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“There are few things that humble me more than my complete and utter buffoonery when it comes to HDL lipidology…” – Peter Attia

“It’s true of all of us.” – Thomas Dayspring (Attia, 2020)

Thomas Dayspring is a nationally recognized lipidologist. That means he’s an expert on cholesterol, fat, and oil metabolism. And Peter Attia is no slouch in this area. If you’d like to spend a few hours hearing cutting-edge concepts in this area, try listening to episodes 20-24 of Attia’s podcast “THE DRIVE.” 

But be warned; that video is very technical. Less than 600 people have started even one of these podcasts. We can only guess how many finished the full 5 hours. I did. 

Some information wasn’t that new. For example, Attia and Dayspring 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. A few of their concepts also seemed to contradict some basics mentioned later in this article. 

Why would I focus this article on such simple concepts? 

Because the basics of triglycerides and HDL are critical to health. But the complicated version just isn’t understandable, let alone actionable. 

I did a simple version of the TG/HDL in a video 3 years ago. It was one of our popular videos. 

 

Many people told me the information saved their lives. Chuck Smith is one of those people.

Chuck Smith’s story

Chuck is a business owner living in Cocoa Beach, Florida. He saw Caldwell Esselstyn for his preventive care. He lost 50 pounds on Esselstyn’s low-fat diet.

Then Chuck had a heart attack. It happened while Chuck was traveling on US Highway 1 in his Tesla at 55 mph. Chuck had nitro pills in his back seat. So he put the Tesla on autopilot, driving him to the hospital. 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. He found my channel. He was one of 60,000 people that watched my video on the basics of TG/HDL.

He measured his own TG/HDL. It was 5. It had been as high as 7. So he switched his diet from low fat to low carb. 

Two years later, he lost 20 more pounds. His TG/HDL is now routinely 1 or less. His heart attack risk has plummeted. His artery scan has improved. His cardiovascular (CV) inflammation panel is perfect. And he’s ready for another 50 years of healthy living.

Watch Chuck’s full story here.

 

The rest of this article will ask and answer a few basic questions about the TG/HDL.

What is triglyceride?

Triglycerides (TG) are fats. Each triglyceride molecule contains 3 fatty acid molecules held together by a glycerol molecule. Fatty acids are fats, while glycerol is a carbohydrate.

The image below of triglyceride components is from Chemistry Libre Texts.

Triglyceride components

What are good blood levels of TG?

Target TG levels between 100 and 200 mg/dL (or about 1 to 2 mmol/L) are usually considered borderline. Lower levels are optimal. Some disease states feature TG levels over 500 mg/dL or 5.7 mmol/L.  

Why is there TG in the blood? 

The most common reason for elevated triglycerides is prediabetes. Chronically high insulin stimulates adipokines 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. 

TG can also become elevated in several inherited diseases. 

What is HDL?

HDL is an acronym for high-density lipoprotein.

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. That’s the reason some people are still calling LDL the “bad cholesterol” and HDL the “good cholesterol.” 

This is an image of HDL from Biosciencenotes.com.

HDL Structure from Biosciencenotes

Will an improvement in HDL level lead to better health?

Yes. Improvement of HDL function improves arterial health (Chiesa 2019). How? By: 

  1. Improving nitric oxide;
  2. Decreasing oxidase enzyme function;
  3. Decreasing adhesion molecules; 
  4. Decreasing monocyte infiltration; and 
  5. (Possibly) improving reverse cholesterol transport.

HDL & Arterial Health

What is remnant cholesterol?

We’ve talked about TG, HDL, and a bit about LDL. There’s another thing we ought to cover—remnant cholesterol.

Remnant cholesterol (RC) is the most dangerous type of cholesterol particle. It’s also called triglyceride-rich lipoproteins (TGRLs), which consists primarily of VLDL (very low density lipoproteins) and IDL (intermediate density lipoproteins) (Dhindsa, 2019). 

