We have excitement at the HDL. A marvelous band of ambitious and inquisitive folks are taking charge of critical health concerns. Something new and important in the history of health care is happening here.

We know that pure EPA has reversed HD symptoms in a small group of patients. Pure EPA is not readily available. We found alternative sources. The HDL EPA Study has about two dozen pioneers, taking EPA from various sources. We have data for about six months.

We know that CNTF reversed HD symptoms in a primate model of HD. It could be that with the help of our resident chemist and detectives that we have found a way to get the benefits of CNTF.

This is serious stuff. The criticism, that this is not the best of science, is valid. We are inspired by science. We are making the best use of the time and the resources we have. We may just improve the treatment of HD. God speed my heroes that are on this Forum.

Another class of drugs to consider:

My theory is that HD is immune related. If HD is immune related then drugs that decrease inflammation may treat HD. The statins are used to treat heart patients. The statins are also strongly anti-inflammatory. I believe statins cross the blood-brain barrier because they treat Alzheimer's disease. One study showed that about two-thirds of HD patients have early but mild AD pathology. It has been found that old guys that happen to be on statins are strongly protected from AD. I believe this is because of the immune properties of the statins. There are other theories. Bring on the HD fruit flies. --Jerry 17-Mar-2001
Proc Natl Acad Sci U S A 2001 Apr 10; [epub ahead of print], Fassbender K, et al.

Recent epidemiological studies show a strong reduction in the incidence of Alzheimer's disease in patients treated with cholesterol-lowering statins.

Moreover, elevated Abeta42 levels and the varepsilon4 allele of the lipid-carrier apolipoprotein E are regarded as risk factors for sporadic and familial Alzheimer's disease.

Here we demonstrate that the widely used cholesterol-lowering drugs simvastatin and lovastatin reduce intracellular and extracellular levels of Abeta42 and Abeta40 peptides in primary cultures of hippocampal neurons and mixed cortical neurons. Likewise, guinea pigs treated with high doses of simvastatin showed a strong and reversible reduction of cerebral Abeta42 and Abeta40 levels in the cerebrospinal fluid and brain homogenate.

These results suggest that lipids are playing an important role in the development of Alzheimer's disease. Lowered levels of Abeta42 may provide the mechanism for the observed reduced incidence of dementia in statin-treated patients and may open up avenues for therapeutic interventions.