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‘The Biophotonic Scammer’

saxophoneIn the summer of 2015, I received a message on Facebook from a faint acquaintance whom I got to know over the course of the previous year, having played in a jazz orchestra with the fellow. We exchanged the occasional pleasantry from across the trumpet section during rehearsals, and surely he knew that I studied medicine, though we lost contact with one another at the end of the school year. He had messaged me about a “new business project” with some “very interesting science type stuffs [sic].” We set up a time where he and his mentor could unload a 30-minute presentation on my easily impressionable mind.

We met in early September at a Starbucks in downtown Toronto. Amidst the low chatter of students preparing to return to classes, I sat, while protégé and mentor explained to me the miracle of ageloc technology, patent pending.

Based on Nobel-prize winning technology, the biophotonic pharmanex scanner can measure carotenoid levels in the skin, which I was told, correlates to antioxidant levels in the body. This medical technology, I was told, was used by some highly-regarded doctors here in Toronto were fervent adherents of the photonic scanner along with a pharmacopoeia of ancillary products to be pushed after paying for a scan. This dubious product, which after a scan would spew out spurious data hardly correlating to a client’s health becomes the perfect inroad to sell supplements to ‘improve’ one’s results. After a course of supplements, a client would scan themselves once again to see if their results had changed.

The scanner was one of the many flagship products offered through a company called Nu Skin (which trades on the New York Stock Exchange, I was told), who’s chief quack Joe Chang has been discredited time after time. Another product, called the Galvanic Spa purports to alter the charges in collagen molecules, while their Ageloc Technology, alluded to before, fleetingly grasps at buzzwords like ‘epigenetics’ to for you to ponder at while your pockets are unsuspectingly emptied.

Having finished with the pseudoscience, we moved on to how I could get involved. I vibrated with excitement anticipating what I could only expect to be a phenomenal pitch. I was asked first whether I considered myself a successful person, and then to suggest reasons for what drove me to this success. It was most certainly my personality, of course! Now what if I could drive my success financially? Who would not be interested in that? Other doctors had taken advantage of offering the Nu Skin line of products, and it had benefitted them beyond their greatest expectations. For the low cost of $200 per month, I could lease my very own photonic scanner, and charge people $55 per scan. I could then grow a roster of clients to scan and enlist a team of my own to recruit other people who would scan even more clients. The mentor pulled out a small cardboard pamphlet and pointed at a six-figure number representing my potential earnings. I slowly sketched a pyramid in my notebook.

The pitch had finally concluded, and I was asked if I would like to have my antioxidant levels measured. I knew the machine to be harmless, but I declined, told them I would not likely be in touch, and walked out. On my way to the subway I began to ponder this curious encounter. Before the meeting I thought about how lucky I was to have an opportunity like this fall right before me – the chance to write an exposé on this most absurdflim flam. Was it really such a rare occasion as I had previously suspected? The reality is that pseudoscience is on the rise. Today, with the great advances we have made in medical sciences, with our armamentarium of treatments for diseases which were once deadly, doctors and scientists are losing the public battle to quacks of the highest order. The concern over this movement cannot be understated. It is clear however, that our greatest asset is a healthy balance of ridicule and education, and we must fight back.

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Hepatitis A From Frozen Berries

berriesOn April 15, 2016, the Canadian Food Inspection Agency (CFIA) announced a food recall warning regarding the possible contamination with Hepatitis A, a viral liver disease, of the frozen fruit product, “Nature’s Touch Organic Berry Cherry Blend”. Canadians have been advised that the food recall is in effect in the provinces of Ontario, Quebec, New Brunswick, Nova Scotia, and Newfoundland and Labrador, where the product has been sold. As of April 22, 2016, there are eleven related Hepatitis A cases in three provinces (1): Ontario (8 cases), Quebec (2 cases), and Newfoundland and Labrador (1 case).


