Monday, November 7, 2011

Guest Post: Natural Alternatives for Arthritis Treatment

Natural Alternatives for Arthritis Treatment
Glucosamine is also found in seashells. (Photo by DavidRPhoto)

Guest post by Emily Matthews

Glucosamine sulfate and chondroitin sulfate have long been used as supplements to ease the pain of arthritis. Both compounds are found naturally in animal cartilage and glucosamine can also be found in seashells. A person who wishes to increase the amount of glucosamine and chondroitin in their diet should take them together as supplements, but only from a reputable manufacturer of vitamins and supplements. Medical professionals are uncertain as to the dosage for the average person.


Chondroitin is a more complex molecule than glucosamine. It's made up of intact or hydrolyzed glycosaminoglycans with attached sugar molecules. Studies from masters degree programs show that it’s not as effective as glucosamine in treating arthritis, as the body doesn’t absorb as much of it; chondroitin is such a large molecule that it's difficult to pass through the normal intestinal barrier. The benefit of chondroitin comes because at least some of it can be broken down into glucosamine in the digestive track.


Glucosamine is a simple molecule made up of glucose and an amine, which is a building lock of protein. The main effect of glucosamine is to stimulate the creation of glycosaminoglycans, which helps cartilage remain spongelike and act as a cushion between joints. As some people age, their bodies lose the ability to manufacture glucosamine and so the cushioning effect of cartilage is lost. Some studies claim that glucosamine supplements are more effective than placebos or non-steroidal anti-inflammatory drugs in easing arthritis pain

GAIT Trials

In a recent study, the National Center for Complementary and Alternative Medicine conducted the Glucosamine Chondroitin Arthritis Intervention Trial, or GAIT to see if glucosamine and chondroitin sulfate gave any benefits in the treatment of arthritis of the knee. The study was conducted to see if the supplements, used alone or separately, eased the pain of 1583 sufferers of this form of arthritis.

In GAIT, the people who participated in the double blind trial took glucosamine alone, chondroitin sulfate alone, the two supplements together, the prescription drug celecoxib, or a placebo. The results of the trial were that celecoxib significantly reduced the pain of knee arthritis and that glucosamine and chondroitin, taken alone or separately, were no better than the placebo in reducing pain. However, there was a small group of participants with what they described as "moderate to severe pain" who found that the glucosamine and chondroitin sulfate combination reduced their pain significantly.

The efficacy of glucosamine and chondroitin in treating arthritis is uncertain. Glucosamine seems to provide some relief for some arthritis sufferers. Chondroitin is too large a molecule to be absorbed by the body in any appreciable amount. If the glucosamine and chondroitin combination works for some people, it’s probably because enough chondroitin is broken down to increase the effect of the glucosamine.

Emily Matthews is currently applying to masters degree programs across the U.S., and loves to read about new research into health care, gender issues, and literature. She lives and writes in Seattle, Washington.

For more information on glucosamine, chondroitin and arthritis, see these posts:

Green Tea Protects Cartilage from Arthritis in Vitro
Green Tea Protects from Arthritis in Rats
MSM + Chondroitin + Glucosamine for Hair & Nail Growth - Results after Seven Weeks
MSM + Chondroitin + Glucosamine: A Sulfur Cocktail for Hair and Nails

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Monday, September 19, 2011

Topical vs. Oral Antioxidants for Sun Protection – Which Is Better?

Eating the right foods can protect your skin from the sun.
Eating the right foods can protect your skin from the sun. (Photo by Extra Medium)

While studies on antioxidants are generally pretty disappointing when it comes to life extension, they do have some use as anti-aging treatments for the skin.

While all or most antioxidants appear to protect from the harmful effects of the sun, some antioxidants are more effective than others. Carotenoids are a case in point. One example is lycopene, which is found in tomatoes. For example, one study showed that people who ate tomato paste daily had 33% more protection against sunburn compared to the control group.

Among carotenoids, lutein seems to give the best bang for the buck. In addition to photo-protection, lutein increases skin hydration and lipid levels while reducing lipid peroxidation.

But is it better to use antioxidants topically or orally? Some folks swear by their skin creams, while others maintain that eating the right foods is the best way to improve the skin. In the lutein study, the combination of taking a lutein supplement and using a lutein cream gave the best results. Not all that surprising – by using topical and oral treatments you're covering both grounds and playing it safe, after all.

However, a recent paper got me thinking whether "attacking the problem from all angles" is really the best way to go at it. The study looked at carotenoid levels in the skin after using carotenoids topically and systemically (link). 129 healthy women, aged between 21 and 72 years, were divided into seven different groups and given topical creams, oral supplements, both, or a placebo.

The first cream contained a basic mixture of antioxidants from sources such as vitamin E, vitamin C and green tea. The second cream contained the same antioxidant mix complemented by beta-carotene and lycopene. Similarly, the first supplement contained antioxidants from sources like green tea, green coffee, and pongamia pinnata seeds, while the second also contained carotenoids.

The placebo treatments did not increase carotenoid concentration in the skin, while the carotenoid cream increased it by 30% in the forehead and 35% in the cheek. That's not bad – until you look at the results in those subjects who used the tablets instead. Taking the antioxidant supplement containing carotenoids resulted in an 80% increase in the forehead and 70% in the cheek after just four weeks.

The interesting part is the group who used both the cream and the supplements. After four weeks, the results were similar to the group using only the supplement, with the supplement-only group actually scoring better in some areas. After eight weeks the group using both treatments saw the best results.

However, whereas the effect from using the cream lasted for only 10 days after stopping treatment, the results from taking the supplement were sustained for up to 5 weeks. The authors also point out that "surprisingly, the combined application of both tablets and creams containing carotenoids did not reach the satisfying result obtained with the application of tablets only".

The result is indeed unexpected, since using the antioxidant + carotenoid cream along with the antioxidant + carotenoid supplement did in fact yield the largest carotenoid concentration. However, using the antioxidant + no carotenoids cream together with the antioxidant + carotenoid supplement gave worse results than skipping the cream altogether. That is, using the cream somehow negated some of the benefits of the supplement.

According to the authors, it's possible that systemically applied antioxidants are absorbed and transported onto the skin surface with sweat and sebum and that applying a cream won't increase the concentration any further. This is because the strateum corneum, the outermost layer of the epidermis, acts as a reservoir for topically applied substances.

Hence, when you apply a skin cream, it penetrates into this layer and saturates the reservoir, which makes it impossible for systemically absorbed antioxidants to penetrate into the same layer through sweat and sebum. The authors state that compared to taking only an oral supplement, taking a supplement and applying a cream results in a lower carotenoid concentration.

To avoid this problem, the authors suggest that the formulation of the topical cream should be such that it does not saturate the reservoir and prevent the oral antioxidants from being transported into the skin. In effect, they advise against using lipid-rich formulations.

Many people seem to have seen good results in photo-protection from using oral supplements only. While combining it with topical creams may potentially give the optimal result, this study suggests that finding the right kind of product is important.

