Monday, 31 July 2017
Source: HealthDay via Exercise and Physical Fitness New Links: MedlinePlus RSS Feed Read More Here..
Sunday, 30 July 2017
Saturday, 29 July 2017
Friday, 28 July 2017
"Drinking a moderate amount of certain drinks such as wine three to four times a week reduced diabetes risk by about 30%," The Guardian reports. That was the main reported finding of a Danish study looking at the impact of alcohol on diabetes risk.
Researchers looked at a group of more than 70,000 people who had completed a survey about their health and lifestyle in 2007-2008, which included questions about their drinking habits. They then checked whether any of the participants had been diagnosed with diabetes (either type 1 or 2) about four years after completing the survey, and looked at survey data for these people.
The researchers noticed a pattern that suggested people who developed diabetes were less likely to have drunk alcohol moderately and frequently compared with those who did not develop diabetes. The researchers reported that the lower risk for diabetes was associated with 14 units per week for men and seven units for women (current recommendations are that men and women shouldn't regularly drink more than 14 units per week).
However, the study had various weaknesses, which means it cannot conclusively show that drinking frequently and moderately protects against diabetes. For example, people were only asked about their drinking habits and other lifestyle choices at a single time point. Also, the study doesn't tell us whether those habits changed over the period in which people were monitored for diabetes.
Even if an association does exist, there are far healthier ways to reduce your diabetes risk, such as achieving or maintaining a healthy weight.
Where did the story come from?
This study was an analysis of data from the general Danish population that had been recorded in a previous cohort study. This particular piece of research was carried out with no specific funding, but the survey data had been funded by the Ministry of the Interior and Health, and the Tryg Foundation. It was published in the peer-reviewed journal Diabetologia.
The suggestion that regularly drinking alcohol may be good for you was met with glee by the UK media. The limitations of the study, or the lack of a definitive cause and effect, were not reported fully.
However, some sources carried sensible advice from independent experts, such as Dr Emily Burns, the head of research communications at Diabetes UK, who was quoted in The Guardian as saying: "While these findings are interesting, we wouldn't recommend people see them as a green light to drink in excess of the existing NHS guidelines, especially as the impact of regular alcohol consumption on the risk of type 2 will be different from one person to the next."
There were several reports that wine was particularly beneficial because it has "a role in helping to manage blood sugar", but this was based only on the authors' comments rather than on the results of the research.
What kind of research was this?
This cohort study assessed people for diabetes in 2012 about four years after their lifestyles had been assessed in 2007-2008. The researchers aimed to examine whether there was any association between alcohol drinking patterns and the risk of developing diabetes in people who did not already have the condition. They looked at the amount that people drank, how often they drank, and what types of alcohol were consumed.
The study benefitted from involving a large number of people in the Danish population, which meant a range of drinking patterns were found, and there were sufficient numbers of cases of diabetes to look for associations.
However, a major weakness of the study was that it only looked at alcohol drinking patterns at a single point in time. And people's drinking habits are known to change over time according to their circumstances, preferences and other health issues.
The researchers did attempt to take into account other confounding factors (such as diet and exercise) that may have influenced the results, but these factors may not have been recorded in enough detail to be useful, and other factors might not have been recorded at all.
What did the research involve?
The researchers identified 70,551 people from the Danish Health Examination Survey (an ongoing nationwide study) who were eligible to participate. These people had already completed a questionnaire in 2007-2008 about their lifestyle and health. People had to meet the following criteria to be selected for participation:
- no existing diagnosis of diabetes at the start of the study
- not pregnant and haven't recently given birth (within the last six months)
- have provided at least some information about their drinking habits in the questionnaire
Information about drinking patterns was collected from questionnaires that people completed by themselves on how often they drank, whether they ever binged and how often this happened, and how much they drank different types of drinks (beers, wines or spirits).
The researchers also looked at information that had been collected at the start of the study on the following confounding factors:
- body mass index
- smoking status
- leisure-time physical activity
- high blood pressure (current or previous)
- family history of diabetes
A diagnosis of diabetes was recorded using the Danish National Diabetes Register, which uses five different sources to detect diabetes cases, but does not distinguish between type 1 and type 2. During the course of the study the researchers carried out a "sensitivity analysis", where they excluded two of the diabetes cases because of concerns the data was unreliable.
The participants were followed up in the study until it ended in December 2012, unless they emigrated, died or developed diabetes before then. The researchers carried out an analysis that looked at the risk of developing diabetes over time, taking into account different risk factors. They used appropriate statistical methods for dealing with missing data.
