Thursday, October 11, 2007


No wonder this research is described as "unfunded"! They say that two ailments have a common cause but out of more than 900 patients with either condition, they found only FOUR cases of overlap! Better proof that the ailments are NOT related would be hard to come by. Another pet theory bites the dust. Popular summary followed by journal abstract below

MULTIPLE sclerosis (MS) and ulcerative colitis (UC) -- a type of inflammatory bowel disease that causes colon ulcers and diarrhoea -- may have common causes, according to new Australian research published in the Internal Medicine Journal. Led by Dr Christopher Pokorny from Liverpool Hospital and the University of NSW in Sydney, the research team examined medical records at Liverpool Hospital dated between 1996 and 2006 and identified 496 patients with MS and 414 patients with UC. There were four patients with both UC and MS, two of whom developed UC after they were diagnosed with MS. Given that some treatments for UC can damage the protective covering of brain cells -- the same process that occurs in MS -- the authors claim that common underlying causes of the two diseases should be further investigated.


Association between ulcerative colitis and multiple sclerosis

By C. S. Pokorny et al.

An association between inflammatory bowel disease (IBD) and multiple sclerosis (MS) has been described. The current study was undertaken to explore this association further. Personal records of patients with IBD and MS were reviewed. In addition, a search of medical records at a large tertiary teaching hospital in Sydney was carried out for the years 1996-2006. Four patients (three women and one man) with both ulcerative colitis and MS were identified. MS did not occur in any of our patients with Crohn's disease. The association between ulcerative colitis and MS appears to be real and may help identify common factors involved in the cause of these two diseases. No association was found in this study between MS and Crohn's disease, sparking consideration why such difference should occur. With the increasing use of biological therapies in IBD and their reported propensity to cause demyelination, recognition of an association is all the more important.

Internal Medicine Journal, Volume 37 Issue 10 Page 721-724, October 2007

Chilli anaesthetic turns off pain

An injection that can block the pain of a dentist's drill but does not cause, numbness, paralysis or drooling could be available within a few years, thanks to an advance that could benefit millions of people. "We've introduced a local anaesthetic selectively into pain-sensing neurons," explains Harvard's Prof Bruce Bean, an author on the paper today in Nature. "Now we can block the activity of pain-sensing neurons without disrupting electrical signalling of other kinds of neurons that control movements or non-painful sensations." "The expectation is that it should block pain but avoid general numbness when applied in dentistry. Also it may minimise drooling."

"We're optimistic that this method will eventually be applied to humans and change our experience during procedures ranging from knee surgery to tooth extractions," adds Prof Clifford Woolf of Massachusetts General Hospital, senior author. "I think by 2010 proof of concept trials in humans are likely and the appropriate safety and efficacy studies will take a few years more."

Despite enormous investments by industry, pain management has changed little since the first successful demonstration of ether general anaesthesia at MGH in 1846. General and local anesthetics work by interfering with electrical signalling by all nerve cells, not just pain-sensing ones. Thus, these drugs produce dramatic side effects, such as loss of consciousness in the case of general anaesthetics or temporary paralysis for local anaesthetics. "We're offering a targeted approach to pain management that avoids these problems," says Prof Woolf.

The new work, done in the lab by Alexander Binshtok, builds on research done since the 1970s showing how the signals sent along nerves depend on microscopic openings in them, in proteins called ion channels. Previous research showed that a protein channel called TRPV1, which is unique to pain-sensing neurons, could be put to work to deliver the anaesthetic.

TRPV1 channels are usually shut but can be opened either by painful heat or by the chilli-pepper ingredient capsaicin. When the TRP1 channels are propped opened by capsaicin they form a pore large enough to be traversed by QX-314, which unlike its close chemical relative lignocaine, normally has no anaesthetic effect because it cannot penetrate cells. Presented in combination with capsaicin, it can selectively enter pain sensitive nerves and shut down their electrical activity.

The team must overcome several hurdles before this method can be applied to humans, notably working out the right blend of agents with similar actions to OX-314 and capsaicin to work with the minimum of pain and side effects. But Prof Woolf said "We have very good leads and I am therfore optimistic that progress will be relatively rapid." "Eventually this method could completely transform surgical and post-surgical analgesia, allowing patients to remain fully alert without experiencing pain or paralysis," he added. "In fact, the possibilities seem endless. I could even imagine using this method to treat itch, as itch-sensitive neurons fall into the same group as pain-sensing ones."

"The Holy Grail in pain science is to eliminate pathologic pain without impairing thinking, alertness, coordination, or other vital functions of the nervous system. "This finding shows that a specific combination of two molecules can block only pain-related neurons. It holds the promise of major future breakthroughs for the millions of persons who suffer with disabling pain," commented Story Landis, director of the National Institute of Neurological Disorders and Stroke, in Bethesda, Maryland.



Just some problems with the "Obesity" war:

1). It tries to impose behavior change on everybody -- when most of those targeted are not obese and hence have no reason to change their behaviour. It is a form of punishing the innocent and the guilty alike. (It is also typical of Leftist thinking: Scorning the individual and capable of dealing with large groups only).

2). The longevity research all leads to the conclusion that it is people of MIDDLING weight who live longest -- not slim people. So the "epidemic" of obesity is in fact largely an "epidemic" of living longer.

3). It is total calorie intake that makes you fat -- not where you get your calories. Policies that attack only the source of the calories (e.g. "junk food") without addressing total calorie intake are hence pissing into the wind. People involuntarily deprived of their preferred calorie intake from one source are highly likely to seek and find their calories elsewhere.

4). So-called junk food is perfectly nutritious. A big Mac meal comprises meat, bread, salad and potatoes -- which is a mainstream Western diet. If that is bad then we are all in big trouble.

5). Food warriors demonize salt and fat. But we need a daily salt intake to counter salt-loss through perspiration and the research shows that people on salt-restricted diets die SOONER. And Eskimos eat huge amounts of fat with no apparent ill-effects. And the average home-cooked roast dinner has LOTS of fat. Will we ban roast dinners?

6). The foods restricted are often no more calorific than those permitted -- such as milk and fruit-juice drinks.

7). Tendency to weight is mostly genetic and is therefore not readily susceptible to voluntary behaviour change.

8). And when are we going to ban cheese? Cheese is a concentrated calorie bomb and has lots of that wicked animal fat in it too. Wouldn't we all be better off without it? And what about butter and margarine? They are just about pure fat. Surely they should be treated as contraband in kids' lunchboxes! [/sarcasm].

Trans fats:

For one summary of the weak science behind the "trans-fat" hysteria, see here. Trans fats have only a temporary effect on blood chemistry and the evidence of lasting harm from them is dubious. By taking extreme groups in trans fats intake, some weak association with coronary heart disease has at times been shown in some sub-populations but extreme group studies are inherently at risk of confounding with other factors and are intrinsically of little interest to the average person.


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