Today’s competitive society is full of stressed people. Extreme and debilitating distress, along with the fear of being judged and criticized by other people can cause panic and social anxiety, characterized by intense sweating, shaking, muscular tension, confusion, and an elevated heart rate. Social anxiety can make social situations very difficult, and if it occurs often, it can severely interfere with day-to-day activities, to the point where socially anxious people will avoid social interactions all together.
Social anxiety is also known as social phobia, as defined by the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). With up to 10.7% of people experiencing this condition at some point in their life, it is the third most common lifetime anxiety and mood disorder in the United States.
Social anxiety, a debilitating disorder that makes social situations extremely distressful and difficult to navigate, is the third most common lifetime anxiety and mood disorder in the United States.
Some research suggests that phobias are, at least in part, hereditary. In fact, a recent twin-study found that the sibling more likely to develop social phobia was the one that inherited genes predisposing them to neuroticism, a personality trait characterized by the tendency to respond poorly to stressors, often leading to the experience of negative emotions, such as anger, envy, nervousness, guilt, anxiety, and depression.
Fortunately, there are a variety of potential treatments for this disorder. Traditionally, cognitive behavioral therapy and selective serotonin reuptake inhibitors (SSRIs) are used. Recently, probiotics (defined as “live microorganisms that, when administered in adequate amounts, confer a health benefit to the host”) have shown promise as a supplement to the traditional treatments for social anxiety. Even though the research is still in its infancy, the fact that probiotics have excellent safety profiles and traditional treatments often only provide partial symptom relief makes them enticing treatment targets.
Research suggests that social anxiety may have a hereditary component. A couple common treatments exist, but they only provide a partial relief of symptoms. Fortunately, probiotics have shown some very early promise as a potential safe supplement to traditional treatments.
A recent study has been touted in the media as providing evidence for the anti-anxiety efficacy of consuming fermented foods that are likely to contain active probiotic cultures. Tantalizing headlines included “Sauerkraut Could Be The Secret To Curing Social Anxiety”. However, there were several limitations, warranting a much deeper look than most media outlets took. Let’s see what this study can really tell us, if anything.
Researchers provided surveys to 710 university students to determine their level of social anxiety, neuroticism, and agoraphobia. The survey also asked how often the students exercised, and how often they ate fermented food. As hypothesized, students that ate more fermented foods tended to experience less social anxiety. Moreover, they found that, as seen in the figure below, social anxiety and neuroticism were positively correlated, and the more neurotic a person was the greater that chance that high fermented food intake might help reduce levels of predicted social anxiety.
However, before jumping to conclusions, there are a few extremely important limitations to consider. This was a cross-sectional study, which only shows correlation, not direct causality. The authors cannot be sure if it was the high fermented food intake that led to low levels of social anxiety or if low levels of social anxiety led to increased consumption of fermented food. It is also possible that an unknown variable caused both the increased consumption of fermented foods and the decreased social anxiety.
It’s also possible that some property of the foods other than their probiotic content affected social anxiety. Furthermore, the nature of a survey or questionnaire is subject to self-report bias. The authors can’t be sure if the participants were being truthful or could even remember exactly what they ate or how much they exercised over the past thirty days. And since the sample was made up of college students, the findings may not be applicable to the general population. Finally, and most importantly, lower levels of predicted social anxiety were also observed in participants that ate more fruit and vegetables, as well as those who exercised frequently. It’s not possible to determine whether exercise or fruit and vegetable consumption are confounding variables or not. This is especially important in light of a recent randomized control trial that found a reduction in symptoms of social anxiety following two months of aerobic exercise.
Based on survey data from 710 university students, a recent study found that consumption of fermented food likely to contain active probiotic cultures was inversely associated with predicted levels of social anxiety. However, due to many limitations and confounding variables, further research is needed before any assertions can be made.
