No, I haven’t received my doctorate yet (that won’t be happening for awhile!) Instead my rogue bastardized blogging days are over – I’ve been made an official Nature Publishing Group blogger, writing for the Nature Education site Scitable. I’ll be blogging on all things brain and biology on the psychology group blog, Mind Read, with the fantastic Jordan Gaines of Gaines, on Brains. We’ll be posting weekly on the latest nerdy neuro papers and fascinating psychological phenomena – think similar Brain Study content but now on a legitimate platform.

As always though, Brain Study is dearest to my blogging heart, and I’ll be sure to post Mind Read pieces here, as well as trying out slightly “edgier” content perhaps not suitable for the corporate science blogosphere.

My first post is on one of my personal favorite topics, synesthesia, exploring Hearing, Touching and Tasting in Color. A sneak-peek with some insight into my own form is below:

I don’t know about you, but to me Wednesday is sun-shiney yellow. Tuesday is hunter green, Thursday purple-ish blue and Friday a deep red. Monday is white, a blank slate and a chance for a new week, whereas Saturday is sparkly black. Sunday is gray, the depressing slouch towards the beginning of the work-week, but also a convenient mix of Saturday and Monday.

This color-word association is not a figment of my imagination or an indication that I’m going crazy, but is instead a recognized neuropsychological phenomenon called synesthesia.

So please check out the new site, and let me know what you think!

And now it turns out that hormonal contraception, or The Pill, our revolutionary defense against the inherent misogyny of biology, could be tricking us into choosing the wrong men.

Two studies led by Dr. Craig Roberts from the University of Stirling in Scotland have suggested that taking oral contraception can change your attraction to and preferences for men. In an initial study, Dr. Roberts and his team asked women who were about to go on the pill to rate the attractiveness of a selection of male faces, considering them as both short-term and long-term partners. They were then tested again approximately three months later to see if their preferences had changed. Sure enough, in the second test session women who had started hormonal contraception had significant shifts in their partner preferences, now preferring significantly less masculine-looking faces than they had three months earlier. Conversely, control women who had not started the pill did not differ in their choices from the first session.

In a follow-up study, real couples who had met while the woman was either on or off the pill were assessed for the male partner’s masculinity. This involved complex photo manipulation and judgment of the pictures by outside individuals, who ranked the male faces on features of masculinity. Though these methods are a bit fuzzy and convoluted, the researchers’ results (surprise surprise) matched those of the first study. That is, male partners of women who were already on the pill when they met were judged to be significantly less masculine looking than men whose female partners were not taking hormonal contraception.

Notable masculine features include squarer face-shapes, stronger jawlines and less prominent cheekbones, all of which are typical signifiers of higher levels of testosterone. The authors claim that this shift to preferring less masculine features is perhaps a transition towards subconsciously choosing more faithful or nurturing partners after starting contraception, which can be beneficial for long-term relationship success. However, a major problem with these partner preference shifts is that presumably at some point during a mature, adult, monogamous relationship women go off their contraception, potentially reversing back their partner preferences. This can lead to dissatisfaction in the relationship, female philandering, and some very awkward conversations: ”Sorry honey, you used to do it for me, but now I find you much too feminine for my liking.”

Another major concern is that genetically we are supposed to be drawn towards mates who are more dissimilar to ourselves. This is evolutionarily advantageous, as greater parental genetic variability reduces the likelihood of heritable diseases in the offspring. Basically, your children are less likely to be born with a genetic disorder if you and your partner’s DNA are more different. It has been proposed that some of the shifts in partner preferences after initiating oral contraception are actually towards men who are more genetically similar to you, which can be problematic, but no theories as to why this might be the case.

However, it’s a pretty big stretch to say that preferring men with slightly rounder faces means you’ve undergone a major change in your list of demands for your partner’s personality and genetic makeup (if you happen to have such a list for that). Also, the first study was only performed with 18 women in the experimental condition, which is a pretty tiny population for measuring significant differences in behavior. So the researchers conducted another follow-up experiment to investigate if these effects mapped onto real-world behavior. Researchers tested 2500 women (a much better sample size) in stable relationships who had started dating their partner while they were either on or off the pill, and compared them on several measures of relationship and sexual satisfaction.