What were the basic results?
During the course of the study, 859 men and 887 women developed diabetes. When looking at the average amount that people drank over the course of a week, they found that the lowest risk of diabetes was observed in:
- men who drank 14 drinks a week (Hazard ratio [HR] 0.57, 95% Confidence Interval [CI] 0.47 to 0.70)
- women who drank nine drinks a week (HR 0.42 (95% CI 0.35 to 0.51))
Frequency of drinking
After adjusting for other factors, the researchers reported the consumption of alcohol on three to four days a week was associated with a lower risk of developing diabetes for men: HR 0.73 (95% CI 0.59 to 0.94) and for women: HR 0.68 (95% CI 0.53 to 0.88).
The researchers also looked at binge drinking and found no clear link between binge drinking and risk of diabetes.
Type of alcohol
Researchers noticed a number of patterns in terms of what types of alcohol people drank.
Men who drank 1-6 glasses of beer a week were found to have lower diabetes risk than those who did not.
In contrast, women who regularly drank spirits seven or more times a week had an increased risk of diabetes compared with those who drank spirits once a week or less. However, the researchers failed to take into account that some people drink a mixture of different types of alcohol either on a single occasion or over a week.
How did the researchers interpret the results?
The authors concluded that "light to moderate" alcohol consumption was associated with a lower risk of diabetes when compared to no alcohol consumption at all. They also noted that frequent consumption was associated with the lowest risk, even after taking into account the amount people drank on average during a week.
They noted that the strengths of their study included its size, the fact that they distinguished between people who currently didn't drink from those who had never drunk at all, and that their results were consistent even when they adjusted various conditions.
Although this study found an interesting association between alcohol drinking habits and risk of developing diabetes, this study does not present strong enough evidence to recommend adopting a particular drinking pattern to reduce diabetes risk.
This study had a number of limitations that weaken confidence in the results:
- People were only asked about their drinking habits and other risk factors at a single time point. The study doesn't tell us whether those habits changed over the period in which people were monitored for diabetes. Most studies related to alcohol consumption also run the risk that people are not always completely accurate when describing what and how much they drink.
- The way diabetes cases were recorded for the study did not distinguish between type 1 and type 2 diabetes, even though these conditions have different causes and treatments.
- The study only followed people up for an average of just under five years, whereas a condition like diabetes may develop due to risk factors experienced over a longer period.
- The information collected on diet may have been too simplistic to properly allow an understanding of how nutrition may also affect the diabetes risk of the people in the study.
- Although the researchers excluded people from the study if they already had a diagnosis of diabetes at baseline, they didn't exclude people if they had other chronic health conditions, some of which may contribute to diabetes risk. The only other condition that was considered in the analysis was high blood pressure.
Overall, it is unclear whether the link between moderate alcohol drinking and diabetes is real. It is not proof that starting to drink more, especially for those who do not currently drink, is useful in preventing diabetes. There are other risks, such as liver damage, to consider when drinking frequent or large volumes of alcohol above recommended limits.
If you are concerned that you might be at risk of developing diabetes, speak to your GP about the ways that lifestyle change can reduce your risk.
Links To The Headlines
Regular alcohol consumption could cut diabetes risk, study finds. The Guardian, July 28 2017
Drinking a few times a week 'reduces diabetes risk'. BBC News, July 28 2017
Drinking alcohol three to four days a week 'could reduce risk of diabetes'. The Independent, July 28 2017
Drinking most days may protect against diabetes - new study. The Daily Telegraph, July 28 2017
Drinking alcohol regularly could cut diabetes risk - and red wine is your 'healthiest' option. Daily Mirror, July 28 2017
Links To Science
Holst C, Becker U, Jørgensen ME, et al. Alcohol drinking patterns and risk of diabetes: a cohort study of 70,551 men and women from the general Danish population. Diabetologia. Published online July 27 2017
Social behavior is important for our survival as a species. But social interaction also gives pathogens a chance to spread, and it thereby increases our exposure to infection. Our immune system is a complex defense system that has evolved to protect us from infections. Therefore, it makes sense to assume that our immune system must have developed ingenious strategies to protect us from new pathogens to which social interaction has exposed us.
