Cholesterol: Explained

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Let me just say first that I am not a physician. But the things I am going to share with you here, you will most likely NOT hear from your healthcare provider. This information is not common knowledge, but it is easily verifiable, and able to be thoroughly researched. The following will provide you with a compilation of studies and material from many experts on cholesterol.

This booklet is a follow up to my first booklet, “Low Carbing with a Whole Food Approach: How a Low Carb Lifestyle Can Help You Lose Weight, Control Your Blood Glucose, and Achieve Total Wellness.” The purpose of this follow up book is that many, when considering adopting a low carb lifestyle, become concerned about the effect of increased fat and cholesterol in the diet.

This booklet is by no means a comprehensive and complete guide to all things related to heart disease. To be honest, there is still no 100% clear answer to the question “what exactly causes heart disease?” Therefore, the intent of this booklet is to educate and better inform ones about their health and to combat the misinformation in the mainstream media about dietary links to heart disease. Hopefully, this book will allay some of the unfounded fears about cholesterol that are in existence. It is meant as a way to open up discussions with your healthcare provider. It is meant to inform and empower individuals to take greater control of their health and give them practical measures to asses their actual risk, and then to reduce or eliminate it.

Cholesterol: The Good and The Bad

Would you be surprised to know that LDL and HDL are not even cholesterol and that there is no such thing as “good cholesterol” and “bad cholesterol?” HDL and LDL are not cholesterol at all. They are lipoproteins. (And they are not the ONLY lipoproteins). HDL stands for high density lipoprotein and LDL stands for low density lipoprotein. Because cholesterol cannot travel directly in the bloodstream, it has to be carried by these lipoproteins. Both HDL and LDL carry cholesterol. So you can see why saying “bad cholesterol” and “good cholesterol” makes no sense.

Cholesterol is a vital substance in the body and plays a significant role in health. The body attempts to maintain a set level of cholesterol at all times, which is why if you deprive your body of dietary cholesterol, your body will just make more cholesterol on its own. In fact, almost all of the cholesterol IN your body is made BY your body. Very little actually comes from the diet. It is so important, that most of the cells of the body can make it. Think about this, if cholesterol was so bad for you, why would the body make it in such abundance?

“Cholesterol is essential for our bodies to function. Without cholesterol, you would die. In fact, the majority of the cholesterol in our blood comes from our own bodies making it. I don’t think that a lot of people understand this concept. People mistakenly think they get most of their cholesterol from their food and that is not true. Cholesterol is used to make hormones like estrogen an testosterone, is transported to the adrenal gland to aid in hormone synthesis, repairs nerves and makes bile for fat digestion, it is a structural component of our cells, it synthesizes vitamin D. It plays such a crucial role in our body that we genuinely need it. If our levels of cholesterol are too low, that can play a negative role in our health too, as a telltale sign of autoimmune disease or even cancer.” Cassie Bjork, Registered Dietician, as quoted in the book Cholesterol Clarity

“Cholesterol, along with saturated fat, gives our cells required stiffness and stability. Cholesterol is vital for the production and function of serotonin receptors in the brain. Serotonin is the body’s “feel good” chemical. Low cholesterol levels have been linked to depression and aggression. Mother’s milk is very high in cholesterol, which is important for the development of infant’s brain and nervous system. Cholesterol acts a precursor to important hormones that help us deal with stress and protect the body against cancer and heart disease. It is also important to our sex hormones like androgen, testosterone, estrogen and progesterone. Cholesterol is necessary for us to use vitamin D, which is a fat-soluble vitamin needed for healthy bones and nervous system, insulin production, reproduction and immune system function, proper growth, mineral metabolism and muscle tone. Bile is vital for digestion and assimilation of fats in the diet; which is made from cholesterol that we eat. Cholesterol performs as an antioxidant, which protects us from free radical damage that leads to heart disease and cancer. This explains why cholesterol levels go up with age. Dietary cholesterol helps maintain the health of the intestinal wall.” Maria Emmerich, Expert in Nutrition and Exercise Physiology, specializing in the study brain chemical transmitters, as quoted in the book Keto Adapted.

So if cholesterol is so important, why have we been led to believe that cholesterol is so bad for us? First, let’s differentiate between DIETARY cholesterol, and cholesterol in the blood. Certain TYPES of “cholesterol” (actually lipoproteins) in the blood CAN have a connection to heart disease risk. It was once reasoned that if cholesterol in the blood can be linked to heart disease, cholesterol in the diet must also be a risk factor. So, the recommendation was made to limit dietary cholesterol. Unfortunately, this reasoning was very flawed. The body tightly maintains cholesterol, a vital nutrient for our survival, in the blood. If one consumes less dietary cholesterol, the body will just make more. The following studies show how dietary cholesterol has little to do with blood cholesterol, and even less to do with cadiovascular risk.