Women who had first met their partners while taking oral contraception scored significantly lower on measures of sexual satisfaction and rated themselves less physically attracted to their partners than those women who had met their partners while not on the pill. However, the women taking the pill did have higher overall relationship non-sexual fulfillment and financial stability than those who were off. And in a related twist, women who were on contraception were actually less likely to have separated from their partners than women not on the pill at ‘partner choice’.

So what’s the take-away from this? Don’t take oral contraception and you’ll have better sex with a more attractive man, but will be more likely to break up with him in the future? Go on the pill and you’ll be dissatisfied sexually by your unattractive mate and your offspring will have genetic disorders, but at least you’ll stay together forever? Maybe. Or maybe being on the pill leads you to choose partners based more on long-term than short-term payouts. Or means that you have different priorities in your partner preferences to begin with. Either way, make the decision wisely, your future children may depend on it.

Just like can we please not place blame on these people because they are Muslim or Christian (or not), can we not claim psychiatric or neurochemical differences as the “reason” why they committed these crimes?

There are millions of people in the world with autism. There are millions of former boxers and football and rugby players who have suffered concussions and do not build bombs. There are billions of us who have successfully passed through adolescence without ever committing an act of terror. So can we please not say that these attributes are the “reasons” why these men have committed these horrendous atrocities?

I fully agree we need better mental health care, better education, better outreach and assimilation to immigrants. But I also believe we need better gun laws to prevent people from having the capacity to commit some of these crimes in the first place. I understand the need to try and find reason behind these acts as they are truly devastating, seeming to stem from a place of pure evil. But let’s not forget that similar atrocities, and worse, are currently being committed around the world in war-torn areas. And placing the blame on a generic mental illness or neurological state, rather than on societal shortcomings or personal perversion, does not help. It only garners distrust and hurts those who do suffer from these illnesses and need help, rather than persecution.

So please, can we just not?

(Thanks to Torey Van Oot for first bringing the boxing article to my attention.)

Yes, fecal matter. That embarrassing brown lumpy bodily expulsion. We learned from an early age that Everyone Poops, and now a recent study has hinted that with the right transfer, somebody else’s poop could help you lose weight.

But let’s not get too far ahead of ourselves and take a look at the real science first. The concept of a personal microbiome, a unique bacterial make-up as individual as our DNA, has been gaining traction over the last few years. Gut bacteria, or ‘microbiota’, have been implicated in everything from food allergies to obesity, with some studies suggesting that these bacteria may account for up to 20% of our differences in body weight. Stool samples are teeming with these microbiota, and previous studies have used fecal transfers to replenish lost essential bacteria that help fight infections after they’ve been wiped out with antibiotics.

Research from scientists at Cedars-Sinai Medical Center in Los Angeles has recently confirmed that some strains of bacteria can contribute to weight gain, helping people to retain and store calories more easily by aiding in the digestion of nutrients. These bacteria appear to make the stomach and intestines more productive, breaking down food faster and more efficiently so that more nutrients and calories can be absorbed. While this may have been beneficial to our hunter-gatherer ancestors, when food was scarce and mostly consisted of difficult-to-digest plants and animals, today it may be contributing to our problems with over-nourishment and obesity. In the current study, people with greater levels of these bacteria, determined either through stool samples or breath tests measuring hydrogen and methane – by-products of this nutrient break-down – had higher BMIs and body fat percentages than those with lower trace products of the bacteria.

But if your breath tastes especially methaney, don’t despair. According to recent research, there are now several ways to change your gut microbiota.

Physicians have long used gastric bypass surgery to aid in weight loss in cases of extreme obesity. The procedure involves removing up to 80% of an individual’s stomach and can result in weight loss of 75% of excess body weight. This dramatic success was initially thought to be driven by the reduction in stomach size, resulting in a lower capacity for consumption and absorption calories. Simply put, the smaller your stomach, the less food you can eat. However, new evidence suggests that a shift in gut bacteria may also aid in this change.

