Which Oils and Fats Are Best for Cooking?

Avocado oil has the highest smoking point. (Photo by Muffet)

If you've wondered which oils and fats are the best choices for cooking your meals, this post is for you. The first question we need to ask is what makes an oil good or bad for cooking? Putting the cholesterol issue aside for a moment, we can say that perhaps the most important thing is how well the oil tolerates heat. We are using it for cooking, after all. Two factors that affect heat tolerance are smoking point and oxidation. Smoking point is, as you might have guessed, the temperature at which the oil begins to smoke. It's also the point the oil starts to break down chemically. This is something you generally want to avoid, so it's usually recommended that you don't heat the oil to its smoking point. This, of course, rules out using oils with a low smoking point for cooking at high temperatures. The second factor, oxidation, is related to smoking point in the sense that both are affected by temperature. However, oxidation also happens at lower temperatures than are needed for the oil to start smoking. Oxidation is problematic because the lipid peroxidation end-products (ALEs) it creates can wreak havoc inside the body. These products have been shown to accumulate with aging and cause problems such as liver spots on the skin. So which oils are most susceptible to oxidation? If you've read this blog before then you already know the answer: polyunsaturated fats. In fact, polyunsaturated fatty acids (or PUFAs) tolerate heat very poorly. Not only do they oxidize when you heat them on a frying pan, they do so inside the body as well. On the other hand, monounsaturated fats are much more resistant to oxidation than polyunsaturated fats. Saturated fats are the most resistant. This gives us a good rule of thumb when looking for fats to use in cooking: avoid oils high in polyunsaturated fatty acids. Because of their potential to undergo lipid peroxidation inside the body, I tend to restrict their consumption altogether, but even if you are a fan of vegetable oils and omega-3, using them for cooking is not a very good idea. The table above shows the relative percentages of saturated (SA), monounsaturated (MUFA) and polyunsaturated fatty acids (PUFA) in various cooking oils and fats (data from US and Finnish food databases). They are in a decreasing order of PUFA content, meaning that the oils moist suitable for cooking are on the left and the least suitable oils are on the right. Coconut oil has the highest SA content and the lowest PUFA content of all oils, making it very resistant to oxidation. Ghee and butter also have very little PUFA and lots of saturated fat. Based on this, butter is actually one of the best choices for cooking, although the high AGE content of butter and its tendency to brown quickly suggest to me that perhaps ghee is a better option. The reason might be that butter also contains some protein and a small amount of carbohydrate. Palm oil and lard are somewhat lower in saturated fat than the first three, but since their MUFA content is quite high, they still make good choices for cooking. The rest to the right of these five are less than optimal. Corn oil, sesame oil, rapeseed oil, peanut oil, and canola oil are all high in polyunsaturates, making them prone to lipid peroxidation. And unless you buy them cold-pressed, they will have been heated during refining anyway, so some oxidation has probably happened before you even use them. What about olive oil then? Even though everyone seems to love olive oil in general, there's something of a debate going on over whether it should be used for cooking purposes. My opinion is that, like the graph suggests, it's not the worst choice but it's not the best either. The smoking point of extra virgin olive oil seems to vary from 160 to 190 °C, depending on the free fatty acid content. Virgin olive oil, however, has some properties that make it more heat-tolerant than most other oils (link). In general, the less refined the oil, the lower the smoke point. Unrefined oils high in PUFAs have the lowest smoking points (link), but high saturated fatty acid content does not necessarily guarantee a high smoking point. Coconut oil, for example, has a fairly low smoking point (177 °C, about the same as butter and lard) compared to peanut oil (227 °C). Refined avocado oil, which is mostly monounsaturated fat, appears to have one of the highest smoking points at 255-270 °C (link). Ghee is another oil with a very high smoking point (252 °C). So which oils should you use for cooking? For sautéing and cooking at light to medium temperatures, my choice would be the ones on the left of the graph: coconut oil, ghee, butter, palm oil, and lard. If you stay below 170 °C, you're in pretty safe waters in terms of oxidation regardless of which one of them you choose. Virgin olive oil seems like a viable choice, too; just make sure the particular olive oil you're using it doesn't start smoking. For searing, browning and other methods of cooking requiring higher temperatures, ghee and avocado oil seem like the best choices. When it comes to resistance to oxidation, ghee might take the cake, but avocado oil appears to have the highest smoking point of all oils, even though it does have 13.5% PUFAs. Still, keep in mind that when cooking at very high temperatures, some advanced glycation end-products (AGEs) are bound to be generated. For more information on fats and health, see these posts: Coconut Lowers LDL, VLDL and Triglycerides, Raises HDL My Current Health Regimen Blood Test Analysis: The Cholesterol and Saturated Fat Issue Revisited Should Saturated Fat Be Avoided in Low-Carb Diets?

