Dr David L. J. Freed, MB, MD, MIBiol
NB These lecture notes refer in shorthand to the likely effects of the lectins that we consume daily in our food. For full explanation, see references below. The key to many of the chronic degenerative diseases of the civilised world (heart disease, diabetes, many kidney diseases, rheumatic conditions etc etc) is likely to be found in this newly-emerging discipline.
There are thousands of lectins; virtually every plant food has at least one. Only relatively few have been studied for interactions with animal or human tissues, but those that have (wheat, bean, lentil, pea etc) tend to be rather relevant to human nutrition. The interactions noted below are mainly taken from this group. We cannot be sure that they are universal among ingested lectins, but they are likely to be highly representative.
Lectins and digestion
Lectins tend to be resistant to cooking and digestion. Lectins disrupt the mucus overlying mucous membranes, sucking it out of goblet cells and causing it to "heap up", leaving patches of naked membrane exposed. Since the mucus layer is the principle protection for mucosae and the site for intraluminal digestion, its disruption would be expected to lead to incomplete digestion and increased susceptibility to dietary toxins. It certainly leads to abnormal bacterial, fungal and protozoal colonization. In addition, many lectins are anti-enzymes.
Stomach
Lectins stimulate mast cells, which in turn (in the stomach) increase acid. Given the above noted effects of stripping off patches of mucus and encouraging abnormal bacteria, you have an ideal scenario for peptic ulcer. Peptic ulcers, at least in my experience, often (not always) respond to stone-age diet.
Small intestine
Effects on mucus and enzymes as noted above. In rats, increased shedding of surface mucosal cells, much loss of protein, compensatory hyperplasia of crypts and increased gut weight but overall protein-losing with wasting of muscles. Hence bloated abdomen with wasted limbs. Virtually identical to human coeliac disease and very reminiscent of many human allergy-type patients. Gut has tremendous capacity to protect itself, by mucus and by throwing away its mucosal surface cells, but lectins on respiratory mucosae causes inflammation (bronchopneumonia) and in gut presumably would cause inflammatory bowel disease if gut's self-protective mechanisms were overwhelmed.
Pancreas and Fat cells
Initially stimulate release of insulin, causing hypoglycaemia, but after days leads to beta-cell exhaustion and hyperglycaemia (rats). Many dietary lectins (typical example: wheat) act similar to insulin, stimulating fat cells to take up glucose and lay it down as fat - leading simultaneously both to obesity and "lack of energy".
Rheumatism & Arthritis
Lectins bind to interfibrillar connective tissue in muscles and to muscle sheaths; likely there to cause stiffening and rheumatic patches. Intra-articular lectin injection in rabbits causes rheumatoid-like arthritis with associated immunological abnormalities.
Kidney
Theoretical involvement of lectins in IgA nephritis.
Atopy
Lectins in pollen. Evidence that lectins may divert an immune response into IgE mode.
Auto-immunity
Self tissues normally protected against autoimmune attack because they lack foreign epitopes and class II histocompatability antigens. Lectins provide the first and cause aberrant expression of the second.
Virus infections
People on stone-age diets rarely catch colds, even during epidemics. Note effect on mucus above; viruses can't attach readily to mucus-coated surfaces but attach easily to naked mucosa, so a much smaller inoculum is required to cause colonization. Complex interactions between infectious agents and lectins have been demonstrated.
References:
(1)Freed, DLJ: 'Lectins', British Medical Journal (1985) 290: 584-6.
(2) Freed, DLJ: 'Lectins in food: their importance in health and disease'.
Journal of Nutritional Medicine (1991) 2: 45-64.
(3) Freed DLJ: 'Do dietary lectins cause disease?'
British Medical Journal 1999, 318: 1023-4