The microbiota of obese people is markedly different from those of lean individuals, contributing to and perpetuating weight problems. This bacterial profile is partly influenced by what we eat, and it turns out that changing the size of the stomach and intestines can also dramatically alter the make-up of these bacteria. A study published in Science Translational Medicine by researchers from Massachusetts General Hospital recently demonstrated this effect in mice, hinting that it also might apply to people.

In the study, animals who had undergone gastric bypass operations showed not only significant weight loss, but also a dramatic change in microbiota, potentially both resulting from and furthering their weight-loss. Notably, this change was larger and more stable in mice who had had the surgery than in those who lost a similar amount of weight through diet changes, but without the operation. The bypass mice also had greater fecal fat content (yes, we’re back to poop again), suggesting that the new gut bacteria make-up was limiting the break-down and digestion of fat, meaning more was passed through the body without being absorbed.

Previous research has suggested that body weight and fat can also be influenced by transferring lean animals’ intestinal bacteria into obese mice, and vice versa. To test this effect in the current study, gut bacteria from the bypass mice were inserted into new animals through intestinal content transfers – i.e. fecal matter transplants. Sure enough, these ‘donations’ from the bypass mice resulted in significant reductions in body weight and fat levels in the receiving animals, but interestingly did not affect food intake.

As fascinating as these results are, some important questions remain. Firstly, is this a long-lasting effect? Could stool bacterial transfers from lean individuals be a long-term solution to obesity, or would these effects fade away as the transferred super-bacteria die off and are replaced by the host’s natural ones? To date, no studies have followed up these effects long-term, so this remains to be seen. Also, like much innovative scientific research, these results come with ethical questions to consider. Does having a different type of gut bacteria change our responsibility for our own weight and healthy diet? And should we all receive an injection of lean bacteria to prevent future obesity and related health problems?

So what do you think, would you do it?

These visceral, gut reactions are physiological fear responses our brain and body automatically initiate when in a perceived threatening situation. These experiences are thought to be subserved by the amygdala, an old and deeply rooted part of the brain that is essential in processing emotion, particularly fear. This is partly through connections the amygdala has to the sympathetic nervous system, which controls our basic ‘fight-or-flight’ reactions to danger – preparing us to either stand and fight or flee as fast as we can.

However, some people don’t experience this sensation of fear. Individuals who have undergone damage to the amygdala, either through a stroke or head injury, or from the rare genetic condition Urbach-Wiethe disease, report an inability to feel this emotion. One famous example of this absence is in the patient SM, who reported no feelings of fear when faced with snakes, spiders, horror films or haunted houses. Even after being threatened with a real life knife attack SM had no experience of fear sensations. However, there was one thing that was able to instill in her these feelings of anxiety and terror – asphyxiation.

Researchers at the University of Iowa have been studying SM over the last decade to try to find something, anything, that would scare her. After exhausting all the typical psychological stressors to no avail, they decided to try a physical stressor that can elicit the same reactions. Published last month in Nature Neuroscience, the researchers had SM and two other people with similar amygdala lesions inhale carbon dioxide for several seconds, cutting off their oxygen flow and essentially suffocating them. This experience typically causes panic attacks and fear responses in people, including extreme distress, pounding heart and an immediate desire to escape the situation. All three participants – none of whom had previously experienced fear – had these exact same panicky reactions to the CO2. In fact, when compared with normal healthy individuals, the amygdala patients had significantly greater fear responses, both physically and psychologically, than those with intact amygdalas.

So what’s behind this phenomenon? The researchers believe that these panic reactions are distinct from learned fear responses, such as phobias of snakes or spiders. Instead, there appears to be a unique pathway involved in panic from inherent physiological stressors that passes through the amygdala. In fact, this response may actually be inhibited in the amygdala, as the control participants had less dramatic reactions to the carbon dioxide than the amygdala patients. However, learned fears or perceived outside dangers may rely on the amygdala to integrate these scary sensory situations – such as seeing someone with a gun – as a threat. Thus, those with amygdala lesions do not learn and incorporate the proper fear associations with these triggers, but they do still have the capacity to experience these dramatic panic responses to internal physical stressors.

