I came across this article on lifehacker today on what alcohol does to the human body. Surprisingly absent from the text was anything more than a brief mention of arguably the most important aspect of alcohol consumption: addiction. This post is the result of what started as a two line comment and ballooned out, admittedly, pretty far.
I would like to add a bit of a disclaimer first, just to cut off any silly ideas: I am not a doctor, this is not legally binding advice and this is a constantly changing area of research; take everything on here with a grain of salt; I am just a student who studies biology. If you have serious questions about this, please please please don't google it. Ask your doctor, it's their job to know about this sort of thing. I am completely serious about this, substance addiction is no joke.
Ok, so there is a very important signalling chemical in the body known as "N-Methyl-D-aspartic acid" or NMDA. NMDA is used by the body to send signals in many different ways, but the one we are interested is nociception (although there is an important difference, this is more commonly known as pain). Even though it might seem annoying at times, pain is a very important survival mechanism for the body; it tells you that what you are doing needs to stop or you risk doing serious damage to your body. NMDA can't do anything on its own though, it triggers a special receptor in the brain to send pain signals which is known as the NMDA receptor [1]. It should be noted here that several other substances activate NMDA receptors to send pain but the exact chemical is not important to this simplified explanation.
Now here's the interesting bit: in the presence of ethanol (that's the part of alcohol that we are interested in), it has been shown that NMDA receptors don't work so well. Following on from this, it has been shown that ethanol decreases the size of pain signals sent by neurones [2]. Over the short term, this doesn't really matter too much; the ethanol is eventually removed and the NMDA receptors return to normal.
Inhibiting NMDA receptors in the long term is a bit different though. Remember how I said pain was an important part of survival? If you try and switch off pain by drinking a lot of alcohol, your body will wise up to it pretty fast. It knows that pain signalling is important and so to restore it, the body starts building more NMDA receptors and increasing the levels of chemicals that will activate them until it can effectively send pain signals again [2]. The increase in sensitivity is known as tolerance, that is, the body can tolerate the presence of ethanol and still function correctly.
Increased sensitivity is fine if we combat it with the decrease in sensitivity from ethanol. But you might already see the problem here: what happens when we remove the ethanol? The NMDA receptors go haywire and start firing pain signals everywhere. This can translate to something as minimal as a headache or agitation, but it can also have very serious consequences like vomiting and, in extreme cases, seizures [3]. These resulting conditions are known as withdrawal symptoms. And the way to quickly combat these uncomfortable symptoms is to desensitise the NMDA receptors again with, you guessed it, more ethanol. This is the never-ending addiction cycle; pain exists without ethanol but the presence of ethanol eventually leads to greater sensitivity to pain. While I have no personal experience with this, my understanding is that pain caused by withdrawal symptoms would be a sort of dull, long term aching. In short: horrible.
Fortunately, the body can readapt if ethanol is taken away for good. It will realise that pain signals are being amplified and start to take NMDA receptors away and break them down. But this takes a great deal of time and willpower, something which may be lacking in alcoholics. However there are many, many, many other factors that influence addiction, both physical and psychological. Although willpower may be all that is needed for some, more potent methods may be required in extreme cases.
References
[1] - Peripheral NMDA and non-NMDA glutamate receptors contribute to nociceptive behaviors in the rat formalin test - http://goo.gl/uoTib
[2] - Ethanol and the NMDA receptor - http://goo.gl/XiGvs
[3] - Ethanol withdrawal seizures and the NMDA receptor complex - http://goo.gl/HRqYP
The reflex that keeps your eyes looking in the same spot as you turn your head is called the vestibulo-ocular reflex. This is triggered by small organs in your head known as otoliths; these little organs are filled with a viscous fluid and tiny little particles. When your head turns, the inertia of these tiny particles causes them to push on nerve connected hairs on the walls of the organ. Through this, the brain can not only determine that your head has moved but also very accurately determine how fast, how far and even in what direction gravity is now pulling. interesting stuff!
In one of my [bored] trawls through the internet, I came across this article on a speech given the founder of TechCrunch (which appears to be a successful blog/news website on internet startup companies). The article is pretty much a [well written] rehash of the tertiary education vs self-taught argument. Since this is the internet and everyone has to give their opinion, I'll say I am for the tertiary group but with the condition that no one should ever be forced to go to university if they don't feel it would do them any good.
What I found particularly interesting was how little the commenters seemed to understand about chance, luck and randomness (hint: they are all the same thing!). Perhaps I am being obnoxious and I understand that it is an extraordinarily difficult topic, but the idea that dropping out of university increases your chances of making a significant amount of money is absolutely and completely absurd. It just is, I don't even see how there can be an argument the other way. To make the abstracted argument that it will increase your chances of having a "successful business" makes me want to explode with vitriol. And for all of you "no risk no reward" types (which admittedly I am to some extent), that actually means "calculated risk, calculated reward" and not "I do whatever the hell I want with other peoples' money because I've been right in the past and will certainly be in the future" (hello wall st!).
On top of this, the amount of hindsight and survivorship bias displayed by some commenters is breathtaking. Personally I wouldn't have put a cent into facebook in the early stages, just as I probably would not have signed JK Rowling for her books. Using the information available at the time and my feeble mind I just can't see how they would be smart investments (at least for my tiny amount of captial!). If there is a single person in the world who accurately predicted the rise of both facebook and harry potter for purely rational reasons then I will start a religion worshipping them because they are nothing short of godly. So what if investors made containerload of money out of these investments? Hindsight is a bitch, but not as much as being broke.
