Tag: small dense LDL

June 7, 2019

What You MUST Know about Total Cholesterol & LDL-C on a Ketogenic Diet

Is following your Total Cholesterol and LDL-C really that important?

You may be quite surprised.

Watch as we discuss the important markers of heart disease and vascular disease risk. We will talk about how these markers can help you understand what your body is doing in the process of making or reversing atherosclerosis (plaque in the vessels). And, should you really be taking that STATIN (cholesterol lowering) drug? Get the scoop here as Dr. Nally very simply points out how the right diet can and will lower your cholesterol without the use of medications.

Research in the last 10 years points to the small-dense LDL particle as the atherogenic component of cholesterol (Hoogeveen RC et al., Arterioscler Thoromb Vasc Biol, 2014 May; Ivanova EA et al., Oxidative Med Cell Longevity, 2017 Apr). Studies in the last five years have identified that elevated small-dense LDL cholesterol correlates much more closely with risk for inflammation, heart disease and vascular disease (Williams PT, et al. Atherosclerosis. 2014 April; 233(2): 713-720.)

Recent research in the last three years demonstrates that small dense LDL cholesterol is a better marker for prediction of cardiovascular disease than total LDL-C (Hoogeveen RC et al., Arterioscler Thromb Vasc Biol. May 2014, 34(5): 1069-1077l; Ivanova EA et al., Oxidative Med Cell Longev. 2017).

Additionally, higher LDL-C is actually predictive of longer life and has been demonstrated to correlate with longevity (Ravnskov U et al., BMJ Open, 2016 Jun 12;6(6): e010401). And, a low LDL-C actually increases risk of early mortality (Schwartz I et al., Lancet 2001, 358: 351-55).

It is commonly understood that LDL-C will rise with increased saturated fat intake on a ketogenic diet. This has been know and reported in the scientific literature for over twenty years. This is to be expected, because LDL-C is really a measurement of three different LDL sub-particles (“big fluffy, medium, and small dense”). Increased saturated fat intake, while at the same time lowering carbohydrate intake, actually causes a shift in these low density particles to a bigger “fluffier” particle conformation (Griffin BA et al., Clin Sci (Lond), 1999 Sep).
The 2015 British Medical Journal, referenced above, analyzed the relevant 19 peer reviewed medical articles that included over 68,000 participants. This review showed that there is no association of high LDL-C with mortality (meaning that an elevated LDL-C does not lead to an increased risk of death from heart or vascular disease). I realize that, in stark opposition to the landmark review above, The American Heart Association’s Presidential Advisory published their position in the June 20, 2017 issue of Circulation. They stated that saturated fat is the cause of increased LDL-C and they further extrapolated that elevated LDL-C is associated with an increase in death by cardiovascular disease. This boldfaced claim is only based on one single small four year (2009-2013) literature review completed by the World Health Organization with a total of only 2353 participants, most of these studies only lasting 3-5 weeks (not nearly long enough to see fully effective cholesterol changes) and none of which had any focus on carbohydrate intake, insulin levels or LDL sub-particle measurement (Mensink RP, Geneva: WHO Library Cataloguing-in-Publication Data, 2016).

Based upon the most current scientific evidence above and my clinical experience, the large body of evidence above demonstrates the use of total cholesterol and LDL-C to determine vascular disease risk to be ineffective tools. A low carbohydrate/ketogenic diet lowers small dense LDL cholesterol, triglycerides and blood sugar and in many cases, the use of cholesterol drug (STATIN) therapy is not needed and ineffective in comparison with a ketogenic/carbohydrate restricted lifestyle.

January 25, 2017

The Conundrum of Cholesterol & Ketones

Watch as Dr. Nally discusses how eating more fat actually lowers your cholesterol and your risk for heart disease. Is a ketogenic lifestyle more effective than cholesterol medication? Find out as we discuss this an many fascinating cholesterol questions from Dr. Nally’s Periscope watchers from around the world. He also answers questions about his KetoEssentials Multi-Vitamin, Exogenous Ketones, and Pork Rinds (his favorite are the Pork Clouds brand).

So, mix up a bowel of fluff and grab a spoon while you listen and lower your cholesterol.

November 9, 2015

How Fat Makes You Skinny . . . (Eating Fat Lowers Your Cholesterol?!)

