"Gene mutation evolved to cope with modern high-sugar diets"

#1

Has any one comments one way or another on the article refered to at https://www.sciencedaily.com/releases/2019/06/190604084857.htm ?

"Summary:
A common gene (CLTCL1) mutation helps people cope with modern diets by keeping blood sugar low, but close to half of people still have an older variant that may be better suited to prehistoric diets, finds a new study. "

Lead author: Dr Frances Brodsky; co-author: Professor Mark Thomas (UCL Genetics, Evolution & Environment)

The latter is quoted as saying " “Our analyses strongly suggest that we have found yet another example of how prehistoric changes in dietary habits have shaped human evolution. Understanding how we have adapted to these changes doesn’t only inform us about why people lived or died in the past, but also helps us to better understand the relationship between diet, health and disease today.”

Is this old or new news? Is it a partial answer/comment on the topic Is a high-sugar diet ok for any subset of people](https://www.ketogenicforums.com/t/is-a-high-sugar-diet-ok-for-any-subset-of-people/6182)

Has anyone on this forum checked out his/her CLTCL1 gene variant, and if so, did it help explain anything, or suggest a particular course of action?

#2

I should add that the full article can be read at https://elifesciences.org/articles/41517 and that the wider range of work being done at the “Brodsky Lab” can be reviewed at https://www.ucl.ac.uk/biosciences/departments/structural-and-molecular-biology/smb-labs/brodsky-lab.

For those who would like to follow developments more closely.

(CharleyD) #3

Huh, wierd. I don’t think my 23andme sequenced that one, at least from what my Promethease service let’s me reasearch
I’ve got:
https://www.snpedia.com/index.php/Rs797044884(-;-)

and the only SNP for the CLTC gene is https://www.snpedia.com/index.php/rs797044884

Nothing on SNPedia for “CLTC1”

(Bunny) #4

”…CLTCL1 gene, which directs production of the CHC22 protein that plays a key role in regulating a glucose transporter in our fat and muscle cells. …” “…“In more recent years, with our high-carb diets that often provide us too much sugar, the newer variant may be advantageous,” Dr. Fumagalli added …” …More

Glucose transporter? I imagine they are talking more specifically about this specific gene and its protein synthesis in relation to the transporter GLUT4[1] …

I can assure myself that the human body was never intended to process 100% pure highly refined sugars and additionally with-out (bleached with granular carbon or charred animal bones[2]) its accompanying natural nutrients like minerals, vitamins and now rare trace elements, you might as well do highly refined and concentrated 100% pure cocaine which will kill you dead and much faster than highly refined and processed 100% pure sugar?

Footnotes:

[1] Fourteen Glut: Most mammalian cells import glucose by a process of facilitative diffusion mediated by members of the Glut (SLC2A) family of membrane transport proteins. Fourteen Glut proteins are expressed in the human and they include transporters for substrates other than glucose, including fructose, myoinositol, and urate. …More

[2] “…It gets even more confusing: While bone char is used to bleach and filter cane sugar, not all cane sugar is refined with bone char. Some companies rely on alternatives like granular carbon, which does not contain animal products, during the filtering process. …More

#5

Strange. There’s another snp that doesn’t even appear in my test results. No CLTC anything. But it was a free test so I can’t complain too much.

(Marius the butter craving dude) #6

Next study on this line should be:
Get a room full of people with this gene mutation and another room with with people without this gene mutation.
Feed them high sugar and carb diets and observe the weight gain. My intuition tells me that the test group will just get fat later than the control group.
I mean I had in highschool friends who would eat all the junk food I eat and be skinny; yet 10 years later they are having beer belly and laughing at my diet. All of this can equally be interpretated as: “Some people have higher carb tolerance before they also get fat”.
Secondly I really do not find the constant obsession with evolution as relevant… TO play the game of evolution and reference Garry taubes: The dinosaurs did not have the time to evolve mechanism to cope hith high levels of space rocks in the atmospheres; Or more directly: Those mutations do not make us carbvors !!

#7

Yes, I think they are talking about GLUT4 too, the insulin mediated transporter. So if it stays active between meals instead of just in response to post-prandial insulin release, it will scavenge more glucose all the time. But if de novo lipogenesis (DNL) can occur in fat cells all the time, does that imply the people with this gene mutation might be able to get fatter but be less IR? That is, they are likely to be the healthy-fat genotype? Or is it more likely that are more constant DNL will cause adipocyte damage sooner?

Either way, would having GLUT4 active more of the time inhibit lipolysis? If it isn’t insulin-dependant, then reducing insulin would affect it less in terms of weight loss.

All about GLUT4

(Bunny) #8

To tell you the truth I don’t think nutrigenomics, genotypes and SNP polymorphism mutations even matter, the bigger question is, how and why is this happening to begin with?

I think Dr. Michael Eades and Hyperlipid touch on that very subject in the way of macrophages (hyperphagic) surrounding adipocytes (immune response) from hydrogenated vegetable and animal fats, then you have HFCS mixed with sucrose (and whatever else mixed with that) and then throwing more table sugar on top of that and then the IR follows with fatty liver, fatty pancreas (visceral adipose fat) etc…

Ever build mud pies as a child? That is kind of what we allow adults to do now and you can’t stop them from doing it to your food…lol

Being GLUT 4 assists enzymes in muscle tissue like the heart which can also use fatty acids directly for fuel and liver tissue to digest glucose.

Some scientists think we may not even need insulin[1]?

What is really strange also is that cancer and tumor cells are very abundant (over-expressed) with GLUT 1 transporters (genes) that also assist enzymes in the cancer cells to digest glucose or other substances for fuel. Thermal conditions like heat seem to be a denominator to inhibiting its functionality.

Footnotes:

[1] “…Contrary to popular belief, insulin is not needed for glucose uptake and utilization in man. Finally, both muscle fat and carbohydrate burn in an amino acid flame. …” …More