Male Odor Bride

By: Ross Federman

If you have ever been sexually attracted to someone, you likely know how powerful a feeling it can be.  You may have also made the discovery that the person you’re attracted to smells really great.  And while you find that they smell amazing, your friends may not always react the same way.  Why is this? The answer is surely a laundry list of factors that we don't understand fully and plenty that we don't even know exist yet.  However, some of how this process works has been studied, and indeed much of what you’re smelling are pheromones—chemicals secreted in sweat and other bodily fluids that have purportedly evolved to attract mates. Several studies have found a fairly significant link between how attractive a potential partner’s pheromones are and how well their combined genetic codes would render their offspring in fighting disease. Evidence really does seem to suggest that one is more attracted to those that will make their future children together healthier.

Although we are very adept at battling infections in general, one of the most powerful aspects of our immune system is its ability to adapt and focus its power on a very specific virus, bacteria, fungus, or toxin that has invaded the body, and to remember that same target if it ever shows up again.  There are two analogous molecules in mammalian immune systems known as the Major Histocompatability Complexes one and two (MHC I/MHC II) that allow little bits and pieces of these pathogens to be "presented" to other components of your immune system.  Under the right confluence of events these bits and pieces of proteins presented by MHC I and II trigger your adaptive immune response to know what to look for.  For example, if some punk kid in a red t-shirt sneaks into a black tie charity gala to get free food and drinks, the MHCs would basically show the red t-shirt to other cells, training them to look for it amongst the crowd.  I can't underscore enough how incredibly important the activity of MHC I and II is to your immune system.

The MHC proteins are made by various genes in the HLA family, and these HLA genes are the most diverse in the entire human genome.  That is to say, within the human population, there are many more varieties of MHC proteins than any of the other proteins that your genome codes for.  Each MHC has its own unique ability to present various types of peptides (which are chopped up bits of larger proteins) to your immune system.  In this case, these peptides are considered "antigens" by your immune system, small molecular signatures that allow for specific recognition, much like the red t-shirt on the moocher in the example above.  And while each unique MHC can present a wide variety of peptides and antigens, no single MHC can do this for all possible peptide antigens.  To answer this, we have evolved to each have several copies of HLA genes instead of just one.  This gives us the ability to try to cover as wide a range as possible in what our immune system can recognize and mount an attack against.

At the population level, this variety is crucial.  It ensures that the human race will have a spectrum of susceptibility to any given pathogen, so that even the worst mega pandemic virus will find some humans whose MHC molecules will present the viral antigens so efficiently that they will (hopefully) survive.  Essentially, evolution has given us the ability, as a whole species, be more suited to survive these horrible occurrences like the plague, the 1918 flu, and countless other similar events that undoubtedly occurred before recorded history.

But back to you and the awesome kids you'd have with that person that smells delicious and you’re finding yourself attracted to.  You and your partner each have a unique set of HLA genes creating a unique blend in ability to present various different antigens.  When you and your mate have very different MHC molecules, your offspring will ultimately get an even greater variety, and since HLA diversity has been so evolutionarily beneficial to our immune systems, our bodies seemed to have developed the ability to pick up on this as a cue.  Thus, we find a far more attractive scent or odor from a potential mate whose HLA genes differ from our own.  So it appears that our senses have been evolutionarily tuned to help us find sexual partners that will give our offspring a survival advantage when it comes to fending off disease, though it is still mysterious as to how this phenomenon occurs at a molecular level.

So take a second to forget about all of the crazy things going on in your head and your body when flirting, dating, or just meeting someone for the first time.  If you find yourself drawn to their scent, it could very well be nature's way of saying, "Hey if you two have kids, they'll have well equipped immune systems to fend off disease."  And with the lower and lower numbers of parents vaccinating their children recently, it might not be such a bad idea to keep this mind.

I Kid You Not, A Disease Exists That Makes You Drunk, Constantly

By: Ross Federman

A bar I used to frequent serves a delicious frozen drink known as a “Constant Buzz.”  It sounds like an appealing concept, a nice basal level of ongoing intoxication, but did you know that in some incredibly rare cases, individuals find themselves in this situation without any choice?  Auto-Brewery Syndrome (or gut fermentation syndrome) is a disease whereby patients literally brew alcohol in their guts.  Imagine not taking a single sip of beer, wine, or liquor, yet still constantly registering above the legal limit on any manner of blood alcohol or breathalyzer tests.  This is the unfortunate case for those rare few that find themselves with this disorder.

