T2D Type 2 diabetes

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Hypothesizes

There is no confirmed theory of what causes obesity/T2D/metabolic disease - appears to be permanent damage - symptoms can be worked around via Low-Carb, but regression seems limited.

T2D has high BG - and chronically elevated insulin. Might be better called insulin tolerance.

Much of what is claimed falls under 'post hoc ergo propter hoc' (after this, therefore because of this) - a fallacy known from the example that the rooster crowing does not make the sun rise. Correlations do not show causation.

Careful treading - with high waders on is required. Strangely, despite T2D rising for decades we don't even know which tissue/organ is damaged.

If we accept that the damage is permanent - it begs the question: "Which tissue is damaged?"

Which tissue is damaged?

Liver

Pancreas

Adipose tissue

Brain and Sympathetic nervous system

Inflammation

Muscle Tissue

Theories pushed by people

Lustig Hypothesizes

Leptin based.
Fructose - NAFLD - causative?
Mitochondrial dysfunction
Insulin makes liver sick - pancreas portal to liver.
Liver backs up causing pancreas to hyper secrete more insulin.
Elevated insulin blocks Leptin - increasing appetite.
Elevated insulin thus causes elevated leptin.
Cause: processed foods - particularly sugar and lack of fiber.
Sugar causes Methylglyoxal - poisons mitochondria in liver
(Seems unaware of sweetness receptors in intestine?).
(Seems aware of the proton-switch - but not PUFAs roll?)
fructose induces leaky-gut
Mucous layer attacked due to lack of fiber? - (this theory doesn't work ???)
Trans-fats make ROSes
Fructose produces AGEs at a high rate.
Emulsifiers create leaky gut
Thickeners also produce leaky-gut
Monoglycerides - glycol ethers - leaky gut
3-MCPD carcinogen
NAFPD (Non Alcoholic Fatty Panaceas Disease) T1D? reduces insulin..
Re-normalization of ALT levels on blood tests hides fatty liver.. should be under 25 - the old limit
Re-normalization of uric-acid levels - high from fructose - should be below 5 - not 7

Mucous layer attacked due to lack of fiber? - (this theory doesn't work ??? - Feed the bacteria that eat mucous fiber and you have more)
Lustig appears wrong about fructose not used in human biology - seems to be manufactured and important for sperm? - (not that dietary fructose is a good thing). Body converts glucose to fructose in some cases.
He is also appears wrong about the role of Cholesterol in CVD.
Also, is more way sure about transfats than he should be - confounded with PUFAs
Seems certain about things that are not well grounded.

Tucker Goodrich

Seed oils damage liver - elevates 4-HNE, 4-ONE, 4-HHE, pentanal( valeraldehyde), methylglyoxal, and glyoxal
Seed Oils Oxidize Cardiolipin and Damage Your Mitochondria
impairs GSIS(Glucose‐stimulated insulin secretion)

Unger

Unger which is called glucagon-centric view of diabetes, there is no damage to liver, but the critical thing is impaired communication between alpha and beta cells of pancreas leading to hyperglucagonemia and excessive production of hepatic glucose.

Marc Gerardot

Other Hypothesizes

Epigenetic effect on GLP-1? (GLP-1 is packaged in secretory granules and secreted into the hepatic portal system by the intestinal L-cells located primarily in the distal ileum and colon, but also found in the jejunum and duodenum - info on this is contradictory and varies by source) Glucagon and GLP-1 are catabolic hormones.

Proton switch (burning or growth)

Kinase phosphorylation status tells whether they are on or off - the ROS switch controls the phosphorylation status.
PI3- kinase - opens cell to glucose
AMP kinase - make more MT (metformin mucks with this).
mTOR kinase - tells cell to divide ( ups protein synthesis)
Increases insulin release

ROS

ROS seems to be confounded with the 'proton switch' which appears to be a normal - very ancient signal that uses ROS as the signal. ROS outside normal ranges is different.

That everything is ROS vs antiox is quite ungrounded - Most antiox are very poorly absorbed - might act only on intestinal flora? real antiox can do harm.
tributal tin ups ROS

Western diet ups ROS

AGE (Advanced Glycation End-products)

Artificial Sweeteners

Uric acid (fructose in sugar(sucrose) drives uric acid)

Uric acid causes cellular dysfunction and insulin resistance, including oxidative stress, inflammation, and even preventing insulin from getting out of the blood stream effectively. dietary and environmental factors that generate uric acid, including fructose, purine rich foods and umami foods, dehydration, alcohol, and more. Glocose to fructose conversion may have evolved to deal with dehydration.

Is Uric acid a signal to get ready for food scarcity in fall (fructose => uric acid )?

uric acid is a signal of tissue injury, a mobilizer of repair systems and, in particular, a recruiter of endothelial progenitor cells

There seems to be little doubt that an acute rise in uric acid is beneficial and chronically elevated uric acid may be less so

quite a lot of evidence to suggest that physiological levels of uric acid production might be beneficial

Type-2 Diabetes

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