It turns out berry is actually a botanical term, not a common English one. It turns out that blackberries, mulberries, and raspberries are not berries at all, but bananas, pumpkins, avocados and cucumbers are. So what makes a berry?
Take-home message: – THC is very dangerous to most companion animals – Medical cannabis has only a few uses in humans, and even fewer in animals – Cannabis, hemp or CBD treats, food or supplements are not approved or regulated by Health Canada. They are illegal and could be quite dangerous for your pets.
While medical marijuana has been available to varying degrees for decades, with recreational marijuana legalized this week in Canada, discussions about what (if anything) cannabis can treat seem to be at an all-time high (see what I did there?)
Discussions of treating medical problems with cannabis are not limited to humans. If cannabis may benefit humans, it may similarity benefit companion animals like dogs or cats. Considering that some of the major ailments cannabis is touted to treat are prime concerns for pet owners (anxiety, arthritis, pain) it makes sense for pet owners to be curious about cannabis.
Cannabis can be very dangerous for pets
When discussing cannabis and companion animals, it’s important to define a few terms.
Tetrahydrocannabinol or THC is the main psychoactive component of cannabis. As most pet owners aren’t interested in getting their furry friends high, the vast majority of pet-marketed cannabis products are free, or almost free, from THC. Which is good, because THC is quite dangerous for animals.
Since it’s difficult to study cannabis (due to it’s soon-to-expire illegal nature) we lack recent numbers on the dose based effects of THC in dogs. Early studies report intoxication effects in dogs with doses between0.25 and 0.5 mg/kg of body weight. If your average German Shepard is about 30 kg, they would show THC’s effects after ingesting 7.5 – 15 mg, or about a 10th of your average “special” brownie.
Though cannabis intoxication and adverse effects have been reported in other animals like cats, horses and ferrets, it’s much more common in dogs. Why? Because dogs like to eat. As Dr Sarah Silcox, the President of the Canadian Association of Veterinary Cannabinoid Medicine explained to me, “edibles, in particular, are very attractive to dogs, and if left within reach of pets, will often be gobbled up quickly.”
While it’s not likely that pets will die from cannabis exposure (through smoke or edibles) there can still be serious effects, especially if left untreated. Fluffy and Rover probably won’t get a kick out of the intoxicating effects of cannabis, given that they can’t understand what’s happening. Pets may experience significant anxiety, agitation or lethargy. Smoke of any kind can cause respiratory distress and potentially lung cancer to pets who inhale it regularly, due to the polyaromatic hydrocarbons created during incomplete combustion. Cats in particular are at risk of developing malignant lymphomas when exposed to secondhand cigarette smoke, a risk that may transfer to other types of smoke. .
So what’s with all the cannabis products for pets then?
Pet treats, foods and supplements in general feature no THC. They instead contain a different cannabinoid found in cannabis: cannabidiol or CBD. CBD is not toxic to animals like THC, and it does not cause the same psychoactive effects.
This study of 16 dogs with osteoarthritis showed a significant decrease in pain after treatment with CBD oil, but similar studies, or studies looking at cannabis to treat other conditions are seriously lacking.
Dr Silcox mentioned many anecdotes of positive effects of CBD products on pets, and this survey have found that that well over half of all owners polled who have used cannabis products on their pets felt it helped. But anecdotes are never evidence enough. We need good, large, controlled studies to properly evaluate the potential benefits and risks of cannabis products on cats, dogs and other pets.
For pain treatment however, the evidence for cannabis hasn’t looked wonderful. This 2015 review found evidence for use of low dose cannabis for neuropathic pain, but not for other pain. This 2018 Cochrane review states that the use of cannabis for “chronic neuropathic pain might be outweighed by their potential harms.”
Second, as Dr Silcox wrote, there is a “concern that that pet owners will attempt to medicate their pets with cannabis products and without appropriate guidance, put their pets at risk of adverse effects.” When we give our pets, children or ourselves any medication we first check dosage information, but the problem is that it isn’t available in any well researched, accurate or well-defined way for most species.