How does it happen?  It was a mystery for years.  In fact, it’s likely that some may have been incarcerated, fired from jobs, suspended from school, you name it, all because they were drunk against their will with no explanation to offer as to their erratic behavior.  Recently, we have gained significant insight into the nature of our gut microbiota and the profound role that it plays in human health.  The microbiota is usually discussed in terms of the species of bacteria that comprise it; yet other microorganisms are present, as well.  In most healthy microbiota, a small population of the commonplace fungal yeast species Saccharomyces cerevisiae lives in your gut with all the other microorganisms.  S. cerevisiae is also known as “Baker’s Yeast” and is the species often simply referred to as “yeast” in the majority of baking and beer brewing applications. You and everyone around you likely have some S. cerevisiae hanging around in your guts, and the amount of it is largely kept in check by your immune system, other microorganism species, and competition for nutrients.  However, in some rare cases, this population is not kept to the proper minimal levels and grows wildly out of control. 

At the heart of this phenomenon is the fermentation process.  It is found in both yeast and bacteria, though the specific fermentation products differ.  In both cases, sugars or carbohydrates are broken down to carbon dioxide in order for the microbes to produce energy in an environment lacking oxygen (such as our guts).  For bacteria, lactic acid is the second byproduct along with carbon dioxide, but in yeast, ethanol is produced in lieu of lactic acid.  Thus by increasing the ratio of S. cerevisiae to bacterial species in the gut, greater amounts of ethanol are produced, and past a certain threshold, the ethanol metabolic product seems to reach levels where it is in a great enough concentration to equate to imbibing ethanol in the form of an alcoholic beverage.  It should also be noted that this same fermentation process is used to achieve the alcohol content in said beverages, though this, of course, does not take place directly in our stomachs.

Even with a greater understanding of the microbiota, the precise nature of why these yeast populations can grow so large and lead to ongoing intoxication remains unknown. Cases are so rare that really everything we know about this disease is almost entirely anecdotal.  Perhaps the patients ate an absurd amount of sourdough after taking antibiotics that would have wiped out many of the bacteria just prior to yeast colonization?  Whatever oddball circumstance lead to this, the end result?  Enough yeast in your gut to lead to fermentation levels that are actually sufficient enough to influence blood alcohol levels.  Sounds pretty awesome if it only lasts for the three days you spend at Coachella, but week in and week out, it would probably get old pretty quickly.

Did someone really prove that eating red meat causes cancer?

By: Ross Federman

One frustration facing many scientists today is the manner in which primary research articles are interpreted by other writers and subsequently reported to the general public.  Often, important subtleties and details regarding the experimental design are disregarded, and while researchers are careful to qualify their conclusions based on this, other writers may not be. The past few weeks has provided a clear example of this.  This research article provides some implications, and promises to guide future research to gain more insight into the question at hand. However, many articles covering the research, such as this one from The Telegraph, are stating these implications as a concept that the article “proved,” in this case, that eating red meat will cause cancer.

First off, it should be noted that there is long standing epidemiological data to show that those who consume meat in their diets, on average, have a higher risk of developing cancer than those who abstain from meat consumption.  It’s also a widely held opinion that this is likely due to increased chronic inflammation that is present in meat eaters.  To date, there was very little mechanistic evidence or insight into why meat eaters suffer from more inflammation and thus higher risk of cancer.  An article published at the end of last year in The Proceedings of the National Academy of Sciences, a very reputable and highly respected journal, provided some a possible mechanism to account for this.  They showed that there is a specific sialic acid molecule (N-Glycolylneuraminic acid or Neu5Gc for short) present in almost all meat consumed by humans, and that this molecule becomes incorporated into the human body after consumption.  The molecule is of course also present in any animal that the meat came from.  To these animals, Neu5Gc is considered “self.” That is, their immune systems are trained to ignore it.  Humans however, do not produce this molecule on their own, so their immune systems likely see it as foreign.  This in theory could lead to an antibody response whereby antibodies specific for the molecule are created, and induce inflammatory conditions wherever it is present. In a meat consumer, this would be all over the place.  The resultant chronic inflammation would thus increase an individual’s risk of cancer.