Diseases seem to arrive in three’s each day in my office. Today I had three different patients with cholesterol concerns who were notably confused about what actually makes the cholesterol worse, and what causes weight gain. Each of them, like many patients that I see, were stuck in a state of confusion between low fat and low carbohydrate lifestyle change. My hope is to give my patients and anyone reading this blog a little more clarity regarding what cholesterol is, how it is influenced and how it affect our individual health.

First, the standard cholesterol profile does not give us a true picture of what is occurring at a cellular level. The standard cholesterol panel includes: total cholesterol (all the forms of cholesterol), HDL (the good stuff), LDL-C (the “bad” stuff) and triglycerides. It is important to recognize that the “-C” in these measurements stands for “a calculation” usually completed by the lab, and not an actual measurement. Total cholesterol, HDL-C and triglycerides are usually measured and LDL-C is calculated using the Friedewald equation [LDL = total cholesterol – HDL – (triglycerides/5)]. (No, there won’t be a quiz on this at the end . . . so relax.)

However, an ever increasing body evidence reveals that the concentration and size of the LDL particles correlates much more powerfully to the degree of atherosclerosis progression (arterial blockage) than the calculated LDL concentration or weight (1, 2, 3).

There are three sub-types of LDL that we each need to be aware of: Large “fluffy” LDL particles (type I), medium LDL particles (type II & III), and small dense LDL particles (type IV).

Weight & Size of VLDL, LDL & HDL

Why LDL-C is misleading: Identical LDL-C of 130 mg/dL can have a low risk (Pattern A) with a few “big fluffy LDL particles or high risk (Pattern B) with many small dense LDL particles.

Second, it is important to realize that HDL and LDL types are actually transport molecules for triglyceride – they are essentially buses for the triglycerides (the passengers). HDL can be simplistically thought of as taking triglycerides to the fat cells and LDL can be thought of as taking triglycerides from the fat cells to the muscles and other organs for use as fuel.

Third, it is the small dense LDL particles that are more easily oxidized and because of their size, are more likely to cause damage to the lining of the blood vessel leading to damage and blockage. The large boyant LDL (“big fluffy LDL particles”) contain more Vitamin E and are much less susceptible to oxidation and vascular wall damage.

Eating more fat or cholesterol DOES NOT raise small dense LDL particle number. Eating eggs, bacon and cheese does not raise your cholesterol! What increases small dense LDL particles then? It is the presence of higher levels of insulin. Insulin is increased because of carbohydrate (sugars, starches or fruits) ingestion. It is the bread or the oatmeal you eat with the bacon that is the culprit. The bread or starch stimulates and insulin response. Insulin stimulates the production of triglycerides and “calls out more small buses” to transport the increased triglyceride to the fat cells (4, 5, 6, 7).

Fourth, following a very low carbohydrate diet or ketogenic diet has been demonstrated to decreased small dense LDL particle number and correlates with a regression in vascular blockage (8, 9). So, what does this really mean to you and me? It means that the low-fat diet dogma that that has been touted from the rooftops and plastered across the cover of every magazine and health journal for the last 50 years is wrong. . . absolutely wrong.

I talk about this and answers questions on today’s Periscope. You can see the recording on Katch.me with the comments in real time here:

https://www.katch.me/docmuscles/v/2f0b6d07-d56a-368b-b4f6-34a5ab3da916

Or, you can watch the video below:

References:

Superko HR, Gadesam RR. Is it LDL particle size or number that correlates with risk for cardiovascular disease? Curr Atheroscler Rep. 2008 Oct;10(5):377-85. PMID: 18706278
Rizzo M, Berneis K. Low-density lipoprotein size and cardiovascular risk assessment. QJM. 2006 Jan;99(1):1-14. PMID: 16371404
Rizzo M, Berneis K, Corrado E, Novo S. The significance of low-density-lipoproteins size in vascular diseases. Int Angiol. 2006 Mar;25(1):4-9. PMID:16520717
Howard BV, Wylie-Rosett J. Sugar and cardiovascular disease: A statement for healthcare professionals from the Committee on Nutrition of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association. Circulation. 2002 Jul 23;106(4):523-7. PMID: 12135957
Elkeles RS. Blood glucose and coronary heart disease. European Heart Journal (2000) 21, 1735–1737 doi:10.1053/euhj.2000.2331
Stanhope KL, Bremer AA, Medici V, et al. Consumption of Fructose and High Fructose Corn Syrup Increase Postprandial Triglycerides, LDL-Cholesterol, and Apolipoprotein-B in Young Men and Women. The Journal of Clinical Endocrinology and Metabolism. 2011;96(10):E1596-E1605.
Shai I et al. Cirulation. 2010; 121:1200-1208
Krauss RM, et al. Prevalence of LDL subclass pattern B as a function of dietary carbohydrate content for each experimental diet before and after weight loss and stabilization with the diets. American Journal of Clinical Nutrition. 2006; 83:1025-1031
Gentile M, Panico S, et al., Clinica Chimica Acta, 2013, Association between small dense LDL and early atherosclerosis in a sample of menopausal women, Department of Clinical Medicine and Surgery, University “Federico II” Medical School, Naples, Italy Division of Cardiology, Moscati Hospital, Aversa, Italy A. Cardarelli Hospital, Naples, Italy

