The Examine.com editors have finished a page on Polygala tenuifolia, or as it’s known in traditional Chinese medicine, Yuan Zhi. Polygala tenuifolia is one of the 50 fundamental herbs in traditional Chinese medicine, and it’s often included in decoctions intended to improve cognitive health and well-being.
Unfortunately, only one human study has been conducted on Polygala tenuifolia. Researchers observed that healthy people supplementing Polygala tenuifolia experienced benefits to spatial organization, making it easier to organize and order diagrams and pictures. Memory retention and formation was not affected.
Animal research, however, suggests Polygala tenuifolia may have a restorative effect on cognition. Studies investigating animal models of cognitive decline and aging found that Polygala tenuifolia has a powerful effect when given to aging rodents. Healthy rodents, however, experienced no major benefits to cognition.
The aging rodents may have experienced cognitive benefits because Polygala tenuifolia supplementation increases brain growth factors, like brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF). It also has an antioxidant effect in the brain. Much more research is needed to investigate these mechanisms and how they may apply to supplementation.
Polygala tenuifolia may also have an antidepressant effect similar to ketamine, a rarely-prescribed antidepressant, since it has hallucinogenic and habit forming properties. After oral supplementation, both Polygala tenuifolia and ketamine cause a fast-acting and potent antidepressant effect. These compounds have a similar effect because both interact with the N-methyl-D-aspartate (NMDA) receptor.
Polygala tenuifolia is a promising brain enhancing herb, but much more research is needed before it can be recommended as a supplement. Preliminary evidence suggests it provides the most benefit when supplemented by people suffering from cognitive decline, while healthy people experience little to no benefit.
If you're a savvy nutrition enthusiast, you probably know that a variety of diets can improve health and lead to weight loss. But in the media, low-carb and low-fat diets have waged an epic battle over the past few decades. The latest comes from a year-long study of obese patients, which claims to shed new light on the topic.
Does this study tell us anything helpful, or does it just confirm what we already know? Headlines in the past 24 hours have largely touted the study as eye-opening, even tying it into the newly low-carb (and much thinner) Lebron James.
While most journalists are chasing the sensationalist story: “low carb proven to be superior,” few actually delved into the study to see what researchers found. When you read the full study, key nuggets jump out that most people have missed. Let's dive right in and break down the details. If you're short on time, read the blue boxes now and then come back and read the details later.
We'll analyze this paper using the PICO method, which researchers often use to frame randomized trials. It stands for:
[P]opulation - The study focused on obese people in Louisiana. Unlike most previous trials, this one included a sizable non-white population. Black people made up a little over half of the group.
[I]ntervention - Participants were split into two groups: the low carb group were told to eat less than 40 grams of carbs per day while the low fat group was to take in less than 30% of their calories from fat. The low fat group also aimed to keep saturated fat under 7% and carbs around 55%, which is in line with the current U.S. dietary guidelines.
[C]omparator - This just refers to the control group. The researchers wanted to know the effects of a low-carb diet (the intervention) and compared it against a low-fat diet (the comparator). The comparator is often the current standard of care. In this case, the low-fat diet was very close to what physicians typically prescribe for people at risk for heart disease.
[O]utcome - The outcomes researchers were most interested in were weight loss and cardiovascular risk factors like LDL, HDL, and waist circumference. They also measured a few other factors, like markers for diabetes.
This study was a bit different than previous low-carb trials. None of the participants had diabetes, heart disease, or kidney disease. Having healthier participants means that the researchers could apply the results to a broader group, not just people who were already sick. One thing that wasn't emphasized in the paper or media: almost 90% of the participants were female! If you're using this study to guide dietary recommendations for obese males, just note that only 9 out of 75 people in the low-carb group were men.
It should be noted that calories were not directly controlled. The participants reported an average intake of 2,000 calories per day before either diet - this seems implausible and emphasizes how inaccurate self-reporting can be.
Furthermore, The low-carb group started at a lower daily caloric intake than the low-fat group. By the end, both were eating slightly more and at roughly the same amount of calories.
Study participants were mostly obese women who didn't have diabetes or heart disease. The low carb group was told to eat less than 40 grams of carbs per day while the low fat group was to take in less than 30% of their calories from fat.