Evidence of a link between the immune system and our social behavior has been accumulating in the last years. A direct connection between the brain and the immune system, through lymphatic vessels in the meninges, was recently revealed. Then it was shown that the immune system can directly affect, and even control social behavior and the desire for social interaction – an impaired immunity was shown to induce deficits in social behavior. This sounds like a clever preventive self-defense mechanism designed to avoid contagion – in times of poor immunity, our brain gets the message to reduce social interaction and, consequently, exposure to pathogens.
This is a self-defense mechanism that is activated when our body signals a poor immunological status; it’s an internal chemical communication system. But is there an external threat signaling system? The ability to detect and avoid infected individuals would clearly be a great evolutionary asset in strengthening our protection mechanisms. Many animals can detect sickness via odors, leading to a restraint in social interaction, most likely intended to reduce exposure to disease. Do humans have a similar sensory sickness detection system, something that allows us to detect infectious threat in others?
To answer this question, a new study aimed at determining whether humans can detect sickness in others from visual and olfactory cues. Sickness was experimentally induced through the injection of lipopolysaccharide (LPS), a molecule found in the membrane of Gram-negative bacteria that provokes robust immune responses. The activation of immune responses leads to an increase in the production of pro-inflammatory molecules that activate sickness responses and behaviors. It is known that visual cues of sickness, such as redness of the skin, allow us to infer the health of others. But although LPS induces a strong sickness response, its observable effects are subtle, and odor cues are difficult to perceive.
Photos of the face and samples of body odors of both sick and healthy individuals were presented to a group of naïve participants while their cerebral responses were recorded using fMRI. These participants were not aware that they would be seeing and smelling sick and healthy people. They were asked to focus on the faces while the odors were also presented and rate how much they liked the person. Faces were also rated on attractiveness, health, and desired social interaction, and odors were rated on intensity, pleasantness and health. This allowed the assessment of the “liking behavior” towards the faces, an indication of the will to approach and interact with others.
The rating of sick and healthy faces showed that photos obtained during acute sickness were generally considered less attractive, less healthy, and less socially desirable than the faces of participants receiving the placebo treatment. When faces were presented concomitantly with an odor, there was a lower liking of sick than of healthy faces, regardless of the odor presented with the face. Although participants were not able to perceive sickness in the odors, nor did they rate sick odors as more unpleasant or more intense than healthy odors, faces, regardless of being sick or healthy, were also less liked when paired with sick body odor.
These results show that we can detect early and subtle signs of sickness in others from both facial and olfactory cues, even just a couple of hours after activation of their immune system. Moreover, fMRI data revealed that visual and olfactory sickness cues activated their respective visual face processing and olfactory sensory cortices, as well as multisensory convergence zones. And even though odors were often too weak to be consciously detected, these olfactory sickness cues still led to activation of the olfactory cortex.
The study also revealed that this perception of subtle cues of sickness leads to reduced liking and decreased will for social interaction. This response may represent a human behavioral defense system against disease. The integration of olfactory and visual sickness cues in the brain may be part of a mechanism designed to detect sickness, resulting in behavioral avoidance of sick individuals, and in avoidance of impending threats of infection.
Filiano AJ, et al (2016). Unexpected role of interferon-? in regulating neuronal connectivity and social behaviour. Nature, 535(7612):425-9. doi: 10.1038/nature18626
Kipnis J (2016). Multifaceted interactions between adaptive immunity and the central nervous system. Science, 353(6301):766-71. doi: 10.1126/science.aag2638
Louveau A, et al (2015). Structural and functional features of central nervous system lymphatic vessels. Nature, 523(7560):337-41. doi: 10.1038/nature14432
Regenbogen C, et al (2017). Behavioral and neural correlates to multisensory detection of sick humans. Proc Natl Acad Sci U S A, pii: 201617357. doi: 10.1073/pnas.1617357114. [Epub ahead of print]
Shattuck EC, Muehlenbein MP (2015). Human sickness behavior: Ultimate and proximate explanations.Am J Phys Anthropol, 157(1):1-18. doi: 10.1002/ajpa.22698.Read More Here..
Thursday, 27 July 2017
On World Hepatitis Day, WHO is calling on countries to continue to translate their commitments into increased services to eliminate hepatitis. This week, WHO has also added a new generic treatment to its list of WHO-prequalified hepatitis C medicines to increase access to therapy, and is promoting prevention through injection safety: a key factor in reducing hepatitis B and C transmission. via WHO news Read More Here..
