Friday, April 29, 2016

Another reason not to take human growth supplements

Nature, the British scientific journal founded in 1869, is not in the business of fear-mongering. But its March cover story may have raised some eyebrows about the nature of Alzheimer’s disease. The article, written by Allison Abbott, considers the notion that, under very specific conditions, Alzheimer’s could be transmitted to other people.
How could this occur? A key element is human growth hormone, which is produced naturally by the pituitary gland and governs growth. For many decades, pituitary glands have been salvaged from cadavers for the hormone that can be used to address growth-related problems. I first learned about HGH in the sports pages. After decades of allegations that many baseball players and other athletes were using steroids to gain a competitive advantage, major league baseball belatedly cracked down on the practice. But as steroid use declined, human growth hormone gained in popularity.
How could human growth hormone transmit Alzheimer’s? Abbott interviewed John Collinge, who has been examining human brains for the past quarter-century. While studying the brains of people who at some point had been injected with growth hormone, “It turned out that some of the preparations were contaminated with a misfolded protein—a prion—that causes a rare but deadly condition,” Creutzfeldt-Jakob disease. Unlike Alzheimer’s, which often takes at least a decade to do its dirty work, Creutzfeldt-Jakob typically kills within a single year.
For Collinge, according to Abbott, “the reason that these brains looked extraordinary was not the damage wrought from a prion disease, such as Alzheimer’s; it was they were scarred in another way. It was very clear that something was there beyond what you would expect,” Collinge was quoted as saying. “The brains were spotted with the whitish plaques typical of people with Alzheimer’s disease.”
Collinge, Abbott wrote, was disturbed by the implications: “That the plaques might have been transmitted from one person to another. If true, they could have far-reaching implications: the possibility that the seeds of the amyloid-β protein involved in Alzheimer’s could be transferred during other procedures from one person to another,” through common medical procedures such as blood tranfusions and organ transplants.
Not surprisingly, the news caused a stir, particularly in Britain, where the tabloid Daily Mail featured the headline, “Can you CATCH Alzheimer’s?”
Should the U.S. public be alarmed? Abbot suggests not, though she poses a range of questions that researchers are trying to answer. “Could seeds of amyloid-β proteins really be transmitted and, if so, are they harmless or do they cause disease? And could seeds of other related diseases involving misfolded proteins be transmitted in a similar way? In the past decade or so, evidence has been mounting for a controversial theory that rogue proteins, known collectively as amyloids and associated with diverse neurodegenerative diseases,”  including Alzheimer’s, “that might share some properties of prions, including their transmissibility.”
My takeaway is this: It’s always good policy to take precautions in a timely fashion. But, at this point, the odds of any one person being afflicted by this disease is exceedingly small.

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