Third, pet owners may use cannabis in lieu of other evidence-based treatments, putting their pets at risk or hurting their quality of life. We don’t really know what cannabis can or should be used for in animals, but that hasn’t stopped many owners from using it for things like pain, anxiety management and diabetes management. My fear, simply put, is that owners will choose cannabis over NSAIDS, over other pain killers, over insulin, and even over euthanasia. I hope that no animals are suffering as a result of receiving cannabis as an alternative treatment to conventional veterinary medicine, but my fear is that it’s already happening and will begin to happen more with legalization.
Whether they work or not, they’re illegal and unregulated.
Until October 17th, 2018 all products containing plant-derived cannabinoids (which includes THC and CBD) fall under the Controlled Drugs and Substances Act. But even after the 17th, it isn’t open season for cannabis products. The new Cannabis Act will regulate the approval and sales of cannabis products, meaning that anything sold legally will need to be approved by Health Canada.
Health Canada currently has no products approved for veterinary or animal use. So CBD and cannabis products currently have, as Dr Silcox explains, “no regulatory oversight to ensure their quality, safety, or effectiveness. While they are marketed to treat a range of ailments, these health claims are unsubstantiated by Health Canada, the products are not approved, and as such, are not compliant with Canadian law.”
Now, that could soon change. With legalization around the corner, studies on cannabis and its effects are about to become a lot more feasible. With more evidence we will be able to hash out which CBD claims have merit, and which are baseless.
With entire conferences being held on veterinary use of cannabis we can hopefully expect some answers soon. In the meantime, a few things remain really important.
Take-home message: – gamma-Aminobutyric acid (GABA) is a major neurotransmitter that regulates much of our brain function. It was previously thought that ingested GABA could not cross the blood-brain barrier, but new research suggests that it may be able to. – Drugs that mimic the action of GABA are numerous, work in a variety of ways, and can have effects ranging from treating epilepsy to causing it. – GABA supplements have shown some promise in early, small-scale studies, but a lot more research is needed to know if they truly help.
Lately, it seems that GABA supplements are being hawked on the corner of every pharmacy aisle and health food shelf. Marketed to promote relaxation, mental focus and sleep, GABA is even being sold by David’s Tea in the form of GABA guava tea. I found it while trying to buy some matcha powder. I don’t even like guava, never mind guava with a side of inflated claims.
While promotions by influencers like Olivia Culpoand Sarah Couture are pretty standard for any trendy supplement, (regardless of efficacy) the attention GABA has been given by known quacks like Dr. Oz,Joseph Mercola orMike Adams has left me wondering about the science behind, and evidence for, these supplements.
Let’s start with the basics: what is GABA?
gamma-Aminobutyric acid (also written as γ-aminobutyric acid) is a neurotransmitter, specifically the major inhibitory one in all mammal’s central nervous systems (CNS). That means that it’s a chemical that binds to nerve cell receptors and hinders their ability to receive, create or send messages to other nerve cells (neurons).
Functionally, GABA is incredibly important. A lack of GABA leaves your central nervous system with too many neuronal signals and causes conditions like epilepsy, seizures or mood disorders. Meanwhile, too much GABA means not enough brain activity and can lead to hypersomnia or daytime sleepiness.
You can learn more about GABA in this lovely video, and more about neurotransmitters in general in this one, although I’ve said all you’ll need to know for this article.
As the chief inhibitory neurotransmitter in the CNS, GABA and its receptors have been major targets for drug development. Drugs that activate GABA receptors (called agonists) or increase the receptors’ sensitivity to GABA (positive allosteric modulators) work to reduce the neuronal signals in the user’s brain, similar to what happens when you sleep. Logically, they include many common sedatives like barbital or Quaaludes, tranquillizers like Valium, Ativanor Xanax and the most commonly used sedative, alcohol.
On the flip side, substances that inhibit the activity of GABA (called antagonists) increase brain activity. That only sounds like a good thing. The results are less Scarlett Johansson in Lucy, more uncontrollable seizures and death.
GABA antagonists, like gabazine or bicuculline are only useful when studying seizures or to counteract overdoses of sedatives and tranquillizers. Some GABA antagonists are particularly scary poisons, causing death by disrupting the CNS’s control of basic body functions like breathing.
