CARBOTOXICITY [screaming face emoji]
Noxious Effects of Exaggerated Carbohydrate Intake (Kroemer et al., 2018)

This blog post is about the above mentioned article. Disclaimer (qualm #1): it is very pro-low carb and refused to include any neutral or negative points about low carb. For example, had it been within the scope of the article, the authors may have said despite excluding the majority of carbohydrate-containing foods, low carb diets actually aren't restrictive at all. In other words, this is not an unbiased review article.

Qualm #2: the authors say people have long-recognized the problems of lipid excess and it even has a name, "lipotoxicity." But these revolutionaries thought the problems of carbohydrate excess need to be recognized so they coined the term "carbotoxicity." Are we to believe these dorks never heard of "glucotoxicity" even though it was coined before lipotoxicity even was?!

The review is about the molecular, cellular, and neuroendocrine mechanisms that link a prolonged energy surplus to disease and accelerated aging. It doesn't really distinguish how the energy surplus is established, specifically, but every now and then they throw out there "carbz." Ignoring that, there are actually some pretty good points.

The history of dietary carbs had three major, transformative steps. The first was the transition from hunter-gatherers to agriculture which shifted the carbs from fruits, seeds, tubers, nuts, roots, and bulbs to a range of cereals (in Europe), rice (in Asia), corn (in Mesoamerica), and potatoes (in South America). And in Weston Price fashion, this was associated with an increase in dental cavities (probably more cause than correlation here).

Acarbose blocks carb digestion, D-glucosamine blocks glycolysis.

The second phase occurred in the last couple hundred years where it got WAY easier to make sugar. Instead of the labor-intensive cultivation and extraction of sugarcane, people figured out how to easily get sugar from beets.

"Before sugar became a low-cost commodity, overweight and obesity was a privilege of the aristocracy" !

Phase three is now. A mysterious combination of sugar, fat, and salt is in everything. Our carbs shifted from fibrous, nutrient-dense foods to sugar, fat, and salt. The epi studies have linked this shift with all imaginable diseases.

MECHANISMS

Imho, they largely plagiarized Michael Brownlee's "Unifying Mechanism" here, but Tl;dr: see the figures above.

To summarize: fructose in fruit is cool because micronutrients, phytochemicals, and fibres. It barely even makes it into the bloodstream. Fructose in industrial foods is usually much higher of a dose. This is problematic and promotes visceral fat deposition and insulin resistance. Remember, the #context of this article is a prolonged energy surplus.

Classic Biochemistry: a little bit of fructose can enhance hepatic glucose uptake, so a high intake of fructose & glucose as sugar in conducive of fatty liver.

Interesting: fructokinase deficiency protects mice against high salt-induced leptin resistance and hyperphagia that cause metabolic syndrome including fatty liver, transaminitis, insulin resistance, hypertension, and obesity. Fructokinase deficiency would counter the Classic Biochemistry note above.

The authors mentioned some stuff about artificial sweeteners which is a boat I've never been on because the evidence is weaksauce.

Some cells and tissues absolutely require glucose. Gluconeogenesis is pretty cool.

Ketones do stuff: suppress class 1 histone deacetylases which influences epigenetics, inhibits NLRP3 inflammasome which suppresses IL-1b, activates a GPCR which suppresses lipolysis, etc.

Ketogenic diets per se are perfectly safe but can be made otherwise. For example, good luck with a deep-fried bacon-wrapped cheese dog keto diet long-term. The same can be said for vegetarianism: whole-food, plant-based vegetarian is probably A-OK, but refined grains, processed vegetable oils, and regular soda is also vegetarian but "no bueno."

That's all for now!

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