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5 Reasons Why Dark Chocolate Is Better than Milk Chocolate

Look good? Forget it, there's way too much sugar. (Photo by .craig)

You may have thought of chocolate as a guilty pleasure, but the ancient Maya considered it the food of gods. Granted, the Maya also thought cutting out someone's heart in a ritual ceremony was a good fun, but they did get one thing right: chocolate really is a health food. That is, as long as you buy the dark kind. In fact, the darker the chocolate the healthier it is. As good as that sugar-laden milk chocolate bar may taste, it wouldn't have made its way into any self-respecting Maya feast. If you don't believe me, read further for three good reasons to choose dark chocolate instead of milk chocolate. 1. Dark chocolate is better for weight loss. Even though the amount of calories in milk chocolate and dark chocolate are pretty similar (and in fact milk chocolate sometimes contains fewer calories), dark chocolate contains significantly less carbohydrates. Milk chocolate usually has about 50 grams of carbs per 100 g, while the amount of carbs in dark chocolate ranges from 8 to 35 carbs, depending on how dark it is. A chocolate with 70% cocoa has ~30 grams; a 85% chocolate has ~20 grams. If weight loss or maintenance is your goal, the combination of large amounts of carbohydrates and fat is something to avoid. A high carbohydrate load will increase insulin secretion, which is a signal for the body to store energy as fat. The reason why low-carb diets are so effective for weight loss is their effect on insulin: even if you eat lots of fat, if there are no carbs present to drive insulin up, the energy from dietary fat won't be stored into fat cells. Unless you consume only a small quantity or restrict other carb sources to a minimum, combining milk chocolate with a low-carb diet is going to be difficult. If your goal is to stay under 50 grams per day, 100 grams of milk chocolate fills up your entire quota. But 100 grams of 85% dark chocolate still leaves you with 30 grams to spend on other carb sources, making dark chocolate a viable option even for low-carb dieters. 2. Dark chocolate causes less aging. Okay, so perhaps a bit of an exaggeration there, since we don't know exactly how big a role advanced glycation end-products play in the aging process. We do know, however, that the accumulation of AGEs is one of the seven biomarkers of aging, which makes avoiding them a sensible goal. As it happens, weight gain is not the only problem with the carbs in milk chocolate. Almost all of the carbohydrate in chocolate is sucrose, which is half glucose and half fructose. Even though the word 'glycation' in 'AGE' implies that glucose is the culprit, the fact is that fructose is much more prone to cause AGEs in the body. Since the main ingredient in milk chocolate is sugar, a 100 grams of milk chocolate will also give you a hefty dose of fructose. Dark chocolate, on the other hand, is mostly composed of fat – cocoa butter, to be specific. The fatty acid composition is 61% saturated fat, 36% monounsaturated and only 3% polyunsaturated fat, making cocoa butter very resistant to oxidation. And if you're worried about cholesterol, here's something to ease your mind: almost all of the saturated fat in cocoa butter is cholesterol-neutral stearic acid. Fructose, however, may increase triglycerides levels. Unlike dark chocolate, milk chocolate also contains some lactose. In addition to making milk chocolate an impossible treat for some lactose intolerants, lactose also causes glycation. Lactose breaks down to glucose and galactose, and like fructose, galactose appears to form AGEs more rapidly than glucose. 3. Dark chocolate has more cocoa polyphenols. The health benefits of chocolate are almost entirely due to the polyphenols found in cocoa. As a rule of thumb, whenever you read something good about chocolate, what they're really talking about is cocoa. Therefore, as the cocoa content of chocolate increases, so do its positive effects on health. A standard milk chocolate will contain about 30% cocoa, while premium dark chocolates usually have more than 70%. Another thing that reduces the polyphenol content of chocolate (by 60-90%) is alkalization (link), also known as Dutch processing or simply Dutching. Alkalization was invented in the 19th century to get rid of some of the bitterness of cocoa powder and to make it more palatable. Non-alkalized cocoa powder is a more light brown in color and tastes less sweet than alkalized cocoa powder. Nowadays Dutch processing is very common among industrial chocolate makers (link), which suggests that there's a good chance the average high-sugar milk chocolate will contain alkalized cocoa. Many dark chocolates seem to use non-alkalized cocoa, however, probably because the bitterness is perceived as preferable among chocolate enthusiasts. 4. The cocoa polyphenols in dark chocolate are more bioavailable. Even if your dark chocolate happens to be made from alkalized cocoa, you'll still get more bang for your buck in terms of polyphenols, because the polyphenols will be more bioavailable. This is again related to differences in the macronutrient composition of chocolates. First, the bioavailability of cocoa polyphenols depends partly on the fat content of chocolate. One in vitro study showed that cocoa liquor (which is about 50% fat) retained more polyphenols than cocoa powder (about 15% fat) when submitted to a digestion model (link). The reason appears to be that the higher fat content increases the stability of cocoa polyphenols during digestion. Second, sucrose and milk protein may affect the absorption of polyphenols negatively (link). Dark chocolate contains no milk protein, less sucrose and much more cocoa liquor than milk chocolate. The actual content varies, since different countries have different regulations on what kind of chocolates can be called "dark chocolate". The FDA, for example, states that dark chocolate must contain at least 35% chocolate liquor, while milk chocolate only needs to have more than 10%. Also, chocolates with 40-70% cocoa are also sometimes sold as "dark chocolate", so be sure to check the ingredient list before purchase. The words "cocoa mass", "cocoa liquor", "cocoa powder", "cocoa paste", "cocoa solids", or something to that effect should be first on the list – if "sugar" is mentioned first, it's definitely not real dark chocolate. 5. Dark chocolate is more filling. Anyone who has tried both milk chocolate and dark chocolate must have noticed that it takes much less to satisfy chocolate cravings with the latter than the former. I can personally eat 200 grams of milk chocolate (more than 1,000 kcal) in one go without having my craving satisfied. With 99% dark chocolate, a few pieces is enough. A similar effect was shown in a study from last year (link). This, as mentioned before, is not related to energy content, because milk chocolate and dark chocolate have virtually the same amount of calories. Rather, the reason why a smaller quantity of dark chocolate is enough is probably a combination of less sugar and more nutrients. Humans generally have a preference for sweet foods, which is why we love candy when we're kids. But part of the reason why we can't stop eating candy until we feel sick is that there are no nutrients in candy, only calories. This lack of nutrients causes our body to send the satiety signal way too late. Since dark chocolate is higher in cocoa powder, it's also higher in many nutrients, such as iron, magnesium, phosphorus, copper and manganese. Combined with the lower amount of sugar and high amount of fat, it's no surprise you get your daily chocolate fix quicker with dark chocolate than milk chocolate. Summary Dark chocolate contains less sugar, more cholesterol-neutral fat, and more cocoa polyphenols in a more bioavailable form than milk chocolate. Dark chocolate is also more filling, which means it takes less calories to satisfy your chocolate cravings. Keep in mind, however, that excess consumption of dark chocolate has its downsides too. Cocoa powder is high in iron and oxalates, which are harmful in high quantities. We'll return to the subject of optimal intakes in future posts, but for now, I limit mine to 50-100 grams of chocolate per day. For more information on chocolate, sugar, fat, and health, see these posts: Tea, Coffee and Cocoa: All Good for Your Teeth SAs, MUFAs vs. PUFAs: Fat Storage Depends on Type of Fatty Acid in Rabbits Fats and AGEs: PUFAs Are Even Worse than Fructose Low-Carb vs. Low-Fat: Effects on Weight Loss and Cholesterol in Overweight Men

