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

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

Many of you have probably heard that soy isoflavones may be good for hair loss. How exactly dietary isoflavones work to promote hair growth is less clear, however. In male rats even a relatively low amount of soy isoflavones reduces DHT and increases testosterone. This alone would probably be enough to explain hair growth in rodents. Of course, humans are a more difficult case. Most of the things that show promise in mice or rats don't work for humans with androgenic alopecia in the end. The good news is that soy isoflavones reduce DHT even in humans. The bad news is that the reduction may not be great enough. About 60 mg of isoflavones daily reduced serum DHT in healthy young men by only 15%. Even this moderate drop would suggest a reduction in 5-alpha-reductase, which converts testosterone to DHT. However, the markers of 5-alpha-reductase looked at in the study did not show a difference between the treated and the control group. And yet, a combination of capsaicin and soy isoflavones grows hair in both animals and humans. In this study, capsaicin injected into the skin was enough to grow hair in animals, although the combination was more effective. In humans, orally administered isoflavones and capsaicin resulted in hair growth in 88% of the participants with androgenic alopecia, which is a remarkable result for a supplement that reduces DHT by so little. The authors speculated that capsaicin and soy isoflavones promote hair growth by increasing dermal levels of insulin-like growth factor (IGF-1). They suggested that a key factor was calcitonin gene-related peptide (CGRP), which acts as a vasodilator, among other things. It also increases IGF-1 in various tissues, including the skin. This theory is supported by the fact that subcutaneous capsaicin increased CGRP release and IGF-1 expression in hair follicle cells in normal mice but not in CGRP-knockout mice. Soy isoflavones increased the production of CGRP, which explains why the combination was more effective than capsaicin alone. Based on these studies, it was still unclear whether dietary isoflavones alone promote hair growth. Now, the same authors have investigated their idea further. In their new study, they fed isoflavones to mice whose backs were shaved and measured their hair growth (link). Again, both wild-type mice and CGRP-knockout were used. The isoflavone supplement used was Fujiflavone P40, which contains 43.5% isoflavones. 5 g of the product was mixed per each kg of standard chow. On average, the mice ate 4.6 grams of food daily, which means that their daily intake of isoflavones was 0.0046 * 0.005 * 0.435 = ~10 mg (correct me if my calculation is wrong). After three weeks of isoflavone administration, dermal CGRP and IGF-1 levels in wild-type mice increased significantly compared to the control group. In the knockout mice, no difference was seen between mice given isoflavones and the control group. Hair follicle number also increased in wild-type mice given isoflavones. Compared to the control group, they had about 40% more hair follicles. The knockout mice had less hair follicles to begin with, and when they were given isoflavones, no improvement was seen. Thus, it seems that isoflavones grow new hairs through increasing dermal levels of CGRP and IGF-1. Compared to the mice given isoflavones, the control mice seemed to take a longer time growing their existing hair back. Even the knockout mice that saw no increase in IGF-1 grew their hair back quicker when they were given isoflavones. This might be due to other effects of isoflavones, such as reducing DHT levels. Based on the pictures in the full paper, the wild-type mice grew their hair back even quicker, however. Wild-type mice given isoflavones also had a more pronounced darkening of hair than their control group. So what is the take home message? Based on all these studies, it looks like soy isoflavones show very good potential for promoting hair growth. A part of their effectiveness may come from the fact that they reduce serum DHT and increase testosterone, but based on the rodent data, the real kick is from the increase in skin levels of IGF-1. At the moment, there is no data comparing the effectiveness of soy isoflavones vs. capsaicin in humans. However, we do know that the combination is superior in increasing dermal IGF-1 in animals, and that the combination of both taken orally grows hair in humans with androgenic alopecia. For more information on hair growth, see these posts: Topical Retinoids Increase Hair Growth in Most People BioSil, JarroSil & Beer – Silicon Experiment Conclusion Zinc Pyrithione Reduces Shedding and Moderately Promotes Hair Growth Hair Growth with Ayurveda – The Nutrich Oil Experiment