There was more to the intervention and comparator than just "low-carb" and "low-fat." Each group actually had two co-interventions along with their recommended macronutrient targets: Meal replacement: Participant were given a meal replacement bar or shake every day. These meal replacements were either low-carb or low-fat, as was appropriate based on their prescribed diet.
Counseling: The participants met up in small group counseling sessions, along with a dietician, in order to learn about dietary guidelines and receive support.
Both of these co-interventions likely impacted the real-world applicability of the study. If we assume that the best diet is one that a person can stick to, the addition of counseling and meal replacement (to ease the transition) greatly helped to prevent dropout. The completion rate was about 80%, which is very high for a diet study.
Both groups got a daily meal replacement shake or bar, and both groups also had regular dietary counseling. This likely increased compliance but might reduce applicability, especially if sticking to the diet is the hardest part.
Regardless of what the researchers intended, the study ended up comparing a diet that was just barely low-carb (with added protein) and a diet that could barely be classified as low-fat.
The low-carb group, while instructed to consume under 40 grams of carbs, did not manage that low of a number. The lowest average carb intake for the group as a whole was 93 grams per day at six months in, and the highest was 127 grams at 12 months in (down from 242 grams a day). Even the low-fat group ended up decreasing their carb intake considerably, but much less than the low-carb group.
That being said, the similarity of the low-fat diet to the macros of the standard American diet might have played a small role in the study results. The intervention group was prescribed a diet that many of the participants were not familiar with. Shiny new diets often provide benefits just because they are new. On the other hand, the low fat group underwent less drastic dietary changes. Unfortunately it's tough to design the perfect control group, and the perfect control group might even control for too many variables and be too difficult to follow, making the trial results difficult to apply.
As an example, let's say an astute researcher realizes that "low-carb" and "low-fat" are not indeed monolithic diets, and that two fat sources can have drastically different effects (e.g. fish oil versus hydrogenated soybean oil), as can two carb sources (e.g. fruit and a twix bar). If this researcher decides to test low-carb against low-fat but control for food quality and carb/fat sources, the trial could get very messy. Recommending an entirely new diet is hard enough, but getting extremely specific with food recommendations could lead to half the sample dropping out. Point being: everyone's a critic when it comes to analyzing studies, but designing a realistic trial is not that easy.
The low-fat group wasn’t that different in fat content from the standard American diet. The low-carb group was barely low-carb and also ate more protein.
Why did the low-carb group miss their carb targets so badly, not even getting close to 40 grams a day? Well, they are human. Some got close to 40 grams, some probably had life get in the way or just found out they really can't handle low-carb diets. Despite not reaching the target, the group did cut their carb intake by about 50% by the end of the trial, compared to baseline levels.
The low-fat group had a much easier change to make. Their baseline fat intake was around 35%, so to target 30% or less was not a very drastic change. Indeed, they ended up hitting 30% fat almost right on the nose after 12 months. Interestingly, at three months in, 25% of the low-fat group reported headaches, compared to only 8% of the low-carb group. Headache rates were much closer at later time points, and other adverse events were fairly similar between groups.
The low-carb group didn’t get close to the target of 40 grams of carbs - they were roughly 300% higher (127 grams on average). Changing your diet is difficult.
Note that the study did not report much on what exactly the participants ate. But we can surmise that the participants didn't end up eating diets much more rich in whole foods than they did before. Both groups ate around 17-18 grams of fiber at the beginning of the study. The new diets caused the groups to eat less fiber. Although eating less in general can lower fiber intake, the two groups likely did not adhere very strongly to the dietary guidelines encouraged by their counseling sessions, since women were recommended 22-28 grams of fiber a day.
It's also interesting that the low-carb group had a similar fiber intake as the low-fat group, so the argument that avoiding carb-rich grains is detrimental due to lower fiber intake doesn't hold true here.
The study didn’t report on the specifics of what foods were eaten, and neither group likely had large increases in fruit and vegetable intake. Both ate an almost equivalent amounts of fibre.
The most publicized result from this trial was weight loss - that the low-carb group had greater weight loss than the low-fat group. Both groups ate about the same number of calories (low-carb clocking in a bit lower). Both groups also ate more calories as the trial went on, with both experiencing an initial drop of about 500 kcal when their diets were given. Although non-significant, the low-fat group ate around 100 calories more at 12 months than at 3 months and the low-carb group ate around 200 calories more.