That being said, this study is consistent with other clinical trials that have also demonstrated anxiolytic effects of pre and probiotics in humans. Unfortunately, the exact biological mechanism behind this is still unclear. However, according to preclinical animal trials, there is mounting evidence that certain gut microbiota can have anxiolytic effects through gut-brain pathways, possibly via the vagus nerve. Supporting these findings, the ability of the gut and brain to bidirectionally communicate through neural, endocrine, and immune pathways, also known as the gut-brain axis, has long been recognized, and recent research has made it increasingly clear that interactions with intestinal microbiota are an important part of this communication.
Furthermore, a couple more specific potential mechanisms for how the probiotics confer their anxiolytic effects have been proposed. For instance, given that research has found a positive association between gut inflammation and anxiety-like behaviors, some have hypothesized that probiotics could potentially colonize the gut, displacing species that are harmful to health, and, in turn, may reduce gut inflammation and the associated anxiety-like behaviors. Others have proposed the involvement of the serotonergic system in the neurobiology of anxiety, especially since research surfaced suggesting that certain intestinal microbiota can increase levels of tryptophan in the blood, and therefore potentially facilitate the turnover of serotonin in the brain.
Overall, research on probiotics and anxiety is still in its early stages. According to the authors, this is the first study to provide some extremely limited observational evidence for the efficacy of probiotic supplementation to fight, specifically, social anxiety, and thus, they did not mean to infer causality. Regardless, due to several limitations imposed by the study design, and the huge number of possible confounding variables, this study should solely serve as preliminary evidence, especially considering how strong of a confounding variable exercise is, as several papers have demonstrated its anxiolytic effects. However, if further well-conducted RCTs can suggest a causal role, independent of exercise and other possible confounding variables, probiotics or fermented foods consumption could potentially serve as great low-risk supplement to traditional treatment for social anxiety.
While the study results seem to support probiotic supplementation to help treat social anxiety, they can easily be misinterpreted in the midst of several limitations and confounding variables. The only thing we can state for certain is that further well-conducted RCTs are necessary before we make any conclusions about probiotics and their possible, low-risk health benefits.
On June 16, 2015, the United States Food and Drug Administration (FDA) announced their decision to eliminate trans fat from food in the United States by 2018, with a gradual phase-out period beginning immediately.
Take THAT, trans fat advocates! Hold on ... are there any trans fat advocates? While some dislike government regulation of foods and nutrients, there isn’t much debate about trans fat health effects anymore.
This brings up a question … if we all know that trans fat is bad, why is it still a public and personal health issue? Well, it is true that trans fat consumption has dipped considerably, with blood levels dropping by 58% in the 2000s. But incremental consumption of industrially produced trans fat is incrementally harmful, and the National Academy of Science has concluded that there is no safe trans fat dose.
So out of all the nutrient and nutrient-like substances out there, trans fat hold the dubious distinction of being one of the only categorically harmful ones. And you might not always know that you’re consuming trans fat, since some soybean and canola oils can have hidden trans fat inside.
Trans fat is an unsaturated fatty acid and a byproduct of partially hydrogenated oils (PHOs.) It is found in many processed food products, including margarine, coffee creamer, fast food, frozen pizza, snack foods and other baked goods. Trans fat is also found in some peanut butter. It is frequently used by the food industry because it improves flavor stability and shelf life of food. Since trans fat has a different melting point depending on how processed it is, it’s also a very flexible ingredient. But aside from these benefits, it seems that the primary reason trans-fat was added into the food system was the demonization of saturated fat by the USDA in the 1950s. By the 1980s, activist organizations were denouncing food manufacturers for using ‘unhealthy’ saturated fats in their foods, and endorsing trans fat as a ‘healthier’ alternative. Considering the benefits to shelf life, flavor stability, and flexibility, manufacturers gladly made the change.
Some types of trans fat are naturally produced by ruminant animals. This group of animals includes cattle, sheep, goats, buffalo, deer, and other animals with four stomach compartments. The first, and largest, part of the stomach, called the rumen, is where trans fat is produced. Humans can create trans fat through a commercial process called hydrogenation, in which hydrogen gas is boiled through oil (usually vegetable oil) to allow the oil to saturate, which determines its thickness.