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AGE Content of Foods

Hot dogs are high in AGEs. (Photo by TheBusyBrain)

There are two ways that advanced glycation endproducts (AGEs) are formed: inside the body or outside the body. These are known as endogenous and exogenous AGEs, respectively. The accumulation of AGEs is one of the seven types of aging damage. While it's uncertain just how big a role exogenous crosslinks play in aging, consuming excess amounts of AGEs through diet has been shown to cause serious health problems in animals and humans. Therefore, it seems useful to have some idea of which foods are especially high in AGEs. The following is a list of the AGE contents of commonly consumed foods. The data is based on one study (link). The authors state:

Two-hundred fifty foods were tested for their content in a common AGE marker (epsilon)N-carboxymethyllysine (CML), using an enzyme-linked immunosorbent assay based on an anti-CML monoclonal antibody. Lipid and protein AGEs were represented in units of AGEs per gram of food. -- -- A limitation of the present data is reliance on CML, a single AGE marker, while many other AGEs/ALEs are generated in food, albeit of unknown significance. In practical terms, however, CML is a commonly measured AGE/ALE compound, used routinely as an indicator of the AGE/ALE burden in numerous animal and human studies

Other ways of measuring AGEs might produce different values, so the numbers below serve mostly to give a rough idea of the relative AGE contents of foods. If you want to compare your own intake with others, here's a quote from the full paper:

In a preliminary survey of the usual daily AGE intake, we analyzed 3-day food records from healthy individuals (n=34). Mean daily AGE intake was 16,000±5,000 kU AGE. These data were used to define a high- or low-AGE diet, depending on whether the estimated daily AGE intake is significantly greater or less than 16,000 kU AGE. A similar investigation in 40 type 2 diabetic patients showed a daily AGE intake of 18,000±7,000 kU AGE, with major proportions of AGE contributed by broiled, fried, grilled, and roasted meat and meat alternatives.

So anything above 16,000 kU (see the list below for values) per day would put you in the high-AGE category. Again, keep in mind that we are talking about crosslinks produces outside body; whatever happens once the foods are digested, important as it may be, is beyond the scope of this post. Based on the data, we can make the following generalizations:

• Fats and meat products contain the most AGEs
• Carbohydrates are relatively low in AGEs
• Higher cooking temperatures increase AGEs
• Longer cooking times increase AGEs
• The presence of liquids in cooking reduces AGEs
• Processed foods have more AGEs than natural or homemade foods

I will try to keep this post updated as I come across new data to include in the list, so remember to check back every now and then. Below, AGEs are expressed either as units per gram (for solids) or units per milliliter (for liquids). Serving sizes are grams, and AGEs per serving are expressed as kilounits.