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Topical Retinoids Increase Hair Growth in Most People

Retinoids – slap them on your scalp and let nature do the rest. (Photo by Steve Rhode)

Retinoid creams and gels are probably the most effective skin care products out there at the moment. They seem to do just about everything you could hope for: increase skin firmness and hydration, reduce wrinkles, improve skin tone, you name it. But what about hair growth? The effects of retinoids on hair growth have been much less studied, even though the positive data on skin health suggests they might rejuvenate scalp skin also. My own experiment with retinol (the milder cousin of retinoids) and the resulting new hairs certainly supports this idea. And yet, while my ongoing experiment with tretinoin has visibly improved my skin, I can't say I've seen much of an increase in hair growth. I find this somewhat surprising, given that tretinoin is much stronger than retinol. Time to take a look at what the science says on retinoids and hair growth. The earliest paper I could find compared the effects of various treatments on hair regrowth in mice (link). According to the paper, retinoic acid applied topically was the least effective of the three treatments but still caused some hair regrowth after shaving the backs of the mice. Interestingly, UV irradiation was more effective, while estradiol suppressed hair regrowth. Then, in 1986, a group of scientists decided to try topical retinoids and minoxidil on humans with androgenic alopecia (link). After one year of using the combination, 66% of the participants saw regrowth of terminal hairs. None of the participants used minoxidil alone, but some of them did use only retinoids. Applying 0.025% tretinoin topically resulted in hair growth in 58% of the subjects. The picture below shows one subject before and after using tretinoin. According to the authors, the hair growth may be due to increased cell proliferation and differentation and the generation of new blood vessels. Another paper that appeared a few years later also speculates on how retinoids might cause hair growth (link). The authors of this paper suggest that certain retinoids increase the rate of hair of hair growth, prolong the anagen phase, and help convert vellus hairs to terminal hairs. At least in mice, levels of cellular retinoic acid binding protein are higher during the anagen phase and lower during the telogen phase of hair growth. Applying some retinoids topically increases the level of this protein in the skin, which might explain how retinoids prolong the growth phase (link). Both isotretinoin (also called 13-cis-retinoic acid) and tretinoin (also called all-trans-retinoic acid) seem to shorten the telogen phase and increase the anagen phase; however, they also differ in their effects, at least in vitro (link). A review on retinoids and hair growth states that according to the studies, only tretinoin and isotretinoin are able to prolong the anagen phase (link). I'm not sure how true this statement is, given that other vitamin A derivatives such as etretinate have been associated with hair darkening and new hair growth (link) and even retinol boosts the effectiveness of minoxidil (link). Not all studies have found the combination of minoxidil and retinoids to be superior to minoxidil alone (link). The hypothesis that retinol and some retinoids increase the absorption of minoxidil is plausible, but this is not the only explanation, since retinoids are effective even on their own. Thus, with or without minoxidil, retinol and retinoids seem worth a shot. Keep in mind, though, that the picture above shows the result after one year of use, and that almost half of the participants did not see an increase in hair growth. For more information on hair growth, see these posts: Zinc Pyrithione Reduces Shedding and Moderately Promotes Hair Growth Hair Growth with Ayurveda – The Nutrich Oil Experiment Do Flax Lignans Reduce Hair Loss from MPB? Green Tea Extract Grows Hair in Vitro, Might Work in Vivo

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Refined vs Red Palm Oil and Cholesterol

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

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

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

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

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

Palm oil and cholesterol in animals

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

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

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

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

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

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

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

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

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

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

Palm oil and cholesterol in humans

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Summary

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

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

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

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

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

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

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

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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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Selegiline and Lifespan Extension

Deprenyl increases the lifespan of female hamsters. (Photo by MarinaAvila)