Cholesterol Intake and Plasma Cholesterol: An Update
December 16, 1997

“The misconception that dietary cholesterol determines blood cholesterol is held by many consumers in spite of evidence to the contrary. Many studies reported over the last two years have shown that dietary cholesterol is not a significant factor in an individual’s plasma cholesterol level or cardiovascular disease risk.”

http://www.ncbi.nlm.nih.gov/pubmed/9430080

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Rethinking Dietary Cholesterol
March 15, 2012

“PURPOSE OF REVIEW: The perceived notion that dietary cholesterol is associated with increased risk for coronary heart disease (CHD) has led to dietary recommendations of no more than 300mg/day for healthy populations in the USA. This study will review the current dietary restriction regarding cholesterol while it presents some beneficial effects of eggs (an icon for dietary cholesterol) in healthy individuals.

RECENT FINDINGS: the European countries, Australia, Canada, New Zealand, Korea and India among others do not have an upper limit for cholesterol in their dietary guidelines. Further, existing epidemiological data have clearly demonstrated that dietary cholesterol is not correlated with increased risk for CHD.

SUMMARY: The lines of evidence coming from current epidemiological studies and from clinical interventions support the notion that the recommendations limiting dietary cholesterol should be reconsidered.”

http://www.ncbi.nlm.nih.gov/pubmed/22037012

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Revisiting Dietary Cholesterol Recommendations: 
Does the evidence support a limit of 300 mg/day?
November 12, 2010

“The perceived association between dietary cholesterol and risk for coronary heart disease (CHD) has resulted in recommendations of no more than 300 mg/day for healthy persons in the United States. These dietary recommendations proposed in the 1960s had little scientific evidence. In contrast, European countries, Asian countries, and Canada do not have an upper limit for dietary cholesterol. Further, current epidemiologic data have clearly demonstrated that increasing concentrations of dietary cholesterol are NOT correlated with increased risk for CHD.

Clinical studies have shown that…dietary cholesterol increases high-density lipoprotein (HDL) cholesterol. More importantly, dietary cholesterol reduces circulating levels of small, dense LDL particles, a well-defined risk factor for CHD. This article presents recent evidence documenting the lack of effect of dietary cholesterol on CHD risk, suggesting that guidelines for dietary cholesterol should be revisited.”

http://www.ncbi.nlm.nih.gov/pubmed/20683785

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Dietary Cholesterol From Eggs Increases Plasma HDL Cholesterol
In Overweight Men Consuming a Carbohydrate-Restricted Diet.
Feb 13, 2008

“Carbohydrate-restricted diets (CRD) significantly decrease body weight and independently improve plasma triglycerides (TG) and HDL cholesterol. In this study, 28 overweight/obese male subjects were recruited to evaluate the contribution of dietary cholesterol from eggs in a CRD. Subjects were counseled to consume a CRD (10-15% energy from carbohydrate) and they were randomly allocated to the EGG group [intake of 3 eggs per day (640 mg/d additional dietary cholesterol)] or SUB group [equivalent amount of egg substitute (0 dietary cholesterol) per day]. Energy intake decreased in both groups compared with baseline. All subjects irrespective of their assigned group had reduced body weight and waist circumference. Similarly, the plasma TG concentration was reduced in all subjects. The plasma LDL-C concentration, as well as the LDL-C:HDL-C ratio, did not change during the intervention. In contrast, plasma HDL-C concentration INCREASED in the EGG group whereas HDL-C did not change in the SUB group.

Eighteen subjects were classified as having the metabolic syndrome (MetS) at the beginning of the study, whereas 3 subjects had that classification at the end. These results suggest that including eggs in a CRD results in increased HDL-C while decreasing the risk factors associated with MetS.”

http://www.ncbi.nlm.nih.gov/pubmed/18203890

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Eggs Modulate the Inflammatory Response to
Carbohydrate Restricted Diets in Overweight Men.
Feb 20, 2008

“Carbohydrate restricted diets (CRD) consistently lower glucose and insulin levels and improve atherogenic dyslipidemia [decreasing triglycerides and increasing HDL cholesterol (HDL-C)]. We have previously shown that male subjects following a CRD experienced significant increases in HDL-C only if they were consuming a higher intake of cholesterol provided by eggs compared to those individuals who were taking lower concentrations of dietary cholesterol. Here, as a follow up of our previous study, we examined the effects of eggs (a source of both dietary cholesterol and lutein) on adiponectin, a marker of insulin sensitivity, and on inflammatory markers in the context of a CRD.