Medical professionals consider trans fat to be one of the most unhealthy compounds found in today’s food. Trans fat consumption is associated with increased low-density lipoprotein cholesterol (LDL-C and inflammation), and decreased high-density lipoprotein cholesterol (HDL-C). These health risks can speed up the development of atherosclerosis (clogging and hardening arteries) and increase the risk of diabetes, coronary heart disease, and cardiac-related sudden death. However, a recent systematic review strongly suggests that these negative health effects are primarily attributed to the consumption of industrially-produced trans fatty acids (IP-TFA), but not ruminant-derived trans fatty acids (R-TFA). In fact, most animal models have demonstrated that IP-TFA and R-TFA have different effects on CVD risk factors. For instance, a rat study showed that supplementation with an R-TFA called Vaccenic acid had either a neutral or beneficial effect on CVD risk markers such as total cholesterol, LDL-C, and fasting and postprandial triglycerides.
Trans fat can be made commercially, or naturally by certain animals. It is used in the food industry to improve flavor and shelf life, but the FDA has announced it will be phased out of the U.S. food supply because it is damaging to health.
This increased risk is significant. A 2006 meta-analysis found that a 2% increase in trans fat intake is associated with a 23% increase in cardiovascular disease risk. Cutting commercial trans fat intake from 2.1% of daily energy intake to 1.1% could potentially prevent 72,000 cardiovascular deaths. A drop to 0.1% of daily energy intake could potentially prevent 228,000 cardiovascular deaths every year in the U.S.
While the evidence on ruminant-produced trans fat isn’t conclusive regarding potential heart health benefits (especially at the doses commonly ingested), a recent meta-analysis points to no detrimental impact on cardiovascular disease markers.
Even though the FDA has recognized the negative health effects of trans fat and is taking steps to remove it, trans fat is still prevalent in our food. While the American Dietetic Association (ADA) recommends no more than 1% of your daily calories come from trans fat, unclear nutrition labels can sneak a lot of trans fat onto your plate. If a nutrition label claims the product contains “partially hydrogenated” fat or “zero grams of trans fat,” that doesn’t mean there is no trans fat in the product. This is because the FDA previously allowed products to be labeled with zero grams of trans fat as long as the product had less than 0.5 grams. Multiple servings of “zero grams of trans fat” food can result in much more ingested trans fat than the ADA recommends.
Trans fat consumption is a significant contributor to cardiovascular disease. The FDA has long recognized this and finally decided to gradually eliminate it from our food system by 2018. Until then, any industrially produced trans fats still present in our food system should be avoided, though this can be quite difficult due to confusing and misleading nutritional labels.
We all know that marijuana is a popular recreational drug- and that it’s also got a variety of medicinal uses, including reducing nausea and boosting appetite. But what, exactly is marijuana - and how does it affect the appetite and digestive system?
The answer to that first question is pretty simple, so let’s start with that. The term ‘marijuana’ refers to several plants in the cannabis genus, including sativa, indica, and ruderalis.
Doctors typically prescribe marijuana to treat inflammatory, gastrointestinal, and cognitive ailments. Marijuana is also frequently administered to cancer patients, since it helps ease the pain associated with chemotherapy while increasing the patient’s appetite. This is why marijuana is used in an effort to minimize weight loss, which could lead to further health complications.
As you can imagine, this increase in appetite is one of marijuana’s most well-known effects, you might refer to it as “the munchies”. In fact, historical sources confirm that people as early as 300 BCE knew that cannabis stimulates appetite, and noted how these cravings were for sweet and savory food. Let’s dig into why that happens.
One of the main active ingredients in marijuana - a chemical compound known as tetrahydrocannabinol (THC) - is one of the main culprits responsible for “the munchies”. Once the marijuana is consumed (normally by smoking), THC activates a receptor called cannabinoid receptor type 1 (CB1), which helps increase appetite. CB1 is also involved with the receptor for ghrelin, a hormone that contributes to an increase in the sensation of hunger.
CB1 receptors appear in a variety of different areas of the body. In each of these areas, these CB1 receptors act in slightly different ways - and many of those effects help increase the desire to eat. CB1 receptors are found in all of the following areas:
Researchers have found that inhaling cannabis is also associated with lower levels of peptide tyrosine tyrosine (PYY), a peptide that contributes to appetite suppression. People who use marijuana recreationally tend to have increased levels of ghrelin and decreased levels of PYY, which may be one reason why their daily caloric intake tends to be greater.
