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Next up: Dr. Paul Mason #Carnivorycon
If you'd told him some of this five years ago, he'd have laughed in your face.
Nine school boys ate a few kidney beans that had been soaked but not boiled, and all nine of them got severe diarrhea. This was considered such a problem that the U.K. government issued required warning labels on treatment of kidney beans. A diet of 1% kidney beans kills rats.
Plants don't have claws and can't run away. Defenseless? You'd be wrong. Chemical defenses.
Lectins can bind to human cells.
Lectins are denatured by cooking. Recommended to soak kidney beans for 5 hours and then boil for 5 minutes to reduce the lectins to a less harmful level.
Ideally intestinal tract allows absorption of nutrition without allowing incursion of harmful substances.
Intestinal tract has micro-vili, at the tip is a glyco-[something], which means that lectins can bind to the intestine and damage it, which causes "Leaky Gut".
[Yep. Too fast for me to capture everything. Way less dense than the Clemens talk though...]
Unfortunately the consumption of lectins in our diet is increasing, significantly. In part due to selective breeding for crops with stronger builtin pesticides, i.e. lectins.
Weight loss due to cutting out plants -- *even* from a low carb or keto diet -- is because lectins stimulate insulin receptor.
Lectin also impacts regulation of the hormone leptin. Lectin binds to leptin receptor, causing leptin-resistance. 
What about reflux? Also called "heartburn". Lectins can stimulate this, by binding to IG molecules on the Mast cell, stimulating histamine ( ?? I think -Ed) release.
Plant lectins are far more likely to be problematic than animal lectins. Y acid is histamine release
[Okay okay I admit he's in the running for most scientific content per minute.]
Lectins ascend to brain by vagus nerve, possibly causing Parkinson's disease.
Okay now he's turning to auto-immune disease.
All auto-immune diseases are characterized by the body's immune system attacking itself.
Normally, antibodies are used to defend against foreign invaders — pathogens. Antibodies have a strong affinity for a foreign bacteria. Hopefully a healthy cell, the antibody has no affinity for it.
In the case of auto-immune diseases, antibodies have receptors that can bind to healthy cells. That can lead to healthy tissues being destroyed. The presence of these antibodies is what I use to try to diagnose an autoimmune disease.
Now "Leaky Gut", this intestinal permeability that allows lectins to enter into the circulation is a key contributor to autoimmune disease, and lectin is one of the key causes of Leaky Gut.
80% of the protein in wheat is gluten.
Bottom pair is celiacs, one exposed to gluten, top pair is non-celiacs, one exposed to gluten. Gluten impairs intestinal barrier in everyone, not just celiacs.
Tight junction disruption == leaky gut
Which allows lectins into the circulation which prompts an immune response since they are foreign bodies.
Due to "molecular mimicry" antibodies targeting lectins may also target healthy cells.
Molecular mimicry isn't just for lectins -- there are also bacteria that trigger this.
Key point: some lipopolysaccharides promote the inflammatory cascade, others block it.
Animal diet increases phylum that produces anti-inflammatory lipopolysaccharides.
[Oh god he's totally in the running for densest science. I hope we have some more rock star comedians later so my wrists can have a break from typing. —Ed]
[Skipping a couple of slides about type 1 diabetes association with gluten intake, because it's merely associational and I'm behind anyway. —Ed]
[Case study about 4-year-old child on gluten-free diet experiencing remission of Type 1 diabetes.]
Type 1 diabetes is auto-immune-caused. [Not sure if he meant always or sometimes. —Ed]
Okay, so why doens't everyone have an autoimmune disease? Because we've all consumed glutens.
The Swiss cheese model of accident causes. Accidents only happen when deficiencies in the defenses line up.
[Skipping photographing chart about genome association study because it's just a genome association study. —Ed]
Taking alcohol increases intestinal permeability
Anti-inflammatory meds increase intestinal permeability. And they are the meds prescribed for people who have auto-immune problems such as rheumatoid arthritis!
Emulsifiers (non-caloric additives to change the clumpiness of foods) also has a substantial effect, in mouse studies.
Another additive is titanium dioxide nano-particles.
It's an approved food additive. It's often in sweets and chewing gums. Studies in animals show that regular consumption of titanium dioxide will lead to measurable accumulation in organs in 10 days.
Titanium dioxide is used in oral drugs to help the drug penetrate the intestinal wall. [I think that's what he said. I'm behind. —Ed]
Next: pesticides.
Shows pics of mouse cells. The ones exposed to pesticide [which pesticide I wonder] doesn't have tight junctions any more.
Many foodstuffs are contaminated with pesticide residues.
Next: pollution. Really small particles called "PM10's". They've been shown to increase gut permeability. Mouse study -- those exposed to PM10's have increased intestinal permeability.
[I'm obvs gonna have to start abbreviating "Intestinal Permeability" as "IP".]
What about chemicals found in plastic? BPA. Damaging to the gut lining. [Skeptical. —Ed]
BPA is being removed from plastics. Replaced by something called "BPS". 80% of Americans now have detectable levels of BPS in their urine. Maybe stay away from plastics.
[something something consuming fat reduces passage of 100-nanometer spheres across some cellular junction by something 10X or 100X ??]
Glutamine is another candidate for reducing such permeability.
Bovine colostrum
Lectins can bind to sugars because they bind to carbohydrate proteins. [Is that what he said? —Ed]
[something something randomized controlled trial steroids something]
Should we have dairy foods. A1 and A2 proteins. In this study, both kinds still [something something] asthmatic-type [something].
15 patients, average duration 19 years inflammatory bowel disease. 11 of the 15 subjects had remission within 6 weeks.
Not statistically significant but clinically significant results (red circle)
[oookay. I'll call it a tie between Clemens and Mason on the scientific density. Her type of data was much preferable to me: more clinical and experimental than mechanism-explanation. Though they both did both kinds.]