So the next time you’re watching a scary movie, you could try reminding yourself that it’s not real, or you could try hyperventilating – it may actually reduce your panic (assuming your amygdala is still intact).*

Boo!

*I do not actually recommend this as a fear-coping mechanism.

The first, the Human Brain Project, is being spearheaded by Prof Henry Markram of École Polytechnique Fédérale de Lausanne. Together, with collaborators from 86 other European institutions, they aim to simulate the workings of the human brain using a giant super computer.

To achieve this, they will work to compile information about the activity of tons of individual neurons and neuronal circuits throughout the brain in a massive database. They then hope to integrate the biological actions of these neurons to create theoretical maps of different subsystems, and eventually, through the magic of computer simulation, a working model of the entire brain.

Similarly, the Brain Activity Map Project, or BAM! (exclamation added because it’s exciting), is a proposed initiative that would be organized through the United States’ National Institutes of Health and carried out in a number of universities and research institutes throughout the U.S. BAM will attempt to create a functional model of the brain – a ‘connectome’ – mapping its billions of neuronal connections and firing patterns. This would enable scientists to create both a ‘static’ and ‘active’ model of the brain, mapping the physical location and connections of these neurons, as well as how they work and fire together between and within different regions. At the moment, we have small snap-shots into some of these circuits but on only a fraction of the scale of the entire brain. This process would first be done on much smaller models, such as a fruit fly and a mouse, before working up to the complexities of a human brain version.

BAM proposes to create this model by measuring the activity of every single neuron in a circuit. At the moment, this is done using deep brain techniques, a highly invasive process that involves opening up the skull to implant electrodes onto individual cells to read and record their outputs. Understandably, this is only done in patients already undergoing brain surgery, and is a slow and expensive process. Thus, the first task of BAM would be to develop better techniques to acquire this information. Research into this field is already underway, and exciting proposals have included nanoparticles and lasers that could measure electrical outputs from these cells less invasively, or even using DNA to map neural connections.

Neither project has directly acknowledged the other, but it is thought that the recent announcement of the U.S. proposal is a response to the initial European scheme launched earlier this year. And while there are distinct differences between the two initiatives in how they will acquire and store the raw information, as well as how they plan to build their subsequent models, the two projects overlap significantly. Both have the potential to better illuminate how exactly the brain works, and each ultimately hopes to provide us with a clearer picture of not only normal brain functioning, but also what happens when these processes are disrupted. Scientists and doctors could then use computer models to simulate dysfunction involved in neurological or psychiatric disorders, such as Alzheimer’s or schizophrenia. This would also open up possibilities for investigating better treatment options, as well as drastically cutting down on the expense and risk currently involved in clinical drug trials for psychiatric and neurological disorders.

However, there is a long list of obstacles these projects must overcome before we get too excited, not the least of which are the 100,000,000,000,000 connections that need to be measured and modeled. That’s over one million times as many neurons as there were genes to map in the Human Genome Project, the closest approximation to the current endeavors. Additionally, while there was a clear end to the human genome, the ambition of making a human connectome is both much larger and much less well-defined. Indeed, neither proposal yet has a definitive end-goal, and no one is clear on what the final product will look like.

For the Human Brain Project, the collaboration of over 80 different labs across Europe will also be a significant challenge. By collaborating rather than competing, the capacity for productivity and innovation in this and future projects is far higher. However, it will be extremely difficult to manage differences in laboratory methods and communication, not to mention egos, between these institutions.

Another major concern for the American proposal is funding. With the financial crisis, fiscal cliff and federal sequestration of recent months, the U.S. economy (and Congress) do not have a very good track record at the moment. And it is hard to believe they are going to approve a multi-billion dollar project when they cannot even agree to continue funding for health care, education and military spending. Private companies including Google and Microsoft, as well as charities such as the Howard Hughes Medical Institute and Allen Institute for Brain Science have signed on to the project, but the bulk of funding will still have to be provided by government institutions.

