Chinese Herbal Medicine

Competition is certainly good for us. One by one, the big league universities in the Boston neighborhood are going OPEN ACCESS.

Open access publishing means that research works can be read (online) and used freely by the public without paying subscription fees to journals and publishers. I know personally how expensive it is to subscribe to just one journal, and the information from abstracts are really so limited that having more open access journals is just good for the science.

Last January, the University of California and publication giant Springer agreed to have articles written by UP-affiliated authors to be published immediately and in full, even if the rest of Springer’s articles remain subscription-only.

In early February, Harvard University’s Arts and Sciences agreed to support an open access system. Harvard faculty will also be required to only submit to journals that will publish their work online immediately after acceptance for publication. Following suit, Boston U and MIT independently announced that the work of faculties all across their universities will be accessible to the public for free.

Lest anyone get the wrong idea: Open access is not free. University libraries have to pay open-access journals to have their research published, and the cost for pre-pay memberships have gone up in the last few years. The public does not need to pay subscription fees, but the researchers do. So, MIT will now be storing their research materials at the MIT DSpace : http://dspace.mit.edu/. Boston and Harvard are also working on their own online repositories.

Hopefully, more universities will follow and set up their own websites, or partner with publishers to get the cost of publication lowered and open-access more available.

Image: sxc.hu

Asians would know what I’m talking about. You drink a few sips of alcohol and suddenly, you feel nauseated and hot, you face turns beet red, and your heart beats faster. Known as the “Asian Glow” or “Asian Flush”, this reaction to alcohol is a risk factor for cancer of the esophagus, one of the deadliest in the world.

The alcohol flushing response is an inherited genetic trait – deficiency in the enzyme aldehyde dehydrogenase 2 (ALDH2)- common among one third of Japanese, Chinese and Koreans.

Here’s how the enzyme works: In normal individuals, alcohol is broken down into a non-toxic forms by the action of two enzymes.

1. Alcohol dehydrogenase (ADH) oxidizes alcohol into acetaldehyde. Acetaldehyde is a carcinogen that causes DNA damage, so the final steps in the metabolism of alcohol help get rid of this mutagen.
2. Aldehyde dehydrogenase 2 (ALDH2) oxidizes acetaldehyde into acetic acid and CO2.

When ALDH2 is deficient, acetaldehyde accumulates in the body and creates an unpleasant flushing reaction. A person homozygote for the inactive ALDH2 gene has a completely defective enzyme and can not tolerate even small amounts of alcohol, essentially protecting them from the acetaldehyde carcinogen. However, a person heterozygote for the ALDH2 gene would only have decreased enzyme activity, which means they may grow to tolerate the unpleasant reaction to alcohol and become habitual heavy drinkers. It is this group of alcohol consumers that is associated with the greatest risk in esophageal cancer.

A collaboration between Japanese and American scientists found that 8% of the world population (540 million) have ALDH2-deficiency and exhibit the telling flushing response when consuming alcohol. Physicians can counsel ALDH2-deficient patients to lessen alcohol drinking and decrease the risk of esophageal cancer.

Read more about the study in the PLOS Medicine issued on March 24, 2009 - The Alcohol Flushing Response: An Unrecognized Risk Factor for Esophageal Cancer from Alcohol Consumption.

Image: PLoS Med 6(3): e1000050 doi:10.1371/journal.pmed.1000050 (CCAL)

Presently available medical technology is always crude when compared with what's presently taking shape in the laboratory. Take cancer therapies, for example: unpleasant and painful chemotherapy remains the state of the art in the field, but laboratories are turning out targeted therapies with next to no side-effects, or using the immune system to eliminate cancer.

This vast gap between lab and clinic is made particularly pronounced by the heavy burden of regulation that ensures commercial development of new therapies is expensive and slow, where it takes place at all. Yet even with this ball and chain, and even lacking the impressive technology still in trials, trends in results of therapy are still moving in the right direction. This is aptly illustrated by this data on cancer survival:

New data and analyses from a long-running study of cancer survival in Europe have shown that the number of people actually cured of cancer - rather than just surviving for at least five years after diagnosis - is rising steadily.