For more information on skin care, see these posts:

Tretinoin Results After a Year – Experiment Update
BioSil, JarroSil & Beer – Silicon Experiment Conclusion
Topical Vitamin C for Skin: Re-examining the Case
How to Get Natural Sun Protection by Eating the Right Foods

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Tuesday, August 16, 2011

Kudzu Is an Anti-Androgen and Hair Growth Promoter

Kudzu Is an Anti-Androgen and Hair Growth Promoter
Kudzu will grow over anything in its path. (Photo by jjjj56cp)

In traditional Chinese Medicine, kudzu – a quick-growing vine native to China and Japan – is commonly used to treat alcoholism and hangover. This may be due to its potential to increase blood levels of alcohol when taken with an alcoholic beverage. Indeed, at least one study found that giving kudzu to heavy drinkers resulted in lower alcohol consumption (link).

The name kudzu encompasses at least five different species of the plant genus Pueraria. While all of them have very similar properties and are can be used for their medicinal purposes, the most often mentioned species are Pueraria lobata and Pueraria thomsonii. The various species contain a significant amount of isoflavones, which may at least partly be behind their use as a treatment for alcoholism.

Isoflavones, however, also have other uses. Because of their slight estrogenic effect, isoflavones from sources such as soy have been studied as a cure for hair loss. The idea is that isoflavones can inhibit 5-alpha-reductase, which converts testosterone into DHT. Since DHT binds to androgen receptors more potently than testosterone, DHT is a major cause of hair loss in genetically predisposed individuals.

Although the root part of the plant is often used, a recent study showed that the flowers of Pueraria thomsonii were much more effective in inhibiting 5-alpha-reductase than the roots of Pueraria lobata (~51% vs. ~7%). The flowers were powdered and made into a 50% ethanol extract, which was then applied onto the backs of mice after a testosterone treatment (link).

Applying the flower extract improved hair growth in a dose-dependent manner. The mice that got the largest dose (5 mg/day) after testosterone had a hair growth score similar to the control mice that were not treated with testosterone. In other words, the kudzu treatment reversed almost all of the hair loss effects of testosterone.

The authors also applied the extract on C3H/He mice without the testosterone to see whether it would promote hair growth independently of an anti-androgenic effect. The higher dose was almost as effective as minoxidil in promoting hair growth. Although the mechanism was not clear, the authors note that the flowers have been shown to have an angiogenetic effect.

Like soy, kudzu contains significant amounts of the isoflavone daidzein, daidzin and genistein. However, kudzu also contains an isoflavone called puerarin, which is not found in soy. Furthermore, Pueraria thomsonii flowers contain both soyasapones (one of the main components of soy beans) and kaikasaponins (not found in soy), making it rather unique.

I've seen a couple of soaps and shampoos that list kudzu as an ingredient, but I doubt that the amounts are large enough to truly make a difference. If you want to try kudzu topically, you might have better luck buying an extract in powder form and making your own topical. Another possibility is simply taking it orally. There is, after all, evidence that dietary isoflavones promote hair growth.

For more information on hair growth, see these posts:

Biotin Goes Back on the Menu
Soy Isoflavones and Chili Pepper for Hair Growth – Experiment Update
Topical Retinoids Increase Hair Growth in Most People
Zinc Pyrithione Reduces Shedding and Moderately Promotes Hair Growth

Read More......

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Thursday, May 26, 2011

Green Tea Polyphenol Heals Stomach Ulcers

Green Tea Polyphenol Heals Stomach Ulcers
Green tea is a good candidate for treating stomach ulcers. (Photo by toughkidcst)

Non-steroidal anti-inflammatory drugs (NSAID) are generally used for treating pain and reducing fever. The most common NSAIDs are aspirin and ibuprofen. While effective, these drugs have some pretty nasty side effects. For example, up to one in four regular users develop a chronic gastric ulcer at some point.

In addition to causing gastric, peptic and duodenal ulcers, NSAIDs also delay ulcer healing. In the United States, upper gastrointestinal problems from non-steroidal anti-inflammatory drug use result in 16,500 deaths every year. What's worse, almost half of the prescriptions for NSAIDs are estimated to be unnecessary. Anti-ulcer drugs, on the other hand, are expensive and do not prevent the ulcers from recurring.

In a recent Indian study, the effectiveness of the anti-ulcer drug omeprazole and one of green tea's polyphenols, epigallocatechin gallate (EGCG), was compared in mice (link). The mice were first given enough of a NSAID called indomethacin to cause stomach ulceration. After that they were split into three groups: the first group was given a standard effective dose of omeprazole (3 mg/kg), while the second group was given EGCG in various doses (0.5–5 mg/kg). The third group acted as the control group and was given no treatment.

After three days, the ulcers of the mice in the control group had not healed at all. The omeprazole-treated mice had healed ~75% of their stomach ulcers. The effectiveness of the green tea polyphenol was dose-dependent: with 3 mg/kg, the ulcers healed as effectively as with omeprazole, while the largest dose (5 mg/kg) resulted in ~82% healing.

Non-steroidal anti-inflammatory drugs cause gastric ulcers through a variety of mechanisms. They increase the production of reactive oxygen species (ROS), increase lipid peroxidation and cause an imbalance in cytokines which regulate the immune system. In this study, EGCG improved all three factors even more effectively than omeprazole.

Although both omeprazole and epigallocatechin gallate have antioxidant properties, the mechanisms through which they work differ from each other. The main reason omeprazole works is because it reduces the production of gastric acid, whereas green tea is said to increase gastric acid release. While more studies are probably needed, the authors of the paper consider EGCG a promising candidate for treating stomach ulcers because it has not been shown to have negative side effects even with large doses (although there are potential problems with high-dose green tea extracts).

For more information on green tea, see these posts:

Green Tea Protects from the Psychological Effects of Stress in Rats
Tea, Coffee and Cocoa: All Good for Your Teeth
Green Tea and Capsaicin Reduce Hunger and Calorie Intake
Green Tea Extract Increases Insulin Sensitivity & Fat Burning during Exercise

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Wednesday, May 11, 2011

Lithium in Drinking Water May Lead to Longer Life

Water may have an effect on your longevity.
Water may have an effect on your longevity. (Photo by anthony_goto)

Lithium is an essential trace element found mostly in drinking water and vegetables. However, nutritional intake of lithium varies considerably, depending on where you live.

In rats, a deficiency of lithium causes health problems such as behavioral abnormalities, but in humans, lithium deficiency is an unknown concept. On the other hand, there have been studies suggesting that  lithium intake, even at low doses, is inversely correlated with suicide risk. High-dose lithium has been used for decades to treat psychiatric conditions such as bipolar disorder.

Lithium may also have other life-extending properties besides reducing suicide risk. For example, roundworms have been shown to live up to 36% longer when given lithium chloride, but the amounts used are 1000-fold higher than would be obtainable through diet. Such a high dose may not be necessary, however. In a recent paper roundworms were shown to live longer when given a low concentration of lithium chloride throughout their life – with the effect being less pronounced than with high doses (link).

