Their function is to carry triglycerides from the liver, possibly to avoid the development of fatty liver, taking them to the peripheral tissues for storage in adipose tissue or for use in skeletal muscle. In the postprandial period, plasma triglycerides are also found significantly in chylomicrons and their remnants.
Triglycerides are another type of fat that’s used to store extra energy in your cells. LDL and LDL are both considered types of “bad” cholesterol.
LDL is created in your liver to carry triglycerides throughout your body. Most people will get their LDL level tested during a routine physical exam.
The American Heart Association recommends all individuals over the age of 20 get their cholesterol checked every four to six years. Cholesterol levels may need to be followed up more frequently if your risk for heart disease is high or to monitor any treatment.
The strategies for lowering your LDL and LDL levels are the same : increase physical exercise and eat a healthy variety of foods. Eat nuts, avocados, steel-cut oatmeal, and fish rich in omega-3 fatty acids, like salmon and halibut.
Avoid saturated fats, which are found in foods like beef, butter, and cheese. Lipoproteins are important biochemical substances whose main purpose is to carry lipids from one tissue to another.
LDL is produced by liver cells and is an important carrier of triglycerides (TGS) and to a lesser extent cholesterol. Once in the circulation, LDL is broken down in capillary beds by an enzyme called lipoprotein lipase, releasing lipids, mainly TGS, for energy utilization by cells or storage in adipose tissue.
A lipoprotein particle usually consists of a single outer layer of phospholipid covering a central core of TGS and cholesterol esters. Chylomicrons, IDL’s, and Vols are TG-rich lipoproteins, while LDL's and HDL's contain abundant cholesterol.
However, measurements of Lipoprotein(a) are not widely available and seldom used in routine clinical practice, despite the fact that it is a strong risk marker for AS CVD. Measurements of blood cholesterol are frequently performed to assess cardiovascular risk.
However, recent research suggests that TG-rich lipoproteins, such as LDL and IDL may also play a significant role in the development of AS CVD (1). They carry triglyceride, cholesterol, and phospholipids via the lymphatic system from where they enter the bloodstream.
The production of chylomicrons by the enterocytes takes place in an intracellular organ called the endoplasmic reticulum. The spherical ball of outer phospholipid and protein with cholesterol and TG inside (away from the watery environment of the cell) is the chylomicron (2).
Thus, the chylomicrons are the vehicles that enable the transport of lipids such as cholesterol, phospholipids, and TGS from the cells of the small intestine to the blood circulation. A blood sample drawn after a fatty meal often looks milky due to the presence of chylomicrons.
The primary role of chylomicrons is to transport digested lipids to the tissues of the body following a meal. Hence, chylomicrons are not needed in the fasting state, and they usually disappear within a few hours following a fatty meal.
TGS from the liver and adipose tissue need to be mobilized for fatty acids to be available as fuel for the cells of the body. Firstly, during conditions such as obesity, diabetes, and insulin resistance, there is increased fatty acid flux from adipose tissue to the liver.
Secondly, there is an increased DE Nova synthesis of fatty acids in the liver mainly from carbohydrates. Hence, high blood levels of LDL are associated with metabolic syndrome and insulin resistance (3).
Furthermore, high consumption of added sugar and refined carbohydrates will promote LDL production by the liver, a phenomenon, known as carbohydrate-induced hypertriglyceridemia. High consumption of added sugar and refined carbohydrates will promote LDL production by the liver, a phenomenon, known as carbohydrate-induced hypertriglyceridemia.
Dietary fat, on the other hand, is not a significant source of liver TG (5), and high-fat diets usually don’t raise fasting TGS. The entrapment of lipoproteins within the vascular wall may be a key factor in promoting atherosclerosis (7).
Because of their larger size, TG-rich lipoproteins carry 5 to 20 times as much cholesterol per particle as LDL. One study found that a nonfasting remnant cholesterol increase of 1 MML/l (39 mg/DL) is associated with a 2.8-fold causal risk for coronary heart disease (9).
This lipid pattern is typical for patients with insulin resistance and metabolic syndrome. It has been suggested that reducing plasma remnant lipoproteins rather than LDL should be the target for patients with metabolic syndrome.