The class of drugs we’re most interested in, however, are GABA analogues. These molecules are structurally similar to GABA, though they have different targets of action. GABA analogues include some big names you’ve probably heard of: Lyrica and gabapentin.
While both Lyrica and gabapentin are prescribed to stop seizures, treat neuropathic pain, and anxiety disorders, gabapentin is additionally used for the prevention of migraines.
Gabapentin has been a constant in my life for a few years now, as my mother was prescribed it for diabetic neuropathic pain just a few years after my partner was prescribed it for near constant migraines. I’ve personally seen GABA to be quite effective in its on-label uses, as the evidence shows it to be, but it was recently at the heart of one of the largest court settlements in US history.
The manufacturers of gabapentin were found to have been marketing it extensively for off-label uses like the treatment of bipolar disorder, restless leg syndrome, hot flashes and stopping smoking. While off-label prescribing is not uncommon, and usually fairly safe, there is no evidence that gabapentin is effective for the bipolar disorder it was being prescribed to treat or some of the other conditions for which it’s being prescribed.
Presently gabapentin is again making headlines as its use as a recreational drug skyrockets. Many opioid users are misusing gabapentin to extend opioid highs or bypass drugs that block opioids effects, but its status as a non-controlled substance makes it difficult for law enforcement to control its unsanctioned use.
GABA and the Blood-Brain Barrier
GABA drugs are certainly useful, but why do we need all these GABA-receptor-activating or GABA-like molecules in the first place? Why not just give patients GABA?
We have a highly selective membrane that keeps our blood and cerebrospinal fluid (or brain juice, if you will) separate: the blood-brain barrier (BBB). Some molecules, like water, pass through it easily, other things, like bacteria don’t. This membrane also contains special channels to diffuse important molecules one way or the other, like glucose.
It’s a really important border, as drugs that cannot cross into the brain, or do so poorly, have much less of an effect than ones that do. For example, morphine can’t cross the BBB very well, but it’s close relative heroin can! Upon entry to the brain, heroin is converted into morphine, which is why heroin is so much more potent than morphine.
A 1958 study was the first to look at GABA’s relationship with the blood-brain barrier, and it found a lack of one: GABA could not cross the barrier. Later studies in ‘58, ‘71, and ‘88 confirmed the barrier’s impermeability to GABA. The evidence seems all but clear until you throw a few more studies into the mix. Studies done in ‘80, ‘81, ‘82 and ‘02 found that GABA did cross the blood-brain barrier, just in minuscule amounts.
Why the disagreement? Well, a few things. Some studies used a molecule just like GABA in lieu of GABA, assuming the 1 extra OH group featured on 3-hydroxybutyric acid wouldn’t make a difference, but it may have. Since many studies don’t report the type of GABA used, it’s hard to compare results. Some studies administered their GABA by injecting it straight into animal’s body cavities, others by injecting it into veins.
Most importantly, the BBB permeability of GABA has never been studied in humans!
What we do know is that human’s BBB contains transporters for GABA, implying that GABA can enter/exit the brain through these channels. In mice it was found that GABA was removed from the brain 17 times faster than it entered.
This could explain the conflicting study results. It may not be that GABA cannot enter the brain, but just that it’s removed from it very rapidly.
GABA as a Supplement
Even if it cannot cross the BBB however, GABA could still be affecting your brain.
The enteric nervous system (ENS) is the network of neurons that control your gastrointestinal system. The ENS contains many GABA receptors, and GABA itself, and is connected to the brain through the vagal nerve. It’s been proposed that ingested GABA is able to affect the body even without crossing the BBB through its interactions with the ENS.
We don’t know at this point how GABA is affecting the brain, but we have good evidence that it is. Several studies have shown reductions in markers of stress in patients given dietary GABA.
On their own the success stories from the consumers who buy GABA supplements are meaningless but taken along with the research findings, they may just show that there is something to these supplements.
We’ll need a lot more research to know for sure if GABA supplements are helpful or not. That being said, they are expensive (like most supplements) and if you’re not anxious, experiencing insomnia or very stressed out they’re probably not worth it. There don’t appear to be many side effects or drug interactions, but until more research is done I’d tread carefully.
