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Comment Re:Not a surprise, but is it just one ingredient? (Score 4, Interesting) 422

Sodium benzoate

My money is on the sugar/syrup itself, acting through the insulin-like growth factor system. There is substantial evidence that decreased IGF activity lengthens lifespan and reduces cancer risk, while increased activity drives increased cell-division activity and apoptosis.

Comment Research Paper Link (Score 5, Informative) 422

1) What is the name of the paper?

Found it: http://ajph.aphapublications.o...
"Soda and Cell Aging: Associations Between Sugar-Sweetened Beverage Consumption and Leukocyte Telomere Length in Healthy Adults From the National Health and Nutrition Examination Surveys"

Objectives. We tested whether leukocyte telomere length maintenance, which underlies healthy cellular aging, provides a link between sugar-sweetened beverage (SSB) consumption and the risk of cardiometabolic disease.

Methods. We examined cross-sectional associations between the consumption of SSBs, diet soda, and fruit juice and telomere length in a nationally representative sample of healthy adults. The study population included 5309 US adults, aged 20 to 65 years, with no history of diabetes or cardiovascular disease, from the 1999 to 2002 National Health and Nutrition Examination Surveys. Leukocyte telomere length was assayed from DNA specimens. Diet was assessed using 24-hour dietary recalls. Associations were examined using multivariate linear regression for the outcome of log-transformed telomere length.

Results. After adjustment for sociodemographic and health-related characteristics, sugar-sweetened soda consumption was associated with shorter telomeres (b=–0.010; 95% confidence interval [CI]=0.020, 0.001; P=.04). Consumption of 100% fruit juice was marginally associated with longer telomeres (b=0.016; 95% CI=0.000, 0.033; P=.05). No significant associations were observed between consumption of diet sodas or noncarbonated SSBs and telomere length.

Conclusions. Regular consumption of sugar-sweetened sodas might influence metabolic disease development through accelerated cell aging. (Am J Public Health. Published online ahead of print October 16, 2014: e1–e7. doi:10.2105/AJPH.2014.302151)

Comment Good reasons not to rush to unguided usage (Score 1) 193

It also means that for those that are infected, there's so little chance of survival with "traditional" treatments that they have very little to lose by trying something experimental. Even if a treatment gives them cancer, or HIV, or leaves them with something like chronic fatigue syndrome, they're still going to enjoy quality of life better than they would if they're dead.

I would posit that the problem is not that the currently infected individual faces any fate worse than death.

The problem is that lack of high-quality data may forestall the development of more effective therapies, which means you are condemning people infected in the future to death. This latter group seems abstract and hazy, compared to the concrete suffering we can see before us, but eventually the future becomes the now, and we'll have to deal with it.

Researchers may well end up heading down blind alleys, trying to optimize ineffective strategies that end up sucking up resources (money, scientists, labs, mindshare). The history of medicine is full of useless or even harmful therapies that were developed without the benefit of rigorous clinical trials -- difficult to treat conditions like cancer were especially prone to this phenomenon (for instance, the radical mastectomy procedure for breast cancer -- painful, disfiguring and debilitating, developed during an age of heroic surgery... a "gold standard" treatment yet much much later proven to offer no survival benefit in the majority of situations).

Comment Re:A Priority (Score 3, Informative) 55

It has been done during the 1995 Kikwit Ebola outbreak in Zaire. They tried it on eight patients and only one died. I have found no indication that any health care workers were infected.

Just in case anyone is curious, here is the actual paper: http://jid.oxfordjournals.org/...

Between 6 and 22 June 1995, 8 patients in Kikwit, Democratic Republic of the Congo, who met the case definition used in Kikwit for Ebola (EBO) hemorrhagic fever, were transfused with blood donated by 5 convalescent patients. The donated blood contained IgG EBO antibodies but no EBO antigen. EBO antigens were detected in all the transfusion recipients just before transfusion. The 8 transfused patients had clinical symptoms similar to those of other EBO patients seen during the epidemic. All were seriously ill with severe asthenia, 4 presented with hemorrhagic manifestations, and 2 became comatose as their disease progressed. Only 1 transfused patient (12.5%) died; this number is significantly lower than the overall case fatality rate (80%) for the EBO epidemic in Kikwit and than the rates for other EBO epidemics.

Comment Re:Doesn't make sense to me (Score 2) 55

Neither the summary or the linked article use the term, but what they're using is known as "convalescent serum". As the parent poster stated above, it's been in use for over a century now, but has only fallen out of fashion in modern times -- mainly because it has been superseded by vaccines and anti-infectives that are cheaper, more reliable, more convenient, and easier to mass-produce.

Trivia note: While Type-O may be the universal blood donor, the ideal serum donor is Type AB.