Studies have also shown that a person’s method of THC consumption (oral capsules, smoke inhalation, or suppository) can influence their food choice, as well as their overall food consumption. For example, study participants who took a suppository consumed significantly more calories throughout the day than participants who took an oral capsule.
Recent research on CB1 has revealed that a synthetic form of THC (dronabinol) can activate a subset of neurons called proopiomelanocortin neurons (POMC). Though POMC are usually responsible for the feeling of fullness after a meal, these neurons can either release hormones that suppress hunger, or hormones that increase appetite. When CB1 is activated, these hormones prevent POMC from suppressing hunger, and enable it to start increasing your appetite.
Since activating the CB1 receptor contributes to an increase in appetite, blocking it has the opposite effect. Studies on individual cells show that blocking CB1 receptors significantly increases production of adiponectin, a hormone with anti-inflammatory effects and a negative correlation with obesity.
Researchers have also used compounds that can block the CB1 receptor - which are known as endocannabinoid antagonists - to treat obesity associated with eating disorders, which is characterized by compulsive binge eating or cravings for sweets and snacks. Animal studies show that rats given rimonabant, an endocannabinoid antagonist anti-obesity drug, experience weight loss and reduced levels of blood insulin.
Still, a lot more research is needed before we can start recommending these kinds of therapies to human patients. The CB1 drug Rimonabant, for example, failed to earn approval from the U.S. Food and Drug Administration (FDA) - and it’s no longer sold in Europe either, due to side effects associated with its use, which include severe depression and suicidal thoughts. Since CB1 receptors are found all throughout the body, it is difficult to pinpoint the cause of these side effects.
Future endocannabinoid antagonists, however, may play a role in treating obesity by blocking CB1 receptors, increasing adiponectin production, and reducing appetite.
Marijuana has been a part of our society longer than any one civilization, and researchers continue to paint a more complete picture of the compound with every passing year. Follow-up studies will not only need to investigate CB1’s effects throughout the body, but also the different ways THC functions when ingested in various ways. More research on marijuana may also lead to breakthroughs in the fight against obesity because of how effective manipulating hunger can be when it comes to controlling our daily caloric consumption.
However, we want to end this post with a reminder that marijuana use impacts more than just your appetite. If you’re curious, click here to learn more about the health benefits and risks of marijuana.
The Examine.com page on Copper has been completed and our researchers have turned up some interesting results in the process.
The body needs dietary copper for cognitive development during infancy, as well as for optimal immune and bone health.
Too much copper, however, has been linked to Alzheimer’s disease progression. That doesn’t mean copper causes Alzheimer’s disease. Instead, some people appear to have a genetic predisposition to Alzheimer’s disease, which causes copper to harm neurons. Too much copper increases the damage done to neurons in these people.
Copper is abundant in developed countries, where it is found in most food, as well as drinking water. Copper deficiencies in otherwise healthy adults are unheard of, so supplementing copper to prevent a deficiency is not a good idea.
Although copper does play a structural role in the makeup of a potent antioxidant enzyme, Cu,Zn,-superoxide dismutase (SOD1), supplementing copper does not result in increased antioxidant defense.
Copper is an important part of a healthy diet, but supplementing copper may not provide much of a practical benefit. Though some research suggests copper may play a role in fighting heart disease, much more research is needed to confirm this hypothesis. Since too much copper can have negative health effects for older people, copper is not recommended for supplementation at this time.
Every month, it seems like there's always a new diet drink or artificial sweetener popping up in our grocery aisles, claiming that it not only offers all the benefits of its nonfat predecessors, but it also comes with none of the downsides. Meanwhile, it’s hard to avoid the reports that claim to link various artificial sweeteners to weight gain, cancer, and other dangerous effects. So how can you separate fact from fiction?
The most common non-caloric artificial sweeteners (NAS) are substances with a very intense sweet taste. They’re used in small amounts to replace the sweetness of a much higher amount of sugar, or of other derivative substances.
