rates from swine flu have been highest among the 15-40 age group. Healthy young people seem to be in an especially big danger of dying from the influenza.

Swine flu, inflammation and the cytokine storm

The reason behind the deaths seems to be an exaggerated immune response, known as a cytokine storm. Since the body doesn't know what to do with the virus, it triggers an all-out release of inflammatory mediators. The reaction then becomes out of control, and the feedback loop ends up killing the patient (link).

The cytokine storm is the reason why the usual recipe for good health doesn't apply in the case of swine flu. Both inflammatory and anti-inflammatory cytokines have their uses in fighting off infection, and inhibiting inflammation is considered a good way to promote health in general. However, increasing anti-inflammatory cytokines during a cytokine storm is a bad idea.

So how do we shield ourselves from a cytokine storm? No one is really sure at this point. In a cytokine storm from avian influenza, the main cytokines responsible are TNF-alpha, IL-6 and IFN-gamma (link, link), with IP-10 and IFN-beta also being expressed more than usual (link). Reducing the levels of these and other cytokines could, at least in theory, be helpful. There is also some evidence that angiontensin converting enzyme (ACE) inhibitors might help in mediating cytokine storms (link, link, link), though we don't know for certain.

While taking cytokine and ACE inhibitors for swine influenza is currently only a theory, I nevertheless find it an interesting one. Specifically, I think a look into how "health foods" affect cytokines is useful, since conventional wisdom may not apply here due to reasons mentioned earlier. Below, we'll take a look at some natural cytokine and ACE inhibitors and also discuss which health foods may actually be harmful.

ACE inhibitors from natural sources

Procyanidins and flavanols have an inhibitory effect on angiotensin converting enzyme (link). They are found in many plants, such as apples, cocoa, cinnamon, berries and tea. Chokeberries have the highest concentration of procyanidins.

In one study, procyanidins and epigallocatechin were effective while catechin, epicatechin, gallic acid, chlorogenic acid, caffeic acid, quercetin, kaempferol and resveratrol at similar concentrations were ineffective (link). Accordingly, wine, chocolate and tea were all found to inhibit ACE activity, with red wine being more effective than white wine, green tea being more effective than black tea.

A word of caution: cocoa, while inhibiting ACE activity, may increase the secretion of TNF-alpha (link) and IL-1 and IL-4 expression (link), which could be bad news in the case of a cytokine storm. Chocolate may therefore not be a good idea if trying to reduce cytokines.

Quercetin, while ineffective in the study mentioned above, has been shown to have an inhibitory effect on the angiotensin converting enzyme, similarly to captopril (link), while also reducing blood pressure (link) and the angiotensin-induced production of IL-6 (link).

Another study found that both green tea and black tea inhibited ACE activity dose-dependently (link). In addition, all four catechins tested (including epicatechin) were effective. Rooibos tea, however, had no effect.

Pomegranate juice seems to be very effective in inhibiting ACE activity in vitro and in vivo (link). Hypertensive patients given 50 ml of pomegranate juice for two weeks had a 36% decrease in ACE activity and a 5% reduction in systolic blood pressure.

Cytokine inhibitors from natural sources

Epigallocatechin gallate (EGCG) inhibits the production of TNF-alpha, IL-6 and IL-8 (link). The best source of EGCG is green tea. Black tea is not without its merits either, though, as the theaflavins in black tea appear to reduce levels of IL-1 and IL-6 (link).

Several compounds in garlic appear to inhibit cytokines. Ajoene partially inhibits the production of TNF-alpha (link). Allicin inhibits IL-1, IL-8 and IP-10 (link), while alliin increases IL-1 and TNF-alpha (link). Crushing or chopping garlic causes alliin to be converted into allicin, while cooking garlic decreases allicin (link). Therefore, for the purposes of reducing cytokines, it's better to crush garlic and eat it raw.

Chronic garlic administration decreases myocardial TNF-alpha expression in rats (link). One study showed that garlic may increase IL-10 (link), and another one showed it increased IL-4 while reducing IFN-gamma (link). However, in humans, garlic powder extract has been shown to reduce IL-1 and TNF-alpha with no effect on IL-10 (link). The ratio of alliin and allicin may be important here as well.

