Posts Tagged ‘animal research’

Spinal cord injury: Amazing News

Friday, June 1st, 2012

I read an incredible article in The New York Times yesterday; scientists in a Swiss lab have been able to overcome an experimental spinal cord injury in rats, enabling them to walk again. Today I found the original scientific publication and decided it was a major breakthrough, well worth translating into human terms and language.

There may be rocks below

Let’s start with the human statistics; there are about 12,000 non-fatal, but severe spinal cord injury (SCI) cases in the United States every year. Half of those SCI lead to chronic paralysis and a quarter of a million people with significant SCI were alive in the US in 2010. Most of those suffered their injury when they were relatively young and 80% of them are male.

Motor vehicle accidents account for roughly 40% of those cases; the next most common cause is termed “falls,” but a typical story for a fall would be a young guy who dives into a pool or a water-filled abandoned quarry, not knowing its actual depth, and strikes the bottom or a rock.

I found a thoughtful blog post on diving. The author gave five suggestions of which one is clearly the most important: “Think First.” The others included “Steer up,” “Hands up and out” and “Control your dive.” The last was also crucial, “Don’t drink or take drugs and dive.”

Let’s go back to the rats. The article was published online in Science and is densely packed with medical terminology (I’d suggest you read the NYT article). The rodents had a partial severing of their spinal cords at two different levels, leaving normal tissue in between and connecting the parts of the spine involved. This corresponds to somewhere between 25% and 33% of human spinal injuries. A week after their SCI, the rats began training for 30 minutes a day.

They were fitted with little vests, held upright on their rear legs and given a goal, a piece of cheese to move toward. At the same time their spines were stimulated electrically above and below the spinal areas partially cut and they got a chemical infusion of several drugs that affect nerve cell activity.

The initial voluntary steps began after 2-3 weeks of daily training and, at that point, the time of exercise was gradually increased. Five to six weeks after the initial SCI all the rats could initiate full weight-bearing steps while the combined electrical and chemical stimulation was being applied. Eventually they could climb stairs and avoid obstacles. They also had anatomic evidence of new neuron (nerve cell) connections around the injury and, higher up, in the brain stem.

Control rodents placed on treadmills did not recover the ability for voluntary motion.

A neurologist from UCSF who was not involved in the research study was quoted as saying, “There’s a huge potential to refine this model to mimic more humanlike conditions.”

A Stanford medical school website captures the essence of what’s going on; this is neural plasticity, the building of new wiring patterns in the nervous system.

Is it possible?

A simpler comment would be that this research, if extended and then repeated in human subjects, may possibly bring hope to some of those afflicted with spinal cord injuries and maybe even diseases. Perhaps some who otherwise would have been wheelchair bound will be able to walk again.

It’s not at all clear to me that this will work in people who had a SCI some time ago and it doesn’t appear to be applicable to those who have a complete transection (total severing) of the cord.

Time, as always, will tell.

 

 

What sweetener do you use: Part 5; Fructose effects

Saturday, January 28th, 2012

A good place to start researching

I basically knew what happens when we ingest glucose, (eating it or drinking it depending on whether it’s in solid or liquid form, e.g frosting versus sweetened tea) : it goes through the liver and heads off to muscle and other body parts where insulin activity is responsible for energy use. But I wanted to compare its effects to those of fructose. First I found an old article (1986 vintage) in the American Journal of Physiology (AJP), hardly a bedside reading item for me these days, but one I used to proofread for as a research fellow. That, once I translated it into English that I could understand, changed my mind a bit.

Glucose does lead to an increase in insulin levels and an increase in carbohydrate breakdown, while lipid (fat) breakdown slows down. The net result is a considerable bump in energy use. ‘So far, so good,’ I thought. But a comparable amount of fructose resulted in a much smaller increase of insulin, yet considerably more carb breakdown and even less fat breakdown. So even more energy was used. That I hadn’t expected, but this study was a one-time experiment with seventeen healthy folk followed for a few hours.

So my next question, and I thought this one was far more important, was what happen longterm?

Let’s look at animal research first. A group from Princeton published an article online in a journal called Pharmacology, Biochemistry and Behavior in February 2010. Tha basic conclusion from these scientists contradicted what I had read elsewhere, but made sense. They concluded all sweetener calories are not equal– after feeding rats standard foods and adding either table sugar-sweetened water or HFCS-sweetened water. Even if the HFCS water was less sweet overall, the rats gained more weight. Long-term feeding experiments showed rats fed HFCS developed many of the signs of the “metabolic syndrome.” weight gain, fat deposition in the belly and abnormal blood levels of trigclycerides.

So fructose was being metabolized to form fat, while glucose was being used as it normally is. That brought their thoughts back to why fructose in HFCS is different from that in table sugar. According to this research group, HFCS contains free, unbound fructose while that found in table sugar is always tied to a glucose molecule. Their concept is that table sugar fructose has to go through an additional chemical process, freeing it from glucose, before it can be used by the body.

So why should we care what makes rats fatter?

But here's our real target

I found a long article in The Journal of Clinical Investigation (JCI), the other research magazine my boss (and I) reviewed potential articles for in 1970 to 1972. Here people who who overweight or obese to begin with were fed either glucose- or fructose-containing liquids for ten weeks.

And the results were similar. Those getting fructose had more belly fat develop. I think translates to more chance of heart disease  and other long term complications.

The evidence is gradually adding up; I think HFCS is something to be avoided. Let’s feed our kids and ourselves more fruits and vegetables and less processed foods.