Light at night

At the end of June, I will once more ride my bike from Vancouver to Seattle as part of the Ride to Conquer Cancer. In the weeks leading to this event, I log many, many kilometers on the saddle and inevitably my thoughts wander to cancer biology (and sometimes to the excruciating pain emanating from my behind). What triggers cancer? How can cancer be prevented? Why are some cancers like breast cancer more prevalent in industrialized countries? While researching the question, I came across a most unsuspected potential risk factor. I’m especially excited about this piece of relevant science because for once I won’t be writing about how eating healthy and sleeping more can cure all your ailments.

In the study, researchers took groups of female rats and exposed each group to different intensities of white light during the dark phase of their daily cycle (typical lab rats live in a programmed 12-hour light/12-hour dark cycle). After two weeks of this night cycle disruption, the researchers implanted a tumor (derived from human breast cancer tumors) in the female rats, and continued on with the night cycle disruption for many weeks. By the end of the experiment, the rats that had been exposed to the strongest intensity of light showed a marked increase in tumor growth rates. The brighter the light at night, the bigger the tumor.

Ok, light at night makes tumors grow faster, but can too much light be the cause for cancer? To answer this question, it’s best to turn to studies in humans. There is convincing evidence that women who work night shifts have a significantly higher risk of breast cancer. As well, women with the brightest bedrooms also have a higher risk of breast cancer. Scientists believe the reason for these correlations is a molecule called melatonin. At night, in the dark, your body produces melatonin, which is a very effective anti-cancer molecule. Several studies have looked at this link in more detail and have shown that melatonin can block the development and the growth of tumors in non-human models of breast cancer.

The light-cancer link is gaining interest, and researchers even started sprucing things up by using a catchy acronym, LAN (for light-at-night), so it’s something to keep in mind. Based on this research, I’ve decided to break my habit of flicking on the lights for my midnight nature calls. Would this habit necessarily give me cancer? No. But flicking on the lights does interrupt my production of melatonin, and on top of being an anti-cancer molecule, it’s also a powerful antioxidant. So I’m just trying to put all the chances on my side. That being said, I’m running into a different problem, which is waking up everyone in the building when I stub my big toe on the door frame. Nobody said staying healthy was easy…

Training for the ride, thinking about cancer

Reference: Circadian stage-dependent inhibition of human breast cancer metabolism and growth by the nocturnal melatonin signal: consequences of its disruption by light at night in rats and women. (2010) Blask D.E. et al. Integrative Cancer Therapies, 8(4):347-353

Yet another reason for a good night's sleep

How much do you sleep at night?

If you’re like most of the people I know, the answer is “not enough”. There’s a reason Starbucks coffee shops are popping up literally meters away from one another. Everybody has a reason to be sleep-deprived: new kid, big job, World of Warcraft, etc. So what if we’re cutting the night short a few hours? Other than the need for an overpriced coffee (or two, or three), it should be just fine, right?

Maybe not, if you believe the latest research on sleep and Alzheimer’s disease.

Alzheimer’s disease, a debilitating form of memory loss and cognitive decline, is the most common form of dementia. It is thought to be caused at least in part by amyloid beta (A-beta), a peptide (short protein). Your brain cells (neurons) normally make some A-beta. The problem that arises with Alzheimer’s disease is that neurons make too much A-beta, and these molecules aggregate together in chunks. It’s those A-beta chunks that are toxic, and their formation is concentration-dependent, which means the more A-beta you have floating around, the higher the probability of toxic chunks forming.

The recent article published in the journal Science looks at levels of A-beta in the brains of normal mice and in the brains of a mouse model of Alzheimer’s disease. The researchers studied the mice when they were 3 months of age, so well before big deposits and chunks of A-beta start occurring.