While it is frightening to know that Hepatitis A can be contracted by eating frozen berries, a product that is supposed to be healthy, coming into contact with hepatitis A can be quite easy. Hepatitis A is usually linked with the lack of potable water and inadequate sanitation,  and the virus is spread mainly by the faecal-oral route. It can be acquired from any food and drinks prepared by a person who is infected, as an  infected person can carry, due to improper hygiene, traces of their faeces when preparing refreshments. Shellfish derived from waters containing sewage can also carry hepatitis A. The frozen berries sold at Costco in Canada were at some point contaminated with hepatitis A from at least one infected worker (during harvest, manufacturing or processing) who was handling the berries, and who did not take preventative hygienic measures such as frequent hand-washing with soap and water, and the use of gloves. After infection with hepatitis A, symptoms usually reveal themselves two to seven weeks after viral infection. Fever, loss of appetite, abdominal pain, jaundice, dark urine, vomiting, and fatigue are all symptoms. Although cases usually last one to two weeks, a few severe cases can last several months before recovery, and some people can die from liver failure. People with pre-existing liver conditions are at a greater risk of severe illness. Older people tend to get sicker than younger people after infection.The disease is not chronic (there is usually no permanent liver damage), and lifetime immunity is acquired either from recovery after infection, or through immunization with the hepatitis A vaccine.


The hepatitis A virus, a picornavirus, is of an icosahedral shape and does not contain an envelope. It possesses a single-stranded RNA packaged in a protein capsid. There are three different numbered human genotypes of the virus, but type IA is the most commonly occurring. Genetic sequencing of the virus can reveal which molecular subtype of the virus is associated with a particular outbreak (2), thus narrowing down unassociated cases of infection. To determine whether infection has occurred, a blood test to look for IgM anti-hepatitis A antibodies, a particular immune response, can detect the virus as early as two weeks after the initial infection.


Known as a “traveller’s disease”, hepatitis A is usually associated with countries that are less developed, but it does and can occur in Canada. In industrialized countries, outbreaks of hepatitis A are often linked to contaminated produce (3). During March 2012, there was a small outbreak of hepatitis A in British Columbia, Canada that was traced to pomegranate seeds in a frozen fruit product (4). April 2013 saw more than 70 cases of hepatitis A infection in four Nordic countries (5,6). In the United States, there were 165 confirmed cases of hepatitis A infection found across 10 states, in 2013 (7). This outbreak was traced to pomegranate arils found in a frozen berry product sold at Costco, and 44% of the infected patients were hospitalized. Frozen fruit can last for up to a year in the store, and hepatitis A can incubate for up to 50 days, so a hepatitis A outbreak is often detected only after many people have been infected (8). Case-control studies, where patients with (case) and without (control) a disease, such as hepatitis A, are compared retrospectively for frequency of exposure to a risk factor (such as the contaminated frozen fruit), and through this study method the source of the outbreak can be unraveled.


Costco is publicly offering free vaccination clinics to affected individuals of this recent 2016 outbreak, as vaccination can prevent the disease symptoms from occurring if given within two weeks of exposure (9). There are two options for post-exposure prophylaxis of hepatitis A. The first is the vaccine injection, which is an inactivated version of the virus. The second is immunoglobulin (IG), which is injected and consists of antibodies which fight the virus to prevent infection. It is a blood product produced from paid donors. An exposed individual who may be allergic to the vaccine may opt for the IG. A study comparing the two options found that immunoglobulin was slightly more effective than the vaccine (10). However, the vaccine offers a lifetime immunity, whereas the response of immunoglobulin against hepatitis A is only for three months after the IG administration-subsequent exposure to hepatitis A can still result in an infection. Individuals can get a pre-exposure prophylaxis vaccination, which renders permanent immunity before any exposure, and travellers to countries where hepatitis A is endemic are required to receive the vaccination before leaving to their destination.


The recent 2016 hepatitis A outbreak in Canada from frozen fruit is only one of several similar outbreaks that have occurred in the past in different industrialized countries. Hepatitis A is spread through the faecal-oral route, and although it is more common in less developed nations where poor sanitation conditions are prevalent, improper hygiene during food handling can cause an outbreak.  Identifying the specific molecular subtype of hepatitis A can help trace which cases are associated with a particular outbreak. It is recommended that anyone handling food take proper precautions in food safety in order to prevent further hepatitis A outbreaks. If worried, one should obtain a pre-exposure vaccination to acquire permanent immunity to the virus.