Remnant Cholesterol

Image from the Cholesterol Code by Dave Feldman.

Remnant cholesterol is short-lived in the plasma of a healthy person. RC particles appear only briefly after a meal. 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 cholesterol levels from total cholesterol number (Feldman, 2020).

Do high TG levels affect HDL and LDL cholesterol levels?

The image below shows how LDLs and HDLs transport TG. It is from the National Lipid Association’s website, used with permission from Tom Dayspring  (Lillo, 2020).

HDL, LDL, VLDL, triglycerides & CETP

Here, an enzyme called CETP (cholesteryl ester transfer protein) facilitates the exchange of cholesterol in large HDL and large LDL with TG. What CETP does is it takes cholesterol out of large HDL and LDL particles and then transfers TG into these particles. In turn, hepatic (liver) lipase metabolizes TG-rich HDLs and LDLs, leading to smaller HDLs and LDLs. 

In a nutshell, high TG levels affect HDL and LDL levels. And prediabetes leads to high TG levels.

Look at the image below showing what a lipid profile would look like in a patient with prediabetes.

HDL & LDL Distribution in a Prediabetic Patient

  1. The patient has elevated TG levels (216 mg/dL), a low HDL cholesterol level (34 mg/dL), and a high LDL cholesterol level (139 mg/dL).
  2. There was a decrease in the size of HDLs. Normally, the HDL curve should be a smooth bell curve peaking where the red circle is drawn. Here, the large HDLs are taken out.
  3. There was also a decrease in the size of LDLs. Though the LDL has a good bell curve at the right, the curve’s peak shifted to the left. This means there are more smaller and denser LDLs. (We call this a B pattern LDL distribution.) 

Aside from prediabetes, this patient actually has another problem—familial hypercholesterolemia (FH). Neither condition was noticed before the patient came to us.

To make matters worse, the patient also has an elevated TG/HDL—216/34 or 6.4! I recommend a goal of 1.5 or less.

What is the TG/HDL?

TG/HDL is the triglyceride-to-HDL ratio. To find your TG/HDL, simply put your blood triglyceride value over your blood HDL cholesterol level, as measured by your medical laboratory blood test. 

Why is TG/HDL important?

TG/HDL is important because it is an important predictor of risk for heart disease. It is also a marker of insulin resistance, and insulin resistance is the major cause of prediabetes, metabolic syndrome, and type 2 diabetes. (Cordero, 2009)

The Women’s Ischemia Syndrome Evaluation (WISE) study studied 544 women referred for CV disease evaluation (Bittner, 2009). The TG/HDL ranged from 0.3 to 18.4. It was a powerful predictor of all mortality and cardiovascular events. 

This chart shows the WISE study range of TG/HDL. Individuals with lower TG/HDL had lower CV disease risk.

WISE study range of TG HDL Ratio

What is a good TG:HDL ratio?

A lower TG/HDL is better. 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. 

Here are the typical cut points for risk (Sigurdsson, 2014): 

  • In US (mg/dL) – less than 2 is ideal; above 4 is too high
  • In Europe (mmol/L) – less than 0.87 is ideal; above 1.74 is too high 

Does ethnicity matter in terms of TG/HDL? 

TG/HDL appears to vary by ethnicity. Ratios are higher in Hispanic Americans (3.9) than non-Hispanic whites (3.3) and non-Hispanic Blacks (2.9) (Willey, 2011). 

Thus, many say that we should go target different levels based upon ethnicity. Those same scientists have said that a TG/HDL of 2.0 is diagnostic of prediabetes for African-Americans. 

Although the patterns of TG/HDL vary by ethnicity, I do not recommend focusing on this. There are several reasons, such as the fact that ethnicities are often mixed and unknown. 

But the biggest reason is that TG/HDL is an indicator of the health of insulin and glucose metabolism—the lower the ratio, the better the patient’s health. Not to mention that most of the cut points used in research as markers for prediabetes are too high. For example, ratios of 2 and 3 confer risk, no matter what your ethnicity is. 