Selegiline, also known as deprenyl, is an old life extension drug. It's been around since the 80's, but after some conflicting data from Parkinson's Disease studies, interest in selegiline for life extension purposes has been negligible. These days, deprenyl is mostly used to treat Parkinson's Disease, depression and dementia. Still, the early studies showed such promising results that a review of the studies on deprenyl and longevity is in order. Deprenyl extends maximum lifespan in male rats In the first study on selegiline and lifespan, 24-month old male Wistar-Logan rats were treated subcutaneously with selegiline (0.25 mg/kg) or a saline solution three times a week (link). The control group receiving only saline had an average lifespan of 147 weeks, about 34 months. The longest living rat in this group was 164 weeks (~37 months) old. The deprenyl group did significantly better. In fact, even the shortest living rat receiving selegiline managed to outlive the longest living in the control group, making it to 171 weeks (~39 months). The longest living rat survived for a whopping 226 weeks (~52 months). That's a maximum lifespan increase of 38%. The average lifespan in the deprenyl group was 198 weeks (~46 months). The author, Dr. Joseph Knoll, states:

The average lifespan was higher than the estimated maximum age of death in the rat (182 weeks). This is the first instance that by the aid of a well-aimed medication members of a species lived beyond the known lifespan maximum.

In 1994, Dr. Knoll continued his experiments, again using the same dosing but this time on younger Wistar-Logan rats (28 weeks, or ~6 months old), some of which were sexually inactive and some of which were sexually highly active (link). The sexually inactive control rats remained inactive throughout their life and lived 135 weeks (~31 months), whereas their deprenyl-treated peers suddenly developed a hunger for sex and lived 152 weeks (~35 months), the same as the sexually active control group. The highly active rats given deprenyl became even more sexually active than their saline-treated control group, and lived for 185 weeks (~43 months). Only mean lifespan increases in another strain of rats Between Knoll's experiments on male Wistar-Logan rats, another lifespan experiment on selegiline was done. This time, male Fischer rats were given deprenyl (0.25 mg/kg) or saline subcutaneously every other day, starting at 23 to 25 months of age (link). Again, the deprenyl group lived longer, but this time the effect was not as dramatic as in the previous study. The remaining life expectancy of rats given selegiline was increased by only 16%. Then again, as Ben Best points out in his good summary of deprenyl, Fischer rats live only 28 months, much shorter than Wistar-Logan rats. In 1993, Japanese scientists doubled the standard dose of deprenyl and injected male Fischer rats with 0.5 mg/kg, starting from the age of 18 months (link). The abstract states:

The increases in average life expectancies caused by deprenyl treatment (15% from 18 months and 34% from 24 months) were both statistically significant.

I don't have access to the full paper, so I'm not sure what exactly they mean by this. Were there actually two treated groups, with one given deprenyl since 18 months and the other since 24 months of age, or did the control group start dropping dead faster after 24 months? In any case, maximum lifespan was apparently not increased, unlike in the previous studies. A possible explanation is the shorter lifespan of Fischer rats and the higher dose used. On the other hand, Ben Best says on his website:

At the 2004 American Aging Association Conference Kitani (one of the authors of the Fischer study) reported that he had halved the dose to the standard 0.25mg/kg (3 times per week) and increased mean life span 44% for females and 32% for females starting from 24 months. Nonetheless, no significant increase in maximum lifespan was seen.

