While reading an article called The Science of Loneliness, I found this interesting passage:

Functional magnetic resonance imaging scans showed that the experience of being snubbed lit up a part of the subjects’ brains (the dorsal anterior cingulate cortex) that also lights up when the body feels physical pain.

I asked Eisenberger why, if the same part of our brain processes social insult and bodily injury, we don’t confuse the two. She explained that physical harm simultaneously lights up another neural region as well, one whose job is to locate the ache—on an arm or leg, inside the body, and so on. What the dorsal anterior cingulate cortex registers is the emotional fact that pain is distressing, be it social or physical. She calls this the “affective component” of pain. In operations performed to relieve chronic pain, doctors have lesioned, or disabled, the dorsal anterior cingulate cortex. After the surgery, the patients report that they can still sense where the trouble comes from, but, they add, it just doesn’t bother them anymore.

What this means is that emotional pain isn’t a metaphorical, “all in your head” thing. It is literal pain, the difference from physical pain being that it is not located at a specific site in the body. From this we can see why people use alcohol and opiates to cope with emotional distress – they function as literal and functional anaesthetics. Which puts the matter of “substance abuse” in a different perspective. You don’t tell someone with a broken leg that their need for painkillers is a character flaw, do you?

(I must advise those tempted to self-medicate for anxiety that taking large amounts of paracetamol will cause liver damage.)

Somehow this is so telling. A WordPress blog called “People are Garbage” has one “Hello world!” entry (full text: “Welcome to WordPress. This is your first post. Edit or delete it, then start blogging!”) – and 316 comments consisting entirely of robospam.

http://peoplearegarbage.com/?p=1&cpage=1#comments
 

I’ve been taking St. John’s Wort for dysthymia as an experiment. I tried taking all five pills (my daily dose) at once, as I’d heard I could do this, but it made me feel a bit woozy and speedy, so now I take 2 in the morning and 3 at night, which seems to be working out okay. Only side-effect I’ve noticed is dry throat, which is occasionally disturbing if I’ve been lying on my back, but it’s nothing I can’t live with.

Also of note, I believe I have been “edged out” by my best and only friend. Oh well, it’s happened before. It’s depressing and lonely but I’ll survive (and without singing that song made famous by Gloria Gaynor).

I’ve recently had disturbed sleep, probably due to anxiety and mild depression due to my current situation. I’ve also come to the realisation that I have dysthymia (I guess I was aware before, but didn’t know the psychological term).

So I’m starting to self-treat with St. John’s Wort (SJW), active chemical hypericum. Now, there’s only one study on SJW for dysthymia that I know of – it’s the one that always gets cited, from the journal Phytomedicine. This study confirmed that SJW is effective for mild depression (it’s also effective for major depression), but said it was ineffective for dysthymia. However, the study was limited: first, total group was 150 patients, which is a small sample. Second, the study only went to 6 weeks (psych meds can take longer to become effective). Third, dose was typical for these studies, with a maximum of 1200g/day (SJW extract – abstracts don’t say what strength of hypericum in the extract).

What is the difference between minor and major depression, and dysthymia? Depression is generally defined as an episode lasting up to 18 months, whereas dysthymia is a chronic condition. But dysthymia is depression, chronic depression – it’s a difference of duration, not of kind. Therefore, although SJW may not match the latest medications in period of efficacy, it may be effective if taken over a long period.

Therefore, I propose to take SJW for at least 2 months, and in “therapeutic” doses – Cenovis St. John’s Wort tablet formulation, 2g extract (dried flowering head) equivalent 1mg hypericum, x 5 per day. My only real issue is: should I be taking more?

I guess we’ll see what happens!

An interesting article published in the second half of last year went largely uncommented (to my knowledge), despite its potential to “ignite a media firestorm”. It went unnoticed because it was published in an academic journal (popular journalists usually begin and end their research with the latest issue of Popular Science), and because drug researchers in the United States have had enough of being the whipping boy for each “unhelpful” piece of research that is allowed to emerge from their tenuously-funded labs.

I am drawing some small attention to it here because I think such an unusual finding should not be hidden from view. However, I should caution the unwary with one of the most fundamental principles for assessing scientific literature: ONE STUDY PROVES NOTHING. There have been plenty of medical stories published on slow news days that rely on one single paper (or sometimes just a press release), which may be statistically or methodologically flawed, biased, ignorant of relevant discoveries in related research, or just lumbered with a misleading abstract (summary). Only repeated examination by multiple researchers and reviewers will allow us to draw a strong conclusion one way or another.

A.L.C. Chen, T.J.H. Chen, et al. (2008). Hypothesizing that marijuana smokers are at a significantly lower risk of carcinogenicity relative to tobacco-non-marijuana smokers: evidenced based on statistical reevaluation of current literature. Journal of Psychoactive Drugs 40(3): 263-272.

ABSTRACT

A hypothetical link between marijuana smoking and cancer has been established based on a number of misleading assumptions. However, recent studies tend to suggest, if anything, an inverse association between marijuana use and cancers. To test the hypothesis that marijuana smoking significantly lowers the risk of developing cancer in humans, we analyzed published data from a prospective cohort study on cancer incidence among nonsmokers (NS), marijuana-only smokers (MS), tobacco-only smokers (TS), and marijuana and tobacco smokers (MTS). Using the log linear model to calculate the probability of developing each cancer form as a function of the interaction between marijuana and tobacco smoking, as well as functions of marijuana and tobacco smoking main effects whereby chi square statistics were calculated for the interaction and main effect estimates, we found that in all cases tested there was a significantly lower risk for MS compared to TS. Male and female TS had a greater probability of developing lung cancer (r = 0.72) than did MS (r = 0.02). Males and females TS had a greater probability of developing lung cancer (r = 0.72) compared with NS (r = 0.05). Males and female MTS had a slightly higher probability of developing lung cancer (r = 0.73) than did MS (r = 0.07). This difference was statistically significant: c2 = 30.51, p < .00001, with a correlation coefficient of -0.75, Z = -7.84, p < .05. Male and female MTS had a lower probability of developing lung cancer (0.23) than did TS (0.77). This difference was statistically significant: c2 = 71.61, p = .00003, with a correlation coefficient of0 .61, Z = 5.06, p < .05.

The study they examine is in:
S. Sidney, C.P. Quesenberry Jr, G.D. Friedman, I.S. Tekawa (1997). Marijuana use and cancer incidence. Cancer Causes and Control 8(5): 722-8.

As the authors say in their conclusion, “our re-evaluation of a large cohort study indicates that marijuana smokers are at a significantly lower risk of cancer relative to those who smoke tobacco and not marijuana.”

What the authors do not dare to state in their abstract or conclusion is that Marijuana-only smokers have a lower probability of developing lung cancer than Non-smokers. This information is available within the body of the paper (p.269): “For all sites [i.e. all cancer sites examined: colorectal, lung, melanoma, prostate, breast, cervix], males and females had a lower probability of developing cancer if they smoked marijuana and not tobacco (r = 0.13) than if they smoked neither marijuana nor tobacco (r = 0.32).” However, in the discussion, they do suggest that “smoking marijuana may treat lung cancer at its roots early on, while treatment still matters”.

They also cite a number of animal studies to support their thesis, and they assert that, unlike for tobacco smoking, there is no convincing epidemiological link between marijuana smoking and cancer. The role of adulterants in commercially-sold tobacco, as opposed to illegally-produced marijuana, is not considered here.