Working for the AEC in the election was an interesting experience. Just before you check a voter's name off the electoral roll, you have to ask them a simple question: "Have you voted in this election before?" What really surprised me was the number of times I was told "No, once is bad enough!". You could literally feel the disillusionment of the voters in the room, not in the democratic process of voting (in fact I had several people thank me for doing what they felt was an important job), but in the choices available to them on the ballot paper. I can't say I blame them.
Here's hoping the Chaser team can inject some humour into this situation.
(Just in case anyone crazy is reading this: nothing on this page should be taken as fact; all of these opinions are my own and mine only.)
I was talking to a researcher about this last week and the journal article just popped up, so I figured I would write a quick, hopefully jargon-minimal summary.
In the past, Alzheimer's disease (AD, a form of dementia) has been diagnosed in a fairly probabilistic manner; patient histories, clinical observation and cognitive function tests have been the major tools in any doctor's belt. Medical imaging can also be used to some extent as well as exclusion diagnosis (looking for evidence that the patient doesn't have the disease). This is all very useful, but the nature of the condition makes it very difficult for doctors to actually know if a patient has Alzheimer's disease. The only test available previously was a post-mortem autopsy; you can hopefully see is not very appropriate for patients who would like to continue to live after visiting their doctor.
Now though, researchers at the Alzheimer's Disease Neuroimaging Institute have developed a new test with 94 to 100% accuracy. The test involves collecting a sample of the patient's spinal fluid and checking for the concentration of a few special proteins: phosphorylated tau181P and beta-amyloid 1-42.
So why look for these? Tau proteins are responsible for stabilising tiny little tubes in your brain cells that allow the transport of various chemicals. The tau proteins can't do it on their own though; in order to work they must be phosphorylated (which is just biology-speak for switched on). The tau hypothesis states that the disease cascade begins when there are abnormalities in these proteins. They become hyperphosphorylated (switched on several times), and start joining tubes in all sorts of directions, causing the neuron's regular transport pathways to become tangled and degrade. As for how these abnormalities occur, the jury is still out on that one. Very little is known about how beta-amyloid 1-42 is involved in AD but there is significant evidence to suggest that the concentration is greatly increased in patients with the fully developed disease.
The researchers took two datasets: the first with about 400 patients all in various stages of the disease (without AD, with MCI [minor cognitive impairment] and with full blown AD) and the second with 73 autopsy-confirmed cases of AD. For the first set of data, researchers were able to find the unique signature of chemicals in 90% of diagnosed AD cases and 72% of patients with MCI. For a special group of patients with MCI that were rechecked after a further five years, the test results predicted with 100% accuracy whether or not they were going to develop AD. Predictions for the second set came in at 94% accuracy; an incredible number for a disease for which specific clinical tests have previously been difficult.
What does all of this mean? In the next few years (and I don't mean a decade, I mean very soon!), a simple lumbar puncture may be all that is required to determine if a patient is developing AD. If the disease can be caught in the earlier stages it would provide the opportunity for researchers to study the disease as it progresses, as well as giving doctors the ability to provide early treatment to try and improve the quality of life of patients. It's only a small step toward conquering the disease, but as long as we keep poking, prodding and pipetting we'll get there in the end.
note: I am not a doctor, I am just a university student who studies this sort of thing. Please please please ask your doctor if you have any questions.
Sources:
De Meyer, G et al. 2010, 'Diagnosis-Independent Alzheimer Disease Biomarker Signature in Cognitively Normal Elderly People', Archives of Neurology, vol. 67, no. 8, pp. 949-956
In June 2008, the inflation rate was 6.5 quindecillion novemdecillion percent.
In July 2008, a single chicken egg was worth ZW$50 billion.
When the currency was suspended at the end of 2009, US$1 was worth ZW$669 000 000 000 (also: this was the third dollar, with the ratio of first:second being 1 000:1 and the ratio of second to third being 1 000 000 000:1).
The company which provided the Zimbabwe Reserve Bank with the software to print banknotes was required by the EU Union to suspend all licences so that no higher denomination notes could be printed.
As of 1/1/09, an original Zimbabwean dollar was worth US$10-31
This is an awesome video of a dendritic cell performing phagocytosis on a conidia. Maybe I'm just a little weird (well, almost certainly), I just think it is awesome to see that such tiny things can actually have independent function. A quick explanation:
Dendritic cells are important in the innate (primary) immune system. They basically grab bits of antigens (things that should not be in the body) and present them to the rest of the immune system so that an appropriate response can occur.
Source: Wikipedia
Original video authors: Judith Behnsen, Priyanka Narang, Mike Hasenberg, Frank Gunzer, Ursula Bilitewski, Nina Klippel, Manfred Rohde, Matthias Brock, Axel A. Brakhage, Matthias Gunzer
(can't see the video? try using a real browser)
It's nice to see some people looking at the hard science instead of saying "it didn't work for my cousin/brother/sister/uncle so I won't try at all".
(looks like the linked page doesn't exist anymore, so here is the proper source.)