So what did these researchers actually do?  They used a mouse model in which they deleted the gene in mice that produces Neu5Gc. This deletion essentially made the mice more like humans in the sense that they would now see Neu5Gc as foreign.  They artificially introduced antibodies directed at the molecule, found that these antibodies did indeed promote chronic inflammation, and that mice treated with the antibodies had significantly higher incidence of cancer.  This provides a mechanism whereby a mammal that does not produce Neu5Gc inherently may be able to produce antibodies against it that promote inflammation.

What did they not show?  First off, none of this work was done in humans, and while mice provide a great experimental model, they are different animals, and not all conclusions drawn from mouse work can simply be transferred to our understanding of humans.  But more importantly, the antibodies that mediate this mechanism were artificially introduced into the mice, and without them, there was no response to the foreign meat residue whatsoever, or at least not enough to significantly impact tumor development.  The authors justify this by stating that antibody responses to this molecule have been shown in the past, but that they are quite complex and not easily controlled in an experimental system.  That’s not a major problem in terms of the research itself.  This still provides a model mechanism to explain the increased inflammation caused by meat consumption.  However, this does become problematic in others’ interpretations of the work because it is a subtle distinction that any immunologist would look and therefore take some of these implications with a grain of salt.  Those covering this research for broader scope publications however may have either not picked up on this, or simply chosen to ignore it. 

Thus, while this research is well executed and appropriately interpreted by the authors, the interpretation by some of the writers that have covered this article are really not supported by the work.  The interpretation that this work has “proven that meat eating causes cancer” is far too great of an over-simplification, and not a correct conclusion to draw from this particular study.  Again, the mice and human differences cannot be overlooked.  Hopefully, because of this study, researchers may begin to look at human antibody responses to this particular molecule, but until that is examined, the relevance to human health is merely an implication, certainly not a conclusion.  The other elephant in the room here is that the gene deletion was not enough to induce this mechanism without the artificial addition of antibodies specific for the residue.  This implies that the true mechanism at work in a physiological context is likely far too complex to be easily explained by this particular study.  So while this is great science, and certainly contributes to the story of “cancer from carnivore,” it is not sufficient to prove much other than the fact that this particular mechanism is possible given all the right conditions that may or may not be present in human meat eaters, but they could be, potentially, and that is really the heart of the paper. 

In all reality, very few individual research papers “prove” major concepts such as these.  Rather, each paper contributes in a way that creates a larger and larger foundation for future studies, fills in knowledge gaps in the field, or both.  This paper does both.  It sheds light on the knowledge gap between meat consumption, and cancer promoting chronic inflammation, while guiding efforts to begin to examine the human antibody response to the molecule in question.

At the end of the day, this shouldn’t really change what the average person thinks about meat consumption.  It was already known that this diet habit is linked to higher rates of cancer.  There are many similar associations of this nature.  Pilots and other flight crewmembers have significantly higher risk of developing acute myeloid leukemia likely due to the increased UV radiation exposure that occurs at flying altitudes over accumulated flight hours for example. This has not stopped us from taking full advantage of flight as a convenience of the modern age, and for many to pursue careers as pilots. Most people would be amazed to see the list of materials or conditions that cause cancer. It’s astounding. And based on how long mankind has been consuming meat, it is likely that the impact meat consumption has on cancer development is fairly minimal. The long history of meat consumption (as far as our records can tell) would imply that if meat consumption significantly impacted human cancer development to such a great extent that it impacted our fitness, we likely would have evolved to be strictly herbivores.  The bigger concern should always be for those highly potent carcinogens, materials like asbestos, benzenes, or even gamma radiation, all of which are not nearly as enjoyable as eating a nice delicious steak. If you’re not going to eat meat, do it because you don’t like it, or you care too much about animals, not because you think this particular research article proved that doing so causes cancer.