When mice infected with influenza were fed vitamin E, they had significantly lower levels of IL-1beta, IL-6 and TNF-alpha (link, link). A relatively good natural source of vitamin E is red palm oil, which has been shown to reduce TNF in humans (link).

Fats, depending on their omega-3/omega-6 ratio and whether they're saturated or unsaturated, may play an important part in cytokine production. In rats, fish oil (which is high in omega-3) was shown to reduce levels of IL-1 and IL-6 (link). In humans, 4 weeks administration of flaxseed oil followed by 4 weeks of fish oil was shown to inhibit TNF-alpha and IL-1 in healthy humans, with fish oil being more effective (link).

Not all the data is positive, unfortunately. A long-term study comparing various doses of fish oil in humans concluded that supplementation for 1 year did not affect cytokine production (link). In another study, olive oil, coconut oil and fish oil all reduced IL-1 production in rats during the first 4 weeks of administration (link). However, after 4 weeks, olive oil and fish oil increased IL-6 production, and after 8 weeks, olive oil began to increase IL-1 production as well.

While resveratrol was found in the previously mentioned study to be ineffective for inhibiting ACE activity, it appears to suppress the expression of TNF-alpha, IL-6 and IL-8 (link, link). Resveratrol is found in red wine, red grapes and peanuts. Red wine has been shown to reduce levels of TNF-alpha, IL-6 and IL-8 in diabetics (link), although one study found no effect on cytokines from red wine (link) and another one found an increase in IL-6 (link). While those with peanut allergy should obviously avoid peanuts, it is unclear how peanuts affect cytokine levels in non-allergic people.

Quercetin decreases the expression of TNF-alpha, IL-6 and IL-8 (link, link). Food sources of quercetin include green tea, capers, fennel, onions, cocoa, kale and apples with skins (link, link). Compared to supplements, the quercetin content of foods is quite low, however.

Curcumin appears to reduce levels of TNF-alpha along with IL-6 and IL-8 (link, link, link). The main food source of curcumin is the spice turmeric. While the bioavailability of curcumin is very low, heating (link) and the addition of piperine greatly enhances its absorption (link). Piperine, which is found in black peppers, also inhibits inhibits IL-1, IL-6 and TNF-alpha (link).

One study showed that 2,000 IU of vitamin D3 given for nine months resulted in lower TNF-alpha and higher IL-10 levels than the control group (link). Vitamin D3 seems to increase IL-4 but decrease TNF-alpha, INF-gamma and IL-6 (link, link). On the other hand, a vitamin D deficiency reduced IL-1 levels, halved TNF levels and reduced IL-6 levels five-to-tenfold in mice (link). The Vitamin D Council newsletter covers this topic extensively (link); in short, they seem to advocate either not taking any vitamin D3 or taking at least 5,000 IU. Anything in between is potentially harmful for cytokine storms.

Summary

For the purposes of inhibiting ACE and reducing cytokines, the following foods and compounds seem to be the best choices:

• Green tea (ACE inhibitor, reduces cytokines)
• Black tea (ACE inhibitor, reduces cytokines)
• Quercetin (possible ACE inhibitor, reduces cytokines)
• Pomegranate juice (ACE inhibitor)
• Red wine (ACE inhibitor)
• Turmeric (reduces cytokines)
• Black pepper (reduces cytokines)
• Raw crushed garlic (reduces cytokines)
• Red palm oil (reduces cytokines)
• Vitamin E (reduces cytokines)
  
• Coconut oil (reduces cytokines)

The following foods, while beneficial in many other ways, may not be a good idea in terms of reducing cytokine levels:

• Olive oil (may increase cytokines)
• Fish oil (may increase cytokines)
• Chocolate (ACE inhibitor, increases cytokines)

In addition, it seems that vitamin D3 could be on either list, depending on the dosage. Average blood levels of vitamin D may be worse than very low or high levels.

