More on this book
Community
Kindle Notes & Highlights
Read between
March 31 - March 31, 2024
But do they reduce the risk of heart attack across the board? Without a doubt they don’t!
Almost assuredly, statins are reducing the large buoyant LDL but not doing anything about the small dense LDL—therefore the risk of a first heart attack remains unchanged.
There’s now a burgeoning literature that statins increase glucose intolerance and risk for both diabetes and weight gain. Is it that, by acting on the liver, statins worsen insulin resistance? Or could it be the inverse—that statin use makes people think they can eat whatever they want because they are now impervious to any cardiovascular risk? It could be both.
side effect, which could include muscle breakdown, kidney failure, and type 2 diabetes?
But are they good or bad for the insurance company, which gets to increase your rates for a preexisting condition
This is important
because the problematic small dense LDL-C is a sign of insulin resistance and metabolic dysfunction.
Because the real problem is metabolic dysfunction due to insulin resistance—and statins do nothing to fix that.
triglycerides. The level of these particles tells you how your liver is doing.
And the primary driver? Insulin resistance. And its primary driver? Our out-of-control sugar consumption. Insulin resistance can be in part measured
by your triglyceride level
which is a better predictor of death by heart attack than h...
This highlight has been truncated due to consecutive passage length restrictions.
But there’s one thing that inhibits sodium excretion by the kidney—insulin resistance.
High insulin levels increase blood pressure, even with relatively low sodium intake. And many people
are insulin resistant—and those people do need to lower their salt as a treatment of the disease....
This highlight has been truncated due to consecutive passage length restrictions.
it’s also our proces...
This highlight has been truncated due to consecutive passage length restrictions.
Interestingly, only the liver and the brain IRKO mice developed high blood glucose, and only the brain IRKO mouse became obese and developed metabolic syndrome.
And even more interestingly, the kidney IRKO
mouse had normal blood glucose, but developed diabetic kid...
This highlight has been truncated due to consecutive passage length restrictions.
Yet, people with metabolic syndrome (insulin resistant) already have kidney disease even
before their glucose levels start to
and bad for you in that it increases the smooth muscle around the coronary arteries or in the kidney, leading to narrowing, and more risk for a heart attack or kidney failure.
Insulin has two actions in cells:
short-term gain (blood-glucose lowering) for long-term pain (vascular dysfunction and cancer).
We need insulin to survive, but if we are insulin resistant, adding extra insulin lowers glucose only at the expense of contributing to chronic disease.
The Atwater equation neglected to account for the intestinal microbiome and its inherent metabolism of approximately 25 to 30 percent of everything you eat, as well as the role of fiber in altering that percentage (see Chapter 12).
Where those food calories come from determines where they go. It’s not physics, it’s nutritional biochemistry.
Nature abhors a vacuum.
There are three different forms of digestible carbohydrate:
Further, our gut microbiomes have been altered by the antibiotics added to our food supply (see Chapter 18), which also drives systemic inflammation, making us even sicker.
And what do the doctors tell the other 21 percent who aren’t obese but still metabolically ill? What disease do they have?
Metabolic dysfunction is the “disease without a name.” The cells of the body, and often of the brain, are sick, due to eight—count ’em, eight—intracellular processes that have gone awry.
In order to stay alive, a cell has to burn energy.
The liver and adipose (fat) tissue need the hormone insulin
Cells are magicians.
But how and when is the key.
inside the cell
pyruvic acid,
captured within a molecule
(...
This highlight has been truncated due to consecutive passage length restrictions.
mitochondria
Krebs cycle, to yield a lot more ATP
triglyceride particle.
Therefore, the cell has another structure called a peroxisome, which is where various antioxidants are stored to neutralize the oxygen radicals.
Why do we get cataracts and wrinkles as we get older?
a carbohydrate (fructose or glucose),
amino acid (e.g., proteins).
but if the reaction occurs faster than the waste can be cleared,
The question is not if the Maillard reaction will occur, but rather how fast.