The authors also looked at lithium in drinking water and total mortality in 18 neighboring Japanese municipalities. They found that tap water levels of lithium were inversely associated with overall mortality adjusted for age and gender. Since lithium levels have been associated with lower suicide rates, the authors also adjusted for suicide. The inverse association between lithium and overall mortality remained.

Lithium concentrations in drinking water ranged from 0.7 to 59 mcg/L. The highest value equals a concentration of 8.5 micromoles. A lithium concentration of 10 micromoles was enough to extend the lifespan of roundworms, while a concetration of 1 micromole was not.

The inverse association between mortality and lithium in drinking water obviously does not prove that lithium reduces mortality in humans, but the roundworm experiments show that the idea is not so far-fetched. Although the mechanism is still unknown, I wonder if the mental health aspect has something to do with it.

Too bad there doesn't appear to be any lithium in the tap water where I live, or at least they don't report it. It is also available as a supplement, but some countries may have customs restrictions on some or all forms lithium.

For more information on longevity, see these posts:

High HDL Cholesterol Reduces Risk of Dying in Men
Selegiline and Lifespan Extension
Does Intermittent Fasting Increase Lifespan?
The 7 Types of Aging Damage That End up Killing You

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Thursday, May 5, 2011

Drinking Coffee = Higher Adiponectin = Lower Body Fat Percentage?

Drinking coffee increases adiponectin levels
Want to lower your body fat? Coffee might an option. (Photo by annais)

Adiponectin is a protein hormone that modulates several metabolic processes related to weight gain. Adiponectin levels are inversely correlated with body fat percentage (link) – for example, diabetics have lower levels of adiponectin than non-diabetics, and losing weight increases adiponectin levels.

Since adiponectin affects glucose uptake and insulin sensitivity, and low adiponectin levels are a risk factor for developing diabetes and metabolic syndrome, it raises the question of whether increasing adiponectin levels might be a good thing.

A study from last year looked at the effects of coffee on adiponectin levels in 665 Japanese males (link). Adiponectin levels were measured from serum samples, and coffee consumption was assessed using a self-administered questionnaire. The questionnaire also included green tea consumption, so that the effects of green tea and coffee could be compared.

The participants who drank more coffee tended to be younger, more likely to smoke, and less likely to drink alcohol. The mean age of non-drinkers was 49.9, while the mean age of those who drank at least three cups per day was 48.2. Interestingly, non-drinkers had the highest mean blood pressure (systolic 129.5 and diastolic 80.7 mmHg) of all groups, while those who drank 1-2 cups per day had the lowest (123.1 and 76.7) – although this could just be due to the age difference. There were no significant differences in BMI or physical activity between coffee drinkers and non-drinkers. Unfortunately, body fat percentage was not measured.

However, adiponectin levels were significantly higher in those who drank coffee compared to non-drinkers. In those who drank none, 1–5 cups per week, 1–2 cups per day, and >2 cups per day, adiponectin levels were 5.95, 6.51, 7.05 and 6.89 mcg/mL, respectively.

When confounding factors such as age, smoking status and BMI were adjusted for, adiponectin levels were still positively associated with coffee consumption. There was a significant dose-response relationship between coffee consumption and adiponectin levels. However, there were no significant differences in adiponectin levels between those who drank 1–2 cups and those who drank >2 cups per day.

Green tea was not associated with adiponectin levels. There was also no association between coffee consumption and total cholesterol, HDL or LDL.

Although this study included only men, similar findings have been reported in women. In one study, diabetic and non-diabetic women who drank at least four cups of coffee per day had higher adiponectin levels than those who didn't drink coffee regularly (link). Interestingly, caffeine consumption was also associated with adiponectin levels. Perhaps the adiponectin-increasing effect of caffeine is diminished or blocked by other compounds such as L-theanine in green tea.

There's also one interventional study on habitual coffee drinkers that found coffee consumption increased adiponectin levels (link). Unlike in the study on Japanese males, total cholesterol and HDL also increased – possibly because the intake of coffee was higher (8 cups per day) at the end of the experiment.

Based on this and other studies, the key points are:

a) those who drink coffee have higher adiponectin levels than those who don't
b) those who have higher adiponectin levels have lower body fat percentage

All in all, while correlation does not prove causation, it seems plausible that drinking coffee could help maintain a lower body fat percentage and avoid type II diabetes and metabolic syndrome.

If you have personal experiences with coffee and weight loss, feel free to share them in the comment section below. For more information on weight and fat loss, see these posts:

Why Are Thin People Not Fat?
A Year of Intermittent Fasting: ADF, Condensed Eating Window, Weight Loss, And More
Green Tea and Capsaicin Reduce Hunger and Calorie Intake
The Twinkie Diet: Thoughts on Weight Loss and Cholesterol

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Thursday, April 28, 2011

Want to Increase Your HDL Cholesterol by 50%? Sage Tea May Be the Answer

Salvia officinalis tea can increase HDL cholesterol by 50%
Common sage tea increases HDL and reduces LDL. (Photo by Kelly Johnson)

Salvia officinalis, also known as common sage or garden sage, has been used for hundreds of years both for cooking and healing purposes. It's the variety you can find in most grocery stores – not to be confused with the psychoactive herb Salvia divinorum.

While you might not get hallucinations from common sage, it does have a wide range of health benefits. For instance, sage is commonly used for its antibiotic and antispasmodic properties. In medieval times, sage was generally associated with longevity.

One less well known use for common sage is cholesterol. Nonetheless, a 2009 pilot trial with six healthy female volunteers (aged 40–50) looked at how drinking sage tea would affect their blood glucose regulation and lipid profiles (link). They also evaluated the antioxidant properties of sage tea.

To prepare the tea, 300 mL of boiling water was poured over 4 grams of dried Salvia officinalis plant material and allowed to steep for 5 minutes. Each participant drank the tea twice a day for four weeks.

Salvia offinalis tea and total & HDL cholesterol

The graphs above show total cholesterol (A) and HDL cholesterol levels (B) of the participants at baseline (white bar), after two weeks, after four weeks (grey bars) and after a two-week washout period (black bar).

While total cholesterol decreased only marginally after two and four weeks of drinking sage tea, there was a 16% drop in total cholesterol two weeks after the treatment ended. HDL cholesterol, on the other hand, increased after just two weeks. After four weeks, HDL levels were up by ~50%. Two weeks later, they were still ~38% higher than at baseline.

Salvia offinalis tea and LDL cholesterol & LDL/HDL ratio

The graphs above show the LDL cholesterol levels and LDL/HDL ratios of the participants. There was a gradual reduction in LDL levels during and after treatment, with a ~20% drop seen after the two-week washout period. Consequently, the LDL/HDL ratio improved throughout the four weeks and remained significantly better after the washout period compared to baseline.

Although the sample size is very small, and this was a non-randomized crossover trial, the figures look very promising. I mean, a 50% increase in HDL in just four weeks? Where else are you going to see improvements like that in healthy people?

