Vldl Quotes

Of those that appeared to play obvious roles in heart disease, three in particular stood out even in the early 1950s. Two of these are familiar today: the low-density lipoproteins, known as LDL, the bad cholesterol, and the high-density variety, known as HDL, the good cholesterol. (This is an oversimplification, as I will explain shortly.) The third class is known as VLDL, which stands for “very low-density lipoproteins,” and these play a critical role in heart disease. Most of the triglycerides in the blood are carried in VLDL; much of the cholesterol is found in LDL. That LDL and HDL are the two species of lipoproteins that physicians now measure when we get a checkup is a result of the oversimplification of the science, not the physiological importance of the particles themselves. In

The small, dense, reactive LDLs are born from the VLDL that is the product of high-carbohydrate intake.

The real trouble starts when triglycerides are unusually high in the bloodstream, causing your body to convert VLDL into small, dense LDL. This condition can occur routinely when you eat a high-carb diet (even if it’s a low-fat diet), because excessive insulin production drives the conversion of ingested carbohydrate into fat (triglycerides).

There is good evidence that Aborigines are genetically insulin resistant,94 so that some of their metabolic traits ‘are associated with being Aboriginal (mild impairment of glucose tolerance, hyperinsulinemia and elevated total and VLDL [very low density lipoprotein] triglycerides)’.95 In such a population, replacing ancestral food choices with the ‘displacing foods of modern commerce’ must predictably lead to high rates of T2DM.

I monitor several biomarkers related to metabolism, keeping a watchful eye for things like elevated uric acid, elevated homocysteine, chronic inflammation, and even mildly elevated ALT liver enzymes. Lipoproteins, which we will discuss in detail in the next chapter, are also important, especially triglycerides; I watch the ratio of triglycerides to HDL cholesterol (it should be less than 2:1 or better yet, less than 1:1), as well as levels of VLDL, a lipoprotein that carries triglycerides—all of which may show up many years before a patient would meet the textbook definition of metabolic syndrome. These biomarkers help give us a clearer picture of a patient’s overall metabolic health than HbA1c, which is not very specific by itself.

keeping a watchful eye for things like elevated uric acid, elevated homocysteine, chronic inflammation, and even mildly elevated ALT liver enzymes. Lipoproteins, which we will discuss in detail in the next chapter, are also important, especially triglycerides; I watch the ratio of triglycerides to HDL cholesterol (it should be less than 2:1 or better yet, less than 1:1), as well as levels of VLDL, a lipoprotein that carries triglycerides

When I look at a patient’s blood panel for the first time, my eyes immediately dart to two numbers: apoB and Lp(a). I look at the other numbers, too, but these two tell me the most when it comes to predicting their risk of ASCVD. ApoB not only tells me the concentration of LDL particles (which, you’ll recall, is more predictive of disease than the concentration of cholesterol found within LDL particles, LDL-C), but it also captures the concentration of VLDL particles, which as members of the apoB family can also contribute to atherosclerosis. Furthermore, even someone whose apoB is low can still have a dangerously elevated Lp(a).[*6]

I monitor several biomarkers related to metabolism, keeping a watchful eye for things like elevated uric acid, elevated homocysteine, chronic inflammation, and even mildly elevated ALT liver enzymes. Lipoproteins, which we will discuss in detail in the next chapter, are also important, especially triglycerides; I watch the ratio of triglycerides to HDL cholesterol (it should be less than 2:1 or better yet, less than 1:1), as well as levels of VLDL, a lipoprotein that carries triglycerides—all of which may show up many years before a patient would meet the textbook definition of metabolic syndrome. These biomarkers help give us a clearer picture of a patient’s overall metabolic health than HbA1c, which is not

I watch the ratio of triglycerides to HDL cholesterol (it should be less than 2:1 or better yet, less than 1:1), as well as levels of VLDL, a lipoprotein that carries triglycerides—all of which may show up many years before a patient would meet the textbook definition of metabolic syndrome. These biomarkers help give us a clearer picture of a patient’s overall metabolic health than HbA1c, which is not very specific by itself. But the first thing I look for, the canary in the coal mine of metabolic disorder, is elevated insulin. As we’ve seen, the body’s first response to incipient insulin resistance is to produce more insulin.

Lipoproteins come in five species: VLDL, ILDL, LDL, HDL, and chylomicrons. The first four, from large to small, stand for Very Low, Intermediate, Low, and High Density Lipoprotein. All these originate in the liver. The odd one, the chylomicron, is constructed by the intestines while digesting a meal, and released directly into the bloodstream. As blood tests are performed after a 12 to 14-hour fast, almost all the chylomicrons are gone. Its life story is much like VLDL, but without the cholesterol.

A heart that works more efficiently also translates to smooth kidney function, so less vulnerability to stress and unreasonable rage, less chances of bloating, less chances of jet-lagging and improved chances of a drug-free, stress-free life. Like that? As for cholesterol, nothing like weight training and its added advantage of after-burn to bring that LDL, VLDL down and HDL up. Cholesterol is a problem only when the LDL and VLDL along with triglycerides are not being utilized sensibly by the body. As a matter of training response or adaptation (expect this to set in about 12 weeks post consistent exercise), the body learns to preferentially use the triglycerides and cholesterol and to spare the muscle glycogen (muscle fuel stores) for its metabolic needs. No cholesterol lowering drug can do that for you.

As for cholesterol, nothing like weight training and its added advantage of after-burn to bring that LDL, VLDL down and HDL up. Cholesterol is a problem only when the LDL and VLDL along with triglycerides are not being utilized sensibly by the body. As a matter of training response or adaptation (expect this to set in about 12 weeks post consistent exercise), the body learns to preferentially use the triglycerides and cholesterol and to spare the muscle glycogen (muscle fuel stores) for its metabolic needs. No cholesterol lowering drug can do that for you. 10.

Alcohol is metabolized exactly like fructose.  Mostly in the liver (and enough in the brain to affect its function, for better and/or worse), and only through the citric acid cycle.  Excess amounts go directly into fat synthesis, raising triglycerides and VLDL.  Weight gain always follows.  I found it useful to go dry initially, to help my liver clear any accumulated fat.  Later, I settled on small amounts of wine only on weekends.

Once you understand that apoB particles—LDL, VLDL, Lp(a)—are causally linked to ASCVD, the game completely changes. The only way to stop the disease is to remove the cause, and the best time to do that is now.