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The Zika Crisis

mosquitoIn 2015, the Zika virus outbreak began in the northeast region of Brazil. According to the World Health Organization, there has been 3174 suspected cases of microcephaly in Brazil since January 2, 2016, including 38 deaths (1). The northeastern region of Brazil continues to be the area most affected, with the highest number of suspected cases. On April 13, 2016, the US Centers for Disease Control and Prevention (CDC) published a paper in The New England Journal of Medicine which concluded that there is a direct causal relationship between prenatal exposure to Zika virus and the outcome of microcephaly and brain abnormalities in the exposed infants (2). While the common symptoms of Zika infection are fever, rash, joint pain, and conjunctivitis lasting from several days to a week after exposure from an infected mosquito’s bite, a recent study recounts two cases of patients who had contracted the Zika virus and later succumbed to acute disseminated encephalitis (ADEM) (3).  This is a condition in which the immune system attacks the body, producing swelling in the brain and spinal cord and damaging the myelin which serves to protectively encase nerve fibers. The same study also describes four patients who had Zika and then developed Guillain-Barré syndrome, a condition where the immune system attacks the body’s peripheral myelin.

Zika virus is quickly spread through the bite of the female Aedes aegypti mosquito, a mosquito that is usually associated with warmer climates. This species of mosquito bites during the day. The Pan American Health Organization (PAHO) sent out a warning of the first confirmed Zika virus infection in Brazil on May 2015, and on February 2016, the World Health Organization (WHO) declared Zika virus a public health emergency of international concern (PHEIC). The PAHO lists the following areas where local transmission of Zika virus is active (4): Aruba, Barbados, Belize, Bonaire, Brazil, Colombia, Costa Rica, Cuba, Curacao, Dominica, Dominican Republic, Ecuador, El Salvador, French Guiana, Guadeloupe, Guatemala, Guyana, Haiti, Hondruas, Jamaica, Martinique, Mexico, Nicaragua, Panama, Paraguay, Peurto Rico, Saint Vincent and the Grenadines, Saint Lucia, Saint Martin, Sint Maarten, Suriname, Trinidad and Tobago, US Virgin Islands, and Venezuela. Locally transmitted cases of Zika have been reported in the Commonwealth of Puerto Rico, the US Virgin Islands, and American Samoa. There is potential for Zika virus to continue to spread to other countries due to the expanding range of the Aedes aegypti mosquito. A population of this species not carrying Zika was found in Capitol Hill, Washington, DC. Genetic analysis revealed that this particular mosquito population survived five winters in the area (5). Although theAedes aegypti is the species most responsible for spreading the Zika virus, other mosquito species in the Aedes genus can also transmit it to humans. Once the virus enters the bloodstream of a human through the bite of a female mosquito (the male mosquitoes do not bite), another female mosquito can acquire Zika by feeding upon the same host, which can then go on to infect another human. In an area with many Aedes mosquitoes, the process will repeat itself exponentially, leading to widespread viral transmission. A possible solution can be to use genetically modified mosquitoes that are male which reproduce with local female mosquitoes to yield offspring which do not live past the pupae stage. Oxitec (6), a British biotechnology company, developed such a mosquito which has already been released and tested successfully in the Cayman Islands in 2010, leading to a drastic 80 percent reduction in population of Aedes aegypti. Release of the same strain of GMO mosquitoes in the suburb of Juazeiro, Brazil in 2011 resulted in a 81-95 percent reduction of Aedes aegypti in the test region. It is also possible to breed mosquitoes to be genetically resistant to diseases such as dengue, malaria, yellow fever and Zika. Gamma radiation is being used in Brazil to sterilize male mosquitoes. Moscamed, a non-profit organization based in Brazil, took to breeding 12 million male mosquitoes per week, sterilizing them with the cobalt-60 irradiator, and then releasing them into select high-risk areas (7). The released sterile males mosquitoes then meet wild female mosquitoes, but no offspring can be produced. As there is no vaccine available right now, the current method of battling Zika virus is to reduce the population of Aedes mosquitoes.

It has been found that the Zika virus can also be transmitted sexually from an infected human male to his sexual partners via vaginal or anal sex (8), and that the virus can remain for a longer duration in semen than in blood. As of now, it is not known whether a woman can sexually spread Zika virus, or if it can be transmitted through saliva or vaginal fluids. Couples who are pregnant, or men who have travelled to areas affected by Zika are advised by the CDC to abstain from sex or use condoms.