When looking at the maintainability of diet, both groups had similar caloric intake at 12 months.
Low-carb eaters also experienced a significant increase in lean mass as well, whereas the low-fat group actually lost a bit of lean mass.
Unfortunately fat mass was measured by bioelectrical impedance, not DEXA or a comparably accurate method. If you own one of those bodyfat-measurement bathroom scales, you know that their large measurement variances makes it hard to draw conclusions. Bioelectrical impedance relies heavily on total body water to calculate fat mass, and low carb diets are known to reduce water weight fairly rapidly which could potentially explain some of the rapid weight loss observed.
Since body fat and lean mass were measured through bioelectrical impedance, one can safely ignore any claims about exact fat loss and muscle gained.
Don’t make the mistake of attributing the group results to individuals. For example, weight loss in the low-carb group varied considerably, with some participants losing around 3 kg and some losing over 12 kg. The trial results don’t mean that you should expect to lose some specific number of kilograms on a low-carb diet. In addition, the first three months is when the weight loss happened in both groups. After that, each group experienced a slight uptick in weight, on average. This is another finding that is sometimes skimmed over by media reports.
Weight loss varied quite a bit between individuals within groups, and mostly happened within the first 3 months of the 12 month study.
A better gauge of fat loss would be the waist circumference. At 3 and 6 months in, the low carb group had a greater reduction in waist circumference. By 12 months in, the low fat group had caught up, and the decrease was the same in both groups.
Waist circumference decreased most rapidly in the low carb group, but was roughly the same between the groups at 12 months in.
Although the paper doesn't get into mechanisms much, we can guess why the low-carb group did better with weight loss and lean mass gain. Protein intake ended up being significantly higher in the low-carb group, which bodes well for weight loss and muscle preservation. The participants were instructed to not change their activity levels, although this was not really measured in the study. Thus, any potential effects of the diets on physical activity were nipped in the bud.
Fat loss in the low-carb group could have been partially due to a higher protein intake, which has been shown to have a positive effect on fat loss.
Considering the similarity in waist circumference reduction and both groups eating similar amounts of calories by the end, coupled with the increase in protein by the low carb group and water weight lost when reducing carbohydrates, it would be disingenuous to state that “low carb is superior to low fat for long term weight loss”.
The low-carb group had a higher HDL to total cholesterol ratio than the low-fat group, which is a strong predictor of heart disease. They also had lower triglycerides, in addition to a lower calculated heart disease risk score. Plus, their LDL dropped a bit more than in the low-fat group. To top it off, the low-carbers had a greater decrease in C-reactive protein, a measure of inflammation in the body.
Despite these improved markers, we can't be quite sure what caused them. Although the low-carb group increased their percentage of saturated fat out of total daily calories, they ended up eating about the same total grams of saturated fat compared to baseline, due to taking in fewer calories per day. The low-fat group on the other hand drastically cut down their daily grams of saturated fat. How much of the improvement in heart disease predictors was due to macronutrient changes rather than weight loss isn't known.
Also, the trial is not really conclusive on the subject of heart health since it didn't measure actual heart disease events nor did it look at LDL particle count and density, which are important predictors of disease. The researchers also measured blood pressure and some indicators of diabetes, but the groups didn't differ much on those parameters.
Many predictors of heart disease were improved by the low-carb diet, but the study was not designed to isolate the specific dietary cause of the improvement.
There were several important questions that the trial didn't answer. For example, was the weight loss and cholesterol improvement due to the low carb level or some other factor? It's possible that the low-carb group ate less simply because there were fewer options for them to eat, since many packaged foods sold at grocery stores are high in carbs.
Would the same result happen if you restricted, let's say, all packaged foods instead of carb-rich foods? Or taken to a ludicrous extreme, what if you limited foods that started with vowels? All of these reduce your food options, which is one way through which low-carb diets could lead to weight loss. Some of the weight loss could also be the result of a bit less glycogen (stored carbohydrate) in the liver and muscles. Glycogen can weigh a couple pounds or more due to its high water content, but less of it is stored in the body during a low-carb diet.
The researchers touted the trial's wider applicability compared to previous trials, since the study included more black people than previous studies. But the trial also happened to include zero Asian people and very few Hispanic people. Not to mention very few males! Combined with the fact that all of the participants were obese but with no history of heart disease or diabetes, this may limit the applicability of the trial.