The authors also evaluated the antioxidant properties of sage tea by measuring erythrocyte antioxidant status. Both superoxide dismutase (SOD) and catalase (CAT) activity increased significantly after two weeks. Unlike the effect on cholesterol levels, however, there was no significant difference after four weeks compared to baseline. It would be interesting to see a comparison between drinking sage tea daily and cycling it. Who knows, maybe something like two weeks on, two weeks off would be better than drinking it constantly.

Although it has been suggested that sage improves glucose tolerance and insulin sensitivity, the results of oral glucose tolerance tests did not change after four weeks of drinking sage tea. While the participants were healthy, they did belong to a risk group for developing pre-diabetes based on their age. It may be that sage is helpful in those who are already pre-diabetic or diabetic but not in healthy people. On the other hand, the expression of the heat shock protein Hsp70, which is involved in insulin sensitivity, increased by 2.8-fold in lymphocytes after two weeks and remained elevated after the washout period.

For more information on improving HDL and reducing LDL, see these posts:

Hibiscus Tea Increases HDL, Lowers LDL and Triglycerides
Anthocyanins from Berries Increase HDL and Lower LDL
Low-Carb vs. Low-Fat: Effects on Weight Loss and Cholesterol in Overweight Men
Niacin Raises HDL, Lowers LDL, VLDL & Triglycerides

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Wednesday, April 20, 2011

High HDL Cholesterol Reduces Risk of Dying in Men

Strawberry margarita – the perfect longevity drink.
Strawberry margarita – the perfect longevity drink. (Photo by bookgrl)

According to conventional wisdom, LDL is the "bad cholesterol" and HDL is the "good cholesterol". While there is plenty of evidence showing this is an oversimplification, it is generally agreed that the higher your HDL is, the better. In fact, I've never seen anyone suggest a "maximum" HDL level for a healthy person.

One of the many strange things you hear most doctors recommend is that you reduce your total cholesterol once it's above a certain level, despite what your LDL and HDL are. That is, even if HDL makes up most of your total cholesterol, you may still get a warning that your total cholesterol is "too high". But why would you want to reduce your HDL cholesterol?

High HDL is generally believed to be associated with longevity, at least to a degree. For example, centenarians and supercentenarians tend to have higher HDL than the general population. To my knowledge, large population studies on HDL and longevity are relatively rare, however – which is why I found this new paper from the American Journal of Cardiology pretty interesting (link).

The study (which began in 1979) looked at the probability of 652 men, aged 65 years, to reach 85 years of age. The authors hypothesized that men with higher HDL cholesterol levels in middle age would be less likely to die before 85 years of age than men with lower HDL levels.

For the analysis, participants were categorized into three groups based on their HDL cholesterol: <40, 40–50 and >50 mg/dL. Converted to mmol/L, the ranges are <1, 1–1.3 and >1.3 mmol/L. To me, these categories seem like they're in the lower range of the healthy spectrum, but then again, average HDL levels in men in the US are said to be 40-50 mg/dL. According to the American Medical Association, less than 40 mg/dL is undesirable and higher than 60 mg/dL is desirable.

The age-adjusted hazard ratios for death before 85 years of age in the three groups were as follows:  1.00 for those with HDL < 40 mg/dL, 0.99 for those with HDL between 40–50 mg/dL, and 0.77 in those with HDL > 50 mg/dL. In the fully adjusted model (which accounted for age, LDL, hypertension, smoking, BMI, etc), the hazard ratios were 1.00, 1.01 and 0.72, respectively. That is, men with HDL higher than 50 mg/dL had a ~28% lower risk of dying than those with HDL lower than 50 mg/dL.

Immediately we can see that it doesn't make much difference whether the participants' HDL was below 40 or between 40 and 50 mg/dL – the risk of dying before 85 years of age was pretty much the same for both groups. Only once their HDL cholesterol levels were above 50 mg/dL was there a significantly lower risk.

Furthermore, when the authors analyzed the data further, they found that each 10-mg/dL increment in HDL cholesterol was associated with a 14% decrease in risk of dying before 85 years of age. In other words, the higher their HDL, the higher the survival rate.

This is all very good news. Reaching a HDL level of, say, 80 mg/dL (~2.1 mmol/L) is not at all impossible as long as you plan your diet properly, and would give you a significantly lower risk of dying from cardiovascular disease – which is the number one killer in the 65–85 age group.

The baseline characteristics of the participants reveal some interesting things too. First, the LDL cholesterol was pretty much the same in all groups: around 160–168 mg/dL. Body mass index, on the other hand, was inversely correlated with HDL levels: those with the lowest HDL levels had a mean BMI of 27.5, while those with the highest HDL levels had a mean BMI of 25.8.

While alcohol is known to increase triglycerides in the short term, it also increases HDL. Indeed, alcohol consumption was positively correlated with HDL levels. The percentage of participants who drank at least 2 alcoholic beverages per day was ~14% in those with the lowest HDL, ~18% in those with average HDL and ~38% in those with the highest HDL. This might explain, in part, why moderate alcohol consumption is associated with increased longevity.

So, if your total cholesterol is high and it's mostly due to high LDL, that may be a potential cause for worry – although it's good to keep in mind that there are several types of LDL, some more harmful than others. However, if you have high cholesterol due to high HDL, well then you should be happy!

For more information on HDL cholesterol and how to increase it, see these posts:

Hibiscus Tea Increases HDL, Lowers LDL and Triglycerides
Refined vs Red Palm Oil and Cholesterol
What a "Heart-Healthy" Diet Does to Your Cholesterol Levels
Anthocyanins from Berries Increase HDL and Lower LDL

Read More......

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Friday, April 15, 2011

Biotin Goes Back on the Menu

Is there evidence behind biotin and hair growth?
Is there evidence behind biotin and hair growth? (Photo by Martin Neuhof)

Long-time readers of the blog may remember that one of the earliest experiments I did was with biotin, also known as vitamin B7. The purpose was to see whether taking a biotin supplement would affect nail and hair strength.

I wrote back then that although a lot of people seemed to believe biotin is good for hair and nails, there were no studies showing it really did anything except in rare cases when the subject was biotin deficient. After two weeks, I posted a quick update. When I'd been taking 5 mg for a month, I concluded the experiment. As you might expect, I didn't see any results.

I've since learned that one month is way too short for any kind of results when it comes to hair growth experiments. In most cases, six months would be the minimum, otherwise you're just wasting money without really learning anything new.

A pubmed search on biotin and hair growth still doesn't come up with any interesting studies. The only thing biotin seems to be proven to do is help with uncombable hair syndrome (link):

We report a family affected to the fourth generation by uncombable hair syndrome. This syndrome is characterized by unruly, dry, blond hair with a tangled appearance. The family pedigree strongly supports the hypothesis of autosomal dominant inheritance; some members of the family had, apart from uncombable hair, minor signs of atopy and ectodermal dysplasia, such as abnormalities of the nails. The diagnosis was confirmed by means of extensive scanning electron microscopy. A trial with oral biotin 5 mg/day was started on two young patients with excellent results as regards the hair appearance, although scanning electron microscopy did not show structural changes in the hair. After a 2-year-period of follow-up, hair normality was maintained without biotin, while nail fragility still required biotin supplementation for control.