In his State of the Union address, President Obama alluded to the Brain Activity Map Project, and tried to head-off the inevitable financial protests to it by invoking the Human Genome Project, which cost $2.7 billion to complete but has reportedly produced a return of $140 to every dollar spent. This was manifested through pharmaceutical and biotechnology developments, as well as subsequent start-up companies. This turnover has the potential to grow even further through future reductions in health care spending from medical developments, and the hope is that BAM will produce similar high returns. However, the question remains as to whether this investment could be better spent elsewhere, such as improving the medical system, research for drug treatment developments, or health education and prevention programs. Some in the scientific community are also worried that already limited funding to other fields of research will be slashed in order to subsidize the project.

Despite these concerns, it is undeniable that if these programs were to succeed they would be spectacular achievements in scientific research, not unakin to the discovery of the Higgs Boson or even the first space expeditions of the 1960s. Many believe that the human brain is the final frontier for medical research, and it will remain to be seen whether these brain-mapping projects will enable us to finally understand the wild and intricate workings of our own minds.

(Originally posted on King’s Review)

(And an updated version has been published on The Atlantic)

A group of highly talented graduate students at King’s College in Cambridge have launched a new web magazine today, and I’m honored to be a part of it. The first issue tackles everything from US national security and the CIA to the uprising of artists in Germany over state funding cuts. I’ve even contributed my own article, which dedicated Brain Study followers might recognize as the mutant off-spring of a piece I posted last year on ‘pathologizing the norm‘. It’s been beefed up and fleshed out as I attempt to tackle some of the proposed changes in the upcoming DSM-V, slated to be published later this year.

Here’s a brief teaser for the article, Pathologising the Norm: The spread of mental illness, to pique your interest:

One in four of us will struggle with a mental illness this year, the most common being depression and anxiety. The upcoming publication of the fifth edition of the Diagnostic and Statistical Manual for Mental Disorders (DSM) will expand the list of psychiatric classifications, further increasing the number of people who meet criteria for disorder. But will this increase in diagnoses really mean more people are getting the help they need? And to what extent are we pathologising normal human behaviours, reactions and mood swings?

So please check out the full piece, and the rest of the magazine, at King’s Review, and let me know what you think!

And don’t worry, Brain Study will always be my first blogging love.

The pleasure of eating is one of our most natural joys, be it savoring a perfectly cooked steak or delighting in that melt-in-your-mouth chocolate. But with the rise of obesity and related maladies – particularly cardiovascular disease, hypertension and type-II diabetes – such simple pleasures have been perverted, pathologized by experts and classed as a source of harm. With nearly 25% of English adults qualifying as obese, and with ensuing costs to the NHS reaching £5.1 billion each year, the UK is facing a self-induced public health pandemic. But how has this happened? And why can’t we all just put down that second piece of chocolate?

Added sugars have become the focus of widespread concern among doctors and researchers, their effects on our waistlines, livers, and even our brains, giving cause for alarm. Obesity specialist Dr. Robert Lustig has emerged as a crusader for the anti-sugar movement, contending that sugar, not fat, is behind the dramatic rise in ‘western diet’ conditions over the past 30 years. The problem stems from the way our bodies metabolize fructose – half of the refined sugar molecule, sucrose – as opposed to pure glucose, which makes up the other half and is found in foods like potatoes and white bread.

Glucose is metabolized by all cells in the body, whereas fructose is primarily processed by the liver. If the liver cannot adequately break down sugar into energy it is converted into fat, and the faster the body receives fructose, the more likely this is to happen. High fructose sugar solutions, like fizzy soft drinks, are particularly prone to this fat conversion, providing high volumes of fructose that reach the liver much more quickly. This inability to break down sugar and the subsequent rise in liver fat is believed to be at the root of insulin resistance, the main deficiency underlying type-II diabetes.

But regardless of doctors’ warnings and the evidence that increased sugar consumption leads to obesity, as well as liver and heart disease, our sugar intake continues to rise. This may be due to the seemingly addictive qualities of high-sugar foods themselves. For despite our best intentions to cut out the cake, doing so rivals quitting smoking in terms of difficulty. New research indicates that foods high in fat or sugar may qualify as addictive substances, causing similar neurochemical changes in the brain as drugs of abuse.