You’ll probably recognize at least some of the following names of common artificial sweeteners:
But are any of these sweeteners really any better than the others --or perhaps, riskier? Let’s break down what the actual research has to say.
The main benefit of artificial sweeteners (or non-nutritive sweeteners) is to provide a zero-calorie alternative to foods and beverages, while still giving them a sweet taste. Replacing refined sugar with artificial sweeteners in your own diet can be an effective way to lower your calorie intake - which can allow you to bring in some healthier higher-calorie foods instead. Some studies have found that this kind of adjustment can help obesity, diabetes mellitus, and similar problems.
The truth is that only a few artificial sweeteners have been studied in-depth: aspartame, sucralose, acesulfame-K and saccharin. The majority of existing clinical and lab data only cover these sweeteners.
The FDA first approved aspartame in 1974, in light of a large amount of evidence - from labs and clinics in the United States, as well as from more than 90 other countries around the world - that demonstrated its safety for human consumption. So why did people get so paranoid about aspartame? Most likely because of a few studies on rodents, which have found that exposure to aspartame is associated with various cancers in rats and mice.
However, experiments have shown that the doses of aspartame required to pose danger to humans are far larger than what any normal person could consume in a day. The FDA has set the acceptable daily intake (ADI) for aspartame at 50 mg/kg of bodyweight - the equivalent of a whopping 18 to 19 cans of diet soda.
Rodent studies have shown a dose-dependent increase in lymphomas, leukemias, and transitional renal cell tumors in rats and mice who received doses of aspartame lower than the ADI - but while rodents and humans do share some metabolic similarities, the mechanisms our bodies use to process aspartame and other relevant compounds are different from those in rats. This fact has led most researchers to conclude that a comparison between rodent and human effects would be invalid in the case of aspartame.
For people born with phenylketonuria (PKU), a rare inherited disease, aspartame can help create dangerously high levels of the naturally occurring essential amino acid phenylalanine - and there’s also some evidence pointing to a possible relationship between aspartame and migraine headaches. For most people, though, aspartame has always been perfectly safe at reasonable doses.
The human body doesn’t metabolize Ace-k at all, so it provides no calories - but it’s 200 times sweeter than table sugar. One breakdown product of ace-k is a chemical known as acetoacetamide, which is known to be toxic if consumed in very large doses - but the amounts of acetoacetamide found in spoonfuls of Ace-k are far below dangerous levels. Still, although plenty of research has found that Ace-k is safe for animals, human studies are still rare.
Although sucralose is made from sugar, the human body doesn’t recognize it as sugar, so it’s not metabolized - which means it provides no calories. Most of the sucralose we consume is excreted as waste - while another 11% to 27% of it gets absorbed into the bloodstream through the gastrointestinal tract, removed from the blood by the kidneys, and eliminated through our urine.
The acceptable daily intake (ADI) for sucralose is 5 mg/kg bodyweight per day, but the typical person’s estimated daily intake is a significantly lower 1.6 mg/kg per day. Human trials haven’t reported any significant dangerous effects for sucralose at all - but similarly to studies on aspartame, some research has found a relationship between sucralose intake and migraine headaches.
Among all the artificial sweeteners listed here, saccharine is the only one that deserves a stain on its reputation. The FDA tried to ban saccharin in 1977, in the wake of a series of animal studies that found close linkages between saccharin intake and the development of cancer in rodents. And while no study has ever shown a clear causal relationship between saccharin consumption and health risks in humans at normal doses, some studies do show a correlation between saccharine consumption and human cancer incidence.
More recently, researchers have found that saccharine can impair glucose metabolism in rodents. This has become a fairly controversial idea, though, and it’s probably the origin for the bad rap that all artificial sweeteners tend to catch.
A recent study by Suez et al. pooled evidence from animal studies to demonstrate several dangerous effects of saccharine - and those same authors also performed a study in which they administered high doses of saccharin to human subjects, then transplanted feces from two human subjects to two rodents. This transplant, the researchers found, caused some damage to the rats’ intestinal microbes, which in turn lowered their tolerance for glucose.