A TG/HDL of 3 confers a higher risk for heart disease, so all of us should focus on this important number. No matter which ethnicity, the goal should be as low as possible. Like I mentioned in the previous section, I do recommend that my patients target 1.5 or less. 

How can you naturally lower TG and increase HDL levels? 

The most effective ways to improve your TG/HDL (that is, lower TG and raise HDL) are: 

  • Lose weight. Body fat used to be considered as an inert energy storage tissue. Now we know it is an endocrine tissue that releases chemicals (like adipokines) that cause insulin resistance, prediabetes, and CV risk (Kwon, 2013; Rabe 2008). 
  • Eat fewer carbs. Get into a lower carbohydrate diet (Dashti, 2004). 
  • Exercise. Exercise increases HDL levels and lowers TG levels (Sopko, 1985; WebMD, “Will Exercise Really Lower Triglycerides?”).
  • Take niacin. It is one of the few supplements that lowers TG (down by 20-50%), increases HDL cholesterol levels (up by 15-35%), and lowers LDL cholesterol levels (down by 10-25%) (Simon, 2007; Kamanna, 2008).
  • Get dietary and supplemental omega-3s (Yanai, 2018).

Which medications improve TG/HDL? 

  • Statins. The major impact of statins on TG/HDL is to lower TG. But usually, statins are given to lower LDL. Sometimes they can also increase HDL levels but still not as much as how they lower TG. They can lower TG by as much as 50% (Maki, 2012). 
  • Fibrates (Lopid, Fibricor, and Tricor);
  • Prescription-strength niacin (Niaspan);
  • Prescription-strength omega-3s. Icosapent ethyl (Vascepa), Epanova, and Lovaza are prescription forms of omega-3s (Bhatt, 2019; WebMD, “What medicine is used to treat triglycerides?”)

Can lowering carbs actually improve TG/HDL, RC, and CV risk?  

Yes. There is plenty of evidence showing this. Multiple studies range from clinical trials in animals and humans to meta-analyses. Here are 4 of them:  

  • The Abbasi study was a human clinical trial using a crossover design. People ate high carbs (60% of calories) for 2 weeks, then low carbs (40% of calories) for 2 weeks, with a “washout period” of 2 weeks in between. The high-carb diet doubled TG levels, tripled remnant cholesterol, and lowered HDL by 15% (Abbasi, 2004).
  • The Wang study is a randomized clinical trial in laboratory mice (Wang, 2008). 
  • The Volek study is a meta-analysis. It reviews pre-2005 studies which had already shown that low-carb diets decrease triglycerides and remnant cholesterol while increasing HDL cholesterol level (Volek, 2005). 
  • The Ebbeling study was also a human subjects clinical trial. It was done at Harvard. Subjects on a low-carb diet had lower TG and higher HDL cholesterol. Also, researchers showed that low-carb diets were less likely to result in weight rebound due to improved energy expenditure and leptin (Ebbelin, 2012). 

My name is Ford Brewer. My team and I work to prevent heart attack, stroke, cancer, and dementia. Our goal is to help you understand how to prevent major killers and disablers. Most of them are driven by the process of cardiovascular inflammation

If you want to know more about the science of preventive medicine or you have questions about certain aspects of your health, check out our webinars, membership programs, and online courses.

If you’d like to learn about the basics of heart attack & stroke prevention for free, complete this form, and get access to our CV inflammation course. If you’re interested in how we can help you, check out our services page.

References

Abbasi F, McLaughlin T et al. 2004. High carbohydrate diets, triglyceride-rich lipoproteins, and coronary heart disease risk. American Jl of Cardiology, Preventive Cardiology 85,(1) p 45-48.

Attia, P. 2020. THE DRIVE # 22 – Thomas Dayspring Part III of  V: reverse cholesterol transport, CETP inhibitors, & apolipoproteins.

BetaBios, 2020. Have you heard of remnant cholesterol before? 