I did ask my partner, who took gabapentin (a GABA analogue) for years if he ever experienced any focusing of his mind or relaxation as the GABA supplements claim. He said a definitive no.
Want a cheaper option for relaxation? Tea. You can even try some GABA tea, a strain of green tea specially fermented to accumulate GABA. Maybe I’ll pick some up… just not that guava flavoured stuff.
Ghee can be found in the international section of most grocery stores, and clarified butter on the pages of many culinary magazines, but what are these fats, and how do they differ from normal sticks of butter?
Butter is made from milk, which itself is composed of globules of butterfat suspended in water, with carbohydrates, minerals and proteins dissolved in the mix. So, when you melt butter it separates into three layers.
From top to bottom they are milk solids (the proteins, minerals and carbs), butterfat, and a combination of more milk solids and water. Clarified butter is simply this middle layer of butterfat, which can be attained by skimming milk solids off the top, evaporating the water, and decanting the butterfat.
Ghee simply requires an extra step: simmering. After the risen milk solids are skimmed off the top, the butterfat, with sunk milk solid still present, is simmered until it begins to brown. The browning of the milk solids provides the nutty flavour that makes ghee so desirable. The butterfat is then decanted off, leaving the browned milk solids, but taking some of their flavours with it.
Why go through this skimming and decanting hassle? A few reasons. First of all, because you’ve eliminated almost all of the milk solids, clarified butter and ghee are essentially lactose-free, something your lactose intolerant friends will appreciate considerably.
Second, butterfat, unlike the butter is was made from, does not burn at such low temperatures. Where butter’s smoke point (the temperature at which an oil begins to create a smoke, and its associated bad flavour) is 302˚F (150˚C), clarified butter’s smoke point is 482˚F (250˚C), which allows it to be used to cook at higher temperatures than any other standard cooking oil.
Thirdly, ghee and clarified butter are shelf stable. They can last about 12 months once opened, or many years if not opened, making them an attractive option for emergency kits, campers or those in rural areas.
If you’re not cooking at really high temperatures, lactose intolerant, or an adventurer, however, there’s no reason to switch to the clarified variety of your toast spread.
While ghee has been part of traditional Indian medicine (specifically ghee made from breast milk) there’s no evidence to support the many health claims made of this fat. Ghee and clarified butter are almost nutritionally identical to the butter from which they’re made.
In the end, clarified butter is still butter, and butter is not a health food.
Take-home message: – Women have an organ analogous to the male prostate that is able to produce a liquid that can be ejaculated upon orgasm. Not all women produce ejaculate. – The scientific study of female ejaculation and the female prostate has been greatly hindered by bad science, cultural taboos and sexism.
In 1642 a Dutch researcher, Regnier De Graaf, made a clinical description of the female prostate using modern scientific methods. In the 1800’s, Alexander Skene characterized the organ further and replaced its name with his own, calling it theSkene’s glands.
But from here on the story of female ejaculation gets messy. Societal ideas of femininity, masculinity, gender and sexuality seemed to influence the scientific study of female ejaculation. A lot of good studies on the topic got overlooked, and some bad science got overused.
The tale of female ejaculation and the female prostate is important to tell not only because many women still struggle with orgasms, sexual fluids and their sex lives, but also because it serves as a shining example of how culture can influence science.
So, without further ado, let’s get down to the nitty gritty.
A Remake of an Old Classic: Can Women Ejaculate?
At the beginning of the 20thcentury a renaissance of female ejaculation studies occurred. Early papers discussing the phenomenon lacked a unified opinion on whether a liquid may exit a woman’s genitals upon orgasm, and if it did, where it came from or what it was made of.
Ernst Grafenberg (now famous for first describing the G-spot) introduced a controversial idea in the 1950’s when he postulated that stimulation of the G-spot was responsible for the ejaculation of fluid through the Skene’s glands. Despite his status as a respected researcher his thorough descriptions of the female ejaculation were seen by academia as anecdotal at best and falsified at worst.
If the work of experts was not being recognized, it seemed unlikely that others would have luck publishing pro-female ejaculation research. And indeed, after Grafenberg came quite a bit of writing outright rejecting the notion of female ejaculation. Notably, even Alfred Kinsey, famous for inventing the Kinsey scale, and in many ways the father of modern sexology, weighed in on the topic of female ejaculation, claiming that it truly was contractions of the vagina pushing out the fluid from the vaginal walls, and therefore not an “actual ejaculation.”