That's it for this week, I'm off for a holiday (hopefully without swine flu), so no updates for a few weeks. For more information on cytokines and inflammation, see these posts:

Examining Possible Causes for Slower Wound Healing
Green Tea Protects from Arthritis in Rats
Green Tea Protects Cartilage from Arthritis in Vitro
Intermittent Fasting with a Condensed Eating Window – Part III: Fasting Blood Glucose, Cortisol & Conclusion

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

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

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

Tea tree oil – is it anti-androgenic?

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

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

Adding a carrier oil and Korean red ginseng

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

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

Switching from tea tree oil to tea tree conditioner

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

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

The conclusion

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

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

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

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

For more information on hair growth, see these posts:

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

Read More......

Examining Possible Causes for Slower Wound Healing

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

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

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

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

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

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

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

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

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

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

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

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

Read More......

Green Tea Protects from Arthritis in Rats

Could green tea be a treatment for arthritis in humans? (Photo by nyki_m)

I wrote a while ago about a study showing that green tea protects from arthritic cartilage breakdown in vitro. As promising as in vitro studies are, they're not the same thing as testing something on whole organisms. For example, based on that study alone, it's difficult to determine how much green tea would be needed to see effects in animals or humans – or indeed, whether it even works in vivo.

But fear not: the above study is not the only piece in the puzzle. According to a paper by Kim et al., green tea extract is effective in protecting rats from arthritis. Rats with bacteria-induced autoimmune arthritis showed less signs of arthritis when they were given green tea in drinking water.

Study design

The green tea extract used by the authors contained 57.5% catechins (of total weight), of which the most abundant one was epigallocatechin gallate (EGCG). The first group of rats received 8 grams of the extract per liter of drinking water, the second group received 12 grams, and the control group received normal water.

Each group was fed for 1-3 weeks before arthritis was induced. The severity of arthritis was evaluated on the basis of erythema (redness of the skin caused by capillary congestion) and swelling in each paw.

Effect of green tea extract on arthritic symptoms

The groups receiving 8 g/L had less signs of arthritis than the control group. The rats that had received green tea in drinking water for 2 weeks showed much less symptoms compared to rats fed for only 1 week. However, 3 weeks of 8 g/L feeding wasn't more effective than 2 weeks; in fact, it was less effective, although the difference was very small.

A similar pattern was observed with the size of the dose. When the duration of the treatment was 2 weeks, the rats fed 8 grams of green tea extract per liter had less arthritis than rats fed 12 grams. In the group fed for 3 weeks, there was no clear difference.

Even though the data for lower doses of 2 and 4 g/L is not presented, the authors mention that when all the arthritis scores from different doses were compared, 8 g/L and 2 weeks of feeding was the optimal combination, with the scores following an inverted bell-shaped dose-response curve.

Effect of green tea extract on cytokines and inflammation

Green tea extract suppressed the proinflammatory cytokine IL-7. Of the anti-inflammatory cytokines IL-4 was unaffected while IL-10 was increased. Other studies have shown that the suppression of IL-7 and induction of IL-4 and IL-10 can prevent or alleviate arthritic conditions, which makes green tea look quite promising in the treatment of arthritis.

Conclusion and practical considerations

An extract of green tea added to drinking water reduced signs of bacterially induced arthritis in rats. The results are explained in part by green tea's ability to suppress the proinflammatory cytokine IL-7 while increasing the secretion of the anti-inflammatory cytokine IL-10.

The optimal dose in this study was found to be 8 grams of extract per liter of drinking water for 2 weeks before inducing arthritis. The amount of catechins per gram of extract was 57.5%, which gives 4.6 g catechins in a liter of drinking water. If we assume that the rats drank about 50 mL per day, this would amount to an intake of 0.23 g (or 230 mg) of catechins per day.

The catechin content of green tea varies, but assuming a conservative estimate of 100 mg per cup, the amount in the study would be equivalent to about 2-3 cups per day. Keep in mind, however, that this is a very rough figure – the amounts that work in rats may not work in humans.