October 21, 2015

Reversal of Diabetes in the Ketogenic Zone – A Case Report

This week I had the pleasure of seeing a really nice 46 year old Hispanic male who is fairly new to the office. He came back in to see me in follow up on his diabetes. To give you a bit of background history, the patient came to see me about 6 months ago, just not feeling very well. Based on his symptoms of fatigue, history of elevated blood sugar and family history, lab work was completed.He saw us initially with a Hemoglobin A1c of 12.3% in June (normal should be 4.9%-5.6%). This means he had an average blood sugar over the previous three months of about 310 mg/dL (normal should be < 110 mg/dL).

Past Medical History include: Diabetes Mellitus – type II (not on any medications when initially seen), Hypertension (high blood pressure), Dyslipidemia (elevated cholesterol) and a non-specific heart arrhythmia.

Medications: None

Surgeries: Knee & shoulder arthroscopies

Family History: Father Diabetes, Stroke, Heart Disease, Hypertension, Elevated Cholesterol

Social History: Non-Smoker, Limited Alcohol Use

He related to me that he had been on metformin before, however, had some significant diarrhea and was not interested in using this medication EVER again. A previous doctor had tried Victoza© (liraglutide), a GLP-1 inhibitor, but he didn’t use it for very long as he didn’t really see much change with this medication.

After getting his labs back, we had a very long conversation about the need to either fix his diet dramatically, or he may be looking at using 3-4 oral medications or even insulin to control his blood sugar.

When I see average blood sugars (HbA1c) stay over 6.5% (or greater than 140 mg/dL), the risk for retinal, kidney and nerve damage is significant and often irreversible after 4-5 years. Most physican’s are affraid to lower the HbA1c to less than 7.0% with medications due to low blood sugar events, and so the diabetes community has “settled” with 7.0% as being effective. However, it still isn’t low enough. I saw this happen with my father and with other members of me family. I’ve seen it happen over and over with my patients over the last 15 years when they have not lowered their blood sugar and reduced the high insulin loads that occur in response to those high blood sugar levels. It has been my experience that HbA1c can be very safely lowered to the normal range, as low as 5.2-5.6% without symptomatic low blood sugars, with the correct diet and careful use of medications.

So, my patient, above, committed to change. I was worried that diet alone would not be able to lower these levels enough to be effective so we discussed tight carbohydrate restriction, the addition of methlyated folate and chromium and a re-trial of a low dose of Victoza© (liraglutide), which he had at home.

I didn’t see him for about three months. When he followed up this week I was amazed. I was amazed because I rarely see more than 1.5% drop in HbA1c with the addition of Victoza© (liraglutide). The additional 4.5% of drop with diet was dramatically impressive.

When we talked, he told me that all he has done differently is use the Victoza© (liraglutide) and cut his carbohydrate intake to less than 10 grams per meal (Yes, he did admit to occasionally cheating).

You can see the dramatic results:

	June 2015	September 2015
Glucose	258	103
HbA1c	12.3%	6.3%
Urine Creatinine (Random)	208	72

Total Cholesterol (mg/dL)	219	218
Triglycerides (mg/dL)	137	117
HDL-C (mg/dL)	38	37
LDL-C (mg/dL)	154	158
LDL-P (nmol/L)	2172	1691
Small dense LDL-P (nmol/L)	1289	419

TSH (mU/L)	1.75

As you can see, a dramatic change in his blood sugar has occurred in a three month interval. Not only that, we see a significant change in his cholesterol profile.

Some might argue that this is the Victoza© (liraglutide) doing this. I can tell you, in the 15 years I’ve been doing this and in the 5 years that Victoza© (liraglutide) has been available in the U.S., I have never seen a drug reduce blood sugar or cholesterol this dramatically.