The Zika virus is in the Flavivirus genus of viruses, which also include the West Nile virus, dengue virus, tick-borne encephalitis virus, and yellow fever virus. As a flavivirus, the Zika virus is enveloped, has a capsid of icosahedral symmetry, and contains a single-stranded positive-sense RNA genome. The Zika genome is about 10.8 kilobase pairs long. The positive-sense RNA is significant because once the virus enters the host cell, this RNA viral genome can be directly translated into a viral polypeptide, which is then cleaved into structural proteins and proteins to aid in the replication process. The envelope (E) glycoprotein protruding from the membrane of the virus is used for attachment and entrance into human cells.  For the development of a potential vaccine for Zika virus, a segment of the E glycoprotein unique to the Zika virus can be used in the vaccine to mount an antibody-mediated immune response, possibly conferring immunity from future attacks of the virus.

The expanding range of travel of both humans and mosquitoes have allowed for rapidly widespread transmission of the Zika virus. The head and brain abnormalities caused by prenatal exposure from an infected mother are detrimental, and a direct casual link between the virus and microcephaly/brain defects has been determined by the CDC. For instance, the Zika virus genome was found in the brain of an aborted, infected infant (9) that had microcephaly, and Zika virus antigens were found in the brain of one newborn with microcephaly (10). Autopsies found the presence of Zika virus in the brains of infants with severe microcephaly who died. Pregnant women infected with Zika virus have consistently given birth to infants with microcephaly and other brain abnormalities (11). The CDC further found that women who deliver infants with microcephaly were infected with Zika virus during the first and second trimester of gestation, when the brain starts to form and develop (12). There are two hypotheses directed at explaining how the Zika virus causes birth defects such as microcephaly (13). The first hypothesis posits that the placenta transfers the virus directly from mother to the fetus. The second hypothesis refers to the possible reaction of the placenta in response to Zika, which may contribute to or result in birth defects. Pregnant women are advised not to travel to areas where Zika virus is occurring.

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tequila copy 2“ When life gives you lemons, make lemonade,” or so goes a proverbial phrase. But when the lemons come at the most inopportune times, I say forget about the lemonade; I need to make tequila. And when excrement really hits the fan, I make that tequila extra añejo. Let’s just say that there has been a lot of tequila.

The past couple of months have definitely been very trying. Those who have read my previous blog entry know that I faced some pretty impossible scenario regarding my visa to stay in the U.S. to continue my medical training. But after obstinately knocking on every door I could think of, both literally and figuratively, including that of the Prime Minister of Health of Quebec, I was granted an extension on my visa, a lucky exception, allowing me to stay in the U.S. and start my fellowship in Pulmonary and Critical Care Medicine.  It was a much hoped-for and prayed-for triumph, followed by a summer not without its challenges.

It is hard to believe that I started writing this blog as I entered medical school, and this summer marked the end of my training as an internal medicine resident. At the end of residency, one can choose to practice independently as an attending physician, or continue further training in a sub-specialty in a fellowship. I signed up for another three years of training to be a lung and critical care specialists.  Call me nuts. But this means that in three years, I will work with patients afflicted with various pulmonary issues, as well as manage some of the sickest people in the Intensive Care Unit.

July is always a chaotic month for doctors. An old batch of trainees leave, and a new batch of wide-eyed incomers flood in. Add into the equation apartment hunting, car hunting, money scrambling, and oh, how can I forget, studying for one of the biggest exams of my life, the American Board of Internal Medicine, or the ABIM. Everything was on a tight and carefully thought-out schedule, all the while living out of cardboard boxes.

Unfortunately, or perhaps fortunately, depending on how you look at it, doctors are humans, too.  We have lives outside the hospital, we get sick, we get hungry and sleepy, we laugh, we cry, we make mistakes, we try to make lemonades when life gets sour, but sometimes we get overwhelmed by all the bitter lemons thrown at us.

Well, I eventually found an apartment and even managed to move by myself, hopping over fences while carrying heavy boxes.  I moved some money around (euphemism for ‘I borrowed’) and got a car so I can drive between the three different hospitals where I will be working.

Then I found that that I had failed the ABIM on my first try. Never having failed an exam in my life, it was to my surprise that I did not die from failing one exam.  I learned that a bad test score does not equate a failed career and that there are always second chances. So here I am, ready for the challenges and fun that the next three years will offer. Let me dust off that nasty feces that was thrown at me, and cheers!

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FOLLOW DR. KO: What You Never Knew About Canadian Doctors Outside Canada

IMGImagine me, a single thirty year-old living in the bustling city of New York, out at a bar on a Saturday night.
“What do you do for a living?” – someone inevitably always asks.