If the above is correct, then the higher dose is probably not the culprit. Perhaps treatment has to be begun earlier, or perhaps deprenyl doesn't work in all rat strains. Different doses and forms of deprenyl In 1992, two more studies appeared in a Hungarian journal, with Dr. Knoll as the coauthor in both of them. The first one fed male mice either deprenyl, Dinh lang root extract or a combination of the two three times a week, starting at 12 months of age (link). The abstract states only that the combination was the most potent treatment, increasing both memory function and survival time. The second study used the same dosage of deprenyl as before, but this time 6-month old male Wistar rats and a different form of deprenyl known as (-)p-fluoro-deprenyl were used (link). The study lasted for 25 months. Three of the 20 control rats (15%) and 15 of the 40 deprenyl-treated rats (37.5%) survived until the end. Three of the rats receiving selegiline were still sexually active at 31 months, even though normal male Wistar rats lose their ability to ejaculate by the time they're 2 years old. The authors also experimented with a much smaller dose of selegiline, giving 13-month old non-copulator rats only 0.01 mg/kg instead of the usual 0.25 mg/kg. The lifespan of these rats was short, with the control group living only 102 weeks (~23 months) and the (-)p-fluoro-deprenyl group living 106 weeks (~24 months). Rats given the standard deprenyl lived for 104 weeks. Sexual performance was improved in both deprenyl groups, however. Deprenyl in females, mice, and dogs The first study on selegeline and life extension on female rats came a few years later. Once again, the dosing was 0.25 mg/kg injected three times a week (link). The rats were 6 months old and had their ovaries removed. All the control females were dead before hitting 15 months of age, while all of the deprenyl-treated rats were still alive. Three of them even reached 36 months of age. Unlike in the case of males, however, neither group showed much sexual activity. In Syrian hamsters, a low dose of selegiline increased the lifespan of females but not males, even though MAO-B was inhibited in both groups by the same amount (link). Female controls died younger than male controls, but in the deprenyl group this difference disappeared. Deprenyl seems to increase lifespan also in immunosuppressed mice. When 4 mg of selegiline was mixed in 10 kg of feed, survival improved dramatically (link). The last mouse in the control group died 2.5 months after the study was started, at the age of 5 months, whereas the last mouse in the selegiline group made it to 14.5 months. Deprenyl and dogs Rodents are not the only animals that seem to gain extra years from selegiline. A study on beagle dogs, ranging in age from 2.8 to 16.4 years, studied the effects of orally administered deprenyl on lifespan (link). The dose was 1 mg/kg, four times as high as the one originally used by Dr. Knoll on rats. The study lasted for 2 years and 10 weeks. Almost all of the young dogs survived until the end of the study, but older dogs given deprenyl survived longer than those that were given placebo. 80% of dogs in the deprenyl group survived until the end of the study, compared to only 39% in the placebo group. The first deprenyl-treated dog died on day 247, whereas the first untreated dog died on day 295. Summary In the experiments of Dr. Knoll, who first discovered its life-extending properties, selegiline consistently increased the mean and maximum lifespan of male Wistar-Logan rats. The rats given deprenyl had a maximum lifespan that was up to 38% greater than that of the control rats. The longest living rat in these studies was 52 months old. Only one study looked at female rats and life extension, but it too showed an increased lifespan from deprenyl. Extrapolating directly from rats, the 0.25 mg/kg dose used in the experiments would correspond to 20 mg of selegiline every other day, or 10 mg daily, for a man weighing 80 kg (~176 pounds). For a female weighing 60 kg (~132 pounds), the equivalent would be 7.5 mg daily. Not all of the results have been so uniformly positive, however. While mean lifespan was increased in male Fischer rats, maximum lifespan was not. One possible reason is the shorter average lifespan of Fischer rats, but other explanations cannot be ruled out. Also, male Syrian hamsters given deprenyl did not live longer, although females did. For more information on life extension, see these posts: Does Intermittent Fasting Increase Lifespan? How Do People Feel about Life Extension? Dietary Supplement Increases Lifespan by 11% in Healthy Mice Slowing Down Aging with Intermittent Protein Restriction

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How Does Eating Avocados Affect Cholesterol?

Avocados contain plenty of MUFAs, most of which is oleic acid. (Photo by Muffet)

Everyone knows avocados are high in fat, but does that make them healthy or unhealthy? In this post, we'll look at how avocados affect cholesterol levels.

Avocados are technically large berries of the avocado tree, each berry containing a single seed usually called the avocado stone. There are several different cultivars, but on average avocados contain about 15 grams of fat, 9 grams of carbohydrates and 2 grams of protein per 100 grams. Most of the fat (~10 grams) is monounsaturated, while the rest is roughly half saturated and half polyunsaturated.