Fats	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Almonds, roasted	66,514	30	1,995
Avocado	15,772	30	473
Butter	264,873	5	1,324
Cashews, roasted	98,082	30	2,942
Cream cheese, Philadelphia soft	108,843	30	3,265
Margarine, 60% vegetable oil	175,192	5	876
Mayonnaise	94,010	5	470
Mayonnaise, imitation	2,000	5	10
Mayonnaise, low fat	22,011	5	110
Olive, ripe	16,686	30	501
Peanut butter, smooth	75,183	30	2,255
Walnuts, roasted	78,874	30	2,366
Salad dressing, Caesar	7,371	15	111
Salad dressing, French, Lite	11	15	0
Salad dressing, Italian, Lite	8	15	0
Beef	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Frankfurter, boiled 7 min	74,850	90	6,736
Frankfurter, broiled 5 min	112,697	90	10,143
Hamburger, fried 6 min	26,391	90	2,375
Hamburger, fast food	54,176	90	4,876
Meatball, boiled in sauce 1 h	28,519	90	2,567
Meat loaf, crust off, roasted 45 min	18,619	90	1,676
Roast beef	60,708	90	5,464
Shoulder cut, boiled 1 h	22,305	90	2,007
Shoulder cut, broiled 15 min	59,636	90	5,367
Bacon, microwave 3 min	90,228	13	1,173
Deli ham, smoked	23,491	90	2,114
Pork chop, pan fried 7 min	47,526	90	4,277
Beef and pork links, pan fried	54,255	45	2,441
Sausage, pork links, microwave 1 min	59,438	90	5,349
Poultry	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Chicken breast, skinless cubes, pan fried 15 min	61,221	90	5,510
Steamed 10 min and broiled 12 min	56,348	90	5,071
Pan fried 10 min and boiled 12 min	63,398	90	5,706
Chicken breast, skinless cutlet, raw	7,686	90	692
Boiled 1 h	11,236	90	1,011
Broiled 15 min	58,281	90	5,245
Fried 8 min	73,896	90	6,651
Microwave 5 min	15,245	90	1,372
Chicken breast, with skin, roasted 45 min	60,203	90	5,418
Chicken, dark meat, broiled 1 h	82,992	90	7,469
Chicken loaf, roasted, crust off, 45 min	14,195	90	1,278
Chicken nuggets	86,271	90	7,764
Turkey breast, cubes, skinless, broiled	55,747	90	5,017
Turkey breast steak, skinless, broiled	43,873	90	3,949
Smoked turkey breast, seared	60,137	90	5,412
Fish	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Fish loaf, boiled 90 min	7,606	90	685
Salmon, breaded, broiled 10 min	14,973	90	1,348
Salmon, raw	5,573	90	502
Salmon, smoked	5,718	90	515
Trout, raw	7,830	90	705
Trout, roasted 25 min	21,383	90	1,924
Tuna, loaf, roasted 40 min	5,895	90 531
Roasted 25 min	9,189	90	827
White, canned in oil, Albacore	17,396	90	1,566
Cheese	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
American, processed	86,775	30	2,603
American, processed, low fat	40,395	30	1,425
Brie	55,979	30	1,679
Cottage cheese 1% fat	14,532	120	1,744
Feta	84,235	30	2,527
Mozzarella, part skim	16,777	30	503
Parmesan, grated	169,020	15	2,535
Swiss, processed	44,701	30	1,341
Eggs	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Egg yolk, boiled 10 min	12,134	15	182
Boiled 12 min	18,616	15 279
Egg white, boiled 10 min	442	30	13
Boiled 12 min	573	30	17
Egg, fried with margarine	27,494	45	1,237
Tofu	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Broiled	41,067	90	3,696
Raw	7,875	90	709
Sautéed	38,303	90	3,447
Breads	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Bagel	1,075	30	32
Greek, hard	1,514	30	45
Whole wheat, center	536	30	16
Whole wheat, center toasted	1,080	30	25
Whole wheat, crust	730	30	22
Whole wheat, crust, toasted	1,394	30	36
Breakfast foods	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Pancake, frozen, toasted	22,618	30	679
Pancake, homemade	9,722	30	292
Waffle, frozen, toasted	28,711	30	861
Cereals	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Bran Flakes	346	30	10
Corn Flakes	2,320	30	70
Frosted Flakes	4,270	30	128
Corn Pops	12,431	30	373
Oatmeal instant, dry	188	30	4
Oatmeal, instant with honey	175	175	31
Rice Krispies	19,997	30	600
Grains and legumes	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Bean, red kidney, raw	1,158	100	116
Bean, red kidney, canned	1,906	100	191
Bean, red kidney, cooked 1 h	2,983	100	298
Pasta, cooked 8 min	1,123	100	112
Pasta, spiral, cooked 12 min	2,420	100	245
White rice, quick cook, 10 min	88	100	9
White rice, converted, cooked 35 min	91	100	9
Starchy vegetables	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Corn, canned	195	100	20
Sweet potato, roasted, 1 h	723	100	72
White potato, boiled, 25 min	174	100	17
White potato, french fries, homemade	6,939	100	694
White potato, french fries, fast food	15,219	100	1,522
Crackers and snacks	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Chips, corn, Doritos	5,049	30	151
Lay’s Potato Chips	28,818	30	865
Chips Ahoy Chocolate Chip Cookies	16,837	30	505
Oatmeal raisin cookie	13,707	30	411
Cracker, Goldfish, cheddar	21,760	30	653
Chocolate Chunk Granola Bar	5,068	30	152
Peanut Butter Chocolate Chunk Granola Bar	31,761	30	953
Popcorn with butter, air popped	1,340	30	40
Fruits	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Apple	127	100	13
Apple, baked	445	100	45
Banana	87	100	9
Cantaloupe	201	100	20
Raisin	201	30	36
Vegetables	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Broccoli, carrots, celery, grilled	2,260	100	226
Carrots, canned	103	100	10
Green beans, canned	179	100	18
Onion, raw	358	100	36
Tomato, raw	234	100	23
Other carbohydrates	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Sugar, white	0	5	0
Sugar substitute, powder	58	1	0
Milk and milk products	AGEs (U/mL)	Serving (mL)	AGEs/serving (kU)
Milk, whole	48	250	12
Fat free	5	250	1
Fat free, microwave, 1 min	21	250	5
Fat free, microwave, 3 min	345	250	86
Formula, infant	4,861	30	146
Human milk, fresh	52	30	2
Instant, chocolate, skim milk, sugar free	11	120	1
Yogurt, strawberry or cherry, nonfat, sugar free	40	250	10
Syrups, gels and juices	AGEs (U/mL)	Serving (mL)	AGEs/serving (kU)
Honey	87	15	1
Syrup, caramel, sugar free	15	15	0
Dark corn	14	15	0
Apple	20	250	5
Cranberry	32	250	8
Orange, fresh squeezed	3	250	1
Orange, carton	56	250	14
Dishes	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Italian pasta salad, homemade	9,346	100	935
Macaroni and cheese, baked	40,698	100	4,070
Pizza, thin crust	68,248	100	6,825
Sandwich, toasted cheese	43,327	100	4,333
Beverages	AGEs (U/mL)	Serving (mL)	AGEs/serving (kU)
Coffee, decaffeinated, instant	53	250	13
Instant	47	250	12
Drip method	15	250	4
On a heating plate more than 1 h	134	250	34
With milk	66	250	17
With milk and sugar	24	250	6
Cola	65	250	16
Cola, sugar free	12	250	3
Tea	19	250	5
Condiments	AGEs (U/mL)	Serving (mL)	AGEs/serving (kU)
Ketchup	103	15	2
Mustard	29	15	0
Soy sauce	573	15	9
Vinegar, balsamic	352	15	5
Vinegar, white	377	15	6