Sometimes, for fun, I make up stories. I tell people that I specialize in cleaning elephant poo at the Bronx Zoo or something ludicrous like that. It is so much more interesting than just saying, “I’m a doctor.”

But when I do say that I am a doctor, people’s reaction is usually “Oh wow.” They think that I must live in luxury on the Upper East Side, drive a Mercedes-Benz or some other fancy vehicle, and travel to exotic lands every couple of months. They picture a doctor, noble and heroic, who goes to work every day and saves lives. Countless lives. They would imagine me shouting out a patient’s blood pressure, cutting them open, performing chest compressions, while pearls of sweat drip down my face, the sweat of hard work, of responsibility, of grandeur. Then the patient lives, wakes up, and thanks me with hugs and tears.

Well, all that is flattering, but none of it is true.

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Bad breath

halitosisFoul breath—also known as halitosis—is an unpleasant condition that affects almost everyone. Because it is so widespread, determining and subsequently diagnosing each individual patient can be difficult. And it gets even harder because patients really can’t smell their own bad breath. But strong-nosed scientists have been discerning the truth bit by bit: there is now hope for those hoping to remedy their morning dragon’s breath.

Originally many believed that malodors originated in the stomach and blamed things like acid reflux, indigestion and gut flora. But what people are beginning to see is that in most cases of halitosis, the mouth is to blame. Halitosis originates from bacteria on the tongue, a condition known as tongue coating. The byproducts are largely responsible for bad breath in patients.  They produce what are known as volatile sulfur compounds (VSCs) such as hydrogen sulfide and methyl mercaptan. In order to then treat halitosis, efforts have focused on developing products that will either reduce these odiferous bacteria or neutralize the VSCs themselves.

The main form of treatment against halitosis is to simply brush the tongue to remove built-up bacteria. When halitosis persists, patients instead try to stop the creation of VSCs. By neutralizing the VSCs, the malodor does not volatilize, and the mouth does not stink. Some of the most successful neutralizing compounds have been zinc salts, chlorhexidine and hydrogen peroxide. Chlorhexidine can result in stained teeth, tongue numbness and burning; on the other hand, hydrogen peroxide can be highly oxidative and damaging to soft tissues. Zinc seems the best breath-fighting agent out there.

Zinc ions have a very high affinity for sulphur and can therefore inhibit the formation of stinky sulphur compounds by reacting with them before they leave the mouth. Zinc is also non-toxic and does not stain teeth, making it an ideal candidate to treat bad breath. While protocols to measure the efficacy of bad breath levels vary, the best measure of a persons’ breath is when the human nose smells it. And generally, these smell-tests result in accurate and reproducible results. When put to the schnoz studies show that mouthwashes, lozenges, and gums containing zinc in 0.2-0.5% are the most pleasant and effective in treating halitosis. It should not be used alone, however. A careful combination of good dental hygiene, eating plenty of fruits and vegetables, and drinking plenty of water will help minimize the smell.

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Chickens, toads, and gluten sensitivity