For more information on green tea, see these posts:

Vitamin C Protects Green Tea Catechins from Degradation
Green Tea Protects Cartilage from Arthritis in Vitro
Green Tea Extract Enhances Abdominal Fat Loss from Exercise
Caffeine and Polyphenol Contents of Green Tea, Black Tea, Oolong Tea & Pu-erh Tea

Read More......

Intermittent Fasting with a Condensed Eating Window – Part III: Fasting Blood Glucose, Cortisol & Conclusion

Which is better, several small meals or one big meal? (Photo by morbuto)

This is the third and last post in a series discussing the effects of a reduced meal frequency on various health markers. To read the previous posts, see Part I: Poorer Insulin Sensitivity and Glucose Tolerance? and Part II: Blood Pressure, Body Weight & Cholesterol.

As mentioned before, reducing the frequency of meals to just one per day effectively means the participants were on a condensed eating window version of intermittent fasting. They consumed their entire energy intake during four hours in the evening. Macronutrient composition was not significantly different from the control group, but the fasting group ate 65 kcal less than the control group.

Fasting blood glucose levels

As mentioned in Part I, glucose tolerance as measured by an oral glucose tolerance test actually seemed to worsen as a result of consuming only one meal per day. However, there is some doubt over the validity of these results, because the morning glucose tolerance test of the fasters may have been affected by the large meal from the previous day.

Fasting blood glucose levels, on the other hand, were lower in the 1-meal-per-day group (85.9 mg/dL) than in the 3-meals-per-day group (89.4 mg/dL), though this difference was not statistically significant. Again, there is the difficulty of comparing these results, because the blood results were taken in the evening (after an 18-hour fast) in the intermittent fasting group and in the morning (after a 12-hour fast) in the control group.

Cortisol levels

Cortisol, which is also known as the "stress hormone", was significantly lower in the fasting group (7.2 micrograms/dL) than in the control group (14.1 micrograms/dL). In other words, eating one big dinner instead of the usual three meals cut cortisol levels almost by half.

This result is somewhat peculiar considering that higher cortisol levels are usually associated with higher blood pressure. In this study, the intermittent fasting group had much lower cortisol levels but slightly higher blood pressure. Since cortisol levels are typically higher in the morning and lower in the evening, the difference may again be explained by the fact that blood samples were taken at different times between the groups.

Conclusion

Eating one large evening meal and fasting the rest of the day instead of eating breakfast, lunch and dinner did not result in major health benefits in healthy, non-obese subjects. In fact, several health markers appeared to be negatively affected: insulin sensitivity and blood glucose tolerance worsened and blood pressure increased. Since measurements were taken at different times, the results may not be comparable, however.

Body weight and body weight were lower in the intermittent fasting group. This may be partly explained by the fact that energy intake was also lower by 65 kcal in subjects consuming only one meal per day.

Both HDL and LDL levels increased in the intermittent fasting group compared to the control group. Triglycerides appeared to be lower, but the difference did not reach statistical significance.

Cortisol levels, which are indicative of stress and immune function, were significantly lower in the intermittent fasting group. As measurements were taken early in the morning in the control group vs. later in the afternoon in the fasting group, this difference may also be due to diurnal changes in cortisol levels.

Following a condensed eating window version of intermittent fasting, where all of the daily calories are consumed during a few hours, may not improve health markers when calorie intake is not reduced. Whether the effects are in fact negative is unclear based on these results, but for those trying this version of IF, regular monitoring of health markers is recommended.
For more information on intermittent fasting, see these posts:

Intermittent Fasting: Understanding the Hunger Cycle
A Typical Paleolithic High-Fat, Low-Carb Meal of an Intermittent Faster
A Typical Day of Intermittent Fasting
Intermittent Fasting Improves Insulin Sensitivity Even without Weight Loss

Read More......

Green Tea Protects Cartilage from Arthritis in Vitro

Green tea catechins protect cattle and human cartilage from arthritis. (Photo by Vincent Boiteau)

Joint diseases such as arthritis are huge problems in the developed world. In the US, they account for more disabilities than cancer or heart disease.