Conclusion Foods high in fat and/or protein are highest in AGEs, while carbohydrates are low in AGEs. The amount of advanced glycation endproducts increases as cooking temperature and time increases. Processed foods in general have more AGEs than unprocessed foods: for example, infant formula milk contains a 100 times more AGEs than human or cow milk. For more information on glycation, see these posts: Yerba Mate Inhibits AGE Formation Green Tea Reduces the Formation of AGEs My Current Health Regimen The 7 Types of Aging Damage That End up Killing You

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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......

Black Tea vs Green Tea: AGEs and ALEs

Theaflavins are black tea's answer to catechins in green tea. (Photo by Caro Wallis)

In previous posts, I've mentioned studies that have shown contradictory results for the effectiveness of green tea against advanced glycation end-products, or AGEs. At the time when the first post was written, I found five studies showing that green tea reduces AGE formation.

In a later post, I wrote that another in vitro study found yerba mate to inhibit AGE formation as effectively as aminoguanidine, which is one of the strongest anti-glycation drugs around. The bad news was that the same study found only a non-significant effect on AGEs from green tea. So what gives?

One possible reason for this discrepancy is dosage; perhaps low doses of green tea catechins are ineffective against glycation. Indeed, the yerba mate study used concentrations that were easily achievable in humans, whereas some of the others used stronger extracts. While a few cups of green tea may not do much in terms of AGEs, it's nonetheless promising that three of the five positive studies were in vivo. One of them was in diabetic rats and two of them were on normal rodents.

The problem with drinking copious amounts of yerba mate is that several reviews have found it to be carcinogenic. I will probably do another post on this, but based on my current knowledge, it looks like less than half a liter per day is not associated with an increased risk of esophageal cancer, while at higher levels the risk becomes clear. That means drinking enough yerba mate to inhibit AGEs may not be a smart choice.

If drinking 10 cups of green tea per day seems like a daunting task, rooibos tea is one alternative. We know that rooibos tea reduces lipid peroxidation, which causes advanced lipid peroxidation end-products, or ALEs. But there are no studies suggesting it reduces AGEs, so we're left looking for more alternatives to green tea.

Enter black tea. Most people consider green tea to be superior to black tea in all aspects, but that's not entirely true. Granted, green tea does often beat black tea because the latter contains fewer catechins, but there are also cases where black tea prevails. This is because during the longer fermentation process (which separates green tea from black tea), some of the catechins are converted to theaflavins – polyphenols unique to black tea.

AGEs in vitro: comparing black tea and green tea

Methylglyoxal (MGO) and glyoxal (GO) are highly reactive dicarbonyl compounds that modify proteins over time, forming AGEs. Although it's still unclear how harmful they are in healthy people, AGEs are known to be higher in chronic diseases such as diabetes, and levels of MGO are also 2-6 times higher in diabetics than in normal people.

In one study, epigallocatechin gallate (EGCG) – the main catechin in green tea – was found to trap both GO and especially MGO under neutral or alkaline conditions (link). Under acidic conditions (pH less than 4) this effect was not present. EGCG was as effective as aminoguanidine, which also works by trapping reactive dicarbonyl compounds.

The authors then decided to test whether other tea polyphenols might have a similar effect. And indeed they did. All of the catechins tested reduced MGO, with epigallocatechin (EGC) being the best of the four. However, they also found that black tea theaflavins outperformed all green tea catechins in reducing MGO. All theaflavins tested decreased MGO by more than 60%.

The concentration of catechin or theaflavin was the same in each test, which means that theaflavins clearly have the upper hand here. GA and PY in the above graph stand for gallic acid and pyrogallol, respectively. Interestingly, when the molar ratio of polyphenols to MGO was increased from 1:3 to 1:1 in a second experiment, some of the catechins did slightly better than theaflavins.

The difference between in vitro and in vivo

So black tea looks effective in vitro, but what about in vivo? Some studies suggest that even a few cups of green tea or black tea increases antioxidant activity in plasma, but it's not clear whether this translates directly to less AGEs and ALEs. The data on black tea and AGEs in vivo is very limited, so we'll have to focus on ALEs instead.

Green tea or black tea powder seems to protect rat livers from lipid peroxidation (link). Green tea also inhibits lipid peroxidation in their central nervous tissue – which is high in easily oxidizable polyunsaturated fatty acids. Levels of malondialdehyde (MDA), an intermediate in the formation of ALEs, were significantly reduced.

Similar findings were reported in another study, in which rats fed black tea instead of water had lower plasma MDA and protein carbonyl contents (link). Thus, black tea was effective against both ALEs and AGEs.

One study found that while black tea polyphenols strongly reduced plasma lipid peroxidation in vitro, but when human subjects were given a drink containing black tea extract, the rate of lipid peroxidation did not change (link). According to the authors, the concentrations of polyphenols in plasma would have to have been at least five times greater (5 micromoles) to see a significant effect.

