On this chapter of Tim Ferris’ book, alloxan, a toxic glucose analog, was used as a stick model to make people try the “white” carbohydrate aversion rule (one of five rules). I did a small research and found that online most people blog about this stuff as if it is an absolute truth. There isn’t such a thing as absolute.
Alloxan is toxic to mice and other animal species but not humans. It can induce diabetes in lab rats alright. It destroys pancreatic beta cells as it accumulates via the GLUT-2 transporter. Its use is mainly for research for novel therapy against the disease. But it is interesting to note, that as I have said since there is nothing absolute, there is no research regarding its possible induction of type 1 diabetes in susceptible humans.
Type 1 diabetes is a condition, as compared to type 2, wherein the pancreatic beta cells, the ones producing the insulin, is suddenly annihilated in a very inconspicuous way. Most literature agree that there is some sort of trigger event, like an allergy that suddenly reduces the beta cells to nil and then produce insulin deficiency and hyperglycemia, thus diabetes mellitus.
The problem is that current research on alloxan is its effect on “Normal” beta cells. You can’t isolate Type 1 diabetes pancreatic beta cells because there isn’t any or maybe very hard to find (small numbers that keep patients alive for the meantime until they get their insulin from exogenous sources).
My hypothesis is this: Alloxan MAY CAUSE a triggering event that can lead to Type 1 diabetes mellitus. The alternative hypothesis is just the opposite and may close the book on Alloxan being a cause for human induced diabetes. This will also destroy the stick model used by Tim in his book.
The plan is to screen subjects (possibly neonates to 5 year olds) via DNA testing (really expensive for now) for the HLA gene that predisposes to Type 1 diabetes. The problem is even though you have the gene, you are only less than 20% to have Type 1 diabetes (numbers may need future citation, I don’t have the current version of Harrison’s) compared to Type 2’s 60% probability. We get consent to isolate pancreatic aspirates. Isolate beta cells if desired then bombard with Alloxan in vitro or in vivo by transplanting cells in other species then feed that species with Alloxan.
Statistics may play a role in this experiment to determine significance of the results but if I get just one result of a positive beta cell destruction via accumulation of alloxan, i’d mark that as already significant and may be a breakthrough in the pathogenesis of Type 1 diabetes.
Now for the lucky few who happens to chance upon my blog and asked why I would post something like this for all to see. Well, I don’t have the capability yet nor the certification required to do some crazy stunt like this. But if your one in a million who do, I am writing this for you. Take the credit, I just need to know this before I die.
Thank you to Tim Ferris and his wonderful new book: 4-hour body for introducing me to this insane idea. The blog title is from the first chapters. Believe me, I haven’t finished yet but I am hooked to read all the chapters. As a practicing clinician, I would love to give some comments on each questionable subject.
For those who haven’t bought the book, Alloxan is said to be a by-product of treating white carbohydrates during pre-market processing.
There is also a trigger for type 2 diabetes mellitus. This is why we do Fasting Blood Sugar as an annual screen. However, the population for an experimental study would include almost everybody (anybody can have it). It’s largely diet- and lifestyle-related and occurs with other morbidities. The beta cells are minimal and can even be normal in number in type 2. In short, much harder and more expensive to experiment.