In this study, 5 mg biotin was taken daily. Even much smaller doses seem to be helpful for uncombable hair syndrome, however (link):

Three children are reported with uncombable hair syndrome, consisting of slow-growing, straw-colored scalp hair that could not be combed flat. The hairs appeared normal on light microscopy but on scanning electron microscopy were triangular in cross section, with canal-like longitudinal depressions. Oral biotin, 0.3 mg three times a day, produced significant improvement after 4 months in one patient, with increased growth rate and with strength and combability of the hair, although the triangular shape remained. The other two patients were unique in having associated ectodermal dysplasia. Their hair slowly improved in appearance and combability over 5 years without biotin therapy.

These studies confirm the fact that biotin does play a part in hair growth, and that it's possible to affect even the growth rate through biotin supplementation. Although the cause of uncombable hair syndrome is unknown, a biotin deficiency (perhaps due to genetic reasons) may play a part. On the other hand, the syndrome often improves by itself with age.

Studies like this do not really warrant supplementing with biotin if you're suffering from androgenic alopecia or just want to make your hair grow thicker and faster. And yet a lot of people seem to believe biotin will do the trick. They keep saying there's "a lot of evidence" for biotin and hair growth, but the references are missing. The actual studies are always about biotin deficiencies or like the ones I quoted above.

However, a while ago I came across one study from 1992 that actually looked at the effect of biotin supplements on hair loss. It's no wonder I didn't find it earlier, since it's not indexed in pubmed. Nor do I have access to the full paper, but here's the abstract:

An examination of the effect of biotin on alopecia and hair quality.

The effect of a daily oral dose of 2,5 mg biotin was studied in 93 patients with the symptoms hair-loss (mostly androgenetic alopecia) and reduced hair quality. The mean duration of treatment was 7,9 +/- 2,8 months. An obvious improvement of hair-loss was reported in 64%, and a slight improvement in 9%. Hair quality was clearly improved in 70% and slightly in 12%. Brittle finger nails as an additional complaint were improved in 80%. If alopecia, decreased hair quality and brittle finger nails occurred in combination, improvement was observed frequently collectively. The study allows - as already shown in a previous investigation concerning brittle finger nails - to suggest biotin as an effective and well tolerated therapy in cases of alopecia and decreased hair quality.

The majority of subjects had improvements in hair loss and hair quality from taking 2.5 mg biotin daily. Sounds good, right? Makes you wonder why nobody has attempted to repeat the experiment if the results are real. Another thing that strikes me as odd is the duration of the experiment. Why a mean duration of 7.9 months with standard deviation? Weren't all the subjects taking biotin for the same duration? Did they just quit whenever they felt like it? That just sounds like bad study design, which makes me somewhat skeptical of the results.

Still, it's intriguing enough to make me add biotin back on the supplement menu for the time being. Although a "it can't hurt and might help" mentality may be dangerous in some cases, I'm unaware of any negative side effects from taking 5 mg biotin daily. This time I'm aiming for at least six months instead of just one.

For more information on hair growth, see these posts:

Soy Isoflavones and Chili Pepper for Hair Growth – Experiment Update
Emu Oil vs. Hair Again® Topical Gel: Hair Growth Battle Conclusion
Do Flax Lignans Reduce Hair Loss from MPB?
2% Nizoral Shampoo Increases Hair Growth More than 2% Minoxidil

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Tuesday, April 12, 2011

Soy Isoflavones and Chili Pepper for Hair Growth – Experiment Update

Spicy peppers contain capsaicin, which should promote hair growth.
Spicy peppers contain capsaicin, which should promote hair growth. (Photo by Jonathon W)

Several readers have been asking for an update on my hair growth experiment with soy isoflavones and capsaicin. I admit it's long overdue, so here goes!

First some background on the experiment. Why soy isoflavones? I know there are a lot of people who think soy is the ultimate poison, and while I'm not a big fan of soy as a food, the science behind isoflavones and hair growth is strong enough for me to give it a go. Soy isoflavones have been shown to increase IGF-1 in the skin, which in turn promotes hair growth. Although soy also reduces DHT in rats and in humans, the effects on IGF-1 seem to be the primary way through which isoflavones grow hair.

Capsaicin seems to have a similar effect on IGF-1, and in both mice and humans, the combination of soy isoflavones and capsaicin appears to be more effective than capsaicin alone. I have not seen a direct comparison of soy isoflavones and soy isoflavones + capsaicin, however, so it's unclear how important capsaicin really is. Nevertheless, I chose to take both for the experiment.

The participants in the study were given a capsaicin supplement, but I decided to take the natural route and just add cayenne pepper or chili powder into my food instead. It's difficult to determine just how much capsaicin I've been ingesting this way, since the capsaicin content depends on a lot of variables. As I wrote when the experiment began:

The only problem is that it's pretty difficult to estimate the amount of capsaicin; a tablespoon of ground chili will contain anywhere between 0.8 mg and 480 mg of capsaicin. In the study, 7 mg per day was consumed, so if I manage to eat a tablespoon, I should have decent odds of ingesting at least as much capsaicin.

The amount of isoflavones I've been eating, on the other hand, has been easy to measure. One capsule contains 60 mg of isoflavones, which is 15 mg less than in the study.

And what about the results? I've not taken any pictures, since unlike in the retinol experiment, there's not much visible going on. I haven't cut my hair in years, and the length of my hair is still the same as it was before (the maximum length of your hair is genetically determined), so it's safe to say that isoflavones and capsaicin haven't done anything in that department.

I also haven't seen any increase in the rate of hair growth, which is perhaps a bit surprising, since you might expect an increase in IGF-1 to increase the speed at which hairs grow. But then again, I have no reliable way of measuring my IGF-1 levels either. I've simply been looking at a few hairs and measuring how much they grow each month.

The one thing I noticed during this experiment is something of a shed in the beginning. There's no way to be sure it's the isoflavones and capsaicin working, but I haven't noticed anything similar with the other experiments. After a few months, I seemed to not only shed more hairs in general, but especially from the front of the scalp. Moreover, many of these hairs had not grown to their full length yet.

As most of you probably know, that can be a good or a bad sign. A lot hair growth drugs, including finasteride, cause an initial shed, after which the hairs grow back stronger and healthier. Then again, inflammation also causes hairs to shed earlier than they should, only they grow back weaker every time.

At this point, it's still too early to tell, since the new hairs are still growing. At least on the surface they look fine. What's funny is that there are some spots where several hairs are pretty much the exact same length. The two possible reasons is that those hairs were shed at the same time and now regrowing, or that the isoflavones and capsaicin increased the number of hair follicles. I suspect the former, but I can't be sure.

So what's the next step? I've already ordered a second bottle of isoflavone capsules, and since I like to use chili in my food anyway, I'll pretty much keep doing what I've been doing so far. If I see any dramatic changes, I will post about them, but if not, I will just consider the isoflavones and capsaicin thing a preventative measure and move on to more interesting experiments.

That's it for today. I hope you found this update useful, and if you have further questions or you've done a similar experiment of your own, please let us know in the comment section.

