Does a low-carb diet increase LDL Cholesterol?

 Why Choose to Become LMHR? 

 It is not only about slimming

Author: Deborah NG SJ

A Lean Mass Hyper-Responder (LMHR) is typically someone on a low-carb or ketogenic diet who experiences high LDL cholesterol but maintains elevated HDL and low triglycerides.

Despite the LDL increase, LMHRs are often lean, active, exhibit stable blood sugar and low inflammation, suggesting a reduced risk for metabolic diseases, including cancer.

Research also indicates ketogenic diets may help manage non-obesity-related conditions like epilepsy, mood disorders, autoimmune diseases, and inflammatory bowel disease; while also benefiting general health and athletic performance.

In this article, we will explore: 

1.  Why take the risk of rising LDL Cholesterol? 

Since the increase of LDL among the LMHR often raises controversial discussions in the medical industry, it is imperative to use a case study to uncover the truth. 

Here is a real case study: 

LM is a 26-year-old ketogenic diet male who aims to reverse and treat his ulcerative colitis. 

Sickness: 

Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) that primarily affects the colon (large intestine) and rectum. 

UC is characterized by inflammation and ulceration of the colon's innermost lining, leading to various symptoms. The condition is typically chronic, with periods of flare-ups and remission.

His blood test results: 

Test Item	Value
Total Cholesterol level	535mg /dl or 13.84 mmol/L
LDL Cholesterol	411mg/dl or 10.63 mmol/L: previously was  95 (2.46 mmol/L) before the ketogenic diet
HDL Cholesterol	116mg/dl or 3.0 mmol/L
Triglycerides	39mg/dl or 0.44 mmol/L
HbA1c	4.8 - 5.0%
Fasting Insulin	<3 μIU/ml
TG/HDL ratio	0.3

LM's unique profile makes him an excellent case study for LMHR. 

*Note: LM's increase in LDL is not solely dependent on his saturated fat intake but is inversely associated with his BMI and body fat reduction.

2.  Patient's testimony: Being an LMHR                     gave me back my life  

Despite this, conventional medical physicians believed that LM's dramatic increase in LDL indicated hypercholesterolemia and intended to prescribe medication. However, LM insisted on undergoing an angiography test for further validation.

After 2 years of hypercholesterolemia, the angiography revealed NO evidence of calcified or non-calcified plaque. No plaque or stenosis was observed in any vessels, with a CAD-RADS score of 0.

The image below shows his computed tomographic angiogram from three angles: LAD (Left Anterior Descending artery), LCx (Left Circumflex artery), and RCA (Right Coronary artery).

Image extracted from National Library of Medicine (4)

This is what this patient (LM) shared as his testimony, written in the journal: 

3.   What you should be really worried about? From 107,301 heart disease patients

A research with coronary heart disease (CHD) 107,301 patients from over 6 major hospitals in Tianjin, including Tianjin Medical University General Hospital, from a 6-year study duration (Jan 2024 to Sept 2020) discovered that (3):

• Ultimately, 28,476 eligible patients were selected due to the strict screening process, eliminating those with infectious, renal, and liver disease and those with incomplete blood test profiles.

Significant findings:

• As HbA1c levels rise, accompanied by increased fasting blood glucose, there is a corresponding increase in coronary heart disease (CHD) cases, with glucose intolerance being the most significant contributing factor.

• Along with these findings, the higher the TG/HDL ratio, the higher the risks associated with diabetes and CHD events.

Insignificant findings:

• If we look at LDL-C and total Cholesterol (TC), we can see NO significant differences between all groups, meaning LDL has NO predictive effect on CHD. 

4.   Why does LDL increase when you become leaner?

The phenomenon where LDL (Low-Density Lipoprotein) levels increase after HDL (High-Density Lipoprotein) levels increase and triglycerides (TG) decrease, especially in the context of a low-carbohydrate or ketogenic diet, can be understood through the following mechanisms and a simplified mathematical relationship.

LMHR must be accompanied by these 3 changes: 

1. Triglyceride Decrease (TG ↓):

• On a low-carb or ketogenic diet, the body shifts from using glucose as its primary energy source to using fat. As a result, triglycerides stored in fat cells are mobilized and used for energy, leading to a decrease in circulating triglycerides in the blood.

•  These are fats stored in your body's fat cells and are finally utilized as energy sources. In other words, you are using your body fat as energy. 

2. HDL Increase (HDL ↑) :

• As triglycerides decrease, HDL levels often increase; this is where HDL can help reverse cholesterol transport. They help clear excess cholesterol from tissues and arteries, bringing it back to the liver, especially for people consuming good omega-3 fats. 