The news media grabbed the results of this single study and blew them out of all proportion to the facts, spawning outrageous headlines like “Diet Soda Causes Diabetes.” The truth is, a lot more research is needed to determine the effects of saccharin (and most other artificial sweeteners) on the human microbiome in vivo. For now, there’s no compelling evidence to suggest that normal doses of saccharin pose any harm to humans.
Aside from that, saccharin is nearly non-existent in today’s diet foods and beverages. Aspartame and sucralose are found all over the place - but saccharin is only found in Tab and a few other fountain drinks, and in the sweetener Sweet’N Low, where it’s present in tiny amounts. In order to match the dose that Suez et al. found to be dangerous for humans, you’d have to drink four cans of Tab, ten packets of Sweet’N Low, or fifty servings of a saccharin-containing fountain drink. So on the whole, even saccharine is a pretty low-risk sweetener.
What about the effects of artificial sweeteners on your weight-loss plans? Most short-term and long-term studies on humans have found that consuming artificial sweeteners doesn’t seem to decrease dieters’ energy intake - and randomized trials have found that people who use these sweeteners in place of refined sugar can successfully reduce both their weight and their body fat. Only been a few studies have examined the overall effects of artificial sweeteners on body weight - but every study has found reductions in weight and body fat in groups of people who use artificial sweeteners, as opposed to normal calorically dense ones.
So, should you be concerned? Maybe. Generally speaking, the only people who should be worried about artificial sweetener intake are children, pregnant women, nursing mothers, and those prone to seizures, headaches or migraines. If you don’t fall into one of those groups, then you probably shouldn’t be worried about opting for diet soda instead of regular soda.
Our eighth issue of the Examine.com Research Digest is finally out and this month we dive into gut health, vitamin K2 and yet another study on meal-timing.
June’s sneak peek breaks down a recent trial on probiotics and how it might improve cognitive reactivity.
Serious about nutrition? Subscribe now for the latest in nutrition research.
With our recent hiring call, we thought it would be useful to our readers and fans to understand exactly how we hire. With over 500 applicants, it's important we do it right.
While we are not an organization that puts a lot of weight into a resume, the resume and cover letter is important to us as it lets us understand the background a person is coming from. It is most important to us that we work with people who are well-rounded individuals and have relevant experience in the field. It's easy to say "I'm passionate about nutrition," but experience helps you understand and appreciate the nuances and nitty gritty that self-interest does not always expose.
Once we have been able to discern who the potential candidates are, we then operate on a very simple premise: show us your abilities.
We are not interested in how well someone interviews, or how amazing their resume looks, or the full sequence of credentials found after their name. We care about the work you can do.
For a copyeditor, we may give them something a researcher has recently written that needs to be cleaned up and made reader-friendly. For a researcher, we'll send over a study and say "analyze this study." A subject matter expert would be given a few documents and say "make notes on anything that stands out."
None of what we send over is written up specifically for them. We always assign actual work. So if we gave a copyeditor something to clean up, it's something we recently completed and have also cleaned up (we just have not published it). So not only is it real work, it lets us compare and contrast with the work we're already producing.
One important step we do take is that there is always a middlewoman (more specifically, Carolyn, our Director of Ops) between the applicants and the rest of our team. Carolyn then anonymizes all of the applicants so that our team that reviews the work has no clue who they are reviewing. This is our way of ensuring that we remain as unbiased as possible - no consideration for friendship, for gender, for race, for name, for anything.
We care for just the work.
Once we have received completed work, an internal team goes over the work, and judges it based on a variety of criteria, including depth, nuance, clarity, brevity, and more. Comments and concerns are also included by each team member. This information is then passed onto Carolyn and Kamal (our Director), to make the call on which applicants are still under consideration.
It is through this iterative process that we are able to select the best candidates and make sure that Examine.com continues to deliver the highest quality analysis for everyone!
We’re lucky to be in a position where we don’t have any sponsors or donors or advertisers to make happy. It’s what lets us be unbiased. Unfortunately, most people do have to worry about the influence of money.