Wednesday, 26 July 2017
Magnesium is everywhere – it does not occur free in nature, only in combination with other elements, but it is the eighth most abundant chemical element in the Earth’s crust and the third most abundant element in seawater; it is even the ninth most abundant in the Milky Way. In the human body, magnesium is the fourth most abundant ion and the eleventh most abundant element by mass, being stored in bones, muscles, and soft tissues.
Magnesium is fundamental for health: it is essential to all cells and to the function of hundreds of enzymes, including enzymes that synthesize DNA and RNA, and enzymes involved in cellular energy metabolism, many of which are vital. Magnesium is involved in virtually every major metabolic and biochemical process in our cells and it plays a critical role in the physiology of basically every single organ.
Low plasma levels of magnesium are common and are mostly due to poor dietary intake, which has lowered significantly in the last decades. Magnesium can be found in high quantities in foods containing dietary fiber, including green leafy vegetables, legumes, nuts, seeds, and whole grains. But although magnesium is widely distributed in vegetable and animal foods, some types of food processing can lower magnesium content up to 90%. Also, the soil used for conventional agriculture is becoming increasingly deprived of essential minerals. In the last 60 years, the magnesium content in fruit and vegetables has decreased by around 20 to 30%.
Symptomatic magnesium deficiency due to low dietary intake in healthy people is not very frequent, but a consistently poor dietary supply of magnesium has insidious effects. Magnesium deficiency alters biochemical pathways and increases the risk of a wide range of diseases over time, namely hypertension and cardiovascular diseases, metabolic diseases, osteoporosis, and migraine headaches, for example.
In the brain, magnesium is an important regulator of neurotransmitter signaling, particularly glutamate and GABA, the main neurotransmitters by modulating the activation of NMDA glutamate receptors and GABAA receptors. It also contributes to the maintenance of adequate calcium levels in the cell through the regulation of calcium channels’ activity.
These physiological roles make magnesium an essential element in important neuronal processes. Magnesium participates in the mechanisms of synaptic transmission, neuronal plasticity, and consequently, learning and memory. Accordingly, increased levels of magnesium in the brain have been shown to promote multiple mechanisms of synaptic plasticity that enhance different forms of learning and memory, and delay age-related cognitive decline. Increased levels of magnesium in the brain have also been linked to an increased proliferation of neural stem cells, indicating that it may promote the generation of new neurons (neurogenesis) in adulthood. This is an important feature because neurogenesis is a key mechanism in the brain’s structural and functional adaptability, in cognitive flexibility, and in mood regulation.
Magnesium supplementation has also been shown to modulate the neuroendocrine system and to improve sleep quality by promoting slow wave (deep) sleep, which, among many other functions, is also important for cognition and memory consolidation.
Furthermore, magnesium may enhance the beneficial effects of exercise in the brain, since it has been shown to increase the availability of glucose in the blood, muscle, and brain, and diminish the accumulation of lactate in the blood and muscles during exercise.
But just as increasing magnesium levels can be beneficial, magnesium deficiency can have serious harmful effects.
Magnesium has important roles in the regulation of oxidative stress, inflammatory processes and modulation of brain blood flow. In circumstances of magnesium deficiency, all of these functions can potentially be dysregulated, laying ground for neurological disorders. Also, in a context of low magnesium availability in the brain, NMDA glutamate receptors, which are excitatory, may become excessively activated, and GABAA receptors, which are inhibitory, may become insufficiently activated; this can lead to neuronal hyperactivity and to a condition known as glutamate excitotoxicity. This causes an excessive accumulation of calcium in neurons, which in turn leads to the production of toxic reactive oxygen species and, ultimately, to neuronal cell death.
Magnesium deficiency has been associated with several neurological and psychiatric diseases, including migraine, epilepsy, depression, schizophrenia, bipolar disorder, stress, and neurodegenerative diseases. Magnesium supplementation has shown beneficial effects on many of these conditions, as well as in post-stroke, post-traumatic brain injury, and post-spinal cord injury therapies. This therapeutic action is likely due to its action in blocking NMDA glutamate receptors and decreasing excitotoxicity, in reducing oxidative stress and inflammation, and in increasing blood flow to the brain, all of which are determinant in the outcome of these conditions.
There are multiple benefits to be obtained from magnesium, both from a health promotion, and from a disease prevention and management perspective. The recommended daily intake of magnesium is of 320mg for females and 420mg for males. Too much magnesium from food sources has no associated health risks in healthy individuals because the kidneys readily eliminate the excess. However, there is a recommended upper intake level for supplemental magnesium, since it can cause gastrointestinal side effects. So, keep it below 350mg/day.
