ALS Growth Hormone Study

A new study led by Mayo Clinic found that a growth hormone, IGF-1, showed no benefit for patients with ALS. The study included 330 people from 20 different medical centers. Two previous studies of the growth hormone had conflicting results. Eric Sorenson, M.D., a Mayo Clinic neurologist, was the lead author of this study.

ALS causes degeneration of the nerve cells in certain regions of the brain and spinal cord that control the voluntary muscles. Each year about 5,000 Americans are newly diagnosed with ALS, and about 20,000 Americans have the disease.

“Studying a drug and finding out it doesn’t work is actually quite helpful,” says Dr. Sorenson. “By doing these studies, we can prevent ALS patients from wasting their time chasing down expensive, unhelpful and sometimes risky treatments.”

This study will be published in the Nov. 25, 2008 issue of Neurology, the medical journal of the American Academy of Neurology.

Below is a youtube video of Dr. Sorenson discussing the study.

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4 Comments

  1. dougal macdonald
    Posted November 25, 2008 at 7:29 pm | Permalink

    Seems obvious that the reason ALS patients are trying doubtful drugs is that after knowing about ALS for 140 years, researchers have come up with zero,zilch, nada, nothing in the way of treatments (everyone knows Rilutek is slightly better than worthless if that). Further, completing studies of a drug takes a ridiculous amount of time from a patient’s perspective. We’re all excited to check back in another 140 to see if anyone has gotten anywhere.

  2. Posted November 25, 2008 at 9:35 pm | Permalink

    Thanks for your comment, Mr. Macdonald. You are certainly not alone in your frustration. You can view another new video of Dr. Sorenson discussing current ALS research, as well as his optimism for the future of ALS research, at: http://www.youtube.com/watch?v=-Qn-NXI1tqo

  3. Posted November 28, 2008 at 5:55 pm | Permalink

    IGF-1 in the bloodstream (after subq injection) should suppress HGH production which in turn should suppress natural production of IGF-1. Is it possible, due to the natural tendency of the body to seek homeostasis, that the experimental group did not actually experience higher circulating IGF-1 levels for extended periods of time except for the initial bolus?

    The published research report did not specify the amount of difference in circulating IGF-1 between the experimental and control groups. Is this data available?

    I appreciate your resonse.

  4. Posted December 1, 2008 at 2:10 pm | Permalink

    Mr. Rossiter,

    Thank you for your comments and questions regarding our IGF-1 study. In terms of the circulating IGF-1 values, I cannot comment on with data. I know that the company that holds the patent to the drug for ALS did check circulating blood levels on the subjects in phase I, II and the first phase III studies. It was based upon these blood values that the twice daily dosing was based. A bigger question in my mind is whether we were able to alter the IGF-1 level or response at the motor neuron. To my knowledge this question remains unanswered. It seems likely however that if IGF-1 has any effect on ALS it cannot be given subcutaneously.

    Thank you for your questions,

    Eric Sorenson


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