Andy Bellatti has been raising the siren on the cosy relationship between industry and researchers for a while, and he has a must-read article (from the latest issue of our Examine.com Research Digest).
Click here to read "How the food industry spins science to fit its agenda" now.
A lot of people think food is pretty straightforward when it comes to improving how you feel. Just pick your favorite meal, maybe grab a beer or glass of wine, and go to town! Unfortunately, it’s not so simple.
A favorite meal or snack will definitely perk you up for a bit, but the effect won’t be as long-lasting, consistent, or healthy as incorporating a variety of vitamins and minerals into your regular diet. There are even some foods that have natural stress-reducing effects, making them a great way to improve mood without resorting to comfort food.
Zinc and Magnesium are both indirectly associated with improved mood. Studies show that people with depression tend to have lower magnesium levels than people without depression. Some antidepressants, like amitriptyline and sertraline, actually increase magnesium levels in red blood cells. There is animal evidence to suggest a lack of magnesium in the diet is associated with increased anxiety and symptoms of depression, but more research is needed to confirm this kind of direct relationship in people.
Bananas, dark leafy green vegetables, nuts, seeds, avocados, and dark chocolate are good sources of magnesium.
Zinc does not have an antidepressant effect by itself, but it increases the effectiveness of antidepressant effects from other food and supplements. Meat, eggs, legumes, and oysters are high in zinc.
To supplement zinc, take 25 – 30 mg a day, with a meal. Zinc supplementation does not improve mood when supplemented by people suffering from clinical depression.
Need help with your sleep? A great way to avoid feeling tired during the day is a good night's rest, but for most of us, that might be easier said than done. Chamomile (Matricaria recutita or Chamomilla recutita) has traditionally been used for its relaxing and calming effect. It is often brewed into a tea. Two double-blinded studies have shown chamomile to be effective for people struggling with anxiety and troubled sleep, though more research is needed to determine the mechanism for this effect.
Another option for fighting fatigue is supplementing with Ornithine. Ornithine is an amino acid that can alleviate fatigue associated with elevated ammonia levels. Ammonia buildup can be the result of prolonged exercise or long work hours. Several liver disorders, like hepatic encephalopathy, are also associated with high levels of ammonia.
To supplement ornithine, take 2 – 6 grams a day. People with normal ammonia levels will not benefit from ornithine supplementation.
If stress seems to be the root of your problems, supplementing Rhodiola Rosea and Ashwagandha might help. Both these supplements are adaptogen compouds. Adaptogens desensitize the body to stress before it occurs and can alleviate depression, mood swings, and irritability. More specifically, rhodiola rosea has been specifically shown to prevent and relieve burnout caused by stress. Ashwagandha is well-tested and has been shown to be effective for athletes, as well as people suffering from social anxiety.
Daily doses of 50 mg of Rhodiola rosea have been shown to be effective at fighting daily fatigue. To supplement Rhodiola rosea in preparation for a specific stressful event, take 288 – 680 mg. Do not exceed 680 mg, as higher doses have been shown to be ineffective. To supplement ashwagandha, take 300 – 500 mg, with breakfast, in preparation for a stressful day.
Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are omega-3 fatty acids. These fatty acids are associated with a variety of health benefits, and preliminary evidence suggests treatment-resistant depression is associated with a low concentration of EPA in the brain.
Fish Oil, derived from fatty fish like salmon, sardines, tuna, mussels, and trout, is high in EPA and DHA. Fish oil supplementation has been shown to be effective at reducing symptoms of depression, specifically when taken by people suffering from major depression. People that eat a lot of fatty fish don’t need to supplement fish oil. Algae is the best alternative for vegetarians and vegans.
Tryptophan is an amino acid that the body uses to produce serotonin, a neurotransmitter responsible for maintaining mood. Low levels of serotonin are one of the contributing factors to depression. Poultry, seafood, nuts, seeds, dairy, and legumes are all good sources of tryptophan.
Another option for improving serotonin levels is supplementing 5-HTP, the precursor to serotonin. However, eating food that contains tryptophan will enable slower, more prolonged production of serotonin, compared to the rapid production associated with 5-HTP supplementation. Supplementation of tryptophan is not as effective as 5-HTP supplementation.