Chen HY, et al (2014). Magnesium enhances exercise performance via increasing glucose availability in the blood, muscle, and brain during exercise. PLoS One, 9(1):e85486. doi: 10.1371/journal.pone.0085486
de Baaij JH, et al (2015). Magnesium in man: implications for health and disease. Physiol Rev, 95(1):1-46. doi: 10.1152/physrev.00012.2014
Held K, et al (2002). Oral Mg(2+) supplementation reverses age-related neuroendocrine and sleep EEG changes in humans. Pharmacopsychiatry, 35(4):135-43. doi: 10.1016/j.pbb.2004.01.006
Jia S, et al (2016). Elevation of Brain Magnesium Potentiates Neural Stem Cell Proliferation in the Hippocampus of Young and Aged Mice. J Cell Physiol, 231(9):1903-12. doi: 10.1002/jcp.25306
National Institutes of Health, Office of Dietary Supplements. Magnesium Fact Sheet for Health Professionals
Slutsky I, et al (2010). Enhancement of learning and memory by elevating brain magnesium. Neuron. 2010 Jan 28;65(2):165-77. doi: 10.1016/j.neuron.2009.12.026Read More Here..
Statement by UNICEF Executive Director, Anthony Lake, WFP Executive Director, David Beasley and WHO Director-General, Dr. Tedros Adhanom Ghebreyesus, following their joint visit to Yemen
Tuesday, 25 July 2017
Monday, 24 July 2017
The use of smart drugs is becoming “trendy”. Lots of people are taking various substances regularly, many others try them from time to time. The idea of enhancing the brain’s ability, or tapping into its unused reservoir is definitely sexy, and many people are actively looking for information on this subject.
The shortage of scientifically verified information is exactly the reason I’m writing this article. Although thousand of publications on “smart drugs”, “cognitive enhancers”, and “nootropics” etc. can be found online, the overwhelming majority of claims are unsubstantiated or unashamedly commercialized. This means that the info you come across mostly consists of descriptions of personal opinions or experiences, or compilations of facts published elsewhere, or just articles from popular media where people can write whatever they want.
Multiple websites publish all kind of rubbish just to convince you to buy yet another wonderfully effective smart drug. Few people make an effort to refer to their sources of information, not to mention to present scientific and statistical data backing their claims. This is particularly enigmatic when these articles provide recipes for various drug combinations and claim the superiority of some of these combinations/compounds over the others. However, even scientific data on the subject is rather incomplete. Many studies were done using only a small number of participants, or in the absence of any reasonable controls. On their own, studies of such kind are of little, if any, value.
Fortunately, several systematic reviews and meta-analyses on the use of nootropics were published in the last couple of years. Systematic reviews and meta-analyses combine data from multiple individual studies, thus making the data statistically significant. This is a better way of assessing the efficacy of different drugs in the general, healthy population, and these are the publications that I will mostly use as reference points in this article.
How to prove that a smart drug is really smart?
Smart drugs (e.g., nootropics and cognitive enhancers) are defined as substances that improve cognitive function, particularly executive functions, memory, creativity, or motivation, in healthy individuals. The last bit is important: there are many drugs that were specifically developed to enhance brain functions in people with various cognitive disorders or deficits. Such drugs won’t necessarily smarten up healthy people, and when they do, they are not necessarily safe. Nootropics may come in many forms, from classical pharmaceutics in the form of pills to herbal supplements and “functional foods”.
There are only few smart drugs that are proven to improve some aspects of cognition. Proving that a compound has the properties of a nootropic is not a simple task. There is no straightforward way of measuring whatever cognitive enhancement you may experience once the pill is taken. The drug may indeed work and visibly increase your productivity. But it may also simply improve your mood if you anticipate a positive effect. On top of this, any given drug may work for some people and not work for others. Furthermore, the use of any drug is associated with potential side effects (e.g., headaches) that might eliminate its advantages in productivity and creativity. If the changes in productivity can be measured using some tests, creativity still remains something arguably impossible to quantify.
How smart drugs work?
There are several mechanisms that can be involved in the functioning of smart drugs. Some drugs can increase the blood flow (and thus oxygen supply) to the brain. Others can accelerate neuronal communication through increased release of certain neuromediators or through agonistic effects on the receptors of these neuromediators. Some compounds can serve as biochemical precursors of neuromediators, others may prevent oxidative damage to brain cells or provide them with a source of energy. Some of these changes can be achieved quickly making the drugs work almost instantly. Others, such as amendment/prevention of neuronal damage, manifest themselves only after prolonged use of the drug, thus making any changes in cognitive functions not so fast and not so obvious (although they can still be substantial).