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
Eclipta Alba Extract Grows Hair Quicker than Minoxidil

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Wednesday, February 2, 2011

Vegetable vs. Animal Sources of Vitamin A: Why Eating Carrots Isn't Enough

Think you're getting enough vitamin A from carrots? Think again.
Think you're getting enough vitamin A from carrots? Think again. (Photo by Ben Hussman)

In the comment section of my previous post on genes, diet and cavities, a couple of readers commented that vitamin A is necessary for proper dental health. I replied that I get plenty of beta-carotene (the vitamin A precursor found in vegetables and fruits) from red palm oil, which I use for most of my cooking these days.

Today, however, I came across a couple of papers looking at how well humans actually absorb beta-carotene and convert it to vitamin A (link, link). To my surprise, the conversion rate was much poorer than I'd previously thought. The first paper, which looked at beta-carotene absorption in 11 men, had this to say:

The vitamin A activity of ß-carotene is variable. The carotene in fruit, grains, and oils seems to be more effective as a source of vitamin A than that in dark-green leafy vegetables.

So, not all sources of beta-carotene are equally good in terms of absorption. The conversion rate also depends on the amount of beta-carotene (the higher the amount, the lower the rate) and whether fat is included or not.

Strikingly, only 6 of the 11 men included in the study absorbed and converted the beta-carotene they were given. The remaining 5 were classified as non-responders. The authors conclude that the vitamin A activity of beta-carotene can be "surprisingly low and variable". Even in those who did respond to supplementation, mean absorption was only ~4% and the conversion ratio was ~0.05.

In a similar study on 11 women, the same thing happened: only 6 of the women absorbed and converted beta-carotene enough to be measurable, while 5 women were non-responders. In those who did respond, mean absorption was ~6% and the conversion ratio ~0.1. This confirms earlier findings reporting that women absorb and convert beta-carotene more efficiently than men; the same also appears to be true in rats.

These figures suggest that the commonly accepted conversion rates of beta-carotene from plant sources may be too optimistic. Even red palm oil might not be up to par with animal sources. In one study, switching from green leafy vegetables to red palm oil did increase retinol levels, but only in subjects who were vitamin A deficient to begin with (link). And for many Westerners who don't eat palm oil or organ meats, the reality is even worse:

Also, it seems that the vitamin A activity of ß-carotene that is not dissolved in oil and emulsified is low and variable. Most ß-carotene in the American diet is not consumed in an emulsified form with fat. Our intent was to replicate a typical diet to develop better leads for how the body utilizes its given resources. The fat content of the meal that accompanied the doses in our study was the recommended amount, 30%. Many professionals recommend lower-fat diets.

Now there's something for the low-fat raw food vegetarians to chew on. On the other hand, the absorption of retinol, found in animal sources such as liver and eggs, appears to be much higher. Most of the estimates I've seen on various websites are between 60-90%, but even that may be too conservative, as the only actual study I could find showed that absorption was >99% (link).

Since my vitamin D levels are already good, and I take vitamin K2 supplements, the missing link in the trinity of dental health could indeed be vitamin A in my case. While I do eat eggs every now and then, their retinol content is only about 10% of that of liver. I guess it's time to put organs on the menu.

For more information dental health, see these posts:

Genes, Diet and Oral Health: Why Do Some People Get Cavities and Others Don't?
Tea, Coffee and Cocoa: All Good for Your Teeth
Dental Health Effects of Green and Black Tea
Preventing Mouth Ulcers with Tea Tree Oil Toothpaste - Results after Two Months

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Tuesday, January 25, 2011

Genes, Diet and Oral Health: Why Do Some People Get Cavities and Others Don't?

Genes, Diet and Oral Health: Why Do Some People Get Cavities and Others Don't?
Getting rid of candies didn't prevent me from getting caries. (Photo by exper)

As you may know, I have something of an ongoing experiment with dental health. This includes reducing cavities, preventing gingivitis and the receding of gums, and also finding safe ways of whitening teeth.

In previous updates, the main focus has been on the teeth whitening aspect. The last product I purchased was called "Plus White 5 Minute Bleach Whitening Gel". Compared to the supposedly teeth whitening toothpastes out there, this product does seem more effective.

However, in recent months, I've noticed increased sensitivity along the gumline. Specifically, the gums next to two of my upper teeth seem to be the problem. The whitening gel probably has very little to do with it, but it doesn't solve the problem either. In the short term, whitening gels can increase sensitivity, so for the time being, I've turned my focus elsewhere – to preventing caries and improving gum health.

The motivation for this post is that I've struggled with these things my whole life, and despite my various experiments with diet, I've yet to find a proper solution to the problem. When I was a kid, the common explanation was that too much candy and soda was the reason for dental cavities – despite the fact that scientists had already shown that carbohydrates in general give rise to the bacteria that cause caries. So when I got a bit older, I cut back on candy and soda, hoping it would be enough.

Unfortunately, it wasn't. Apart from the Snickers Bars and Coca-Cola I'd occasionally enjoyed that were now gone, my diet remained the same. It took me a long time to discover that all carbs are essentially sugars, that all acidic drinks make the issue worse, and that it's not just Coke and candy that are the problem. You can get cavities just as easily by eating bread and drinking apple juice. Then it was time to get rid of those too.

When I reduced my carb consumption and switched to a more paleo-like diet, my dental health improved, but it still didn't stop me from getting a new cavity every now and then. Furthermore, I knew several people who ate junk food and drank acidic sodas all the time, and yet had never had cavities. Some didn't even brush their teeth every day, let alone floss. When we were kids, my brother and I had very similar diets, and yet I was the only one to get cavities.

These things have led me to believe that genes play a more important part than most dentists would have you believe. Kind of like some people stay thin no matter how much they eat. But, just like in the case of weight loss, your genes do not necessarily determine your fate – it just means you have to know what you're doing. People who don't have the genes for staying naturally thin have to be more careful with what they eat if they want to avoid weight gain. Similarly, people who get cavities easily have to be more careful with dental health.

While keeping your teeth clean by brushing, flossing and chewing gum prevents cavities, I'm wondering whether all the cleaning really strikes the problem at the root (no pun intended). If genetics do play a role, what is it specifically about some people's genes that keeps them from getting cavities, despite their poor dental health habits?

One important factor in cavity formation is saliva. The surfaces of teeth are constantly going through a process of demineralization and remineralization. The balance depends, in part, on salivary flow and the pH of saliva, with the mineral content probably playing a role as well. I know my mouth often feels kind of dry and acidic, which can't be a good thing for remineralization. What is unclear to me is how to affect these things.

There are a million websites out there listing foods that are "acid-forming" or "alkaline-forming", but the classification seems very unscientific. Some list apples as acid-forming because apples themselves are acidic, some list them as alkaline-forming because they claim we should look at what happens after digestion. Here's a quote from one such website:

All foods are "burned" in the body -- more commonly called "digested" -- leaving an ash as the result of the "burning", or the digestion. This food ash can be neutral, acid or alkaline, depending largely on the mineral composition of the foods.