The study didn’t answer the question of what it is about the low-carb diet that encourages weight loss, as it isn’t necessarily due to carb levels.
This trial is a mixed bag. It included a relatively large number of participants and ensured a high completion rate with counseling sessions and meal replacements. And since there was no calorie goal set, the trial could test just how a low-carb diet affected food intake in obese people.
But rather than proving that a low-carb diet leads to weight loss, the study shows that directing people to consume less carbohydrates might increase dietary protein intake. Was it the increased protein? Was it just fewer carbs (remember, this was not truly low carb)? Was the lower carbs/higher protein/higher fat diet simply more filling? And how does that apply to non-obese individuals? These are four very important questions that come out of this study.
Decreasing carbs and increasing protein leads to superior weight loss. The question is: what caused it, the decrease in carbs or the increase in protein?
At 12 months in, both groups were at roughly the same calories and had lost roughly the same amount on their waist circumference.
The claims of muscle gains and superior fat loss should be ignored as they were measured using bioelectrical impedance, which is essentially useless.
How does this trial inform public policy? Well, the U.S. dietary guidelines have long warned against saturated fat and encouraged carbohydrate intake. Unfortunately weight loss is often oversimplified to carb and fat intake, even though protein could have a big impact. When forming public policy on weight loss, a focus on quality foods rather than micromanaging macronutrients would be a step in the right direction. Factors like sleep and stress might have a bigger impact on weight than any one nutritional factor.
Directing people to consume less than 40g of carbs is not feasible policy. Carb intake may go down, but will likely remain over 100 grams/day.
A low-carb diet improved cardiovascular disease predictors, but the study was not designed to isolate whether the cause was weight loss or macronutrient intake.Perhaps the biggest takeaway is that media headlines are not always informative, and it takes a thorough reading of the study and some methodological knowledge (much of the nitty gritty, which wasn't mentioned here) to understand what the paper really says.
A more accurate headline would have been: “If you are obese, decreasing carbs and upping protein may lead to greater weight loss, but sticking to any diet that has you eat less will lead to weight loss.”
Examine.com will soon start publishing a digest that analyses the latest nutritional studies and their context in the bigger picture. Be sure to sign up as an Examine.com Insider below to be notified when we publish our next analysis.
Grab a coffee and get comfortable, because after months of research, we’re about to break down the scientific research on marijuana. And if you want to see all of our research, our marijuana page has 639 citations (and counting).
Marijuana is an herb that contains molecules called cannabinoids. The most famous cannabinoid is tetrahydrocannabinol, also known as THC. THC is responsible for the high that inhaling or ingesting marijuana causes.
Traditionally, marijuana has been used to treat a variety of inflammatory and gastrointestinal ailments. It has also been used to reduce anxiety and help alleviate cognitive decline.
Today, marijuana is used an adjuvant treatment for cancer, meaning it is taken alongside other drugs. It is used alongside chemotherapy because marijuana increases appetite, which prevents the weight loss associated with chemotherapy. Maintaining weight during chemotherapy greatly improves patient survival rates during cancer treatment. Marijuana is not a potent anti-cancer agent by itself.
During cancer treatment, marijuana is used primarily to improve appetite and alleviate pain.
Marijuana has been successfully used to treat other conditions characterized by nerve pain. It can also be used to treat glaucoma due to the reduction in eye pressure it causes. Marijuana is also very promising in the context of treating Parkinson’s and Alzheimer’s disease.
Marijuana is a very popular recreational drug due to its ability to reduce anxiety, alter the perception of your surroundings, and increase euphoria.
Marijuana acts on two receptors, located on cell walls. These cannabinoid receptors are actually named after the plant itself. They are known as the first cannabinoid receptor (CB1) and the second cannabinoid receptor (CB2).
CB1 is responsible for the immediate and psychoactive effects of marijuana, while CB2 determines the long-term and anti-inflammatory effects.
Using marijuana can lead to tolerance, which means more marijuana will be needed to achieve the same effect. Tolerance is caused by a process called internalization. When the CB1 receptor is internalized, it means it withdraws into the cell and can no longer come into contact with THC.
Internalization doesn’t just lead to marijuana tolerance. Other receptors associated with the CB1 receptor will follow CB1 into the cell. For example, the N-methyl-D-aspartate (NMDA) receptor is internalized along with CB1. This leads to protective effects against anxiety and epilepsy, but it also causes the temporarily impaired memory retention associated with marijuana.