• The decrease in triglycerides reduces the exchange of triglycerides for cholesterol esters (chemical reaction) between HDL and VLDL (Very Low-Density Lipoprotein) particles. This results in HDL becoming more cholesterol-rich and thus, more stable.

3. LDL  Increase (LDL ↑):

• LDL levels may increase as a result of changes in lipoprotein metabolism. When triglycerides decrease, fewer VLDL particles are rich in triglycerides. VLDL particles are eventually converted into LDL particles after triglycerides are removed.

• The increase in HDL, alongside the reduction in triglycerides, can mean that more cholesterol is available to be packaged into LDL particles, leading to further increase. 

• In a low-carb diet, the liver will need to increase the production of LDL particles to transport the fat-derived cholesterol to tissues for energy use, particularly when low carbohydrate-derived energy.

                              

Graphic extracted from Cholesterol code: Reverse engineering the mystery (1)

In conclusion, the body adapts to fat metabolism in a low-carb environment, and the increase in LDL is due to two mechanisms. 

The first is that fewer triglycerides (TG) result in less VLDL production and more conversion to LDL. The second is due to reverse cholesterol transport, facilitated by larger and more stable HDL particles.

5.   Only LDL increase doesn't mean

 that you are an LMHR

It is important to note that a sole increase in LDL doesn't mean that you are LMHR; apart from the rise in HDL and decrease of Triglycerides, other bio-markers must also be accompanied. Here are the guidelines:

1) CRP (Inflammation): The increase of LDL is due to the increased lipid turnover for energy; this metabolic state will eventually lead to a metabolic state that reduces inflammation, and the anti-inflammatory effects stem from better glucose management and lower oxidative stress.

2) Waist-to-hip ratio (WHR): As the body is constantly fat-burning,  the effects of lipolysis (fat breakdown) reduce visceral fat around the abdomen and, thus, lower WHR.

3) Improved HbA1c (Glucose): The low-carb diet adopted by LMHR improves insulin sensitivity and leads to minimum to no blood glucose spikes. This fat metabolism, rather than glucose metabolism, helps stabilize blood sugar and reverse diabetes.

 

4) Improved liver function: Fat metabolism helps to reduce fat storage in the liver as the body needs to burn fat as fuel. On the contrary, people suffering from non-alcoholic fatty liver disease often accumulate fat more easily as this fat metabolism is "shut down." This results in lower GGT and ALT levels accompanied by low inflammation. 

6.   How to reduce LDL if an LMHR wants to do so? 

Since raising LDL is often perceived as dangerous by typical modern science and challenges the medical industry, it would be worthwhile to investigate whether LMHR aims to reduce its LDL over a certain period of time. Is this plausible?

Dr. Nicholas G. Norwitz and Dr. William C. Cromwell published an article in Metabolites about how it is possible and effortless if an LMHR aims to do so.

They conducted an unusual experiment by eating Oreo cookies. They showed that this is more effective than a high-intensity statin therapy for an LMHR who usually consumes a ketogenic diet.

1. The experiment method: Dr Norwitz, an LMHR, ate 12 Oreo Cookies per day continuously for 16 days, lowering his LDL-C by 71%. In comparison, those with high-dose statin therapy patients only reduced it by 32.5% in the same period (2).

2. Why use Oreo: We know that Oreo cookies are bad for health, right? Whether you are a low-carb, low-calorie, healthy vegan diet person, we should all agree about this.

Hence, Dr. Norwitz is trying to use a "bad diet" experiment to show that if an LMHR intends to achieve low LDL levels, they can do it quickly; this is an ironic approach or sarcastic method to show the medical field.

3. The result of 71% vs 32.5% (statin treatment): Despite a bad diet, LMHR people demonstrate unusual capabilities to reduce LDL-C if intended. So, why bother about the high LDL-C levels if they do not cause any harm to you and you can reduce it effortlessly if you wish to do so?

References:

(1) Our Paper on Low Carb, LDL Cholesterol, and the LMHR Phenotype is Now Finalized.

(2) “You Have High Cholesterol”: A Science Appetizer Based on the Latest Research Published in Metabolites

(3) Correlation between the triglyceride-to-high-density lipoprotein cholesterol ratio and other unconventional lipid parameters with the risk of prediabetes and Type 2 diabetes in patients with coronary heart disease: a RCSCD-TCM study in China

(4) Case Report: Hypercholesterolemia “Lean Mass Hyper-Responder” Phenotype Presents in the Context of a Low Saturated Fat Carbohydrate-Restricted Diet