The few papers in support of female ejaculation that were published postulated that female ejaculation might originate from small glands located just below the urethra. At the same time, another theory started making waves: that female ejaculation was just urinary incontinence.
But, for all of the papers being published, no actual studies were being performed. It wasn’t until the 80’s that studies of female ejaculation started occurring and turning up evidence for female ejaculation. A couple of literature reviews on this subject in the mid 80’s consider the study by Addiego et al. in 1981 to be the first “hard” research done on this subject. It was a case study and “provided objective evidence supporting the hypothesis that female ejaculation, a partial, infertile homologue of male ejaculation, exists,” and that it was at least in part chemically distinct from urine.
Are You Sure You’re Not Just Peeing? Really Sure?
The landscape of research shifted slightly after this case study, as the goal was no longer to prove or disprove the existence of the female ejaculation, but now to classify its composition and source.
To do this, several more studies were conducted in the1980’s that either definitively classified urine and ejaculate as two distinct fluids or came to no conclusion at all. The only studies opposing this conclusion were performed by Goldberg et al. in 1983, and Alzate in 1985. Goldberg tested six women, Alzate only one. While Goldberg concluded that “the ejaculate and urine seem to be one and the same,” Alzate only wrote that the ejaculate and urine were chemically indistinguishable. Nonetheless it’s Alzate’s study that was cited again and again as proof that female ejaculate was urine.
Most of the urine analysis studies compared female ejaculate with urine across some variation of chemical parameters: creatinine (a muscular waste product), urea (the main component of urine), pH, prostate specific antigen, or glucose. There are many reasons why the concentrations of these components in urine may change. We should not ignore the fact that, just because two liquids are similar across these parameters, it doesn’t mean they are the same.
Alzate’s study did not primarily examine the chemical composition of the fluid, analysed only 1 sample, and even within that sample found some large chemical differences between the urine and ejaculate (like 14 mg of glucose in ejaculate vs 1.9 mg in urine). There is a space between being certain ejaculate is not urine and being certain that it is, and that is where this study lies.
The 80’s and 90’s saw several more studies tha tfurther proved the non-urine nature of female ejaculate, so with the existence and nature of the ejaculate seemingly sorted, research shifted to finding its source.
Do Women Have A Prostate?
De Graaf had initially coined the term female prostate for the female ejaculatory organ, but this terminology had been rejected and reworked into the Skene’s glands, since it wasn’t thought the female prostate (if it even existed) was analogous to the male prostate. Well, the late 80’s saw the resurgence of the name ‘female prostate’ for this organ, as the evidence mounted for the analogous nature of the male prostate gland and Skene’s glands.
The evidence pointed to a female prostate that was the source of female ejaculate, as well as a highly functioning hormone producing organ, with function very similar to the male prostate. Dr Zaviacic, who performed hundreds of autopsies, chemical and clinical experiments, reported that “the female prostate was observed at autopsy in two thirds of women of reproductive age”. He also wrote that there was massive variation in prostate size, function and component ratio from woman to woman. These variations could explain why only some women ejaculate, and why the volume and colour of that ejaculate seemed so variable.
With the name “female prostate” poised to fall back into usage, semantic arguments seemed to dominate the conversation. Scientists argued over minute anatomical points, and whether the prostates found in women could be considered “well developed.” They argued that since female ejaculate served no reproductive function, it shouldn’t be called ejaculate. And they argued over the very definition of ejaculate. Did an ejaculation originate, by definition, exclusively from a penis? Did an ejaculation need to contain sperm?
Thankfully, in 2001 the Federative Committee on Anatomical Terminology officially renamed the Skene’s glands back to female prostate’’ and ended this tedious terminology argument once and for all.
Regardless of what it was called though, it seemed that the world had finally reached a consensus that women have prostates and can expel a fluid upon orgasm that is not urine. Research in support of female ejaculation continued to appear, and systematic reviews, like this one by Pastor, further highlighted that female ejaculation was not due to urinary incontinence.