A special issue of the European Journal of Cancer [1] containing reports from the EUROCARE-4 Working Group, includes, for the first time, an estimate of the proportions of patients who are cured of their cancer in Europe and who, therefore, have a life expectancy equal to that of the rest of the population. The analysis divides patients into two groups - the proportion who may be considered cured of their disease and who are likely to die of something else, and those who will die of their cancer.

The study compared two periods - 1988-1990 and 1997-1999 - and found the proportion of patients estimated to be cured of lung, stomach and colorectal cancers increased from 6% to 8%, from 15% to 18% and from 42% to 49%, respectively.

...

"Geographic variation in the estimated proportion of patients diagnosed in 1988-1999 who were cured ranged from about 4% to 10% for lung cancer, from 9% to 27% for stomach cancer, from 25% to 49% for colon and rectum cancer, and from 55% to 73% for breast cancer."

There's a long way to go in terms of defeating cancer if you just project out that trend - but the work presently taking place in the laboratory goes far beyond trend continuation. The next generation of cancer therapies are completely new approaches and technologies that can be expected to greatly increase survival rates where they are deployed. This makes it all the more frustrating that we are saddled with a regulatory prison that prevents and discourages new medicine.

Regulatory bodies like the FDA have every incentive to stop the release of new medicine: the government employees involved suffer far more from bad press for an approved medical technology than they do from the largely unexamined consequences of heavy regulation. These consequences go far beyond the obvious and announced disapproval of specific medical technologies: the far greater cost lies in all the research, innovation and development that was never undertaken because regulatory burdens ensure there would be no profit for the developer. Personal gain for the regulator is thus to destroy the gains of people they will never meet, the exact opposite of what occurs in an open marketplace.

A short Russian language blog entry provides we decadent Westerners with a picture of the cover of the translated version of Aubrey de Grey and Michael Rae's "Ending Aging".

Congratulations to those involved in the translation process: translation of a scientific work is never easy, especially when its focus is on research that is still cutting edge. Much of the crucial terminology in new fields is essentially made up from whole cloth or built of unusual compound words that draw on language roots and traditions of nomenclature that English and Russian may not have in common. In addition, precision of translation is important, as positions of understanding are built up over many succeeding steps - an incorrectly translated early stage can render whole pages of information nonsense.

Ending Aging is a dense, informative, and valuable book, as well as a call to action for an age in which we could, collectively, be doing far more to reverse the damage of aging than is presently taking place. The more people who have the chance to read Ending Aging, the better.

I'm sure you've all already noticed that Rejuvenation Research Vol 12 Number 1 is available online. I'm late as usual in pointing it out, but better late than never. I should draw your attention to one of the papers, "Unexpected Regeneration in Middle-Aged Mice", as the full PDF version is presently free for access in one of the journal publisher's occasional promotions.

Complete regeneration of damaged extremities, including both the epithelium and the underlying tissues, is thought to occur mainly in embryos, fetuses, and juvenile mammals, but only very rarely in adult mammals. Surprisingly, we found that common strains of mice are able to regenerate all of the tissues necessary to completely fill experimentally punched ear holes, but only if punched at middle age.

Although young postweaning mice regrew the epithelium without typical pre-scar granulation tissue, they showed only minimal regeneration of connective tissues. In contrast, mice punched at 5-11 months of age showed true amphibian-like blastema formation and regrowth of cartilage, fat, and dermis, with blood vessels, sebaceous glands, hair follicles, and, in black mice, melanocytes.

These data suggest that at least partial appendage regeneration may be more common in adult mammals than previously thought and call into question the common view that regenerative ability is lost with age. The data suggest that the age at which various inbred mouse strains become capable of epimorphic regeneration may be correlated with adult body weight.

Now this is interesting indeed. You'll recall the MRL mice that show unexpected regenerative powers, something that has been known for a few years now. What these researchers have shown is that several other species of lab-bred mice have similar unexpected regenerative capabilities. This leads me to expect that, in the years ahead, scientists will uncover a complex and interrelated network of controlling genes and biochemical processes that can be manipulated at several points to produce exceptional healing in mammals. That discovery process will look much like the ongoing work attending metabolic changes in calorie restriction - a lot of potential controlling genes, much confusion and contradiction in the early years, and progress to initial therapies on a timescale of 10 to 15 years.