Are cancer and MS two sides of the same coin?
WGA/lectins attack membranes by forming a ring in the membrane. Some of the damage done is irreparable. This leads to a free diffusion of molecules in and out of the cell, and if enough poores are affected, the cell will not survive. This is called lysis.
The neuron may be affected in two ways: the membranes of the energy intake and; the various functional membranes of the sodium/potassium pump and diffusion. Either way, the pump will run down leading to neuropathy.
http://www.columbia.edu/cu/psychology/c ... aling.html
http://www.columbia.edu/cu/psychology/c ... cells.html
In cancer, cells that lack lectin-binding carbohydrates were resistant to lysis by these lectins.
Lysis of killer-resistant tumor cells by lectins may be an important pathway. And may possibly point to the key mechanism explaining why eating vegetables and fruits lowers cancer risk.
The case of MS and a significantly reduced risk of cancer, and in particular colon cancer with an abundance of lectins available in the gut (before the blood passed and was processed by the liver), could point to an important role of lectins and the lysis/innate immunity to control cancer. The results of these studies, when taken together, are of epidemiological nature and thus very powerful.
http://www.oncologypractice.com/oncolog ... 27a40.html
[The relationship of cancer with Type 2 Diabetes Mellitus is less clear, and results may be obscured because T2DM typically develops when people get older, just as cancer.
This leaves me puzzled with a number of questions:
- Is there something (e.g. carbohydrates, cytokines) that is more expressed in cancer cells because they need an abundance of nutrition? Is this triggering the lectin mechanism to attack to kill the cancer cell, in its early stage?
- Likewise, are some (neuron, oligodendrocytes, myelin, Schwann) cells in MS patients in desperate need of nutrition, because of a mitochondrial energy failure caused by poor gut functioning (e.g. due to failure of large intestine vitamin production and absoption)? Is this triggering (by mistake) the lectin/innate immunity mechanism to kill the cell?
- Does our body make smart use of the lectins produced by nature that leak through the gut (now it is the small intestine), or does the liver also make its own lectins (as suggested on Wikipedia)?
- Are the membranes of neuronal cells in MS patients more vulnerable to the combination of carbohydrates/cytokines and/or lectins, or is the problem just the supply side / higher exposure to lectins from a "broken" gut?
- Is the calcification of veins at older age and the corresponding insulin resistance the result of lectin caused lysis?
- Has the liver a crucial gatekeeper role (to filter out and/or process lectins) as suggested by the case of the Kaukasian women with MS who got a new liver and recovered from MS?
- Is the innate immune system closely related to the lectin mechanism? (the lectin mechanism is one of mechanisms of the innate immune sytem as suggested by wikipedia with lectins produced by the liver, but this may be wrong and lectins may be plant based)
- Are cancer control and T2DM/MS "auto" immunity by the innate immune system the same, i.e. is the binding of killer lectins to control cancer the same thing as easy binding of killer lectins to neurons?
- And what is the role of carbohydrates and possibly other things (cytokines?) to influence lectin binding and how can that be influenced e.g. by low fat/no sugar diet (re: the double hit in inflammatory response)? And what is the role of other food that may disrupt the digestive tract (e.g. modern wheat)?
I don't exclude here the possibility that ultimately a new concept will prevail that embraces both autoimmunity and reactivity or that the understanding of things becomes so fluid that autoimmunity and reactivity loose their meaning...