Don’t miss this podcast as Dr. Nally discusses the sugar alcohol, erythritol, and what the Cleveland Clinic’s study really means to those following a Ketogenic Lifestyle. Is there another reason behind attacking erythritol?
After hearing this podcast, you decide.
“Won’t my cholesterol get worse and increase my risk of heart disease if I eat more fat?”
I get asked this question at least 3-4 times a day. The answer is, “NO. Not if you cut out the sugar and starch.”
“But, wait?! What about my heart? All that fat can’t be good for my heart?” they ask.
Let’s start with the contents of the standard cholesterol panel or “Lipid Panel.”
For the last 20-30 years the following labs have been looked at as the holy grail of heart disease risk:
The first problem with this panel is that it makes you believe that there are four different forms of cholesterol. NOT TRUE!
Actually, cholesterol is a steroid precursor that either makes up a part of the lipoprotein molecule or is transported with the triglycerides as a passenger. The lipoproteins are just transporters made of lipid that are only slightly different from their passenger load (causing increased or decreased density). The proteins that are contained within the wall of the lipoprotein transporter is what makes them different. These lipoprotein particles can be thought of, simplistically as buses, carrying triglyceride passengers. Here size does matter, and size determines the function of the molecule at that moment in time.
These buses, big and small, carry the passengers up and down the vascular system of the body. Glucose can float freely through the blood stream, but the other form of fuel, triglyceride, must be transported via the “lipoprotein bus”. The triglyceride and cholesterol are actually the passengers inside the bus. But triglyceride presence in the system seems to change the density of the lipoproteins. So now picture big, medium and small buses . . . the high density lipoprotein (HDL), intermediate density lipoprotein (IDL) and the low density lipoprotein (LDL) buses.
The density of the bus gets lower as triglyceride levels rise and fewer cholesterol esters and proteins are bound. As HDL goes up, LDL-C goes down (Parker TS et al, Proc Natl Acad Sci USA, Feb 1986)
The second problem is the VLDL-C and LDL-C are actually calculated numbers and don’t actually reflect the true presence of the lipoprotein particles as the triglyceride number rises. For the accountants, mathematicians and engineers reading this that calculation is called the Friedwald Equation and is as follows:
Total Cholesterol is the sum of the HDL, LDL, as well as intermediate density lipoprotein (IDL) & very low density lipoprotein (VLDL) which aren’t reported in the “Lipid Panel” above. So, total cholesterol is basically the sum of all the buses you have driving around.
The third key piece of information that the Lipid Panel above doesn’t tell you is the lipoprotein categories (HDL, LDL, IDL, and VLDL) are actually have three to four sub-types or sub-particles that are further differentiated by weight and size.
Improvement in cardiovascular risk, including improvement in cholesterol, inflammation and plaque formation have been the case with every patient I have used a high fat, low carbohydrate (ketogenic) dietary approach with over the last 12 years.
I’ve had so many people ask me how this works, and then, how to explain the changes to their primary doctors or cardiologist, I decided to write the following article. My intent is not to point the finger where others are wrong; but to identify how we, myself included, took a misstep along the path of scientific discovery. This misstep led to guidelines that, for over 45 years, have been accepted by medical students and clinicians as the “gospel truth.”
The measurement of cholesterol, specifically total cholesterol, started in the 1950’s. There appeared to be a mild correlation of heart disease in countries who’s diets had higher fat intake. Ansel Key’s identified this apparent correlation in his Diet-Heart Hypothesis published in JAMA in 1957. He stated from his observational work that “the results of a fatty diet are hypercholesterolemia [elevated cholesterol].” A number of studies at the time showed that increasing fat intake in the standard diet increased total cholesterol; however, NO LINK to heart disease was ever proven (Ahrens EH, Jr, Lancet, May 1985).
Studies published by E. H. Ahrens, Jr. demonstrated that the cholesterol increased because of carbohydrate intake, not fat alone (Ahrens EH Jr, et al., Trans Assoc Am Physicians, 1961). The actual question, “Does increasing fat alone cause heart disease?” was never answered. The question, as well as known evidence based cholesterol reducing dietary approaches, were ignored in 1984 by the National Institutes of Health (NIH) Consensus Development Conference on Lowering Cholesterol to Prevent Heart Disease that was based heavily on epidemiological data rather than clinical reproducible science (Ahrens EH, Jr, Lancet May 1985).
Despite significant scientific evidence refuting the Diet-Heart Hypothesis, the 1984 NIH decision reflected politics and massive publicity campaigns.
Since 1984, fat and cholesterol containing foods are treated like witches of Salem. As an example, eggs, specifically the egg yolk. (To this day, the chef at every breakfast bar I’ve ever visited asks if I want an egg white only omelet.) Interestingly, there is actually no scientific data association between whole egg consumption and heart disease. The science simply does not exist. Seriously, check for yourself.