Most of the benefits marijuana provides are related to its psychoactive effects. It is effective for reducing stress by alleviating anxiety, increasing euphoria, and causing users to slightly disassociate from their environment.
Marijuana can also help people with low body weight increase their food intake. Since it can also reduce nerve pain, marijuana can be very beneficial to people suffering from conditions characterized by chronic pain.
More research is needed to determine if marijuana can provide benefits for people suffering from Parkinson’s, Alzheimer's, and multiple sclerosis, though preliminary evidence is promising.
The biggest drawback associated with marijuana use is the internalization of the NMDA receptor, which can lead to poor memory retention.
Occasional marijuana use will not impair long term memory, or the capacity to form memories.
Activating the CB1 receptor also increases activity and blood flow in a region of the brain called the anterior cingulate cortex (ACC), which leads to an increase in diastolic blood pressure (the second number on the blood pressure readout). This means that marijuana, when combined with stimulants, can increase the risk of a cardiovascular injury, like a heart attack.
Frequent marijuana use will turn this blood flow increase into a decrease, once the CB1 receptor is internalized. Very heavy usage, meaning five or more joints a day over a period of several years, can actually cause the ACC to shrink. This can hurt attention span and may increase the risk of developing psychosis. If the ACC is affected in this way, it may not return to normal even if marijuana usage is stopped.
Using marijuana causes a temporary state of lowered memory retention, meaning it becomes harder to remember things in the short term. It’s the same feeling that you get when you check your watch, only to realize immediately after that you don’t remember the time. This effect does not cause long lasting memory problems.
Frequent marijuana users may experience slight cognitive impairment, or ‘brain fog’, if they stop using marijuana, but this feeling disappears after two weeks, leaving no long term damage.
Very heavy marijuana users may have more trouble focusing and learning new things if the ACC has been affected.
There is evidence to suggest marijuana use can increase the risk of schizophrenia, but there is also evidence that suggests the opposite. Early studies found that people with schizophrenia sometimes believed that marijuana use would alleviate their symptoms. Since marijuana use does increase blood flow to the ACC, and schizophrenia is characterized by reduced ACC activity, it makes sense that occasional marijuana use could temporarily alleviate symptoms of schizophrenia.
This does not mean marijuana causes schizophrenia, and it should not be considered a treatment option for schizophrenia.
Marijuana use reliably increases appetite, though this effect is subject to tolerance. Still, the effect is powerful enough to make marijuana a popular pharmaceutical, since its appetite-increasing effects help cancer patients stay at a healthy weight, which leads to higher survival rates.
Marijuana’s anti-inflammatory effects are caused by CB2 activation, which makes it a potential therapy for treating cognitive diseases characterized by inflammation, like Parkinson’s and Alzheimer’s.
Unfortunately, since activating CB1 can cause issues with memory retention, more research is needed before marijuana can be recommended specifically to alleviate Parkinson’s and Alzheimer’s.
Marijuana is illegal in many parts of the world, and many sports organizations have explicitly banned its use. In fact, scientists have actually tested how much second hand inhalation is required to test positive on a urine test to determine if athletes could legitimately use the excuse that they were around other users, but didn’t personally partake.
It turns out that to test positive for marijuana after second hand inhalation would require exposure to at least 16 joints in a closed room approximately the size of a bathroom for at least an hour. That’s a lot of inhalation.
Marijuana use increases diastolic blood pressure and thus should not be used alongside stimulants, especially by people already at risk for heart attacks and other cardiac conditions. Otherwise, infrequent marijuana does not pose a serious health risk, provided that the influence of marijuana doesn’t lead you to do something stupid.
The risks of marijuana come with heavy and near-daily usage. Marijuana causes impaired memory retention, so when that effect is repeated daily across multiple joints for years, learning can become difficult.
Chronic heavy users of marijuana can experience reduced ACC weight. This is brain atrophy and should be taken seriously. However, it is the only negative effect of marijuana that persists even after marijuana usage is stopped.
Maintaining sensitivity to the psychoactive effects of marijuana requires infrequent use. Some people’s CB1 receptors may start to internalize even while using marijuana only once a week. Using marijuana twice a month will make you more likely to experience marijuana’s beneficial effects in a safe and sustainable way.