The interesting finding of this study is that the levels of A-beta in the brains of both types of mice were significantly correlated with the amount of time they spent awake. More time spent awake lead to more A-beta. Because the control, normal mice also exhibited this relationship, it means that it is not linked to the disease. It’s just a normal fluctuation of A-beta levels linked to the sleep-wake cycle. To be certain this link was relevant for human physiology, they also tested this in healthy humans and, sure enough, they observed the same correlation.

Not surprisingly, when the researchers proceeded to sleep-deprive the mice, they showed an even larger increase in A-beta levels. This increase was also observed when the mice were given a drug that promotes wakefulness (don’t extrapolate this to coffee just yet… But maybe keep it in mind…). The study also points out that the Alzheimer mice who are sleep-deprived showed much greater numbers of A-beta chunks (the toxic stuff) compared with non sleep-deprived mice.

If you come to Scientific Chick for relevant findings, this one is for you. The study essentially implies that optimizing sleep time could potentially inhibit the formation of chunks of toxic A-beta and slow the progression of Alzheimer’s disease.

We all know that Alzheimer’s disease is terrible, and that sleeping in is glorious. Let’s just put two and two together, shall we? Easier said than done, I know…

Mr. Minou gave up on caloric restriction but approves of this new approach to ward off age-related diseases.

Reference : Amyloid-{beta} dynamics are regulated by orexin and the sleep-wake cycle. (2009) Kang JE, Lim MM, Bateman RJ, Lee JJ, Smyth LP, Cirrito JR, Fujiki N, Nishino S, Holtzman DM. Science Sep 24. [Epub ahead of print]

Your brain's reset key is Zzzz

As a teenager, like many of you I’m sure, I neglected sleep. It seemed that partying all night and then working hard at school all day was the obvious solution to an overbooked schedule. I was rudely awakened a few years later when a good night’s sleep became necessary to merely function the next day (also when I realized what it really meant to have an overbooked schedule). While we know that sleep is essential for survival (at some point, coffee just doesn’t cut it), we know very little about why sleep is so important, and what happens to our brain while we sleep. In a recent issue of Science, a team of researchers made a contribution to this field using sleep-deprived fruit flies.

In the study, researchers looked at synapses, the junctions between brain cells (called neurons). Synapses are important because they relay information from one neuron to the next. Through synaptic connections, neurons form networks, and these networks underlie many complex brain functions like perception and thought.

The researchers cleverly engineered fruit flies to make their synaptic connections fluorescent (for those of you who read my first post, this is an excellent use of GFP). Subsequently, the researchers took images of the flies’ brains, and were able to count the brightly fluorescent synapses. The study first established that flies that hang out with other flies (this is called social enrichment) have more synapses than lonely flies. While this finding is interesting on its own, the researchers didn’t stop there. They took the socially enriched flies and divided them in two groups. The first group of flies was allowed to sleep as much as they wanted for 48 hours while the second group of flies was sleep deprived for 48 hours. Which group of flies do you think had more synapses after the experiment?

Well, the study shows that flies that slept had much fewer synapses than the sleep-deprived ones. Does it surprise you?

Initially, I thought this was a little counter-intuitive. With all this talk about sleep being important for performance and memory, I would have thought that the flies that slept would have had more connections between brain cells. This study suggests exactly the opposite, and shows that sleep acts to downscale the synapses that are created while the flies are awake and experiencing new things. When you think about it, this finding makes sense. If there was no way to “reset” those synapses, we can hypothesize that every time you learn or experience something new, you would get more and more connections between your brain cells. Eventually, we can imagine it would be a complete mess up there, and connections might saturate, leaving no room for anything new. Downscaling your synapses at night while you sleep also helps eliminate the unimportant connections, thereby making the stronger synapses stand out.

So what’s the take-home message? Enough procrastinating on the internet, go to bed!

Reference: Use-dependent plasticity in clock neurons regulates sleep need in Drosophila. Donlea JM, Ramanan N, Shaw PJ. Science. 2009 Apr 3;324(5923):105-8.