You can’t extrapolate mortality risk based on a single small study that doesn’t actually identify correlation or causation. But the AHA did exactly that in 1961, and they are trying to do it again today. The MR-FIT study, largest study ever completed, is incessantly quoted as the study that demonstrates reduction in cholesterol leads to reduction in cardiovascular disease, but this trial was actually a failure and did not demonstrate improved risk by lowering cholesterol. In fact, the Director of the study, Dr. William Castelli actually stated, “. . . the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower people’s serum cholesterol…”
“We found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories weighed the least, and were the most physically active,” he said.
To add to cholesterol confusion, the Diet-Heart Hypothesis does not explain the “European or French Paradox.” The French prefer cooking in butter instead of vegetable oil. In fact, the French eat 40% fat in their diet. And, more than 15% of that is saturated fat.
Interestingly, the French and those that eat the most cheese, butter and whole eggs have the lowest rate of coronary vessel calcification and heart disease. Attempts to explain this away as epidemiological error or diet complexities have been published, but still never answers the underlying question, “Does increasing fat alone cause heart disease?” (Ferrieres J, Heart, Jan 2004).
According to the Diet-Heart Hypothesis, people with familial hypercholesterolemia should have much shorter lifespans and are at increased risk of early mortality or death. However, there is actually no scientific evidence of this. In fact, the Honolulu Heart Program study revealed that people with low cholesterol are the ones at significant risk of early mortality or death (Schwartz I, et al., Lancet 2001 Aug). 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).
I hate to burst your bubble, but saturated fat is NOT linked to vascular disease, diabetes or increased mortality (de Souza RJ et al., BMJ 2015,351:h3978).
It is commonly understood that LDL-C will rise as you eat more saturated fat. This is normal on a ketogenic diet. It has been reported in the scientific literature for over twenty years. It 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). We know that the small dense LDL particles are the atherogenic / inflammatory particles participating in the formation of vascular disease and directly correlate with triglyceride levels. We also know the big “fluffy” LDL particles actually reduce the risk of vascular disease (Griffin BA et al., Clin Sci (Lond), 1999 Sep).
So why have clinicians been pushing the use of STATIN medications to reduce risk of coronary heart disease? It started with the Lipid Research Clinics Coronary Primary Prevention Trial (LRC-CPPT). This was a study of over 3800 men treated with cholestyramine, a cholesterol lowering medication (JAMA, 1984 Jan. 20;251(3):351-64.). There was a very slight “absolute reduction” in coronary heart disease risk, 1.6% to be exact. LDL-C decreased, but there was no reduction in the risk of death. In fact, there was actually an increase in risk of all cause mortality in the cholestyramine group which was never emphasized.
Overall, cholestyramine reduced non-fatal heart attacks in 60 of the 3,806 men. In other words, one in 63 men improved with the use of this medication . . . not very impressive. However, statistics look more impressive expressed in terms of “relative risk.” Relative risk is the percent increase of those with no treatment from those with treatment. This is always a bigger number.
When the LRC-CPPT researchers calculated relative risk, the percent change between the treated and non-treated was 19%. This bigger number was reported as the “risk reduction.” For those that don’t know the difference between actual risk and relative risk, 19% sounds very impressive! (JAMA. 1984 Jan 20;251(3):351-64.)
This relative risk reduction drove the STATIN era we are well aware of today. Lipitor (atorvastatin) reduces heart disease risk by only 1%. However, when you use the term “relative risk reduction,” it has more psychological effect. Relative risk of 36% sells more drugs.
Crestor (rosuvastatin) was show to have an absolute risk reduction in heart disease by 1.2%. When run through the relative risk reduction statistic it has a claim of 44% relative risk reduction.
These big numbers emphasized false evidences in many clinician’s minds that reducing LDL-C must be really effectively reducing heart disease.
Knowing that the LDL-C doesn’t really give you a clear idea of heart disease risk. It becomes essential to know which type of LDL lipoprotein particle is the atherogenic or heart disease causing particle. Research now points to the small-dense LDL particle as the atherogenic molecule (Hoogeveen RC et al., Arterioscler Thoromb Vasc Biol, 2014 May; Ivanova EA et al., Oxidative Med Cell Longevity, 2017 Apr). Studies 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 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).
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).
In stark opposition to the landmark evidences above, the American Heart Association’s Presidential Advisory published their position in the June 20, 2017 issue of Circulation. I am well aware of their position. They claim that saturated fat is the cause of increased LDL-C. Further, they extrapolate that elevated LDL-C is associated with increase in cardiovascular disease death. This boldfaced claim is based on one single small four-year (2009-2013) literature review completed by the World Health Organization. It looked at very small studies lasting only 3-5 weeks and comprised in total only 2353 participants. That’s not nearly long enough to see fully effective cholesterol changes. And, none of the studies had any focus on carbohydrate intake, insulin levels or LDL sub-particle measurement (Mensink RP, Geneva: WHO Library Cataloguing-in-Publication Data, 2016).
In my office, I see up to 10% regression in carotid stenosis (blockage in the carotid arteries) each year when following a ketogenic dietary lifestyle. Evidence points out that higher fat intake and lowering of carbohydrate intake has a regression effect on plaque and thickness of the arterial wall. (Shai I et al., Circulation, Mar 2010.) And, increased small dense LDL cholesterol correlates with thickening of the carotid arterial wall (Gentile M et al., Clinica Chimica Acta,Naples, Italy Division of Cardiology, Nov 2013, DOI: 10.1016 / j.cca.2013.08.010)
Based on the large body of evidence that sits before us today, the use of total cholesterol and LDL-C to determine vascular disease risk are obsolete and ineffective tools. That’s why we focus on insulin, triglycerides and small dense LDL particles.