Bhatt DL, Steg PG, Miller M, et al. 2019. Cardiovascular Risk Reduction with Icosapent Ethyl for Hypertriglyceridemia. N Engl J Med. 380:11-22. 

BioScience Notes. 2020. High density lipoproteins  (HDL)

Bittner V, Johnson BD, Zineh I, et al. 2009. The TG/HDL Cholesterol Ratio Predicts All Cause Mortality in Women With Suspected Myocardial Ischemia A Report from the Women’s Ischemia Syndrome Evaluation (WISE). Am Heart J. 157(3):548-555. 

Brewer, F. 2017. Silent CV Risk: Triglyceride/HDL Ratio.

Brewer, F. 2020. Chuck’s Heart Attack at 55 mph: Switch to Tesla Autopilot

Chemistry LibreTexts. Triglycerides

Chiesa ST, Charakida M. 2019. High-Density Lipoprotein Function and Dysfunction in Health and Disease. Cardiovasc Drugs Ther. 33(2):207-219. 

Cordero A, Alegria-Ezquerra E. 2008. TG/HDL as surrogate marker for insulin resistance. European Society of Cardiology. 

Dashti HM, Mathew TC, Hussein T, et al. 2004. Long-term effects of a ketogenic diet in obese patients. Exp Clin Cardiol. 9(3):200-205. 

Dhindsa D, Shapiro MD. 2019. Triglycerides, Remnant Cholesterol and Atherosclerotic Cardiovascular Disease. 2019. American College of Cardiology.

Ebbeling CB, Swain JF, Feldman HA, et al. 2012. Effects of Dietary Composition on Energy Expenditure During Weight-Loss Maintenance. JAMA. 307(24):2627–2634. 

Feldman D. Remnant Cholesterol – What Every Low Carber Should Know

Kamanna VS, Kashyap ML. 2008. Mechanism of action of niacin. Am J Cardiol. 101(8A):20B-26B. 

Kwon H, Pessin JE. 2013. Adipokines Mediate Inflammation and Insulin Resistance. Front Endocrinol (Lausanne). 4:71. 

Lillo J. 2020. Specialty Corner: Disorders of The Triglyceride-HDL Axis in Insulin Resistance. National Lipid Association. 

Maki KC, Bays JE, Dicklin MR. 2012. Treatment options for the management of hypertriglyceridemia: strategies based on the best-available evidence. J Clin Lipidol. 6(5):413-26.

Rabe K, Lehrke M, Parhofer KG, Broedl UC. 2008. Adipokines and Insulin Resistance. Mol Med. 14(11-12):741-751. 

Sigurdsson A. 2014. The Triglyceride/HDL Cholesterol Ratio. The Doc’s Opinion. 

Simon HB. 2007. On Call: Niacin for Cholesterol. Harvard Men’s Health Watch 

Sopko G, Leon AS, Jacobs DR Jr, et al. 1985. The effects of exercise and weight loss on plasma lipids in young obese men. Metabolism. 34(3):227-236. 

Volek JS et al. 2005. Modification of Lipoproteins by Very Low-Carbohydrate Diets. Jl of Nutrition. 135(6) pp 139-142. 

Wang L, Yu J, Walzem RL. 2008. High-carbohydrate Diets Affect the Size and Composition of Plasma Lipoproteins in Hamsters (Mesocricetus auratus). Comp Med. 58(2):151-160. 

WebMD. What medicine is used to treat triglycerides?  

WebMD. Will Exercise Really Lower Triglycerides? 

Willey JZ, Rodriguez CJ, Carlino RF, et al. 2011. Race-ethnic differences in the association between lipid profile components and risk of myocardial infarction: The Northern Manhattan Study. Am Heart J. 161(5):886-892. 

Yanai H, Masui Y, Katsuyama H, et al. 2018. An Improvement of Cardiovascular Risk Factors by Omega-3 Polyunsaturated Fatty Acids. J Clin Med Res. 10(4):281-289. 

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