Most health enthusiasts are either pro-saturated fatty acids (SAs) or pro-polyunsatured fatty acids (PUFAs) – and if you're a long-time reader of this blog, you already know which category I lean towards. Monounsatured fatty acids (MUFAs), however, seem to represent something of a "neutral" group of fats to many. Olive oil, for example, is high in MUFAs, and almost all studies find it either beneficial or at least neutral: generally, LDL decreases and HDL either increases or stays the same.

So if olive oil is good for you, what about avocados? Since both are high in MUFAs, specifically oleic acid, one might expect to see similar results. In rats, adding avocados to their diet seems to increase HDL and decrease triglycerides (link). Avocado leaf extracts appear to be especially effective (link).

Avocados, cholesterol & healthy subjects

Experiments on humans, unfortunately, are not always as unequivocal. The earliest human study I came across find compared an avocado-enriched diet with a diet high in complex carbohydrates and low in fat – namely, the lipid-lowering diet advocated by the American Heart Association (link). The study included 15 women who were randomly assigned to one of the diets for three weeks, followed by 3 weeks on the other diet. Only the avocado diet, on which the women ate between half and one and a half avocados per day, resulted in a statistically significant decrease (~8%) in total cholesterol levels. This was due to a lowering of LDL without affecting HDL, whereas the complex carbohydrate diet lowered HDL levels by ~14%. So much for the heart-healthy effects of low-fat diets.

The second study included 16 healthy volunteers who were fed three different diets for 2 weeks: a high-MUFA diet consisting of 30% fat (75% of which came from avocados), a free diet including avocados, and a low-saturated fat without avocados (link). Both the high-MUFA diet and the low-SA diet reduced total cholesterol and LDL. However, the low-SA diet also also reduced HDL and increased triglycerides, while the other two diets reduced triglycerides. Again, the low-fat diet with an emphasis on limiting saturated fats was the most harmful for cholesterol levels.

I find it somewhat surprising that the free diet with avocados apparently also reduced HDL, even though the authors say the volunteers ate the same amount of avocados as during the high-MUFA diet. Unfortunately I don't have access to the full paper, so I'm not sure what the free diets were like in reality. Perhaps the volunteers simply ate more during the free diet, which could have skewed the results, or maybe the SA/PUFA ratio was significantly lower on the free diet for some reason.

Avocados and people with high cholesterol

Another study included 13 patients with high LDL cholesterol (link). The patients were given a standard vegetarian diet, a vegetarian diet enriched with avocado or a free diet that included avocados. The standard vegetarian diet consisted of 70% carbs, 20% fat and 10% protein, while the vegetarian avocado diet was 60% carbs, 30% fat and 10% protein. The vegetarian avocado diet reduced LDL, whereas the free diet increased it slightly. Only the standard vegetarian diet significantly reduced triglycerides – however, it also reduced HDL more than the other two.

The results of this study seem to contradict the two earlier studies, since simply adding avocados to the diet resulted in slightly lower HDL and slightly higher LDL – in other words, their cholesterol levels worsened. Genetics may play a role here, as some individuals who are predisposed to higher LDL levels seem to react negatively to foods that generally improve the cholesterol ratio. The authors themselves state:

"Low-fat, carbohydrate-rich vegetarian diets may be harmful to hypercholesterolemic patients. The avocado addition to a vegetarian diet does not correct these undesirable effects. To obtain beneficial effects on lipid profile with avocado, lower amounts of carbohydrates and polyunsaturated fatty acids are probably needed."

Yet another study compared the effect of an avocado-enriched diet on healthy subjects and patients with slightly elevated cholesterol levels (link). In healthy participants, total cholesterol decreased by 16% on the avocado diet. In participants with high cholesterol, total cholesterol decreased similarly, with LDL and triglycerides decreasing by 22% and HDL increasing by 11%. The authors conclude that a high-MUFA diet containing avocados improves lipid profile in healthy and especially in mildly hypercholesterolemic people.

Conclusion

Compared to low-fat diets, diets containing moderate to high amounts of monounsaturated fatty acids from avocados seem to result in better cholesterol levels. In healthy people, replacing carbohydrates with avocados generally lowers LDL without affecting HDL, similar to olive oil. In people with high cholesterol, replacing carbohydrates with avocados appears to reduce LDL and, in some cases, increase HDL.