Comment Humoral vs. Cell-mediated Immune responses (Score 4, Informative) 55

Couldn't this approach be used for any infectious disease for which there's no effective cure but there are some survivors? Are there just no Western diseases that fit the profile? I suppose you need both a person sick with a deadly infection and a recent survivor of a same infection (with the same blood type). So it may just be the case that we simply don't experience that scenario enough to develop this solution. But I'm curious if this approach has been used outside of Ebola in Africa.

It's not used much today, because we've largely conquered the disease agents that such an approach works against. Typically, it works well against infectious agents which are highly vulnerable to a Humoral (antibody-mediated) immune response. Co-incidentally, this also means most vaccines work extremely well against those same disease agents. Unfortunately, Ebola doesn't yet have a commercially available vaccine, but I would expect such a vaccine to work well.

There are only a few examples in the West where we still use this approach -- one that I can think of, is the use of anti-HepB sera in infants born to infected mothers, and for emergency prophylaxis of needlestick injuries involving Hepatitis B exposure. For the bulk of the population, Hepatitis B vaccination works well enough (and is far cheaper).

What it doesn't work well against, are infectious agents that don't respond well to natural antibody defenses. For instance, most anti-HIV antibodies do not defend well against HIV, anti-HepC antibodies do not protect against Hepatitis C, nor do anti-TB antibodies protect against Tuberculosis. For those agents, an effective response depends on cell-mediated immunity.

Comment Re:They didn't build that (Score 3, Insightful) 105

ZMapp is produced by a private firm

If you follow the money, it'll lead back to a grant funded by the Federal government (in this case, both the U.S. and Canadian governments).

Ebola therapeutics were (and probably still are) anticipated to be a profit-less product segment, as far as the civilian commercial market is concerned. The affected population can't afford any resulting product, plus previous outbreaks were sporadic with small numbers of fatalities. The only potential "customers" -- at the time research was initiated over a decade ago -- were governments who might be interested in stockpiling treatments for future bio-defense use.

Now, a few of the large pharmaceutical companies still maintain and fund tropical-diseases divisions, despite the lack of profitability (for instance, Glaxo's division is largely a legacy of British Colonial days, which they've carried ever since). But I highly doubt a small biotech like Mapp Biopharm would ever do so without being paid most of the cost up-front.

Comment Ever-increasing proportion of female physicians (Score 1) 329

According to this data chart [kff.org], about 30% of physicians are female.

As time go on, this will even out. While the ranks of older physicians are male-dominated, females make up just slightly under half the medical school class in the US. In parts of Europe, they already make up the majority:

women make up 54 percent of physicians below the age of 35 in Britain, 58 percent in France and almost 64 percent in Spain, according to the latest figures from the Organization for Economic Cooperation and Development

http://www.nytimes.com/2011/03...

Comment Re:What about nursing?? (Score 3, Informative) 329

Because women who want go into medicine end up nurses instead of doctors. This is the result of stereotypes, peer pressure and a largely male establishment.

In 2011-2012, women represented 47.0% of entering students entering medical school, and it's been hovering at just below half (around 47-49%) for the past decade. This value has also been approximately proportional to the gender mix of applicants, which was 47.3% female in 2011-2012.

Source: https://www.aamc.org/download/...

Comment Tag #WhereIsTheFuckingPaper (Score 4, Informative) 74

Oh, here it is: Pre-Columbian mycobacterial genomes reveal seals as a source of New World human tuberculosis (Paywall -- free Nature summary article here).

Modern strains of Mycobacterium tuberculosis from the Americas are closely related to those from Europe, supporting the assumption that human tuberculosis was introduced post-contact. This notion, however, is incompatible with archaeological evidence of pre-contact tuberculosis in the New World. Comparative genomics of modern isolates suggests that M. tuberculosis attained its worldwide distribution following human dispersals out of Africa during the Pleistocene epoch, although this has yet to be confirmed with ancient calibration points. Here we present three 1,000-year-old mycobacterial genomes from Peruvian human skeletons, revealing that a member of the M. tuberculosis complex caused human disease before contact. The ancient strains are distinct from known human-adapted forms and are most closely related to those adapted to seals and sea lions. Two independent dating approaches suggest a most recent common ancestor for the M. tuberculosis complex less than 6,000 years ago, which supports a Holocene dispersal of the disease. Our results implicate sea mammals as having played a role in transmitting the disease to humans across the ocean.

Comment Re:Home fecal transplant went wrong (Score 1) 53

While the clinical picture and timing suggests the possibility, it's far from certain that this was a primary infection stemming from his home fecal transplant. I would have liked to see an analysis of anti-CMV IgM titers, although in this case it's also possible that his case was recognized too long afterwards to determine whether or not it was an actual primary infection.

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