Are you worried about your cholesterol?
Is a ketogenic lifestyle right for you?
These are great questions that I hope I can answer. Check out this month’s Kickstart program if you’re just getting started. Or, click here to work with me individually on your ketogenic lifestyle and cholesterol.
If you want more information about cholesterol and atherosclerosis, please checkout my latest YouTube video on cholesterol and atherosclerosis.
Coconut oil can be found in just about every grocery store, health food store and coffee shop near you. It was made popular in the last few years by the highly advertised Bullet Proof Coffee claims of health and taste over the last few years. But in the last few days, the news outlets through video and print have made it clear that the American Heart Association (AHA) isn’t happy with our use of this “duct tape for one’s metabolism.” The AHA has long been a proponent of education against activities increasing the risk of heart disease. Since 1961 the AHA has decried the use of saturated fat, based on their support of Ansel Key’s diet heart hypothesis, and leading to over 60 years of preaching against the use of saturated fats from the pulpits of science. The claim is that 85% of coconut oil is saturated fat (this is the fat deemed “evil” by those “disciples of the low-fat cloth”). Yes, coconut oil is predominantly a saturated fat. And approximately 75% of that is medium chain triglycerides, the form that converts most efficiently into ketones, for those of us using ketogenic nutritional approaches to health. But is coconut oil really bad for your heart health?
Those of us using ketogenic diets know that LDL-C will commonly rise with increased saturated fat intake. And, we’ve know this for over twenty years. This is to be expected, because LDL-C is really comprised of three different LDL sub-particles (big fluffy, medium, and small dense). We’ve known for the last twenty years that increased saturated fat actually causes a shift in these particles to bigger “fluffier” particles. We also know that it’s the small dense LDL particles are the atherogenic/inflammatory particles participating in the formation of vascular disease (arterial blockage) and their presence in the blood is directly correlated with the level of triglyceride, and that the big “fluffy” particles actually reduce the risk of vascular disease. Those of us following ketogenic lifestyles and treating disease with these protocols also know that triglycerides levels are increased directly by increasing levels of insulin.
The 2015 British Medical Journal published a study reviewing 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 (a calculated value of all the LDL sub-particles) with mortality (meaning that an elevated LDL-C does not lead to an increased risk of death from heart disease). In stark contrast to this landmark review, The American Heart Association’s Presidential Advisory published this week in the June 20, 2017 issue of Circulation states that saturated fat is the cause of increased LDL-C and elevated LDL-C is associated with an increase in death by cardiovascular disease. This boldfaced claim is based on a single small 4 year (2009-2013) literature review completed by the World Health Organization with a whopping 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. From this singular study, the AHA concludes that elevated LDL-C is an indicator of increased cardiovascular mortality. That’s the equivalent of saying, “you know cars drive on the roads and cause pot holes, so we should all STOP driving cars because it is causing our freeway system to have increased pot holes.”
You can’t extrapolate mortality risk based on a single small study that doesn’t actually identify correlation or causation. But the AHA did exactly that in 1961, and they are trying to do it again today. The MR-FIT study, largest study ever completed, is incessantly quoted as the study that demonstrates reduction in cholesterol leads to reduction in cardiovascular disease, but this trial was actually a failure and did not demonstrate improved risk by lowering cholesterol. In fact, the Director of the study, Dr. William Castelli actually stated, “. . . the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower people’s serum cholesterol…”
“We found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories weighed the least and were the most physically active,” he said.
Isn’t that interesting?
So, is coconut oil, or any other food high in saturated fat to blame? Absolutely not! There is no solid evidence to support these facts and there hasn’t been in over 65 years. In fact, clinically, I find that the addition of coconut oil lowers triglycerides, decreases appetite, improves energy, improves skin tone, and plays a huge role in shifting the Omega 3/6 ratios to a more normal 2:1 level.
[clickToTweet tweet=”Is coconut oil, or any other food high in saturated fat to blame? Absolutely not! #docmuscles” quote=”Is coconut oil, or any other food high in saturated fat to blame? Absolutely not! There is no solid evidence to support these facts and there hasn’t been in over 65 years. #docmuscles”]
So, how does coconut oil help the broken metabolism? The majority of people I see in my office have insulin resistance to some degree. Insulin resistance is an over production of insulin in response to any form of carbohydrate or starch. Increasing your saturated fat, does two things. It provides a fantastic form of fuel, one your body can use very easily. And second, it will decrease your craving for starches and carbohydrates, naturally decreasing production of insulin and helping to improve insulin resistance over time.
If you want to learn more about using fat and improving insulin resistance, see my previous blog post here.
You can learn more about how our acceptance of bad science has lead to an obesity and diabetes epidemic in our country over the last 65 years by reading these books below:
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.