Thus, the long debate seems to have ended.
There was actually one more study, in 2009, that denied female ejaculation. It suffered from some serious flaws however. Ahmed Shafik undertook an electrophysiological study of the female orgasm in 2009, investigating the hypothesis that “female orgasm is not associated with ejaculation.” After testing 38 married, middle-aged women with children via clitoral stimulation alone, he concluded that female ejaculation did not exist.
Now raise your hand if you see problems with this study. A small sample size with no selection for a history of ejaculation, non-varied demographics, and no G-spot stimulation despite evidence that that is the mechanism by which ejaculation is triggered. It’s just bad science.
New studies have found antimicrobial compounds, similar to those found in male ejaculate, in female ejaculate. So, it may be that female ejaculation could confer a protection against UTIs.
One of the last remaining mysteries was highlighted in a 2015 study that took pelvic ultrasounds of seven women who self-reported experiencing ejaculation. It found that before and after orgasm the bladders of the women were empty, but during the build up to orgasm, the bladder rapidly filled, and then rapidly emptied upon ejaculation. This large-volume ejaculate was found to be chemically similar to the women’s urine (though not identical).
The current evidence points to women not only ejaculating but experiencing two types of ejaculations: a small-volume ejaculate that is milky in colour and that originates primarily from the prostate, and a clear, larger-volume ejaculate originating primarily from the bladder.
Bad Science Doesn’t Only Affect Scientists
The bad science that paved the historical road of female ejaculation has had some serious effects. Our sordid history of female prostate denial has created a society unwilling to accept its existence, despite the scientific evidence.
For instance, studies have shown that people with vaginas are only shown reaching orgasm in pornographic movies in 18% of cases, with female ejaculation being shown 5% of the time, (As opposed to 78% and 90% respectively for men).
In 2014 Britain banned pornographic depictions of female ejaculation, claiming that the fluid ejaculated is really urine. They justified this on the basis that urine is unsterile and could cause an infection if a participant had an open wound. That’s true of all sexual fluids, but I don’t see them banning male ejaculation.
It’s hard (if not impossible) to quantify the effects the non-acceptance of female ejaculation has had on women. In the most serious sense, cases of female prostate cancer and chronic UTIs have likely gone undiagnosed or untreated. In a less life-threatening sense, many women have had to face a body of evidence that denies their everyday sexual experience. A quote from a research paper on this topic really highlights what women who ejaculated were up against: “The ignorance and/or confusion still prevalent among women about the anatomy and physiology of their sexual organs may make them mistake either vaginal lubrication or stress urinary incontinence for an ‘ejaculation’.”
We should let the long journey to the “discovery” of the female prostate serve as a cautionary tale. When we let poorly performed studies, misinterpreted results, and gendered assumptions drown out real evidence, we make mistakes, delay discoveries, and end up looking pretty dumb in retrospect.
I am fascinated that there still remain mysteries to uncover about our bodies, and truly excited to see what research is being done on female ejaculation and the female prostate now. I’m also waiting with bated breath to see when Gray’s Anatomy decides include the female prostate in its textbooks.
Goats are really useful creatures. We use their milk, fur, meat and… firefighting skills?
In several places goats and sheep are being herded into fire-prone areas. The hungry herbivores move through the land, munching on shrubs, trees and grass, and creating firebreaks. Since goats only stand about 1 metre tall, they will graze heavily on low-lying plants, creating a gap between the ground and higher trees. This gap can prevent fires from spreading or slow them down. Some places in Spain have even blamed recent wildfire severity on the declining number of herds grazing on the land.
Goats are perfect for the job for a few reasons. Unlike some grazers, goats do not limit themselves to leaves or grass, eating the wood and bark of smaller plants as well. Goats are able to traverse a wide variety of terrains, and they are naturally resistant to several toxic plants. They can also be herded in tandem with sheep or cows, creating an even more effective grazing party. Using goats comes with the added advantage of reducing the carbon footprint, compared to clearing brush with machines, and improving air quality. The waste left by goats is simply absorbed into the ecosystem of the area.