Previously, we looked at LDL-C for heart disease risk, however, I have multiple patients that have had heart disease with normal LDL-C ( <100 mg/dL). LDL-C is just a summation of all the particles. The LDL particle is actually made up of three sub-types and it is specifically the small dense particle that causes the vascular risk. You can see a dramatic normalization of the small dense particle LDL with no change in LDL-C and minimal change in Total Cholesterol in the patient’s labs when he reduces his carbohydrate intake. This is a pattern I see every single day. When serial carotid ultrasound studies are completed, I see reduction in blockage and reduction in the vascular wall thickening. I will be very interested to see the vascular studies on this patient and I will await his results as he tightens up his diet even further.

All in all, he has dramatically brought his diabetes under control with carbohydrate restriction and if he continues this lifestyle, he has reduced his risk for retinal damage, reduced his risk for kidney damage, reduced his risk for nerve damage and essentially added 20 years to his life.

(Disclosures: Dr. Nally has no vested interest, monitary or otherwise, in Novo Nordisc or it’s products including liraglutide.)

May 31, 2014

I Like My Green Eggs & Ham . . .

Green Eggs & Ham

You know, Dr. Seuss was right, the whole egg is actually good for you.
A recent s tudy from the University of Connecticut demonstrated that eating the whole egg actually decreases LDL (the bad cholesterol) sub-particles and insulin resistance in Metabolic Syndrome better than the egg white or the egg substitute.

I like green eggs and ham!
I do!! I like them, Sam-I-am!
And I would eat them in a boat!
And I would eat them with a goat…
And I will eat them in the rain.
And in the dark. And on a train.
And in a car. And in a tree.
They are so good so good you see!

May 31, 2014

Fat Thoughts on Cholesterol

As a medical bariatrician and family practitioner specializing in low-carbohydrate diets, I often see the panic stricken look on people’s faces when they look at their cholesterol profiles just after starting a carbohydrate restriction life-style.

First, it is very important to understand that if you check your cholesterol within the first 4-6 weeks of dietary changes, there will be a transient rise in the cholesterol profile as your adipose tissues (fat cells) release your new fuel source into the blood stream and the mitochondria in the one trillion cells in your body convert from the use of glucose to the use of ketones (derived from triglycerides) as the primary fuel source. This is not a problem as the body is designed to handle this increase in triglyceride and cholesterol. I explain to patient’s that we are essentially making the figurative change from “un-leaded fuel to diesel fuel.”

Second, the standard cholesterol profile does not give you a true picture of what is occurring at a cellular level. The standard cholesterol panel checks Total cholesterol (all the forms of cholesterol), HDL (the good stuff), LDL-C (the bad stuff) and triglycerides. It is important to recognize that the “-C” stands for a calculation usually completed by the lab.

Cholesterol Particle Sizes

Total cholesterol, HDL and triglycerides are usually measured and LDL-C is measured using the Friedewald equation [LDL = total cholesterol – HDL – (triglycerides/5)].

Third, it is also important to realize that HDL and LDL are actually transport molecules (the buses for the triglycerides (the passengers). HDL is taking triglycerides to the fat cells and LDL is taking triglycerides from the fat cells to the muscles and other organs for use as fuel.

When you being a low carbohydrate diet, your blood glucose availability as the primary fuel source drops and triglycerides become the primary source. It takes your body 4-6 weeks to increase the number of mitochondria necessary to effectively use triglycerides as the primary fuel. (This is why many athletes and patients who are active will feel slightly sluggish during their exercise for the first few weeks).

Once your body accommodation to the new fuel, there will be a notable drop in LDL-C and a rise in the HDL.

But this still doesn’t answer the question and relieve the panic seen above. A deep sigh and the look of relief occurs when I explain that LDL-C doesn’t give us the real story.

To make it simple and understandable, LDL is made up of three main sub-types big fluffy ones, medium sized ones, and small dense ones. It’s the small dense ones that contain lipoprotien A [Lp(a)] found in increased vascular risk. Recent studies reveal that heart disease and atherosclerosis is caused by the small dense LDL molecules.

A low carbohydrate diet causes the small dense cholesterol to drop and there is a rise in the two other sub-types This shift in sub-types can actually elevate the Total Cholesterol number and occasionally the LDL-C.

If you are following a low carbohydrate diet, get your cholesterol levels checked. It is more ideal to get an NMR Lipoprofile or VAP Cholesterol test that will give you an LDL particle number and this can be explained more fully by your doctor.

Now, off to the fridge . . . where did I put that package of bacon . . . ?