I was watching a 3 part series on Curiosity Stream called “The Body”.
[URL: https://curiositystream.com/ (requires subscription)]
Here is the synopsis:
“The image of the human body was that the brain is the command center and the other organs obey the orders from the brain. We now know more.”
In one part, they indicate that hyperglycemia triggers an auto-immune response and it is the immune cells attacking the arteries that is a cause of arteriosclerosis. Has anyone else heard of this?
I should probably be more precise and it’s Insulin Resistance that is the actual trigger. I rewatched the segment and they say the fat cells become saturated and won’t let any more lipid cells in, classical insulin resistance.
This then triggers the immune cells to attack the lipid cells hanging around outside the fat cells. These immune cells go crazy throughout the circulation system and eventually break through the artery walls and start attacking any lipid cells they find. Eventually, the immune cells become saturated with lipid cells and explode, releasing their toxins which then attacks the artery wall.
Yes, but indirectly. It has to do with the secretion of insulin to lower the level of serum glucose. Elevated serum glucose causes all sorts of advanced glycation end-products (and haemoglobin, when glycated, makes the blood much likelier to clot, thus elevating the risk of a cardiovascular event). Insulin does at least three relevant things: first, it activates a gene complex that down-regulates the bodies defences against oxidative stress. Second, it activates inflammatory processes throughout the body. Third, it interferes with the production of nitric oxide (NO), thus increasing blood pressure, stiffening the arterial walls, and increasing the risk of arterial tears. When the rate of arterial damage outstrips the body’s ability to repair it, we develop atherosclerosis.
That sounds very dramatic!
Ravnskov and Diamond posit an alternative mechanism for arterial damage, which involves the vasa vasorum, the blood supply to the coronary arteries. Small clots in the capillaries of this system injure the intima media, the tear in the arterial lining is repaired with fibrin and cholesterol. Eventually the clot is shaved down, and arterial cells grow over the clot. The thickened section eventually returns to normal, and as long as a clot doesn’t travel down that stretch of the artery and cause a blockage before then, the heart muscle is fine.
Blame the hyperglycemia not the actual culprit SUGAR? <=== what caused the hypoglycemia to begin with?
Shakes head in disbelief…
These researchers really need to get grip on a thing called REALITY<=== does the body good!
I can just imagine how this got funded? When you do research on sugar burners you get data that DOES NOT APPLY?
If your doing the ketogenic diet correctly or fasting correctly when your individual metabolism adjusts your NOT going to be quote: “hypoglycemic?”
Megan Ramos: But my blood sugar levels are typically between 3 and 3.9 mmol/L, which translates into 50 to … or sorry 54 to 70 mg/dL. So, that 65 to 99 mg/dL is considered to be normal by government standards here in Canada, the 54 to 70 is considered to be common amongst ketogenic population . A lot of my patients too, who follow ketogenic diet, they’re getting sugars between 3 and 3.9 or between 54 and 70 .
What does it mean? What is normal? What is acceptable for someone who’s keto adapted? We’re still learning. I usually gauge how my body’s feeling at a certain blood sugar level. I let that determine whether or not it’s normal for me. Hypoglycemia is not defined as a set of numbers. It’s defined as a set of symptoms, so dizziness, mental fatigue, shaking, palms sweaty, hands. That defines hypoglycemia. It’s a list of symptoms. …More
We can now assemble a hypothesis linking low carb diets to high LDL. If one eats a glucose and/or PROTEIN restricted diet, T3 levels will fall to conserve glucose or PROTEIN. When T3 levels fall, LDL receptor expression is reduced. This prevents LDL from serving its fat transport function, but keeps the LDL particles in the blood where their immune function operates.
If LDL particles were being taken up from the blood via LDL receptors, they would have to be replaced – a resource-expensive operation – or immunity would suffer. Apparently evolution favors immunity, and gives up the lipid-transport functions of LDL in order to maintain immune functions during periods of food scarcity.
High LDL on Low Carb: Good health, bad diet?
Suppose LDL receptors are so thoroughly suppressed by low T3 that the lipid transport function of LDL is abolished. What happens to LDL particles in the blood?
Immunity becomes their only function. They hang around in the blood until they meet up with (bacterial) toxins. This contact causes the LDL lipoprotein to be oxidized, after which the particle attaches to macrophage scavenger receptors and is cleared by immune cells.
So, if T3 hormone levels are very low and there is an infection, LDL particles will get oxidized and cleared by immune cells, and LDL levels will stay low. But if there is no infection and no toxins to oxidize LDL, and the diet creates no oxidative stress (i.e. low levels of omega-6 fats and fructose), then LDL particles may stay in the blood for long periods of time. …More