Another study found that tea flavonoids reduced LDL oxidation in vitro (oxidised LDL seems to be a key player in atherosclerosis), with theaflavins being more effective than catechins (link). Then, human volunteers were given 750 mL of black tea for 4 weeks to see if the same thing happened in vivo. Although the concentration of polyphenols was now much lower, tea consumption still had a significant inhibitory effect on LDL oxidation.

Unfortunately, other studies have failed to validate this finding. Human volunteers given 900 mL (6 cups) of green tea or black tea daily for 4 weeks did not have lower levels of LDL oxidation or lipid peroxidation, even though green tea slightly increased plasma antioxidant activity (link). Since both were effective in vitro, the authors conclude that the amount of polyphenol needed is far greater than what could be achieved by drinking tea.

Another similar study found that 6 cups of green tea or black tea daily did not reduce LDL oxidation in smokers, even though they were found to be effective in vitro (link). Increasing the dose by drinking more tea does not seem feasible. Even a green tea extract equivalent to 18 cups of green tea was ineffective in the same study, and another study found that 1,000-1,250 mL of tea did not reduce markers of lipid peroxidation (link).

In one study, smokers and non-smokers were put on a diet otherwise low in flavonoids and given green tea extract with their food (link). The daily intake of catechins was 18.6 mg. No changes in markers of AGEs or ALEs was seen, although the green tea extract increased plasma antioxidant capacity, especially in smokers.

Conclusion

Black tea polyphenols are effective in inhibiting AGE and ALE formation in vitro, in some cases even more effective than green tea catechins. Green tea and black tea seem to be effective also in vivo in rodents, whereas human data is mostly disappointing.

A probable reason for the mismatch between in vitro and in vivo results is that the bioavailability of tea polyphenols is very low. Even large consumption of tea did not reduce lipid peroxidation in most human studies. Unfortunately, there are no studies looking AGEs and tea polyphenols in humans.

A closer look at the absorption of tea polyphenols and whether their bioavailability can be improved is probably in order, but we'll save that for another post. For more information on tea, AGEs and ALEs, see these posts:

Hibiscus Tea Lowers Blood Pressure
Green Tea Protects from the Psychological Effects of Stress in Rats
Carotenoids and Lipid Peroxidation: Can Vegetables & Fruit Reduce ALEs?
Fats and AGEs: PUFAs Are Even Worse than Fructose

Read More......

The Many Health Benefits of Rooibos Tea

Oxidation gives rooibos its familiar reddish colour. (Photo by Smaku)

The herbal tea made from rooibos has been a popular drink in Southern Africa for generations. The plant, Aspalathus linearis, is grown only in a small area in the Western Cape province of South Africa, but during recent years rooibos has become popular in other parts of the world as well.

Though not technically a tea, the infusion made from oxidised rooibos leaves is commonly referred to as rooibos tea. Traditionally, it is enjoyed hot with a slice of lemon and sugar or honey, but iced tea versions and even a rooibos espresso made from concentrated rooibos are apparently gaining popularity.

While many people have acquired a taste for rooibos and know that it is considered something of a health drink, most of us are clueless as to what exactly the health benefits of rooibos are. In this post, we'll review what the studies say on rooibos tea.

The antioxidant activity of rooibos tea

Like regular tea, rooibos tea contains flavonoids which act as antioxidants. While the most beneficial flavonoids of green tea are catechins such as epigallocatechin gallate (EGCG), the main flavonoids in rooibos tea are aspalathin and nothofagin. One in vitro study found that aspalathin is even more effective at scavenging free radicals than EGCG (link) – a rather surprising result, given that just about everyone knows about antioxidants in green tea but not in rooibos tea. All in all, green tea still seems to beat rooibos tea in antioxidant activity, however (link).

The second flavonoid tested, nothofagin, was not as effective as quercetin but still potent. Oddly enough, an older study found that aspalathin and nothofagin can also act as pro-oxidants under certain in vitro conditions (link). The authors comment:

Fermentation (i.e., oxidation) of rooibos decreased the pro-oxidant activity of aqueous extracts, which was contributed to a decrease in their dihydrochalcone content. The in vitro pro-oxidant activity displayed by flavonoid-enriched fractions of rooibos demonstrates that one must be aware of the potential adverse biological properties of potent antioxidant extracts utilized as dietary supplements.

This is not a unique case, however. Vitamin C, probably the most famous antioxidant, has also been said to act as a pro-oxidant in some conditions in vitro; there is much less evidence to suggest it does so in vivo, however (link).

Feeding normal, healthy rats given rooibos tea instead of water had significantly higher serum superoxide dismutase (SOD) levels than the control rats (link). They also had less DNA damage, a result that confirms the findings of an earlier study (link). Futhermore, when the rats were given dextran sodium sulfate to induce colitis, the rooibos group had higher SOD levels, and the drop in hemoglobin levels seen in the control group was prevented. Thus, rooibos tea seems to be anti-inflammatory and have the potential to prevent DNA damage.

The cardiovascular benefits of rooibos tea

Due to their effects on vasodilation and vasoconstriction, angiotensin I-converting enzyme (ACE) inhibitors and nitric oxide (NO) are used to treat conditions such as high blood pressure and heart failure. In one study, the effect of green tea, black tea and rooibos tea on ACE and NO was compared in healthy human volunteers (link). None of the three had a marked effect on NO concentration, but both green tea and rooibos tea inhibited ACE activity, suggesting that they have cardiovascular benefits. This is in contrast to an earlier in vitro study which found that only green tea and black tea inhibited ACE (link).

