The Blood Type Diet Archives Volume 1
Re: Your New Book "Eat Right for Your Type"
Posted By: Cher Boomhower
Date: February 17, 1998 at 18:56:32
In Response To: Your New Book "Eat Right for Your Type" (Veronica J. McKay)
First of all, I enjoyed your book a lot. Secondly, Iím now doing lectin-cancer research for a naturopath here in Victoria. Iím having some conceptual problems- some missing links, that I wondered if you could help to clear up.
Mody et.al. 1995 has said that when a lectin binds to a cell it gets internalized, which makes it useful in cancer treatment because you can attach tumoricidal drugs to it. Youíve said that the lectin causes agglutination essentially by cross-linking cells. If the lectin is internalized it could not cause cross-linking.
At first I thought that some lectins caused agglutination and some were mitogenic (Yu et.al. 1993), and still others could activate immune cells (eg. WGA with alveolar macrophages in bladder cancer- Ogawara et al 1987, 1997 and Sharon and Lis 1972), and others had still other functions, but by the definition of a lectin, it must cause agglutination (Goldstein et.al. 1980).
At least in the case of ConA Iíve read that agglutination may be a 2 step process (Liener 1976)- "1) simple mono or divalent bonding process which is enough to trigger mitogenesis or to inhibit cell growth, 2)Multivalent process- cross-linking of macromolecules or cell receptor sites causes precipitation of macromolecules or agglutination of cells respectively".
Now from that, I get that the lectin binds to the sugar on the cell surface and triggers an internal response and THEN agglutinates cells, and I have no problem with that except that 1)the ligand canít be internalized in order to trigger an internal response and then cause external cross-linking! And 2)If a lectin is mitogenic AND agglutinates, then youíd think it would be a self-defeating process if there was enough lectin present. Letís take the pokeweed: itís a potent mitogen (Mody et.al 1995, Liener 1976), as youíve said. But if itís going to bind to the leukocytes and cause them to divide rapidly and soon after itís going to cross-link every leukocyte in the area it really should have very little effect on the system except to cause big globs of agglutinated leukocytes to appear. It shouldnít just cause proliferation and not agglutination, by definition. Am I missing something?
I know that ligands donít have to be internalized in order to trigger a cellular response, even though they often are, so thatís just a small point, but I thought Iíd ask what you thought on that. The second point, however, has me completely aggrivated. Another problem I have is with WGA in (eg) bladder cancer with the alveolar macrophages. Supposedly it binds these macrophages and makes them tumoricidal (Ogawara 1987, 1997, Sharon and Lis 1972). What good is this if it will subsequently agglutinate them? Iíve run into this problem with all the lectins that are supposed to enhance the immune system (eg, the mistletoes- Schumacher et.al 1995). In your book you say that (p.25) some lectins interact with the surface of cells and cause the cells to multiply (i.e. mitogens) but that they donít cause agglutination. Is it only mitogens and white blood cells that this applies to? If so, why are these mitogens still called lectins if they donít agglutinate? Is the definition I have out of date? I wonder if thereís a list somewhere of which lectins agglutinate and which are simply mitogenic or activators.
But hereís my next problem- letís say HPA is binding metastatic cancer cells (tons of references for that, Iím not going to list them all). I can see that in vivo HPA could bind cancer cells, and then agglutinate them, If HPA is actually an agglutinin, and again, I havenít read anywhere specifically that it agglutinated them (have you?), but then you said that once the malignant cells are agglutinated the immune system becomes activated. I can not find any specific reference for this. Why would the antibodies suddenly target the cancer cells just because they are agglutinated when they wouldnít target them before? I did read that "recent experimental observations support the notion that the action of cell-adhesion inhibitors may force cells into apoptosis and lectin mediated enhanced homotypic aggregation of metastatic cancer cells MAY INCREASE THEIR RESISTANCE TO APOPTOSIS" (Glinsky et.al 1996). This finding is basically contrary to what you said, although Glinsky is referring to the lectins produced on the surface of the cancer cell and not introduced lectins. Itís implying that tumor cells are stronger while theyíre adhering to eachother. Would this also apply to agglutinated metastatic cells? Probably not, I agree, but unless the binding of lectins both agglutinates and inhibits proliferation, what good is agglutinating them? Really, all Iím looking for here is evidence that once the cancerous cells are agglutinated, that theyíre actually somehow eliminated from the system.
You advise type Aís to increase the soy inn their diets, especially to avoid breast cancer. But soy lectin is specific for N-acetyl-D-galactosamine (Sharon and Lis 1972) so will it not agglutinate type A RBCís? Thereís a lot of evidence that soy lectin will bind breast cancer cells (Morecki et.al.1988) and that itíll bind other transformed cells (Drachenburg et.al 1995, Sharon and Lis 1972) but this is only useful if it will first of all bind these cancer cells at concentrations low enough to not agglutinate blood cells, and then also if it has some kind of magnetic effect on other metastatic cells in the blood stream and, if applicable, at other organ sites. That kind of implies a lot of lectin in the system. Would that not be enough to agglutinate the RBCís? How do you reconcile this? You said that lectins bind cancerous cells with 100x the affinity of normal cells, but thatís quite a blanket statement, and I wondered where I could find more specific statistics.
At one point you advised that type Aís eat peanuts because they contain a cancer-fighting lectin. I have here one paper that says PNA inhibits breast cancer cell proliferation in culture, but that PNA canít bind all breast cancer cell lines (Marth and Dasinbichler 1988). Another paper that supports this is Glinsky et.al. 1996. But I have other papers that show that PNA binds to the TN antigen and acts as a MITOGEN to colon cancer cells (Langkilde et.al 1989 and Yu et.al 1993). I also read that PNA strongly binds to normal mammary epithelium but that this strength is reduced by 50x with progressive malignancy (Rak et.al 1992). Also that itís very common for malignant tissues to start to produce the PNA autoantigen which may play a role in tumor escape from the immune system and hence tumor PROGRESSION (Laderoute et.al. 1994). So the impression that Iím gettin is that if you may have breast cancer, and then only certain types, you should be eating peanuts, but certainly not if thereís any chance at all that you may have colon cancer, and in any case, PNA seems to disappear in high grade malignancies (Langkilde et.al 1989) so shouldnít peanuts all in all be avoided?
As you can see, Iím a bit confused. Basically I need to get these things straight in my head so I can relate them to my boss so she can decide whether or not to use them in treatment, and Iím obviously missing some important connections here! Iíd be eternally grateful if you could nudge me in the right direction by suggesting some additional references for me! Again, thank you for this information. Iím really enjoying learning about all this! Cher Boomhower, Victoria B.C. P.S. If you wouldn't mind emailing me at firstname.lastname@example.org when you have the chance, that'd be great. Thanks again!
Messages in This Thread
Veronica J. McKay -- Tuesday, 17 February 1998, at 6:56 p.m.