Up until about 15 years ago lectins were thought of as laboratory tools, useful for histochemistry and blood transfusion work. The fact that many common foods are rich sources of lectin was not considered by most biomedical scientists. In the last decade, however, there has been a flowering of knowledge about the interactions of lectins with body organs and tissues, and it has become clear that many lectins are resistant to cooking and digestion and are distributed to distant parts of the body after ingestion. There is now abundant evidence that dietary lectins can cause disease in Man and animals. This review will adduce evidence that such hitherto mysterious diseases as inflammatory bowel disease, diabetes mellitus, rheumatoid arthritis, glomerulonephri-tis, psoriasis, multiple sclerosis, retinitis and cataracts in the eye, are all explicable in terms of a lectin aetiology, as are congenital malformations, infertility, IgE-mediated allergies and autoimmune states. Complete proof is still lacking in most cases, but the new hypothesis, if true, offers scope for rational therapy in these hitherto intractable diseases
Paper: https://doi.org/10.3109/13590849109084100
Full Paper on zlibrary
Notes:
Lectins are non-immunologic binding molecules present in virtually all plants, especially in seeds. They bind strongly to single and complex carbohydrates and behave rather like antibodies in vitro, although their structure is totally different… We ingest lectins every time we eat a vegetable foodstuff.
Virtually every cell in the body, and every extracellular substance, will be bound by lectins because of the ubiquity of secreted glycoconjugates
So something only from plants that binds to nearly every cell in the body, that behaves like antibodies.
Insulin itself serves to allow glucose admittance into fat-synthesizing cells and stimulates their activiw, several lectins including WGA, LCA, Pisum sativum agglutinin (PSA) from pea, waxbean lectin and Con A mimic these effects of insulin on isolated adipocytes, in the case of WGA with extreme molecular efficiency [Sl-881. It is tempting to suggest that lectins might be used therapeutically to take the place of insulin in insulindependent diabetes mellitus, but the reactive hyperglycaemia noted above sounds a warning note: the benefit might only be short term, to be followed by accelerated progression of the diabetes
There is a noted interaction in the Pancreas and insulin production and function. This may suggest some link between autoimmune diabetes (t1d) and lectins (very speculative)
Once lectins are bound to these slow-turnover tissues, it would be reasonable to expect them to stay in situ for some time and evoke inflammation, both directly and via auto-immunity (see Lectins and Auto-Immunity).
There could be a arthritis link
Skin: The Link with Psoriasis
Lectin uptake by neurones might be expected to damage the cells, and indeed ‘suicide transport’, in which neurones are persuaded to imbibe ricin or abrin, is popular among neuroanatomists for tracing nerve pathways
Do Lectins Interfere with Ontogeny or Reproduction?
Sex Organs and Fertility. Agglutination of spermatozoa is one of the classic tests for lectin activity in plant extracts. The majority of lectins bind to human and animal testis, epidydymis, spermatids and spermatozoa, and can be toxic to them…WGA prevents fertilization of hamster ova by spermatozoa [180], but lectins do not, curiously, interfere with the function of cervical mucus to any material degree
The interaction with immunoglobulins poses considerable problems in devising useful laboratory tests for food allergy, since when an antibody binds to a food extract it could signify antigedantibody binding, lectid- glycoprotein binding, or a mixtureof both. This gives rise to a series of problems that have yet to be overcome
Lectins and Gut Immunity
Anything that increases the permeability of the intestine to antigens, be it alcohol [230], trauma [231] or lectin [41] is likely to interfere with the normal oral tolerization process [232], giving rise to systemic antibodies against that substance itself [233], as well as against ‘bystander’ gut antigens.
Lectins and Auto-Immunity
Lectins and Virus Infection – WGA prevents herpes simplex virus (HSV) from adhering to rat sensory neurones, by binding to the cell surface and presumably obstructing the virus’s ‘landing pad‘ receptor [264]. Con A also prevents HSV attachment, but in this case by attaching to the virus 12641. Con A also inhibits influenza virus budding-off from infected human cells, presumably by increasing cell-surface rigidity [265]. – However, this anti-virus effect is only one side of the coin, and some lectins (particularly PHA) have a much more sinister interaction with viruses, transforming silent, asymptomatic carriage of adenoviruses [266], bovine leukaemia virus I2671 and HIV (the AIDS virus) [268] into f d y infectious, active disease. The patient could have remained completely well for years, then be struck down by a viral insurrection following the injudicious ingestion of under-cooked beans.
!!! Super interesting
Although absolute proof is lacking, it seems likely that dietary and/or inhaled lectins that escape the dual assaults of cooking and digestion reach the body tissues of humans and animals to cause much hitherto unexplained inflammation and tissue damage. Unexplained diseases of the gut, endocrine system, musculo-skeletal system, kidney, skin (including breast), and nervous system (including the eye) can now tentatively be explained, and rational therapies devised. Lectins are also implicated in congenital malformations and infertility. Inflammatory conditions involving auto-immunity and IgE antibodies are also satisfactorily explained in terms of a lectin aetiology and lectins can also interfere in complex fashion with virus infections.
Appropriate therapy for lectin-induced diseases would include, where appropriate, avoidance and active immunization, but the existence of laboratory-proven sugar inhibitors suggests that lectins might also be blocked in vivo by administration of the appropriate monosaccharides. Wheat-induced diseases, for example, should respond to N-acetyl glucosamine
avoidance would be some form of zero-carb or carnivore intervention.
Issues with this paper:
- It’s a review article
- It’s over 30 years old (where are the newer article? funding issue?)
- Nothing is proven, just suggestive linking of a common source of inflammation