Closely related to cardiovascular disease is diabetes. The good news is that that rooibos tea may help with this as well. In a mouse model of type 2 diabetes, aslapathin suppresses the increase in fasting blood glucose levels. It also improves glucose tolerance, apparently through stimulating glucose uptake in muscle tissues and insulin secretion from the pancreas (link). Drinking rooibos tea during a meal may not be a bad idea.

Rooibos tea for liver disease and respiratory problems

In rats, rooibos tea aids in liver tissue regeneration after prolonged intoxication. Compared to the rats receiving water during the regeneration period, the rooibos group had less fibrotic tissue in their livers and lower tissue malondialdehyde levels. The authors conclude that rooibos tea "can be recommended not only for the prevention but also as a co-adjuvant for the therapy of liver diseases."

Rooibos tea also has therapeutic potential for respiratory ailments. According to a study on rats, in addition to lowering blood pressure, rooibos tea is both a bronchodilator and an antispasmodic (link, link). This helps explain why rooibos tea is commonly used for gastrointestinal and respiratory problems. The flavonoid chrysoeriol seems to be mainly responsible for the bronchodilator and antispasmodic effect.

Rooibos extract fights HIV

Rooibos tea extract seems to be helpful in antigen-specific antibody production by increasing interleukin-2 (IL-2) production in vitro and in vivo (link). According to the authors, rooibos tea intake "may be of value in prophylaxis of the diseases involving a severe defect in Th1 immune response such as cancer, allergy, AIDS, and other infections."

Another study found that an alkaline extract of rooibos tea leaves suppressed HIV-induced cytopathicity (link). Green tea extract, on the other hand, was ineffective. The authors conclude that HIV infection may be suppressed by the daily intake of the alkaline extract of rooibos tea. Note that the extraction mechanism is important here, because regular rooibos tea does not have anti-HIV activity (link). See the abstracts for details.

Rooibos tea, lipid peroxidation and brain aging

The uncontrolled oxidation of lipids, which can happen during cooking or inside the body, leads to the formation of advanced lipid peroxidation end-products (ALEs). The accumulation of such products is one of the types of damage that occurs with aging.

Lipid peroxides also accumulate in the brain. Rooibos tea may help prevent this damage, however. Rats given rooibos tea instead of water accumulate significantly less aging damage in the brain than rats given water (link). In fact, the 24-month old rats given rooibos tea for most of their lives had brains similar to young 5-week-old rats. This is quite a remarkable result.

One study found that out of the flavonoids tested, quercetin and EGCG (found in green tea) were the best inhibitors of lipid peroxidation, while aspalathin had a similar potency as catechin (link). Nothofagin was of no use here, however. Since polyunsaturated fats or PUFAs are especially prone to form ALEs, it seems like a cup of green tea or rooibos tea with a meal containing polyunsaturated fats might be useful.

The difference between red and green rooibos tea

Typically, rooibos leaves are oxidised before they are used to make rooibos tea. This process, which is not exactly the same as the fermentation process used in making black tea, gives them the familiar reddish-brown color and the slightly sweet taste. However, unoxidised rooibos tea is also available, if you know where to look. The color and taste are quite different; I personally prefer the red version, but green rooibos tea is not bad either.

Like in the case of regular tea, the oxidation process also affects the flavonoid content of the tea. Unoxidised rooibos tea contains more about twice as much total flavonoids as oxidised tea and 10-fold higher levels of aspalathin and nothofagin (link, link). In the studies that have directly compared the two, the unoxidised version seems to generally come out on top. For example, unoxidised rooibos tea seems to protect rats from liver cancer more effectively than oxidised tea (link). The antimutagenic activity of the two depends on the mutagen in question, however (link).

Summary

The health benefits of rooibos tea seem to be mostly due to the flavonoids aspalathin and nothofagin, although other compounds in rooibos may also play a part. Here's a summary of the benefits:

• Acts as an antioxidant and increases SOD levels
• Prevents DNA damage
• Cardiovascular protection through ACE inhibition
• Suppresses fasting glucose levels
• Improves glucose uptake and insulin secretion after a meal
• Aids in liver tissue regeneration
• Lowers blood pressure
• Acts as a bronchodilator and antispasmodic
• Inhibits lipid peroxidation and brain aging
• Rooibos extract improves immune defects such as HIV

Since nothofagin and especially aspalathin are not really found in any other plant, rooibos tea looks like a valuable addition to one's health regimen. Even people who are not fans of green tea usually like the taste of rooibos tea. Since rooibos contains no caffeine, it can be also enjoyed in the evening.

For more information on various teas and health, see these posts:

Hibiscus Tea Lowers Blood Pressure
Tea, Coffee and Cocoa: All Good for Your Teeth
Yerba Mate Inhibits AGE Formation
Drinking 3 Cups of Green Tea Increases Plasma Antioxidant Activity in Humans by 12%

Read More......

Carotenoids and Lipid Peroxidation: Can Vegetables & Fruit Reduce ALEs?

Can we reduce ALEs by eating foods rich in carotenoids? (Photo by tibchris)

When you cook foods until they have that delicious brown color, what you're really seeing is advanced glycation end-products, or AGEs. In cooking, they're formed by heating sugars with fats or proteins, but they can also be formed inside the body through normal metabolism. The problem with AGEs is that with time, they accumulate in the body and cause harm.

Similar products are formed when polyunsaturated fats are oxidized, as a result of heating or contact with oxygen. These are known as advanced lipid peroxidation end-products, or ALEs. Lipid peroxidation is even more problematic than glycation, because it leads to ALEs much more rapidly than glycation leads to AGEs.

