Who owns Glycobiology?

A recent article in Science (2 Nov 07(318):734-737) discussed the wealthy Mannatech company that produces aloe-based products such as Acemannan. It has long been used as one of the many alternative approaches to managing HIV infection.  Sugars (carbohydrates) are often found in the body attached to fats (lipids) or proteins where they are known as glycolipids or glycoproteins. As a field of scientific discovery, this is a relatively new area of understanding biological systems and functioning.

Some scientists in the field have taken umbrage against Mannatech for commercializing products that are little understood and applying a patina of science to their own sales efforts. While the science is definitely critical, company-sponsored research is always questionable. With agents like dietary supplements, we suffer the double whammy of little financial interest in paying for these studies due to lower profits as well as lack of interest on the part of mainstream medicine.

However, Mannatech is a well-heeled company, charges a great deal (with a workforce of 500,000 independent sales people according to the article) and some $400 million in sales, they are hardly poor, if not as stinking rich as even relatively small pharmaceutical companies. At issue is a scientific conference that Mannatech has provided some funding for. This conference on glycobiology to take place in Ireland has some scientists up in arms.

Essentially, paid for conferences of this type ARE problematic. The pharmaceutical industry has virtually completely replaced continuing physician education with dog and pony shows designed solely to sell product, while downplaying side effects. (An article from the November 25, 2007 New York Times on the topic is illustrative.)

Unfortunately, there is only one significant study of Acemanna in the context of HIV (J Acquir Immune Defic Syndr Hum Retrovirol. 1996 Jun 1;12(2):153-157) which found no benefit in terms of CD4 count nor in the older p24 antigen assay (prior to viral loads and not very useful as a marker).  The abstract is below.

But this leaves us in a bind. How do we get good data on these types of interventions? How can we figure out what works, what helps? And how can we establish the cost/benefit of such interventions? Perhaps a new administration will reinvigorate the NIH so that more independent studies can be undertaken of the most important questions.

Sadly, the for-profit, privatized approach to discovery, let alone access, has left us with fewer reliable data, misinformed physicians and reduced access to best practices and care.

George M. Carter


Montaner JS, Gill J, Singer J, Raboud J, Arseneau R, McLean BD, Schechter MT, Ruedy J.

Canadian HIV Trials Network, St. Paul’s Hospital/University of British Columbia, Vancouver, Canada.

SUMMARY: We assessed the safety and surrogate markers’ effect of acemannan as an adjunctive to antiretroviral therapy among patients with advanced HIV disease receiving zidovudine (ZDV) or didanosine (ddI) in a randomized, double-blind, placebo-controlled trial of acemannan (400 mg orally four times daily). Eligible patients of either sex had CD4 counts of 50-300/microl twice within 1 month of study entry and had received 26 months of antiretroviral treatment (ZDV or ddI) at a stable dose for the month before entry. CD4 counts were made every 4 weeks for 48 weeks. P24 antigen was measured at entry and every 12 weeks thereafter. Sequential quantitative lymphocyte cultures for HIV and ZDV pharmacokinetics were performed in a subset of patients. Sixty-three patients were randomized. All were males (mean age 39 years). The mean baseline CD4 counts were 165 and 147/microl in the placebo and acemannan groups, respectively; 90 percent of the patients were receiving ZDV at entry. Six patients in the acemannan group and five in the placebo group developed AIDS-defining illnesses. There was no statistically significant difference between the groups at 48 weeks with regard to the absolute change or rate of decline at CD4 count. Among ZDV-treated patients, the median rates of CD4 change (ACD4) in the initial 16 weeks were – 121 and – 120 cells per year in the placebo and acemannan groups, respectively ( p = 0.45), ACD4 from week 16 to 48 was 0 and – 61 cells per year in the acemannan and placebo groups (p = .11), respectively. There was no statistical difference between groups with regard to adverse events, p24 antigen, quantitative virology, or pharmacokinetics. Twenty-four patients, 11 receiving placebo and 13 receiving acemannan, discontinued study therapy prematurely, none due to serious adverse reactions. Our results demonstrate that acemannan at an oral daily dose of 1600 mg does not prevent the decline in CD4 count characteristic of progressive HIV disease. Acemannan showed no significant effect on p24 antigen and quantitative virology. Acemannan was well tolerated and showed no significant pharmacokinetic interaction with ZDV.


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