Keratosis pilarisBy: Laurie Laforest
Keratosis pilaris is one of the many symptoms attributed to non-celiac gluten sensitivity in alternative medicine circles.  Keratosis pilaris – or “chicken skin” – is a benign skin condition reminiscent of permanent goose bumps.  I first heard the term keratosis pilaris on a episode of The Dr. Oz Show about gluten sensitivity [1], the premise being that keratosis pilaris results from fat malabsorption caused by gluten-induced intestinal damage.  Since my family and I have little patches of this on our elbows and knees, I was eager to learn what was really behind it.
It turns out that the link between “chicken skin” and gluten sensitivity is one of mistaken identity.  Keratosis pilaris is a type of follicular hyperkeratosis where excess keratin – a key protein in our outer layer of skin and in our hair and nails – plugs the hair follicule, sometimes trapping a small hair inside. [2]  Enlargement of the follicule and the presence of the hard keratin plug produces the characteristic rough and bumpy appearance; reddening may also occur.  Keratosis pilaris is quite common – it affects around 50% adolescents (80% of females) and 40% of adults – and seems to have a strong hereditary component. [3]
Phrynoderma – or “toad skin” – is another type of follicular hyperkeratosis that is typically related to malnutrition in developing nations.  Phrynoderma is what alternative medicine folks are actually thinking of (or they should be) when they speak about a diet-related bumpy skin problem.  The exact nutrient deficiency behind phrynoderma is not known, but the condition can be reversed by supplementation with essential fatty acids, vitamin A, vitamin E, or B-complex vitamins; different people seem to respond to different nutrients. [4-7]
So “chicken skin” (keratosis pilaris) is common and benign, while “toad skin” (phrynoderma) is uncommon in the developed world and a sign of a serious problem.  But could it still be possible that gluten sensitivity is at the heart of these conditions?  Most likely not.  Keratosis pilaris is not related to diet, although it does seem to occur more often in people with a high body mass index. [8,9]  Hormones could also play a role, since keratosis pilaris is more common during adolescence.  Still, keratosis pilaris can come and go throughout adulthood and may worsen during the drier winter months.
Even for phrynoderma, the gluten connection doesn’t pan out.  Let’s first consider celiac disease, an autoimmune reaction triggered by gluten that damages the small intestine.  Celiac disease is the worst-case scenario when it comes to gluten sensitivity – fat malabsorption is a classic symptom of untreated celiac disease, and there is a risk that celiac sufferers could be deficient in fat-soluble vitamins like A, D, and E.  But even though it might seem like celiac disease could produce the kind of malnutrition that leads to phrynoderma, phrynoderma is not one of the skin conditions seen alongside celiac disease [10], and fat-soluble vitamin deficiencies are also not found in newly-diagnosed celiac patients as often as one is led to believe on TV [11-13].  Now consider that non-celiac gluten sensitivity is not supposed to involve the characteristic intestinal damage (and, hence, the potential vitamin deficiencies) found in celiac disease [14,15], and you have no reason for the average person to suspect that their rough skin is related to gluten.
If you do have “chicken skin” or other roughening or reddening of the skin, it is best to talk to a dermatologist to properly identify your skin condition or to your doctor if you do suspect that you have celiac disease.  Most people with keratosis pilaris don’t even realize that they have it, but others may be plagued by large, unsightly patches of skin.  Mild cases can be improved by over-the-counter moisturizers; more severe cases can be treated by medicated creams that soften keratin and help remove the outer layer of skin.  Even though there is an abundance of advice on treating keratosis pilaris on the Internet, ask a doctor or pharmacist to direct you to the right products to use.

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Opioid peptides: the heroin within?

Screen Shot 2014-11-07 at 10.36.51 PMBy: Emily Brown PhD

If you were to hear the words ‘opioid peptides’, they might not trigger much within your brain, other than that the former sounds a bit like opium and together they sound quite scientific. Opium (also known as poppy tears) is a dried substance or latex that originates, as the alternative name suggests, from the opium poppy. Beautifully intricate pipes of bamboo, ivory, silver, jade and porcelain have been carved over the centuries and used to vaporise and inhale the latex traditionally obtained by scratching immature poppy seed pods by hand. Numerous Empires including the Egyptian, Greek, Roman, Persian and Arab made widespread use of the drug, which was then the most potent form of pain relief available. This analgesic property is conferred by morphine, which constitutes approximately twelve per cent of opium and is chemically processed to produce heroin. Commonly known by the street names H, smack, horse and brown, among others, the effects of heroin will be well known by any ‘Trainspotting’ fans. What writer Irvine Welsh did not reveal, however, is that opiates such as heroin mimic the effects of naturally occurring molecules that can be generated inside our own bodies.

Opioid peptides are small molecules that are produced in the central nervous system (the brain and spinal cord) and in various glands throughout the body such as the pituitary and adrenal glands. These peptides can be divided into three categories (enkephalins, endorphins, and dynorphins), depending on the type of larger precursor molecule from which they are derived. Opioid peptides function both as hormones and as neuromodulators; the former are secreted in the blood system by glands and are delivered to a variety of target tissues where they induce a response, while the later are produced and secreted by nerve cells (or neurons) and act in the central nervous system to modulate the actions of other neurotransmitters.

Neurons are electrically excitable cells that process and transmit information through electrical and chemical signals that travel via synapses, specialised connections with other cells. These signals are transmitted across a synapse from one neuron to another by neurotransmitters. By altering the electrical properties of their target neurons and making them difficult to excite, opioid peptides can influence the release of various neurotransmitters.