Short overview of most popular nootropics
Amphetamines are a class of pharmaceuticals that include adderall, dextroamphetamine, and lisdexamphetamine. The drugs were developed to treat people with ADHD (attention deficit hyperactivity disorder) and this is where their effects are the most prominent. The drugs were also demonstrated to improve episodic memory, working memory, and some aspects of attention in the general population. At low doses they improve memory consolidation, recall of information, and motivation to perform tasks that require high degree of attention. Ritalin is structurally different from amphetamines and works through different mechanisms, although produces similar effects. Both amphetamines and ritalin improve cognitive functions, albeit only at lower doses. At high doses they stimulate other neural pathways not involved in learning that effectively cancel their positive effects on cognition.
Wakefulness-promoting agents, such as modafinil and armodafinil, increase alertness, counteract fatigue, and increase productivity and motivation. Modafinil is praised for its ability to improve reaction time, logical reasoning, and problem-solving. The drug is clinically prescribed for a number of conditions including sleep apnea, narcolepsy, and shift work sleep disorder.
Compounds from the racetam family (piracetam, oxiracetam etc.) are more extensively studied compared than the newer nootropics. Piracetam was developed back in the 1960s and has an almost perfect safety profile. Convincingly, it was shown to improve cognitive abilities, particularly in older people and those with cognitive impairment. Although piracetam is officially recognized as a nootropic, its brain-enhancing effects in healthy people are considered to be moderate. There is a number of other derivatives from this group of drugs which, allegedly, work better. A good example is phenotropil. This compound was developed in Russia where it is available as a prescription drug. It was demonstrated to have a memory enhancing effect. The drug can be used as a stimulant and enhances resistance to extreme temperatures and stress. Due to its stimulating effect, phenotropil is banned by the World Anti-Doping Agency, which means that it cannot be used by athletes intending to compete in official events.
Xanthines, such as caffeine, are some of the most commonly used compounds with nootropic effects. In particular, they increase alertness and performance levels. Caffeine is not what comes to mind when we think of nootropics, but apparently its effect is comparable to many pharmaceuticals.
L-Theanine, a chemical component of green tea, is very well studied and its effects on promoting alertness and attention are confirmed by multiple research.
When it comes to nutraceuticals and herbal supplements, recent studies appear to be contradictory. Some data do support the memory-enhancing effects of such plants as Gingko biloba, Asian ginseng, and Bacopa monnieri, but systematic reviews do not find convincing evidence of their effectiveness. It is likely that herbal supplements may work well over longer periods of time and improve cognitive abilities, but in the short term their effects are not particularly obvious. The same applies to many vitamins, such as vitamin E and B group vitamins, as well as Omega-3 fatty acids: the evidence supporting their benefits are limited at the present time.
To conclude, only few drugs are scientifically proven to be associated with moderate cognitive enhancement effects in the healthy population. Being sceptical when assessing information on smart drugs from the internet is a good idea: lots of ridiculous rubbish is published online. Most nootropics are relatively safe, but side effects are always a possibility since the response to nootropics is highly individual.
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Urban KR and Gao WJ (2014) Performance enhancement at the cost of potential brain plasticity: neural ramifications of nootropic drugs in the healthy developing brain. Front. Syst. Neurosci.| doi: 10.3389/fnsys.2014.00038
Winblad B (2005) Piracetam: a review of pharmacological properties and clinical uses. CNS Drug Rev. 11, 169-182. PMID:16007238
Zvejniece L et al. (2011) Investigation into Stereoselective Pharmacological Activity of Phenotropil. Basic & Clinical Pharmacology & Toxicology 109, 407–412. doi: 10.1111/j.1742-7843.2011.00742.x
Rogers PJ (2007) Caffeine, mood and mental performance in everyday life. Nutrition Bulletin 32, 84–89. doi: 10.1111/j.1467-3010.2007.00607.x
Camfield DA et al. (2014) Acute effects of tea constituents L-theanine, caffeine, and epigallocatechin gallate on cognitive function and mood: a systematic review and meta-analysis. Nutr Rev 72, 507-522. DOI: https://doi.org/10.1111/nure.12120Read More Here..