Researchers at Princeton University have demonstrated this phenomenon by intermittently exposing rats to a sucrose solution in addition to their regular food. After a month, rats began to show binge, craving and withdrawal-like behaviors for sucrose, self-administering extremely large quantities when it was available. Adaptations similar to those seen in cocaine-addicted animals emerged in the rats’ brains, with surges of dopamine released during a binge – a process linked to feelings of reward and novelty, and a key facet of drug addiction. An increase in craving was also seen in the test animals, demonstrated by greater sucrose-seeking when deprived of the solution, even in the face of punishment. Additionally, rats experienced withdrawal-like symptoms when the sugar was removed, exhibiting tremors, head-shakes and signs of anxiety and aggression. Such behavior is typically seen in animals going through opiate withdrawal, and is caused by the release of endogenous opioids in the brain by high-sugar foods, reinforcing their hedonic characteristics and creating a withdrawal effect when removed.

Given sugar’s apparently addictive properties, one proposed response to the obesity epidemic is to regulate its availability in much the same way as tobacco and alcohol. Labeling foods high in sugar and fat as ‘addictive’ could potentially remove the stigma attached to being overweight, re-characterising it as a complex medical condition rather than simply one of personal weakness and poor self-control. Furthermore, tougher regulations on the advertising and availability of junk food might help to reduce the proliferation of cheap high-fat/high-sugar snacks that has made diet control increasingly difficult. However, taking responsibility for diet out of the hands of individuals also diminishes personal accountability and the imperative for each of us to make positive food choices. The fast food industry certainly isn’t helping us to lose weight, but it’s also not forcing the food down our throats. Should we be trusted to control what we put into our bodies, or do we need someone to stop us from taking that second piece of chocolate?

*So this post is a bit cheeky. I originally wrote this as a submission for a writing competition, but seeing as how it was never published, I figured it made an apt piece in honor of New Year’s resolutions!

(Thanks to Paul Sagar for help in editing the original piece.)

Yes, tryptophan. That infamous amino acid we use to justify dozing off during our aunt’s vacation slideshow after the big meal. Tryptophan is an essential amino acid, a protein precursor that the body uses to build various chemical structures. This includes serotonin, one of the primary neurotransmitters in the brain that is involved in everything from decision-making to depression. Serotonin is also a precursor to melatonin, which is important in sleep and wakefulness and is where the tryptophan-tiredness link comes in. However, despite the popular neuro-myth, turkey is actually no higher in tryptophan concentration than other types of poultry. Numerous different plant and animal proteins provide us with our daily doses of tryptophan, with sunflower seeds, egg whites and soy beans having some of the highest concentrations of the amino acid. In fact, turkey comes in at a measly 10th on the list of tryptophan sources.

Instead, the relation between eating and sleeping seems to be more dependent on the amount of food consumed, rather than the type we eat. Insulin is released after every meal, particularly ones high in carbohydrates, and the more carbs consumed, the more insulin is produced. This increase then changes the chemical levels in our bloodstream, affecting the re-uptake and release of various amino acids. Ultimately these changes result in greater amounts of tryptophan crossing the blood-brain-barrier and being taken up into the brain. There the tryptophan is converted to serotonin, some of which is also metabolized into melatonin, causing our postprandial nap.

Tryptophan’s influence on serotonin levels doesn’t just affect sleep cycles. The link between depression and low serotonin levels is well established, and tryptophan supplements have been suggested as less invasive treatments for the disorder. Unfortunately these studies have been mostly unsuccessful to date, as mild modifications of tryptophan seem to have little to no effect on mood in most individuals. However, it is possible that people with low endogenous levels of tryptophan due to specific genetic profiles may be more susceptible to the chemical’s effect on mood, and current research is still ongoing in the matter.

So regardless of whether it’s turkey, stuffing or sweet potatoes you prefer, remember to load up your plate during Thanksgiving to get those happy drowsy effects later. It may just help you feel a little bit calmer, and prevent some of the Black Friday mayhem the next day.