Under these circumstances, it may be crucial to reduce dietary fat intake to lower triglycerides. It is necessary for patients with severe hypertriglyceridemia to avoid alcohol abuse as it can cause substantial increases in triglyceride levels and lead to acute inflammation of the pancreas (pancreatitis).
For example, Attic and Day spring mentioned that the Framingham study indicates that TG/HDL (triglycerides over HDL ratio) is 5 times more predictive of heart attack risk than LDL. They also mentioned that lipoprotein particles pass both cholesterol and fatty acids around like hot potatoes.
Because the basics of triglycerides and HDL are critical to health. I did a simple version of the TG/HDL ratio in a video 3 years ago (Brewer, 2017).
Chuck is a business owner living in Cocoa Beach, Florida. It happened while Chuck was traveling on US Highway 1 in his Tesla at 55 mph.
Meanwhile, he fumbled in the back seat for some nitro tabs, which he spilled on the floor. During his recovery, Chuck investigated how he could have a heart attack after losing 50 pounds.
The rest of this article will ask and answer a few basic questions about the TG/HDL ratio. The image below of triglyceride components is from Chemistry Libra Texts.
Chronically high insulin stimulates adenosines and hormone-sensitive lipase. This results in the release of too many fatty acids from fat cells.
These excess fatty acids take up space in HDL and LDL particles. HDL particles are considered being responsible for bringing cholesterol from the body to be metabolized by the liver.
(That’s opposed to LDL or low-density lipoprotein which brings cholesterol to different parts of the body.) We’ve talked about TG, HDL, and a bit about LDL.
They are then metabolized into other lipoproteins by the breakdown of triglycerides inside an RC particle. This breakdown is accomplished by lipoprotein lipase lining the luminal surface of capillaries.
RC is also higher in the serum of those with CV disease risk (around 15 mg/DL and above). It is calculated by subtracting LDL and HDL from total cholesterol (Feldman, 2020).
The image below shows how LDL's and HDL's transport TG. It is from the National Lipid Association’s website, used with permission from Tom Day spring (Lille, 2020).
Here, an enzyme called CEP (cholesterol ester transfer protein) facilitates the exchange of cholesterol in large HDL and large LDL with TG. In a nutshell, high TG levels affect HDL's and LDL's.
Look at the image below showing what a lipid profile would look like in a patient with prediabetes. The Women’s Ischemia Syndrome Evaluation (WISE) study studied 544 women referred for CV disease evaluation (Bittner, 2009).
In the discussion of science, studies, and treatment, there has been a tendency to go with higher ratios to show the largest impact on CV disease risk and death. TG/HDL ratios are higher in Hispanic Americans (3.9) than non-Hispanic whites (3.3) and non-Hispanic Blacks (2.9) (Willa, 2011).
Although the patterns of TG/HDL ratio vary by ethnicity, I do not recommend focusing on this. Not to mention that most of the cut points used in research as markers for prediabetes are too high.
A TG/HDL ratio of 3 confers a higher risk, so all of us should focus on this important number. Like I mentioned in the previous section, I do recommend that my patients target 1.5 or less.
The most effective ways to improve your TG/HDL ratio (that is, lower TG and raise HDL cholesterol) are: Body fat used to be considered as an inert energy storage tissue.
Now we know it is an endocrine tissue that releases chemicals (like adenosines) that cause insulin resistance, prediabetes, and CV risk (Won, 2013; Race 2008). The major impact of statins on TG/HDL ratio is to lower TG.
Multiple studies range from clinical trials in animals and humans to meta-analyses. The Abbas study was a human clinical trial using a crossover design.
The high-carb diet doubled TG levels, tripled remnant cholesterol, and lowered HDL by 15% (Abbas, 2004). It reviews pre-2005 studies which had already shown that low-carb diets decrease triglycerides and remnant cholesterol while increasing HDL (Voles, 2005).
Also, researchers showed that low-carb diets were less likely to result in weight rebound due to improved energy expenditure and leptin (Begin, 2012). We do heart attack, stroke, cancer & disability prevention.
Here at Premed, we can’t make you do high-Intensity intervals and resistance training or manage an appropriate BMI. But we can help you by telling you what you need to do, why, and how to organize around it, and provide recommendations to support you in staying healthy.