We know that arthritis is associated with varying degrees of inflammation of the joints. Inflammation is accompanied by a loss of the connective tissue of the joint, especially the layer of cartilage covering the ends of bone. When enough damage has accumulated, the joint becomes dysfunctional and needs replacing surgically.

Treating the inflammation will only fix a part of the problem, however. Some studies have reported that the destruction of connective tissue may continue even when inflammation is suppressed, which suggests that ongoing loss of cartilage and inflammation are two separate processes. None of the traditional treatments for arthritis preserve cartilage from being destroyed and may in fact even increase the rate of loss.

Fortunately, green tea may be of help here. Adcocks et al. studied the effects of green tea catechins on the integrity of joint structure and function. Based on the results it seems that in addition to reducing inflammation associated with arthritis, green tea contains catechins that may protect from cartilage breakdown as well.

The authors studied the effects of green tea on cartilage breakdown in vitro by treating cartilage from both humans and cattle with cytokines or all-trans-retinoic acid (Ret), which are known to cause breakdown of cartilage proteoglycan. The cytokines used were recombinant human interleukin-1-alpha & beta (IL-1a & IL-1b) and recombinant human tumor necrosis factor-alpha (TNF). They then treated the cartilages with different catechins from green tea to see whether this breakdown was prevented.

Green tea catechins and breakdown of bovine cartilage

Epigallocatechin gallate (EGCG), the main catechin found in green tea, effectively prevented the TNF-stimulated breakdown of nasal cartilage from cattle. The effect was dose-dependent: with every ten-fold increase in EGCG concentration, the percentage of inhibition doubled. EGCG did not prevent cartilage breakdown caused by Ret or IL-1a, however.

In contrast, two other green tea catechins, epicatechin gallate (ECG) and epicatechin (EC), inhibited breakdown caused by IL-1a but not Ret or TNF. Epigallocatechin (EGC) was ineffective in preventing nasal cartilage breakdown. EGCG, ECG or EGC all decreased loss of type II collagen resulting from IL-1a by 50% or more.

In bovine articular cartilage, EGCG and ECG prevented cartilage breakdown from IL-1a, Ret and TNF. EC and EGC, on the other hand, had no effect.

Green tea catechins, osteoarthritis and rheumatic arthritis

The authors also tested the effect of green tea catechins on cartilage from humans suffering from osteoarthritis (OA) or rheumatic arthritis (RA). Osteoarthritis, also referred to as degenerative joint disease or wear-and-tear arthritis, is caused by a deterioration of cartilage and overgrowth of bone usually due to injury or aging. Rheumatic arthritis, on the other hand, is a chronic inflammation of the connective tissues of joints, which eventually leads to loss cartilage. The cause of RA is less clear.

The catechins of green tea were effective against both types of arthritis. ECG and EGCG inhibited the proteoglycan breakdown of human cartilage treated with IL-1b or TNF. The same effect was seen regardless of whether the cartilage was from OA or RA sufferers. The catechins also inhibited the breakdown of treated cartilage from humans not suffering from arthritis.

Comparing the results in human and bovine cartilages, it seems that EGCG and ECG are the most effective catechins in terms of arthritis. EGCG prevented cartilage loss from TNF in all cases, while ECG was effective against IL-1.

Conclusion

Arthritis is associated with inflammation and deterioration of cartilage, which seem to be two separate processes. Since reducing inflammation may not prevent the loss of cartilage in patients suffering from arthritis, finding ways to inhibit cartilage breakdown is important.

In addition to being anti-inflammatory, green tea catechins protect cartilage from breakdown caused by proinflammatory cytokines in vitro. Catechins were also effective in reducing the loss of type II collagen. Whether drinking green tea provides sufficient levels of catechins to treat arthritis in humans remains to be seen.

For more information on green tea, see these posts:

Green Tea Enhances Abdominal Fat Loss from Exercise
Peak Increase in Antioxidants Occurs 20-40 Minutes After Drinking Green Tea
Green Tea Reverses the Effect of DHT in Prostate Cancer Cells
Caffeine and Polyphenol Contents of Green Tea, Black Tea, Oolong Tea & Pu-Erh Tea

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