If you have not used marijuana before, make sure your first time is with other people you trust in a safe environment. Psychoactive drugs can have unexpected side-effects, so safety is key to a good experience.
When it comes to chronic usage, marijuana’s greatest benefits include a pain reducing effect and an increase in appetite, which is critical during chemotherapy. Conversely, the biggest downside with chronic usage is potential ACC (a component of the brain) shrinkage and the reduced capability for learning and remembering.
During infrequent usage, the risk of reduced learning capability is much lower, whereas the benefits of pain reduction and increased appetite remain, though the effect is not as strong.
Want to read the full science? See our Marijuana page.
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Examine.com editors have finished going over Taraxacum officinale, more commonly known as dandelion. The same yellow plant that pops up in your yard every spring is used around the world in various traditional medicines and as a diuretic. In fact, it’s used so frequently for its urine-inducing property that its French name, pissenlit, actually means ‘wet the bed’.
Traditional medicines that include dandelion usually intend it as a treatment for gastrointestinal ailments or inflammation. Some preliminary rodent evidence does suggest dandelion may be able to increase the rate at which food exits the stomach and enters the small intestine, but much more research is needed to confirm if this effect can be replicated through supplementation.
Though it is frequently used as a diuretic, dandelion lacks research on its effects. It is effective when taken by humans, but the potency of the effect and mechanism through which it occurs requires further investigation. It is possible that the diuretic effect is caused by a high potassium to sodium ratio. Dandelion is very high in potassium, with about 2.45% of its roots, dry weight, being potassium, while sodium makes up only 0.33% of the plant.
Dandelion can be added to salad to increase dietary potassium intake. Just don’t start using the clippings from your lawn. Dandelions growing in urban and suburban environments are frequently exposed to pesticides.
Dandelion is not recommended for supplementation at this time, since it has limited evidence for its effects.
A recent study has revived the supplement market’s interest in a compound called (-)-epicatechin, a molecule found in chocolate. This molecule is claimed to be a myostatin inhibitor. Myostatin deficiencies are well known for their biggest side effect: greatly increased muscle mass without the major side-effects associated with anabolic steroids. Hindering myostatin’s actions would be able to replicate this effect.
Myostatin is a myokine, a kind of regulating molecule released by muscles. The ‘opposite’ of myostatin is a myokine called follistatin. Unlike myostatin, which suppresses muscular growth, follistatin indirectly promotes muscle growth because it hinders myostatin signalling.
While there are a few supplements that are known to interact with myostatin signaling (like sulforaphane), none had been tested in the context of human supplementation, until now.
This recent study examined the effects of (-)-epicatechin when supplemented by people. Already, new supplements are popping up on the shelves, containing (-)-epicatechin and claiming to be myostatin inhibitors.
Myostatin and follistatin both have potential to alter muscle growth rates, but supplements and foods affecting these molecules have limited evidence in humans.
Should you supplement (-)-epicatechin or eat more chocolate to build muscle? Let’s dissect the study and find out.
This was a proof of concept study in three parts. A proof of concept study is designed to test whether a compound will have the effect researchers hypothesized, as well as determine if further studies are appropriate.
The first part of the study was done in vitro, meaning outside the body in a test tube or petri dish. Scientists assessed muscle cells taken from people of different ages. When people age, their muscles tend to have higher myostatin levels and lower follistatin levels. The in vitro part of the study confirmed this relationship.
The second part of the study was the mouse study. After measuring the myostatin and follistatin levels of old and young mice to confirm the age-related difference, researchers gave the rats 1 mg (-)-epicatechin per kg of body weight, twice a day. Over two weeks, young mice experienced a 15% decrease in myostatin with no change to follistatin. Older mice, meanwhile, experienced an 18% reduction in myostatin and a 30% increase in follistatin.
Two weeks is not enough time to notice any changes in muscle tissue mass, so researchers did not measure it.
In the third part of the study, six middle-aged people supplemented 1 mg of (-)-epicatechin per kg of body weight, twice a day. This translated to about 75 mg of (-)-epicatechin, twice a day, for a total daily dose of 150 mg.
The published study reports that the follistatin to myostatin ratio of the six middle-aged subjects increased +49.2% (follistatin)/ -16.6% (myostatin), which suggests an increase in follistatin levels and a decrease in myostatin levels. However, the exact changes in myostatin and follistatin levels were not reported.