Through these two different mechanisms, opioid peptides can produce many effects including pain relief, euphoria and altered behaviour such as food and alcohol consumption. The apparent connection between exercise and happiness has been explained at least somewhat by the release of endorphins, for example. Exercise is commonly recommended as a strategy for stress-relief and mood improvement, but less widely accepted forms of therapy might also be connected to opioid peptides. Evidence suggests that pain relief induced by acupuncture results from stimulation of opioid peptides – these peptides act through receptors on their target neurons, and chemicals that inhibit opioid receptor function have been found to reverse acupuncture-induced analgesia. Painful, stressful or traumatic events or stimuli can induce the release of opioid peptides, with the resulting euphoria and pain relief making the sufferer less sensitive to noxious events. Opioid peptides have been reported to affect the release of specific neurotransmitters such as dopamine and serotonin, but the response of the neurons that receive opioid-peptide stimulation depends on their excitatory versus inhibitory nature, making the outcome difficult to predict.

The words ‘opioid peptides’ may not have left a dazzling feeling of recognition within your memory upon first encounter, but these peptides act within the brain and wider body to influence a number of important functions. Although it is not easy to predict the effect of neuromodulators that alter the release of other neurotransmitters, there is little question that opioid systems play a critical role in modulating a large number of sensory, motivational, emotional and cognitive functions. Alterations in opioid peptide systems may contribute to a variety of clinical conditions, including alcoholism, obesity, depression, diabetes and epilepsy. Many questions still remain, particularly those concerning the exact role of opioid peptides produced within the body in relation to addictive and emotional behaviour and psychiatric disorders. Since these disorders are typically of a complex nature, seeking the answers to these questions is not a simple feat. Advances in genetics and genomics research that aim to explain function by studying our DNA are helping to pave the way. But perhaps if there is one thing that can help motivate our talented scientists to reach their challenging goals, a healthy dose of opioid peptide might be just the thing.

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Protein supplements: powerful powder or powerful promotion?

protein supplementsGoogle the words ‘protein supplements for athletes’ and a number of links will appear in your browser. While apparently just a click away from learning the ‘truth’ about these dietary additions, it is advisable to consider the nature of whichever website you fall upon before hollering hallelujah. Company websites marketing protein supplements claim to give athletes the ability to ‘beat their best competition’ and to ‘get bigger and/or stronger’. Promasil, ‘the athlete’s protein’, for example, features seven of the world’s most powerful proteins. Imagine the industrial strength containers needed to keep these key ingredients from escaping. No more five dozen eggs a day to grow biceps the size of barges (the strategy adopted by Disney’s Gaston), a more palatable and practical solution is delivered in the form of a delicious flavoured powder. Since proteins are a major component of muscle, it surely makes sense that consuming more would result in extra bulk. But protein supplementation is not only about bodybuilding. For those more concerned about beating personal bests and leaving the competition trailing behind, protein supplements are also argued to directly enhance endurance performance and to optimise recovery of muscle function following exercise.

So how does it work? Naming a chocolate bar after a long-distance running event (and later rebranding using a word that sounds like underwear in British vocabulary – ‘Snickers’), no doubt taught the importance of carbohydrate as an energy source. Through reduced breakdown of carbohydrate during prolonged exercise, protein supplements are thought to enhance performance and to more quickly replete muscle glycogen (a specific type of carbohydrate) during recovery. By stimulating muscle protein synthesis, protein supplementation is also theorised to reduce muscle damage and speed up the recovery of muscle function. If you recently ran down a hill or lifted some weights, ideally not at the same time, you may later have felt soreness in your muscles, caused by damage to proteins that are required for muscle contraction. In such circumstances, rates of muscle synthesis and degradation are increased, and without sufficient protein intake, rates of degradation exceed synthesis and a negative net protein balance results. Consuming protein supplements during recovery from exercise should, however, promote the production of skeletal muscle (muscle that is attached to bones and contracts on demand).

Despite the logic behind these claims, a systematic assessment of the evidence to support or refute the relationship between the use of protein supplements and exercise performance, muscle damage and soreness, and recovery of muscle function has until recently been lacking. Earlier this year, Pasaikos, Lierberman and McLellan addressed this dearth by publishing two review articles in the journal Sports Medicine.  Examining publications reporting findings from ‘healthy human adults’ (no chimpanzees thankfully) between 18 and 50 years of age, they found no apparent relationship between recovery of muscle function, muscle soreness and muscle damage when protein supplements were consumed prior to, during or after a bout of endurance or resistance exercise. If supplemental protein was consumed after daily training sessions, however, beneficial effects such as reduced muscle soreness and damage became more evident. They also found that when carbohydrates were at optimal levels during or after exercise, protein supplements provided no performance enhancing effects. In particular, sparing of muscle glycogen stores was not supported as a mechanism leading to enhanced endurance performance.