The controversial result is the lower HDL in free diets with avocados. Does simply adding an avocado to your diet actually make cholesterol levels worse? This is a tricky question, since adding an avocado would mean an increase in total energy intake, unless it also means you eat less of something else – which would be the case, unless avocados somehow increase appetite. One possibility is that when the participants added avocados (and thus MUFAs) to their diet, they reduced their consumption of other fatty acids while keeping total energy intake the same. Reducing saturated fatty acid intake could result in lower HDL, although this doesn't necessarily explain the higher LDL. Without knowing what the participants actually ate during their free diet periods, it's difficult to say what the cause is.

While it's generally taken for granted that a) olive oil reduces LDL and has a neutral or positive effect on HDL and b) this effect is due to the high MUFA content of olive oil, there are differences in the food sources of MUFAs. Both avocados and olive oil are high in oleic acid, but olive oil contains squalene, whereas avocados do not. Squalene is a precursor in cholesterol synthesis and is metabolized to cholesterol in the body. Avocados, on the other hand, contain beta-sitosterol, which lowers LDL.

Finally, genes play a major role in cholesterol levels. Apolipoprotein E genotype affects how individuals react to dietary fatty acids and also cholesterol-lowering drugs like statins. Without knowing the genotypes of the participants in the studies, it's hard to say how generalizable the results are.

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

Want to Increase Your HDL Cholesterol by 50%? Sage Tea May Be the Answer
High HDL Cholesterol Reduces Risk of Dying in Men
Hibiscus Tea Increases HDL, Lowers LDL and Triglycerides
The Twinkie Diet: Thoughts on Weight Loss and Cholesterol

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Rinsing with Green Tea Improves Oral Health

Rinse with green tea and keep your teeth happy. (Photo by Daria)

I've written before about the protective effects of green tea against dental caries. Several studies have shown that green tea helps tooth and gum health by reducing harmful bacteria, increasing enamel strength and inhibiting the breakdown of starch to sugar.

Black tea, cocoa and coffee protect against oral problems too, but green tea seems to be the most effective. A new study sheds more light on how drinking green tea improve oral defense mechanisms through oral peroxidases (OPOs) (link).

The two major defensive peroxidases of the mouth are salivary peroxidase (SPO) and myeloperoxidase (MPO). Their function depends partly on diet and probably also on genes.
In the abstract, the authors mention that their earlier study showed that elderly people who drank green tea for 3 months had higher levels of oral peroxidase activity than non-drinkers. In this study, they compared the effects of green tea on OPO in vivo and in vitro.

Adding a green tea infusion to saliva increased oral peroxidase activity by 280%, while black tea increased it by only 54%. Adding only epigallocatechin gallate (EGCG), the main polyphenol in green tea, increased activity by 42%. The effect was dose-dependent, which I assume here means that the stronger the tea, the greater the effect.

In human subjects, green tea gave a very similar result. Mouth rinsing with a green tea infusion resulted in a 268% increase in OPO activity. Thus, while green tea extracts may be more useful than just drinking regular green tea for some purposes, for dental health drinking and/or rinsing is probably the most effective way.

Note, however, that higher levels of salivary peroxidase don't necessarily mean better oral health; in fact, people with more dental caries and gingivitis tend to have higher SPO activity (link). My guess is that this is a defense mechanism against the harmful effects of excess hydrogen peroxide, which is excreted by oral bacteria. In other words, the stronger the attack, the stronger the defense.

In the case of green tea it seems that increasing SPO really does lead to better oral health, though.

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

Drinking 10 Cups of Green Tea Daily and Not Smoking Could Add 12 Years to Your Life
Green Tea Extract Enhances Abdominal Fat Loss from Exercise
Vegetable vs. Animal Sources of Vitamin A: Why Eating Carrots Isn't Enough
Genes, Diet and Oral Health: Why Do Some People Get Cavities and Others Don't?

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