I'm not sure how scientifically valid this theory is in the first place, but I do know that even those who promote the "food ash" theory disagree on which foods leave acid or alkaline ash. One person will tell you plums are acid-forming, while others will tell you they're alkaline-forming. I doubt any of them have actually burned plums and studied the ashes.

So, expect some dental health related posts in the upcoming weeks and months, as I go through some of the papers on the subject. I'm also interested in hearing your comments, especially if you've previously suffered from cavities but managed to find a solution.

Meanwhile, for more information on dental health, see these posts:

Tea, Coffee and Cocoa: All Good for Your Teeth
Dental Health Effects of Green and Black Tea
The Role of Coenzyme Q10 in Oral Health
Whitening Teeth & Healing Gums: In Search of the Perfect Toothpaste

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Monday, January 10, 2011

Green Tea as a Pro-oxidant: Too Much of a Good Thing?

Is too much green tea harmful for you?
Is too much green tea harmful for you? (Photo by tornado_twister)

I was browsing through the latest studies on green tea and came across a paper saying EGCG, one of the green tea polyphenols, increases protein cross-linking (link). I was intrigued, because this was the first time I'd heard of such an effect. The abstract also mentions that there's increasing evidence EGCG can generate reactive oxygen species and break DNA strands in biological systems. In effect, it says that the antioxidant is actually a pro-oxidant.

I looked up some of the references and indeed, even green tea's polyphenols (at least EGCG, possibly some others) have oxidative effects under certain in vitro conditions. For example, in human whole blood lymphocytes, EGCG either suppresses or induces DNA strand breakage, depending on the concentration.

In concentrations between 0.01-10 μM (micromoles/L), strand breakage decreases, but once the concetration gets higher than 1000 μM, it increases instead. In purified blood lymphocytes, concentrations of 1-100 μM induce and concentrations of 0.01-0.1 μM suppress DNA strand breakage.

Sounds an awfully lot like hormesis, doesn't it? As with everything, the dose makes the poison. The interesting part, of course, is whether drinking green tea can cause similar harmful effects in real life.

Luckily, one study looked at the effect of green tea on DNA strand breaks in rats (link). The smaller dose (which according to the authors is equivalent to one desiliter of green tea in humans) had no effect, but the larger dose (equivalent to half a liter) significantly reduced strand breaks.

Half a liter of green tea, equal to about three cups, increase total plasma antioxidant capacity only moderately. When only EGCG is taken into account, the results vary somewhat from study to study, but concentrations rarely exceed 1 μM (link). Also, plasma antioxidant activity has a plateau, which suggests that the absorption mechanism of green tea polyphenols becomes saturated after a certain point:

To make the tea used in the study, 500 ml of boiling water was poured on 20 grams of green tea leaves (8-10 tea bags), and the tea was then allowed to infuse for 10 minutes. That makes for a very strong tea, much stronger than the ones used in the other studies. The volunteers drank 300-400 ml of the tea, after which blood samples were collected at different time intervals

In this study, there was no difference between those who drank 300 and 400 ml of the tea. Even then, the increase in antioxidant activity was only 4% at the peak. Thus, it seems unlikely that harmful levels could be reached by simply drinking plenty of green tea. In one Asian population, 10 cups of green tea daily reduced total mortality compared to those who drank less green tea and/or smoked.

Theoretically at least, extracts and supplements could be a different matter, because they often contain a higher percentage of EGCG than green tea and come with things that increase absorption. For example, piperine increases plasma levels of EGCG.

One green tea extract containing 40% EGCG resulted in a peak  of 0.8 μg/mL in human subjects; when the same extract was complexed with phospholipids, the peak was 1.9 μg/mL. If my calculations are correct (which they often aren't; please correct me if I'm wrong), then these would be ~1.75 μM and ~4.14 μM, respectively. Again, in whole blood lymphocytes concentrations between 0.01-10 μM, strand breakage was decreased, and it took concentrations higher than 1000 μM to increase strand breakage.

All in all, it appears that green tea in reasonable quantities (at least up to 10 cups) does not cause it to act as an oxidant in vivo. It's unknown what a much higher amount would do, assuming you could somehow bring yourself to drink 50 cups. I haven't seen any human studies on such amounts. But if the plateau effect is indeed true, then you might not be able to reach high plasma levels of EGCG no matter how much you drink.

With supplements, the situation is different. Piperine and phospholipids make reaching higher plasma values possible, which can be a good thing or a bad thing, depending on what you're using the supplements for. Some conditions require higher doses than others, so you'll have to judge the proper approach on a case by case basis. However, since EGCG does have the potential of being a pro-oxidant in vitro and is toxic to the liver in very high amounts, be careful not to overdo it with green tea supplements.

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

Green Tea Protects from the Psychological Effects of Stress in Rats
Tea, Coffee and Cocoa: All Good for Your Teeth
Green Tea and Capsaicin Reduce Hunger and Calorie Intake
Green Tea Catechin Reverses the Effect of DHT in Prostate Cancer Cells

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Wednesday, January 5, 2011

Dark Chocolate Reduces Blood Pressure and Improves Insulin Sensitivity in Just Two Weeks

Dark Chocolate Reduces Blood Pressure and Improves Insulin Sensitivity in Just Two Weeks
Not all things that are good for you taste bad. (Photo by CC Chapman)

Everyone knows that dark chocolate is healthy, but how many of us really know why exactly it's healthy? It's the same as with red wine: it's common knowledge that it's healthy – it contains those magical polyphenols, after all – but the actual effects are mentioned less frequently.

Most things that are labeled healthy by mainstream media are things that reduce the risk of cardiovascular disease. The same is true of red wine and dark chocolate, although I'm sure there's more to them than just heart health. Resveratrol, found in red wine, for example has a multitude of effects. What I found interesting, however, is how quickly dark chocolate can have a beneficial effect on two common health problems: blood pressure and glucose intolerance (link).

Study design

To study how dark chocolate affects glucose tolerance, insulin sensitivity and blood pressure, 19 subjects with hypertension and impaired glucose tolerance were chosen for the experiment. Smokers and those with significant overweight (BMI > 30) or diabetes were excluded.

The subjects were then randomized and given either 100 grams of flavonol-rich dark chocolate or flavonol-free white chocolate for 15 days. They were told to eat the chocolate in two 50 gram doses, one for breakfast and one for lunch. After a washout period of one week the two treatments were switched, so that those who had been eating dark chocolate got white chocolate instead and vice versa.


Two weeks of dark chocolate consumption decreased insulin resistance significantly compared to baseline and white chocolate. The graphs below show the results from various measurements.

Insulin sensitivity and dark chocolate

The graph on the left show the results from the homeostasis model asssessment of insulin resistance (HOMA-IR) for baseline, flavonoid-rich dark chocolate (FRDC) and flavonoid-free white chocolate (FFWC). The three other graphs show the differences in insulin sensitivity. White chocolate had no effect on any of the tests, while dark chocolate improved glucose and insulin responses to the oral glucose tolerance test.

Compared to baseline, blood pressure decreased after dark chocolate consumption. White chocolate had no effect on 24-h, daytime or nighttime blood pressure. The graphs below show the changes in systolic and diastolic blood pressure.