Pasaikos et al. warned, however, that small numbers of participating adults and lack of dietary control limited the effectiveness of several of the investigations they examined. Since studies did not measure the effects of protein supplementation on direct indices of muscle damage or muscle glycogen, for example, the interpretation of the data was often limited. What does seem clear, however, is that if athletes maintain a healthy diet, by consuming enough protein and carbohydrate through traditional means (for example regular food), protein supplements are unlikely to generate record breaking results. Only when the healthy human adults involved in the studies examined by Pasaikos et al. were lacking in nitrogen (found in amino acids that make up proteins) and/or energy balance were performance enhancing effects of protein supplements found to be greatest. Endurance is of course built by training and not protein alone. Whilst Pasaikos et al. demonstrated the need for further high quality research on the potential benefits of protein supplements, a healthy diet, sufficient rest and undeterred dedication seem to be best recipe for success.

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An Apple a Day!

appleAn apple a day may keep the doctor away and is a good idea title for a book, but it’s probably a bad premise for a scientific study. The other day, a friend of mine drew my attention to a headline in the UK Telegraph “Eating an apple a day improves women’s sex lives, study shows.” Bad grammar not withstanding, I defied my better judgment and decided to read the article. The Telegraph doesn’t have the best track record of health reporting. Recently they wildly misreported a study about edible flowers and true to form they botched this one as well.

The article makes a number of claims. It says that that apples have “been show to be an aphrodisiac,” that “an apple a day can improve the sex lives of women” and that they “boost sexual pleasure in healthy women.” These are impressive attributes for a simple fruit, so I decided to read the actual study this report was based on.

The study was published in the Archives of Gynecology and Obstetrics. Essentially researchers took 731 women and asked them how many apples they ate every day and then asked them to fill out a questionnaire about their sex lives in areas such as desire, arousal, satisfaction, pain, etc. Researchers found an improvement in lubrication and consequently in the total score, but not in any other area of the questionnaire. Here is an actual quote from the study, “No significant differences between the two study groups were observed concerning desire, sexual arousal, satisfaction, pain and orgasm.” (Interestingly, the group that ate less apples had a slightly higher satisfaction score 4.5 vs. 4.3). This strikes me as fairly convincing that apples are don’t affect the quality of women’s sex lives at least in terms of the metrics that actually matter. Having read this study, I cannot for the life of me figure out how the Telegraph could have generated their headline. I can only assume they didn’t actually read it and just parroted the press release.

Even if you accepted their one single positive finding, the study has a lot wrong with it. First off, it is not a randomized clinical trial. Even though the newspaper story seemed to imply that it was, here researchers simply asked women how many apples they ate and did not actually conduct an experiment. It is easy to image why women who ate apples on a daily basis would be different than women who did not. They were likely more health conscious, probably exercised more, and probably had a better diet overall. Those who ate more apples probably ate more bananas, more oranges, more pears and more fruits in general. Researchers did not ask about other fruits and they likely could have just as easily shown an association with kiwis or pomegranates. So why apples? I guess the link to the biblical story of Adam and Eve was too good to pass up. Of course, the fruit of the tree of knowledge wasn’t actually an apple but why quibble on details.

The newspaper article also then makes a number of claims that the benefits of apples are due to phloridizin and polyphenols.  This is pure speculation. This study, as I mentioned, did not measure any hormone levels or perform any tests on the apples themselves. It was purely the analysis of questionnaire sent out to women.  Clearly, throwing in a few “sciency” terms (and adding the requisite photo of an alluring women biting into an apple) made the article more appealing to the newspaper editors.

Apples are unlikely to improve your sex life and, while we’re at it, neither will oysters, chocolate, or ginseng. An overall healthy lifestyle with regular exercise and a balanced diet is probably your best bet (but admittedly this would make for a lousy headline). So what can we conclude overall about eating an apple day? No effect on sexual desire or satisfaction, great title for a book, and (from my point of view) it’s bad for business.

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