So what can we do to reduce the accumulation of ALEs? As we've seen, one obvious way is to avoid cooking with fats that contain lots of polyunsaturated fatty acids. Still, as in the case of AGEs, ALEs are formed not only on the frying pan but also inside the body as a result of metabolism. Since completely avoiding polyunsaturated fats is probably not feasible (and they may even have certain benefits), looking for ways to inhibit metabolic lipid peroxidation seems very useful.

In addition to fatty acids, other components of the diet play a role in the accumulation of AGEs and ALEs. One particular group of micronutrients that may be beneficial is carotenoids, the compounds which give vegetables and fruit their bright color. In this post, we'll take a look at what the studies say on carotenoids and lipid peroxidation.

Various carotenoids and lipid peroxidation

One study found that carotenoids inhibited lipid peroxidation in mouse embryo cells (link). The carotenoids tested were alpha-carotene, beta-carotene, canthaxanthin, lutein, lycopene, and bixin. Bixin, which is extracted from annatto seeds, was the most effective out of the six.

In another study, the effect of various carotenoids on lipid peroxidation were measured in membranes enriched with polyunsaturated fatty acids (link). Surprisingly, only astaxanthin reduced peroxide formation, while beta-carotene and lycopene increased it significantly. Zeaxanthin and lutein also increased peroxide formation slightly.

The authors of the second paper note that this may be because conventional antioxidant assays use high concentrations of free radicals over a period of a few hours, whereas this study observed the effects over a longer period (48 hours). The relevance to biological systems is not entirely clear, but these results might help explain some of the controversial effects of carotenoids (for example, beta-carotene increasing lung cancer risk in smokers).

Zooming in on lutein

While the above studies suggest that other carotenoids such as astaxanthin may be useful, many of the studies on lipid peroxidation focus mainly on lutein. One paper I've posted earlier about as part of my self-experiment claimed an improvement in skin elasticity, hydration and photoprotection from a supplement containing lutein. Interestingly, a reduction in lipid peroxidation was also seen.

In another study, when spinach or perilla preparations containing 5 mg lutein were given to healthy volunteers for 10 days, their plasma concentrations of lutein increased significantly (link). The increase was more pronounced after consumption of perilla, even though the amount of lutein in both preparations was the same. In other words, other micronutrients in the food in question have an effect on lutein absorption.

Glutathione peroxidase was unchanged, but superoxide dismutase increased slightly. Both of these enzymes protect the body from oxidative damage. As for lipid peroxidation, the concentration of malondialdehyde (MDA) in plasma tended to decrease and the time span until a rapid increase in oxidation (known as lag time) tended to increase after spinach and perilla. MDA is a product of lipid peroxidation which eventually forms ALEs.

It's interesting to note that while lutein is absorbed rather well from vegetable foods, it is also absorbed from carotenoid supplements. In fact, the bioavailability of lutein from vegetables is only 67% compared to a preparation of pure carotenoids (link). In contrast to some of the findings in other studies, in this study healthy volunteers fed a high-vegetable diet or given 9 mg lutein and 6 mg beta-carotene daily for 4 weeks did not show an increased resistance to LDL oxidation ex vivo. The authors suggest that one possible explanation is that while lutein and beta-carotene concentrations increased, plasma lycopene concentrations decreased on both diets.

In one human study on healthy men, subjects were first put on a low carotenoid diet and then given either 330 mL tomato juice, 330 mL carrot juice or 10 g spinach powder for 2 weeks to see how the diets affected LDL oxidation. This time it was tomato juice that reduced the lag time of lipoprotein oxidizability, while carrot juice and spinach powder had no effect (link). Glutathione peroxidase was again unchanged. Given that tomatoes contain both lutein and lycopene, perhaps this hints at some kind of a synergy between the two?

Finally, let's take a brief look at two studies suggesting that lutein might be useful in treating diseases related to lipid peroxidation.

Lipid hydroperoxides are non-radical intermediates of lipid peroxidation that are involved in many diseases. For example in dementia, the number of phospholipid hydroperoxides (PLOOH) in red blood cells is greatly increased. When six healthy subjects took 9.67 mg lutein daily for 4 weeks, PLOOH levels decreased in red blood cells (link). An antioxidant effect was confirmed in red blood cells but not in plasma.

Genetically modified mice (ApoE-/-) that have high cholesterol and develop atherosclerosis as a result. They also have increased levels of systemic and retinal lipid peroxidation compared to wild mice. Supplementing them with 0.09 mg/kg lutein per day protects their retinas from this oxidative damage (link), suggesting that lutein might be helpful for patients with hypercholesterolemia.

Conclusion

Carotenoids may be effective in reducing lipid peroxidation and thus the accumulation of ALEs. Lutein in particular seems useful: at doses of 5-10 mg per day, it has been shown to increase plasma levels of lutein and reduce some of the markers of lipid peroxidation. Other carotenoids, such as astaxanthin and bixin, may be beneficial as well.

It should be noted that some of the evidence is contradictory. Some studies have found no benefit, and one study even found a slight increase in lipid peroxidation from various carotenoids. A certain balance of carotenoids may be necessary for inhibiting the formation ALEs; lycopene in particular may be important.

For more information on AGEs, ALEs and aging, see these posts:

Sugar and AGEs: Fructose Is 10 Times Worse than Glucose
Eating Meat or Going Vegan? Comparing AGE Levels in Vegetarians and Omnivores
AGE Content of Foods
Green Tea Reduces the Formation of AGEs

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