Study: Gene helped humans adapt to higher-carb world — but 50% of us don’t have it

Why is it that one person eating a high-carb meal will not have her blood sugar rise, and yet another person, eating exactly the same food, sees her blood sugar climb?
It might be related to whether or not she carries a specific variant of a single gene enabling more efficient blood glucose regulation. This newer gene variant spread among farming populations during the dawn of the agricultural revolution, when higher carb foods became more common.
But here’s the rub: Half of us don’t have it.
If you are among the 50% of the population who still carries the older variant that is less efficient with glucose regulation, your body may have a harder time managing your blood sugar levels in a high-carb world.
That is one of the findings of a fascinating new genetic study by researchers at the University College London, released early this month.
Science Daily News: Gene mutation evolved to cope with modern high-sugar diets
The study brought together specialists in population genetics, evolutionary biology, cell biology, and ancient DNA analysis to examine the evolutionary history of a gene involved the transport of glucose out of our blood and into our fat and muscle cells. The study examines the selective pressure on two existing variants of the gene, one that maintains glucose in blood and one that clears it faster.
The researchers compared the genomes of 2504 modern-day people from around the world, 61 animals including chimpanzees, gorillas, bears and fish, ancient fossilized human DNA, and DNA from Neanderthals and Denisovans to see how the gene had evolved over time.
The gene, called CLTCL1, codes for a specific protein called CHC22 clathrin, involved in glucose metabolism. The 56-page paper was published in eLife in early June 2019.
eLife: Genetic diversity of CHC22 clathrin impacts its function in glucose metabolism
CHC22 acts almost like a traffic cop that lets vehicles — GLUT4 transporters — carry glucose across the cell membranes. The older variant holds the transporters back in the cells for longer, resulting in slower removal of glucose from the blood. The newer variant does not keep the glucose transporter held inside the cells, enabling faster removal of glucose from the blood.
“The older version of this genetic variant likely would have been helpful to our ancestors as it would have helped maintain higher levels of blood sugar during periods of fasting… this would have helped us evolve our large brains,” explained first author Dr. Matteo Fumagalli.
The research found that a mutation in the ancient CLTCL1 gene first appeared about 450,000 years ago when humans started cooking food — when cooked carbohydrate starches would have first become more digestible. However, selective pressure on the gene during the time of the agricultural revolution 12,500 years ago spread the gene more widely into farming populations.
Nowadays the study found half of us still carry the ancient gene. The researchers say more research is needed to understand how these genetic variants impact our health and physiology, however, “people with the older variant may need to be more careful with their carb intake.”
So far, genetic testing companies like 23andme are not offering tests for the CLTCL1 gene, but any bet is that soon you will be able find out which variant you carry.
Earlier
Your thin friends can scarf down carbs? It may be their genes
Prediction: Even healthy people will be tracking blood sugar
And then suddenly my thyroid went ...Hashimotos.....weight gain of 58 lbs
Eating less and less
Then NA fatty liver disease..Metabolic Syndrome...glucose intolerance
Now not able to eat sugars and high carb foods
So which gene do I have?
As I have lived both sides of the situation
In this case, the not-so-subtle suggestion is the primacy of the Central Dogma of biology: genes are responsible for everything. While there are truthful observations in it, the extrapolation that one gene is "the" single point of failure in a complex physiological system, is not at all likely. It is merely one part in a very large puzzle.
The allele is in 23AndMe, but they don't tell you much about it:
The name of it is rs1061325.
CC is for grain/plant adaptation.
CT is the so-called "superior" heterozygous version that lets you more efficiently handle both fat/protein and carbs.
TT is the hunter-gatherer polymorphism that lets you handle fat/protein.
It turns out I'm CC. Before the age of about 45, I could eat anything and not gain weight, after that I ultimately gained about 50 pounds before keto.
I am not a doctor or otherwise qualified to give you medical advice. However due to experience with my health issues and needing to educate myself, I have some questions for you to investigate.
Have you been tested for coeliac disease (celiac disease, CD) or non-celiac gluten sensitivity (NCGS)
Many people with Hashimoto's also have CD. In the USA, the CD testing starts with a simple blood test called the "celiac panel". If the celiac panel tests positive, doctors usually order an endoscopy in which up to 8 biopsy samples are taken from the intestine. If any of the 8 samples, under microscope, show damage to the intestinal villi, the person is diagnosed with CD.
If none of the 8 samples show villi damage, the person is diagnosed as not having CD. If this happens, my questions are, (1) why did the celiac panel test positive if the person does not have CD, was it a false positive, (2) can a second celiac panel test be taken to confirm if the first test was a positive or false positive, (3) since villi damage can happen in patches, were the patches missed when the 8 samples were taken?
If the person tests negative for CD, the person can possibly have NCGS. I do not know of any scientifically validated test for NCGS. Since people with CD and NCGS produce excessive amounts of the hormone zonulin when these people ingest gluten, researchers can test for zonulin level in research settings. But, this test is not available to the general public in the USA.
So in the USA, the only NCGS test is to eat 100% gluten free and see if health problems go way. Doctors usually say to refrain from gluten for up to 2 weeks. However for an adult with CD, the intestinal damage can take up to 12 months to heal. [A very small percentage of CD adults age 50 and over, have refractory CD (RCD) which doesn't heal or is very unresponsive to healing attempts.]. Here's another question: is there, as yet, undetected damage to intestinal microvilli or another intestinal structure that needs to heal for NCGS? If so, how long does the healing take for a NCGS person?
My personal experience is that I had to go meticulous 100% gluten free for 10 months before starting to rid myself of the first health problem (loss of sense of smell). I got rid of 18 or 19 health problems over a period of 2 years 4 months. Since I'm not wealthy and didn't have access to a doctor, I had to do all of this experimenting on my own. I would be very happy to participate in scientific research if a scientist would like to confirm what my experimenting leads me to think. I don't have the HLA-DQ2 or HLA-DQ8 genetic markers for CD. However, I have at least two close relatives who have concluded that they have NCGS, one before and one after I concluded that I have NCGS. When I get glutened, my skin gets extremely itchy patches that get red, rise up, and get water blisters (dyshidrotic eczema or something else?).
After all of my self-experimentation, I was able to go to a medical doctor who confirmed that it appears I have NCGS.
There are at least 300 possible symptoms for CD. With NCGS, I had 18-19 of those symptoms.
I invite anyone, who has better or more current scientific information to correct or add to my above post.
So, Maggie, I hope that the above proves useful if you would like to explore the above questions with your medical doctor.