To supplement 5-HTP, take 300 – 500 mg a day. Do not take 5-HTP if you are taking any neurological drug or antidepressant. High levels of serotonin are very dangerous and potentially lethal.
St. John’s Wort is a well-researched herbal antidepressant, comparable in strength to pharmaceutical alternatives like tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs). Do not supplement St. John’s Wort if you are taking antidepressants like SSRIs, SNRIs, or MAOIs. St. John’s Wort increases serotonin signaling in the brain and, like 5-HTP, can result in an overdose if taken alongside medication.
Agmatine is a neurotransmitter that works synergistically to increase the effects of other antidepressant compounds, including bupropion, SSRIs, adenosine, imipramine, and folic acid. Agmatine does possess some antidepressant effects, but they are weaker than comparable reference drugs, like imipramine.
Before supplementing a compound to alleviate symptoms of depression, talk to your doctor.
Comfort foods tend to be loaded with sodium and packed with calories, without a lot of nutrients to show for them.Don’t give in to the temporary pick-me-up, no matter how tempting it is. Instead, evaluate your weekly diet to determine if you could include some additional healthy foods that will also improve your day-to-day mood.
Change your diet one step at a time. Start by adding a dark, leafy salad to your lunch, or replace burger night with fish night. As you change your diet, take note of your mood. Taking the time to track results will help you stick to your goals.
Supplementation should be the last step in a dietary overhaul. Eating better food to become a happier person is cheaper, delicious, and more effective than supplementation.
If you’re a marathoner (or training to be one), you may have noticed that many popular supplements intended to improve your physical performance, fall flat when used during endurance events. Pre-workout supplements and stimulants, for example, don’t work because a marathon typically lasts longer than the stimulant itself, leaving you crashing mid race. Even Creatine, a supplement used to improve physical performance, is counterproductive because it results in temporary water weight gain, which makes running harder.
Carbohydrate supplements however, are far more effective than traditional physical performance enhancers. Gel packs, or energy gels, are ideal for improving marathon performance because they are easy to ingest during a race.
So what makes gel packs so effective? Runners talk about eating a big bowl of pasta the night before a race because “carb-loading” is a good way to increase glycogen levels. A lot of glycogen is used in the first 10 minutes of exercise, and the rate of glycogen use falls until it is depleted altogether.
Have you ever ‘hit the wall’ during a marathon?
Glycogen depletion is responsible for that feeling. Eating a lot of carbohydrates the night before might delay the wall, but it won’t necessarily prevent it altogether. This is why energy gels are an ideal way to get mid-race carbohydrates. They are dense and viscous, which reduces the risk of intestinal upset, even during exercise. Plus, they’re light and portable, which means you can carry them with you or easily snag a few from an aid station. Just don’t forget to properly dispose of the wrapper!
A recent study investigated whether energy gel supplementation in the middle of a race can help delay or prevent hitting the wall during a marathon. Researchers split non-elite marathon runners into two groups. One group was provided energy gels containing 20 grams of carbohydrates and 30 milligrams of caffeine (equivalent to one cup of tea), and were told to eat two before the race, one when they believed they had hit the wall, and another every 20 minutes afterward. The runners in the second group were left to fend for themselves. Researchers also monitored the water intake of both groups.
The results show that the energy gel group was able to maintain its speed throughout the marathon, while the control group began to drop off around the halfway point. Though both groups were running at about the same speed at the beginning of the marathon, researchers found significant differences at the last three checkpoints of the race, beginning at the 18 mile mark.
The runners supplementing energy gels averaged a completion time of 3:38.31 while the control group had an average completion time of 3:49.26. Energy gel supplementation was found to improve time by just over 10 minutes, or by about 5%.
Runners having trouble with energy levels or anxious about hitting ‘the wall’ for the first time can consider energy gel supplementation to improve their time and avoid getting hit by a ton of bricks.
Never try anything for the first time during a race. If energy gels sound right for you, try taking one or two during a long training run. You don’t want to find out gels disagree with you when you’re lining up at the starting line.