Studies have shown that a herd of 250 sheep can reduce the available plant mass by 75% in 30 days. When a wildfire in Utah with 15-foot-high flames reached an area that had been cleared by goats, the flames dropped to only 3 feet tall in lightly-grazed areas and stopped entirely in more heavily-grazed ones.
The biggest barrier to using goats in this way is a lack of trained and skilled herders and herding dogs to manage the goats. So, if you’re looking for a career change, a position in goat herding is probably available. Given goats’ relative quietness and lack of air-polluting outputs, they could be especially useful for grooming areas near residences and towns, so you may not even have to commute very far.
While this question seems simple, it turns out there are a lot of complex processes behind your development of a particular body size or shape.
Some biologic aspects are controlled by individual genes. Take for example sickle cell anemia. This red blood cell disorder is caused by inheriting just one abnormal gene from each parent. There is, similarly, just one gene implicated in people having or not having cleft chins.
Body size is not controlled by only one gene, but many, making it hard to predict the size of individuals before they reach adulthood. To further complicate matters, it’s not only genetics that influence body size. Factors like diet, nutrition, climate and health status all change how you grow.
As Manuel Will, an anthropologist and archaeologist with the universities of Cambridge and Tübingen, explained to me: “your genes define a range for the potential body size you might achieve as an adult, and factors duringyour development determine how much you realize of it.”
So how did different ranges of body size develop in the first place? We can look to random genetic mutations, competitive living and environmental influences in early Homo species to explain how such a range of human sizes developed.
It could be that a random mutation made an individual taller-therefore able to reach more food-or the opposite. Taller individuals would likely be more successful, so reproduce more, passing these genes to the next generation, but a certain number of less-successful shorter individuals would still reproduce and pass their genes on.
A trend develops wherein the gene pool contains more “tall genes”, and when you go fishing in it, you’re more likely to catch a tall person. There is still a range of heights available to catch, but the pool is overstocked with tall. But, gene pools are often destroyed, subdivided, reduced or impacted by natural events.
Famines, earthquakes or floods can cause population bottlenecks. This means that the gene pool is reduced to include only those who survived the disaster. It could be that every tall individual was killed, so that the tall trait goes extinct in future generations.
Since gene pools only exist between breeding populations, if a few of individuals left the main group to establish their own population, they are also establishing their own gene pool. Within this new pool though, certain genes can be over represented (maybe most of the new pool’s founders happened to be short). This is called a founder effect.
As humans began to migrate around and out of Africa, founder effects and population bottlenecks would have occurred frequently. Combine these genetic effects (nature) with the environmental effects (nurture) different groups of humans would experience as they moved around, like fires or plagues, and you can see why the world has so many different types of bodies.
So, there isn’t really a hard-and-fast rule for body sizes based on genetics, since location, nutrition and other factors play such a role. But, we can pick out some general trends. Individuals from colder environments tend to have shorter limbs and larger body sizes, while those from warmer climates are taller and thinner. Those from richer countries tend to be taller than those from poorer ones.
While it may seem universally beneficial to be a larger human, there are some drawbacks. Larger bodies take longer to grow and require more resources. They’re more likely to experience joint pain, and generally put more strain on their internal organs.
As modern humans continue living in an economically successful and stable countries their nutrition and health improve, allowing them to grow larger. There will always be variation in a population (some people shorter than average, some taller) but we can expect a general increase in average heights and body sizes of Canadians as time goes on.
I’ve been eating veggie burgers for a long time. If it’s sold in Canadian grocery stores or fast food restaurants, there’s a good chance I’ve tried it. There are some I like more, and some I like less, but they all fall into one of two categories: fake meat and veggie.
I like a veggie burger that knows it’s made of veggies, not one that’s pretending it’s beef. Mostly because all fake meat patties seem to come out as bad imitations. But, that seems to be changing in a big way.
What makes this burger different? The same thing that makes Fireball taste so good and Buckleys taste so bad. Chemistry!
The molecule responsible for the “meaty” taste of meat is heme and it’s found in animal muscle cells in the protein myoglobin. Sadly, there are no non-animal sources of myoglobin, but there is something pretty close: leghemoglobin.