Dark chocolate also increased flow-mediated dilation, which measures endothelial function. Again, white chocolate had no effect compared to baseline. Interestingly, dark chocolate also reduced LDL cholesterol compared to baseline and white chocolate but had no effect on triglycerides and HDL.


In people with hypertension and impaired insulin sensitivity, dark chocolate (but not white chocolate) reduced blood pressure and improved glucose tolerance and insulin sensitivity. Endothelial function was also improved.

What's interesting about this study is that the duration was so short: the participants saw improvements in just two weeks. And, unlike in many studies, they weren't given cocoa powder or a small dose of dark chocolate, but an entire 100 gram chocolate bar for each day. Also, the subjects were not diabetic, and they only had stage 1 hypertension (systolic 140-159 mmHg, diastolic 90-99 mmHg), which suggests that dark chocolate is helpful even before things get really bad.

I try to keep my intake at around 50 grams per day on average, but at least this study shows that higher amounts are not bad for cholesterol, blood pressure or insulin sensitivity. The reasons I try to stay below 100 grams are the high iron and copper contents and possible lead contamination in cocoa powder.

Still, if you're eating milk chocolate with a low cocoa content (typically around 30%), consider upping the ante and slowly progressing towards darker chocolates. It's the better choice in at least five different ways.

For more information on blood pressure, insulin and cholesterol, see these posts:

Hibiscus Tea Increases HDL, Lowers LDL and Triglycerides
The Many Health Benefits of Rooibos Tea
Intermittent Fasting Improves Insulin Sensitivity Even without Weight Loss
Intermittent Fasting with a Condensed Eating Window – Part III: Fasting Blood Glucose, Cortisol & Conclusion

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Monday, January 3, 2011

Nootropics, Longevity and More: The Year 2010 in Review

Comments or suggestions for the year 2011? Drop a comment!
Comments or suggestions for the year 2011? Drop a comment! (Photo by Altus)

Happy New Year everyone! I hope your holidays went well and you're ready to make 2011 even better than last year. But before we do that, let's take a look at some of the best bits and pieces from 2010.

In January, I finally got a chance to see Aubrey de Grey for the first time. His presentation in Helsinki, Finland was mostly familiar to me already, but I enjoyed it nonetheless. Perhaps the most interesting part was when the audience got to ask questions; I thought Aubrey's answers were good, especially given that some of the comments were pretty frustrating (apparently some people think going through their entire family history somehow qualifies as a question). If you want to check out the presentation, the video is still available online through the link above. And in case you want to know more about Aubrey himself, he was also interviewed in a while ago.

Nootropics are gaining more and more attention these days. Even 60 minutes ran a segment on students boosting brain power to do better in their studies. Amphetamine derivatives are still the most popular choice – but whoever comes up with an "organic herbal formula" that actually works as well as Adderrall is going to be rich. I also did an experiment with Ashwagandha to see whether it had a nootropic effect. It didn't, at least not the brand I was using.

And then there was the experiment with BioSil, the stuff that is supposed to make your hair and nails stronger. The science seems solid, but as I wrote in my conclusion, the price of the liquid supplement doesn't seem worth it, since orthosilicic acid, the active ingredient, is also present in my favourite beverage.

Speaking of hair, a lot of people have asked for an update on the soy isoflavones + capsaicin experiment, another one of my attempts at finding a magical hair growth formula that will make me filthy rich. The experiment has been going on for six months now, which is longer than the five months that the original study lasted, so perhaps a proper update is indeed due. So far I haven't seen much visible changes, however. I'm now adding various kinds of chili powders and pastes to almost all my foods, but I'm thinking of ordering capsaicin supplements to be sure I'm getting enough to match the study. And I also need another bottle of soy isoflavones.

I've tried a lot of useless supplements and topicals, but last year I came across something that really, actually works: retinoids. I've now been using them for over a year and I can really see the difference. My advice to anyone looking for real results is to forget about all the overpriced skin creams that are really nothing but moisturizers and go for tretinoin instead. Of course, since it actually works it's prescription stuff, so you can't just buy it from the store, you'll have to order it online and hope your package doesn't get confiscated by the customs officers who surely know better what you need than you do. Thank god for regulations!

Probably the longest and most throrough post of last year was about human hibernation and how it might relate to longevity. In addition to a look at the current state of hibernation science, there's also the odd legend of lotska, the art of hibernation allegedly practiced by poor Russian peasants:

At the first fall of snow the whole family gathers round the stove, lies down, ceases to wrestle with the problems of human existence, and quietly goes to sleep. Once a day every one wakes up to eat a piece of hard bread, of which an amount sufficient to last six months has providently been baked in the previous autumn. When the bread has been washed down with a draught of water, everyone goes to sleep again. The members of the family take it in turn to watch and keep the fire alight.

And of course, no post on slowing down metabolism would be complete without Indian fakirs and frozen mountain climbers. Check it out if you have the time, it's fascinating stuff.

While the Russian peasants may have spent most of their winter sleeping to avoid starving, there are also those who can eat as much as they like and still avoid getting fat. Even without any exercise. I'll let other bloggers fight it out over the details of the energy equation and whether a calorie truly is a calorie, but take a look at the BBC documentary in the link to see what I mean. Also check out the comment section, some interesting anecdotes in there.

How is the life extension movement doing these days? Well, the same old (and false) arguments against longer lifespans are still there, but the overall mood is pretty optimistic. Personally, I've noticed that younger people tend to be more open to the possibility of life extension than middle-aged people. Go figure. Meanwhile, the Russians have apparently found the cure for aging, although I haven't heard anything new on SkQ1 since September. But that's okay, because the next fountain of youth is already here.

Long-time readers of this blog probably remember that I did intermittent fasting for over a year. Part of the reason was that I wanted to see if 24-hour fasts could be done – I wanted to be the master of my hunger, so to speak. However, the most important reason were the studies showing positive effects from intermittent fasting without restricting total calories. You know, the whole "cleaning cells from junk through autophagy" thing.

But alas, after going through the studies more carefully, I was disappointed to find out that whenever intermittent fasting increased lifespan in mice, total calories had also been restricted. In effect, intermittent fasting extends lifespan only in conjuction with caloric restriction. Some of the other benefits of fasting may still be valid, to a degree at least, but without potential gains in lifespan, I don't see the point in doing a strict 24/24-hour cycle of fasting and feasting anymore. Besides, I now think that even full-blown calorie restriction would only give me a few extra years. Why? Because humans just can't do CR the same way rodents can. More on this later. Meanwhile, see my updated health regimen.

Of course, there were also several other posts which I didn't mention here; see the archives section in case you missed them. And just so you don't miss anything interesting in the future, remember to subscribe to my feed and to follow me on Twitter, which I use to post stuff (life extension, health, science) I don't have time to blog about in depth. Oh yeah, and tell your friends to do so too!

For summaries of previous years, see these posts:

10 Human Experiments of 2009 – Year in Review
7 Human Experiments of 2008 – Year in Review

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