Though a minor (7%) increase in hand grip strength was observed, muscle tissue mass was not measured, and there was no placebo group for comparison.
This study fulfilled the goals of a proof of concept study, because it provides evidence to suggest a possible relationship between (-)-epicatechin, follistatin, and myostatin levels, which can be investigated in future studies.
A recent study is the first to show that supplemental (-)-epicatechin increases the follistatin to myostatin ratio in humans.
The biggest difference between this study and the new myostatin supplements are the doses. The study used a 150 mg daily dose, while the supplements range from 250 - 500 mg (-)-epicatechin per dose, for a total daily dose of 500 mg - 1,000 mg.
The 75 mg used in the study can be supplemented through dark chocolate consumption. Eating 50g of pure dark chocolate containing at least 50% cocoa a day will provide a similar amount of (-)-epicatechin as the dose used in the study. The higher the cocoa content in the chocolate, the less you need to eat. For example, if you eat dark chocolate containing 85% cocoa, you’d only need to eat 30 g for an equivalent dose.
Milk and white chocolate have a much lower cocoa content and subsequently, contain little to no (-)-epicatechin.
It’s easy to obtain the studied levels of (-)-epicatechin by consuming a small to moderate amount of dark chocolate daily.
Keep in mind, this study had a very small sample size, just six people, and there was no placebo control. Furthermore, only the ratio of myostatin and follistatin changes were published, not the actual numbers. This study does not provide evidence to recommend (-)-epicatechin as a muscle growth agent, but it does lay the groundwork for future research and suggests (-)-epicatechin is a promising muscle growth supplement.
Since (-)-epicatechin provides other health benefits and is very safe, it is possible to test this potential muscle growth agent for yourself by eating dark chocolate twice a day.
In the future, (-)-epicatechin may be a novel and exciting muscle growth enhancing compound, but there is not enough evidence to recommended it as a dedicated dietary supplement today.
Due to the preliminary nature of studies, there is not currently enough evidence to support (-)-epicatechin for muscle growth. However, dark chocolate is safe and provides other health benefits, so consuming it regularly may not be a bad idea.
To bring you up to speed: kombucha is a fermented drink product, made by fermenting already-fermented green or black tea. This is why kombucha is called ‘doubly-fermented’ tea. However, if kombucha is fermented for too long or in unsanitary conditions, it can develop very dangerous properties.
One of the molecules found in kombucha is called D-saccharic acid 1,4 lactone (D-saccharolactone). D-saccharolactone has been studied for its ability to prevent colon cancer, diabetes and hyperglycemia.
Unfortunately, more research is needed to determine if D-saccharolactone is an effective protective compound when supplemented or consumed through products like kombucha. D-saccharolactone has been shown to be effective when studied in vitro, meaning outside of the body, in a test tube or petri dish, but more studies are needed to determine if these effects extend to oral consumption of kombucha. It is not uncommon for a compound to be very promising in vitro but not do much when consumed (for example, see glutamine).
What sets kombucha apart from other potentially dangerous food products is how little is known about the strains of toxic bacteria and fungi that make improperly brewed kombucha dangerous.
Dangerous food products can fall into several groups:
Spirulina, an algae sometimes used as a supplement, can be dangerous if it is contaminated with microcystin, a kind of toxin. Spirulina producers are aware of this potential danger, and test spirulina for microcystin.
Some herbal supplements can be toxic if they are contaminated with other species of herbs. Herbal producers run tests to make sure their herbal supplements are pure, and subsequently, safe. For example, Stephania tetrandra is one of the four plants that can make up the traditional Chinese medicine Fang Ji. In the past, it has been contaminated with a toxic plant called Aristolochia fangchi, which can also be called Fang Ji. Anyone that produces Stepania supplements knows to test for Aristolochia.
Other food products, when prepared improperly, become toxic or dangerous. Chicken, for example, can be dangerous if it is eaten raw or undercooked. But while you can use a thermometer to determine how safe chicken is to eat, there is no easy test for determining kombucha’s safety. Unlike spirulina, researchers don’t know what fungi and/or bacteria strains are dangerous in kombucha, and which provide the health effects.