Like much of the advice our parents give us (like always take out your contacts before you go to bed), this one is also true. The THC (tetrahydrocannabinol – the primary psychoactive compound in cannabis) concentration in marijuana has increased by as much as 12% over the last 30 years. This rise in THC levels is related to increases in the subjective ‘high’ feelings associated with smoking cannabis, like changes in perceptual sensations, contentedness, and increased appetite. However, THC is also linked to many of the negative consequences of cannabis use, including risk for dependence, attentional bias or distraction, impaired memory and cognition, and the potential emergence of psychotic symptoms.

Alternatively, CBD (cannabidiol – one of the other major chemicals in cannabis that works by increasing endogenous cannabinoid levels in the brain) is associated with the anxiolytic or anti-anxiety effects of marijuana. Additionally, it is thought to act as a protective factor against many of the negative effects the drug can have, including the development of abuse, cognitive impairments, and even psychotic symptoms.

Unfortunately, in addition to the high levels of THC seen in today’s cannabis, there is also a significant depletion of CBD. ’Skunk’, as it is referred to by users and dealers alike, is the strain of this new high-THC, low-CBD cannabis that is flooding the marijuana market. And it is this drug that is thought to be at the root of the increase in cannabis dependence diagnoses seen over the last decade.

Recent changes in policy and public perception of the risks associated with cannabis have also resulted in an increase in use, particularly among adolescents and young adults, with roughly 50% of high school students reporting having used the drug at some point in their lives. However, despite a previous belief that cannabis was not addictive, there has also been a substantial increase in the number of users seeking treatment for dependence, and nearly 11% of current users qualify as addicted. Skunk smokers in particular are more likely to experience cravings for the drug, go through their stash in shorter amounts of time, and have greater attentional bias to cannabis cues.

Professor Val Curran’s group from University College London has been leading the charge on research into the effects of cannabis use, comparing recreational and chronic smokers, and studying the varying effects different strains of cannabis have on the brain. Her group is particularly interested in comparing skunk to THC-CBD strains, and they have discovered much of the evidence for the protective effects CBD has against the development of psychosis and dependence. CBD’s action upon the endogenous cannabinoid anandamide seems to be behind the reduction in psychotic experiences in regular smokers, and CBD has even been looked at as a potential treatment for schizophrenia, reducing psychotic symptoms as effectively as some of the anti-psychotic drugs currently prescribed. THC-CBD users also show less distraction to marijuana stimuli than skunk smokers, and they report significantly reduced feelings of craving. There were also no differences in the subjective intoxication effects of smoking either skunk or THC-CBD, indicating it does not alter the psychoactive properties of the drug.

So the question is, where has all the CBD gone? Modern day growing methods using indoor marijuana farms have greatly decreased the risk of detection for cannabis producers by circumventing the need to import cannabis internationally. Cannabis greenhouses also guarantee a more reliable crop, as they are not dependent on changes in weather patterns. However, the 24-hour lighting used in these farms results in an inadvertent destruction of the CBD levels in the plant. Thus, these new strains not only have increased potency with higher THC contents, they also have reduced protective factors against the drug’s negative effects. In the producers’ eyes, these are just additional economic advantages to growing on an indoor farm, as more dependent users who go through the drug more quickly will result in more cannabis being sold.

These changes in potency raise interesting questions regarding the recent legalization of recreational and medicinal marijuana use in some states. Most pressingly, where and how is this cannabis being produced? And what are the differing levels of THC and CBD present in it? Also, would it be possible to better control cannabis production to avoid its addictive or psychotic-inducing effects? And should we start to think about prescribing CBD to patients currently suffering from THC dependence?

While the developments in cannabis policy may potentially reduce the harm caused to individuals from incarceration or criminal records for minor possession, in terms of the potential psychological effects caused by the drug, it appears we’d be better off smoking our parents’ pot.

*Apologies to my parents, who have never actually uttered the above phrase.

**Title pun credit to Claire Gillan.