Leghemoglobin is found in the roots of legumes and can provide a “meaty” taste very similar to its animal-based brother. It’s not especially environmentally friendly or affordable to dig up bean plants for their roots, so Impossible Foods had to get creative. They genetically engineered yeast to make leghemoglobin, so that by growing the yeast in fermentation vats they were able to create all the heme needed to make a meaty tasting veggie burger.
Other than heme, the ingredients of an Impossible burger are pretty similar to any other fake meat product. Wheat and potato protein, coconut and soy oil, some binders. All perfectly safe (despitesome cries of outrageover soy and GMOs).
How does it taste? On a recent trip to New York I went out of my way to find one and was not disappointed. The texture isn’t perfectly meat-like (or at least how I remember the texture of meat) but the taste was very similar, as was the look. But don’t just take my vegetarian opinion on the matter, here’s what Michael Marshall, The Project Director of the Good Thinking Society, had to say on it:
“If I hadn’t known what the Impossible Burger was – and, more to the point, what it wasn’t – I’m not sure I’d have been able to tell. It definitely wasn’t the best burger I’ve ever had, but it also wasn’t the worst, and that’s pretty impressive given that the rest of them (at least, I hope the rest of them) had the head start of actually being a burger. Possibly the most remarkable thing about the Impossible Burger is that they’ve managed to make a meat-substitute that differs from meat so little as to be unremarkable. If you’re looking to reduce or cut out meat but fear you’ll miss the experience of eating meat, it’s a pretty solid substitute.”
Sadly, the Impossible burger still isn’t available in Canada. A rival product however is being pushed by A&W: The Beyond Meat Burger.
This meat alternative also makes claimsabout tasting, smelling and having a meat-like texture. However, as far as I can tell it contains similar ingredients to any other veggie burger, with some beet added to dye the uncooked patty red. A&W’s website proudly states (several times) that their product is GMO free, a big change from Impossible Food’s pride in their GM technology.
Never one to pass up a veggie burger, I obviously went and tried the Beyond Meat Burger too. I was, to put it nicely, underwhelmed. It didn’t taste like meat. It didn’t really taste like anything other than a typical cheap veggie patty, and I honestly think I preferred A&W’s old veggie burger. It was boring enough that I’ll probably just opt for some French fries next time we make a road trip stop at an A&W.
But it’s not all about taste, right? Maybe the Impossible burger is delicious but very unhealthy? Well, nutrition-wise the two new veggie burgers actually beat out their meat competitors in terms of protein and iron (two of the nutrients vegetarians often struggle to consume). The Beyond Meat Burger has a lot more fat than the Impossible burger, but is still on par with the meat burgers. Perhaps the biggest lesson to learn from comparing the burgers is that while veggie burgers tend to cost the same (or less) as meat ones, at least at A&W they’re much larger!
There is also the animal welfare aspect of the meat industry to consider, as well as the documented health benefits to minimizing your meat intake. Technologies like lab grown meat or ethically raised animals can help your conscience, but not your wallet or heart. Part of what makes meat-like alternatives so compelling is their affordability.
While there are issues with replacing all meat with vegetable proteins, such as plant sources lacking some nutrients and ethical issues of putting herders out of work, there is a lot to be gained by embracing a vegetarian diet (or just going veggie sometimes). The Impossible Burger, and other products I hope are available shortly, might be a simple way to do that.
Until then, I guess I’ll stick to grilling Portobello mushrooms. Not such an impossible task.
A New York Times’ study of 500,000 race times, set wearing Vaporflys and other shoes, confirmed Nike’s claims. They found that Vaporflys allowed a runner to run 1% faster than the next-fastest shoe, and 3-4% faster than a similarly skilled runner running in different shoes.
These results, taken from race entries on the app Strava, show that runners were more likely to set a personal record when wearing Vaporflys (though not quite as likely as those wearing Nike Streak shoes). Runners were also more likely to run faster when switching to Vaporflys and complained of less leg fatigue.
So, what’s so great about these shoes? Carbon fibres. Each sneaker features a carbon fibre plate in the midsole which absorbs and releases energy, throwing the runner forward with every step.
Since the shoes don’t contain any springs or elastics, they’re not likely to be banned from future sports competitions. But given their $250 price tag, don’t expect to see me wearing them anytime soon.