My big health issue was diabetes until I dislocated my shoulder. Now that my shoulder is merely a little awkward and the OTC pain meds brain-shudder seems to be backing off, I return to thinking about diabetes. Neuropathy of the feet is sneaking in and out, though no doc ever checks that. Eye troubles seem to be due to overuse rather than diabetic influence. What I discover is that in my absence the idea grew that diabetes is a process disturbance and that the process can be interrupted at any point in its function, which means the mishandling of sugar can be due to many possible glitches, rather than One Big Thing like diseases due to microbe invaders.
Doctors hate the particalization of causes. It was not taught in Med School and those of us who cruise Google all the time are always asking things they can't answer. More and more I run into doctors who were either in a different field for most of their practise or who have changed geography or who are just doing locums until they have enough money to retire, an amount that keeps going up.
The insurance claim people have not caught up either, but the docs compensate for their gaps in knowledge by standing up without explanation and going to their office, where they use Google or some specialized medical version. They never explain what they are doing. It would be more honest to bring the computer, even a tablet, into the exam room and make their search in plain sight, maybe with coaching from the patient. But they feel they need the mystique to maintain dominance and many are resistant to even admitting computers exist.
The human body is made up of cumulative mutations arranged on top of each other in the order that they happened. One change in a few atoms in a molecule of DNA makes something good happen, so it is kept and handed on because the mutation made the person a little more fitting. Or at least it didn't do any damage so the people who carry it forward are not affected. Now that we can actually detect these little mutations, we get a better idea of what's happening.
"CHC22 clathrin plays a key role in intracellular membrane traffic of the insulin-responsive glucose transporter GLUT4 in humans." It's a protein that escorts glucose in the blood to storage in muscle and fat. A process called "endocytosis" is a matter of the cell wall membrane making a little bag out of its surface, folded around the molecule so it can be taken into the cell. Or it could work the other way and throw the little bag with something in it OUT of the cell. Or there is a third way, taking in the fluid from around all the cells. If the clathrin doesn't remove the glucose from the blood stream by pushing it into a cell, you may have diabetes. The real point of the glucose is storage for a time of need. Too much glucose is poison. Too little is lack of energy.
These little bits have acronymic names like Clathrin Heavy Chain (CHC with a number which separates the various versions though they hardly vary. It must be important because mice have no CHC22 but people seem to need it. A protein molecule is very big and there are more characteristics of CHC than 22, so more indicators are attached.
"CHC22-V1316, which is more frequent in farming populations than in hunter-gatherers, has different cellular dynamics than M1316-CHC22 and is less effective at controlling GLUT4 membrane traffic, altering its insulin-regulated response. These analyses suggest that ancestral human dietary change influenced selection of allotypes that affect CHC22’s role in metabolism and have potential to differentially influence the human insulin response." Presumably the major change is the result of eating grain. Carbs.
When foundational food sources like wheat are genetically altered (frankenfoods) they may or may not play into the variability of the consumers. We know about gluten and there are other tiny genes in altered grain that might change something like CHC enough to hamper cell function but not kill or sicken the person entirely. There is a lot of theory about all this. A fellow named Fumagalli and his team find that CHC22 "first evolved around the time animals began developing a backbone and complex nervous systems." Mice, sheep and pigs then dropped it. CHC varies from one person to another. Some CHC allows higher levels of brain function. No one I know of has studied whether more glucose circulates in smarter people.
What is CLTCL, I ask google and it gives me:
Crazy Little Thing Called Love
Song by Queen
I gotta be cool, relax, get hip
And get on my track's
Take a back seat, hitch-hike
And take a long ride on my motorbike. . .
That was fun, but a quick look at this vid may help some people more. https://www.youtube.com/watch?v=GaIPFs52cUU
Rereading, I finally get it that CLTC and CLTCL1 are the names of genes and that the adepts talk about "CLD (Clathrin light chain subunits) and CCV's, lysosome biogenesis and maturation of regulated secretory granules." Okay. I'll just leave that to the adepts. A person can carry this search for understanding too far and become resistant.
Mostly, this information has little immediate helpful use for people who are trying to manage diabetes or related phenomena. One of my secondary concerns is why I've been so lethargic lifelong. I thought it was laziness and so did people who wanted me to do things, but it may be this business of moving glucose in and out of muscle cells. Much more pressing is the need for conscientious genomic interference by those trying to improve basic food origins. If we are accidentally breeding diabetes triggers into our daily bread, we need to stop as soon as we figure out how to do that. Some people have better results when baking with wheat flour made from very early versions of the grain, but that's too preoccupying and vulnerable to placebo effects for all of us to get into. After all, how many of us know where to test to find out even whether they have CHC17 or CHC22? Still, I like thinking about clathrin.
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