This was a multicenter, prospective, randomized, open-label, blinded, end-point trial conducted from December 2002 through April 2008 at 163 institutions throughout Japan, involving 2539 patients with type 2 diabetes without a history of atherosclerotic disease and had a median follow-up of 4.37 years.

Patients took either 81 or 100 mg of aspirin per day, or nothing.

Although there were less atherosclerotic events in the aspirin group (68 vs 86), given the size of the groups, the results did not reveal any significant differences (p=0.16).

So, as far as this study is concerned, low-dose aspirin did nothing for those with type-2 diabetes.

Why does low-dose aspirin has a reputation for lowering the risk of untoward cardiac events? Daily low-dose aspirin is known as anti-platelet therapy, due to its ability to prevent platelets aggregating and causing the blood to clot. It is via this mechanism that it reduces the likelihood of cardiovascular events, and it is currently endorsed by the American Heart Association specifically for this purpose:

The American Heart Association recommends aspirin use for patients who’ve had a myocardial infarction (heart attack), unstable angina, ischemic stroke (caused by blood clot) or transient ischemic attacks (TIAs or “little strokes”), if not contraindicated. This recommendation is based on sound evidence from clinical trials showing that aspirin helps prevent the recurrence of such events as heart attack, hospitalization for recurrent angina, second strokes, etc. (secondary prevention). Studies show aspirin also helps prevent these events from occurring in people at high risk (primary prevention).

Given the apparent weight of evidence supporting the daily use of aspirin as a preventative therapy, it’s quite strange that there appear to be few effects in type-2 diabetes sufferers. The Japanese study could be considered to be underpowered due to the very small number of cardiovascular events occurring in either group; another weakness was that it was not double-blinded nor randomized.

The authors of the study admit that the results do not suggest that low-dose aspirin is ineffective, but rather that their study design did not produce conclusive results, and possibly that overriding factors in diabetes sufferers contribute to cardiovascular problems far more than the protective effect conferred by aspirin therapy.

So there you go.

In the past, this kind of approach was only used on those extremely short children in whom a growth hormone deficiency was detected, but it turns out that it doesn’t matter – all children can benefit from a bit of the old juice!

This was a very long term study, looking at the effects on 150 children over the course of 20 years.

Apparently the technique works better when the child is unusually short compared to its parents, but remained efficacious even when it was a case of short+short=short.

Does this mean that if one’s not satisfied with their stature, and their parter brings no improvement to their collective gene pool that preemptive treatment will become the norm?

Do you, like me, foresee a future populated exclusively with monster men?

If largeness were so inherently desirable, however, why are aliens so small and diminutive? Obviously possessing far greater genetic engineering technology that we do, surely if extreme head altitude were truly a better state of being, then they’d have super-sized themselves millions of years ago.

They probably did and immediately realized that it’s actually a bit annoying being tall, and the only benefit is that people have to look up to you, and that they equate tallness with goodness. It’s not real though, no more so than big breasts being indicative of job suitability.

I know it’s a tough road for short guys. I can see their daily struggle from up here and I pity them, I really do! So, for their sake I’m declaring this medical advancement ‘absolutely brilliant’, and I’ll join them in their prayers for a solution that works on people who have already passed through puberty.

The study has been accepted for publication in the Journal of Clinical Endocrinology & Metabolism (JCEM).

Adapted from a Eurekalert press release

I guess most of us wonder why we evolved in such a way that when our fingers or limbs are severed they don’t regrow, and why a severed spinal cord can’t just heal up. And, I guess we’ll never know the answer to that question, but the irrepressible forces of human ingenuity seem set to fix this problem once and for all.

Previous efforts at regrowing damaged nerves have focused on removing from the damaged region the molecules that inhibited regeneration, but this yielded only modest results.

The growth of neurons depends on a pathway called mTOR, which is active during early development but its activity is almost totally stopped in mature nerve cells. The researchers used genetic techniques to delete two key inhibitory regulators of the mTOR pathway, TEN and TSC1, in the brains of mice.

The mice then had their optic nerves severed and were left to fend for themselves (!), and after two weeks they found that 50% of the mutant blind mice survived compared with only 20% of the controls. The mutant mice experienced marked regeneration of their optic nerves, which continued to improve over time.

While genetic techniques were used to achieve this outcome (which means, essentially, that it’s not applicable to humans because at present we have no real way of modifying our DNA in this way), it’s an important proof-of-concept that will lead the way to the development of pharmaceutical agents that promote neuronal regeneration by targeting these genes.

So, it’s another step in the right direction, towards that day when we can all go out and enjoy extreme sports without the niggling worry that we’ll wind up in a wheelchair. I guess death itself is still on the cards for base jumpers et al., but by the time this technology matures, we might just have overcome that too.

Adapted from materials provided by Eurekalert

The National Center for Homeopathy points out today, however, that the researchers must have borrowed some tricks from their opponents in neglecting to properly exercise the scientific rigor involved in good quality research.

It seems that shoddy research plagues both sides of the homeopathy debate.

The review compared six clinical trials of conventional medicine with eight of homeopathy but failed to properly include details of the trials examined. The review then concluded that there is ‘weak evidence for a specific effect of homeopathic remedies, but strong evidence for specific effects of conventional interventions’.

This then prompted the homeopathy proponents to somehow reconstruct the conditions of the Lancet review, ultimately ‘revealing’ that:

• Analysis of all high quality trials of homeopathy yields a positive conclusion.
• The 8 larger higher quality trials of homeopathy were all for different conditions; if homeopathy works for some of these but not others the result changes, implying that it is not placebo.
• The comparison with conventional medicine was meaningless.
• Doubts remain about the opaque, unpublished criteria used in the review, including the definition of ‘higher quality’.

The charge was that because actual scientific studies into the efficacy of homeopathy are so lacking, it was easy to pick and choose unfavorable ones to arrive at their desired conclusion of homeopathy being bunkum.

So, no doubt to the jubilation of the quacks out there, there is again hope that homeopathy may just be a miraculous cure that defies all conventional science and general common sense. The reinvigorated uncertainty is likely to strengthen the placebo effect, and once again people can go back to curing their hypochondria with sugar pills.

I can probably understand what drove the authors of the Lancet paper to be so lax in their method. It would all seem such a waste of time that the futility of it all started to get to them, and they started cutting corners just to get the thing finished.

Similar laxness was exhibited on the part of those conducting the peer review process and given that it’s taken three years to hear about this again, most of the scientific community. They just don’t care. How closely would you scrutinize a paper that sought to determine whether water really does run down hill?

But now look what you’ve done! You’ve inadvertently kicked an own goal for the side you wished to shut down once and for all. This new uncertainty will make the idiocy of homeopathy even more difficult to extinguish. Good job, guys.

References

• Lüdtke R, Rutten ALB. The conclusions on the effectiveness of homeopathy highly depend on the set of analyzed trials. J Clin Epidemiol 2008. doi:10.1016/j.jclinepi.2008.06.015
• Rutten ALB, Stolper CF. The 2005 meta-analysis of homeopathy: the importance of post-publication data. Homeopathy 2008. doi:10.1016/j.homp.2008.09.008