Though kombucha may have potential health benefits, it can be dangerous to drink because many of its risks are still unknown. Unsanitary kombucha can cause death, organ failure, and there’s even been one report of cutaneous anthrax.
Any compound that provides unique benefits, but has also been shown to be toxic, can still be supplemented if the toxicity is carefully controlled for. Unfortunately, the specific toxins in kombucha have yet to be identified. More importantly, more research is needed to determine whether kombucha really does provide unique health benefits. With little proven health benefits, and questionable toxicity, Kombucha cannot be recommended for supplementation or consumption at this time. Future evidence must identify the toxic strains in kombucha, or confirm the unique therapeutic effect of saccharolactone (when consumed through kombucha), for kombucha to be recommended as a health drink.
If you do choose to drink kombucha, it is very important to research the producer. Only purchase kombucha from sanitary producers with properly trained staff. Kombucha is not recommended as a therapeutic or preventative drink. Instead, consider options like black or green tea, or fermented food products like kimchi or sauerkraut.
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Kombucha is a tea product, known as doubly fermented tea or fungal tea. It’s often claimed to have stronger anti-cancer properties than other teas.
Kombucha comes from the same plant that produces green and black tea, Camellia sinensis. The process of brewing kombucha involves fermenting already-fermented black tea with fungi and bacteria. During fermentation, the tea becomes mildly carbonated, acidic, and acquires its distinct vinegary taste. The fermentation process also produces new bioactive compounds and alcohol. Don’t try getting drunk off of kombucha, since the alcohol content is low and drinking a lot of kombucha can be dangerous.
The most important bioactive compound in kombucha is called D-saccharic acid 1,4-lactone, also known as saccharolactone. Saccharolactone is claimed to exert anti-cancer effects in the colon, and it’s supposed to help with detoxification too.
Unfortunately, the potential potency of saccharolactone, as seen in vitro, is difficult to apply to the human body, for two reasons:
There have not been any human studies done on saccharolactone by itself, or in kombucha.
Improper preparation of kombucha results in toxicity and the risk of death.
While kombucha can be prepared safely, improper sanitation can cause cross-contamination, which leads to the growth of toxic fungi and bacteria. Kombucha is a risky supplement option, since it is difficult to identify toxic strains of fungi. Moreover, further research is needed to identify the bacteria strains responsible for kombucha’s health effects. If kombucha is fermented for longer than a week, it will start to develop these toxic properties.
Kombucha made incorrectly can do a lot of damage to the human body. Case studies examining harm done by kombucha consumption have noted death, organ failure, and even one report of cutaneous anthrax.
Ultimately, there is no proven and significant benefit of drinking kombucha. It’s not a very practical health supplement, considering there’s hardly any evidence for its health effects, but plenty of evidence for the damage it can do. If you do choose to drink kombucha, make sure to purchase it from trustworthy producers with sanitary working conditions and properly trained staff.
NOTE: You can see all sources on our Kombucha page.
Added July 21 2014: An Update on Kombucha: Understanding Risk and Evaluating Toxicity
As Examine.com continues to grow (over 33,000 scientific references now), it's important that we remain versatile and ready for the future. A lot of companies start off successfully but get bogged down as they struggle to scale their operations.
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The good news: stepping up as the new Director of Examine.com is Kamal Patel. With an MBA and an MPH (Master of Public Health) from Johns Hopkins, and on hiatus from his PhD in nutrition at Tufts, Kamal Patel brings the perfect blend of business savvy, big-picture health applications, and understanding the nitty gritty of scientific research (he's been published in peer-review over a dozen times). His larger involvement in our future will only be good news for us (for those that remember us linking to a LifeHacker article on why there's so much confusion over health and nutrition, it was Kamal's broad knowledge that contributed heavily to that article).
Secondly, as we grow, we realize that having a large breadth of expert individuals looking over our research and ensuring we haven't missed any crucial detail only helps everyone. Thus, we are now adding Reviewers to Examine.com. While the Editors will continue to perform the bulk of the primary research, Reviewers will be brought in after our internal discussion has concluded to ensure that nothing is amiss and no theoretical or practical points have been overlooked. The addition of Reviewers lets our team remain versatile and lets us work with knowledge experts without greatly slowing down our research.
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Please be sure to give Kamal and Dr. Cass a very warm welcome on our Facebook page. We're extremely excited to have them onboard.