Twenty eight overweight consumed a CRD. Body weight, percent total body fat and trunk fat were reduced for all. Subjects in the EGG group had a 21% increase in this adipokine compared to a 7% increase in the SUB group. Plasma CRP was significantly decreased only in the EGG group.

CONCLUSION: A CRD with daily intake of eggs decreased plasma CRP and increased plasma adiponectin compared to a CRD without eggs. These findings indicate that eggs make a significant contribution to the anti-inflammatory effects of CRD, possibly due to the presence of cholesterol, which increases HDL-C and to the antioxidant lutein which modulates certain inflammatory responses.”

http://www.ncbi.nlm.nih.gov/pubmed/18289377

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So let’s get the full impact of these findings:

A carbohydrate restricted diet:

*Decreases body weight
*Decreases waist circumference
(Meaning a decrease in dangerous visceral fat)
*Decreases glucose levels
*Decreases insulin levels
*Decreases atherogenic dyslipidemia
(Meaning a decrease in the type of “cholesterol”
that causes heart disease)
*Lowers triglycerides
*Increases HDL
*Decreases risk factors for metabolic syndrome
(A cluster of medial conditions characterized by obesity, insulin resistance, type 2 diabetes, hypertension and dyslipidemia)

Adding eggs, causes further benefit:

*Decreases plasma CRP
(Meaning inflammation is decreased)
*Increases plasma adiponectin
(Meaning insulin sensitivity is increased)

So how does cholesterol relate to our risk of for heart disease?

In the past, before we knew about HDL and LDL, the marker of “total” cholesterol was used as a predictor of heart disease. But then study after study began to show that many with low total cholesterol actually had higher incidences of death compared to those with high total cholesterol. This is still true today. Approximately half of those suffering heart attacks have “normal” total cholesterol levels. (In my experience as a registered nurse specializing in care of cardiac patients, I can attest to seeing patients with total cholesterol levels of 125, having cardiac artery bypasses.)

Later, the lipid panel we use today was developed, measuring both HDL and LDL. Although total cholesterol is still used as a goal for predicting heart disease, we know this is majorly flawed. The new proposed upper limit for total cholesterol is 180. However, , if you had a client with an HDL of 100 and an LDL of 75 and a triglyceride of 50, making their total cholesterol 185, (HDL+LDL+TRG/5) would you be worried? No way! So it is widely accepted that the components that make up the total cholesterol is a far more important marker than the total cholesterol itself.

Well, now lipid panels have further evolved. The current lipid panel is as outdated as the total-cholesterol of times past was. Newer lipid panels, such as the NMR lipoprofile and the VAP test, are gaining wide use. These tests actually measure, rather than calculate, total cholesterol and each of its components. They also measures particle number and particle size. It is tests like these, that greater determine the actual risk for heart disease based on cholesterol numbers.

Why is Particle NUMBER Relevant?

What does LDL number and particle size have to do with cardiovascular risk? Let’s explore particle number first. The current lab work that tests for cholesterol, tests only the cholesterol contained within the LDL particle (LDL-C). More recent studies suggest that it is not the amount of cholesterol contained in the LDL particle that creates the greatest risk factor for heart disease, but more likely the actual number of particles floating around in the bloodstream (LDL-P). In other words, the greater the number of particles there are, the greater the risk for heart disease. (images courtesy of NMR Lipoprofile.)

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As you can see in the illustration, LDL particles also carry around other fats, ie. triglycerides. “As you might expect, there’s a limit to how much “stuff” that each LDL particle can carry. As the number of triglycerides increases, the amount of cholesterol it can carry decreases, and the liver will have to make more LDL particles to carry a given amount of cholesterol around the body. This person will end up with a higher number of LDL particles.

Consider two hypothetical people. Both have an LDL cholesterol level of 130 mg/dL, but one has high triglycerides and the other has low triglycerides. The one with the high triglyceride level will need more LDL particles to transport that same amount of cholesterol around the body than the one with a low triglyceride level.” Chris Kresser, Integrative Medicine Practitioner.

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To borrow an illustration…our bloodstream is like a highway. Each of the LDL particles can be represented by cars on the highway. The amount of cholesterol within the particle can be represented by the number of passengers in the cars. The more cars there are on the highway, the greater chance there is for an accident to occur. It doesn’t matter how many passengers are in the cars.imageSo once again, when there is a large NUMBER of LDL particles (LDL-P) circulating in the blood (represented by the number of cars on the highway), cardiovascular risk is likely to increase. Cholesterol WITHIN the particles (LDL-C – represented by the passengers in the car) is not an accurate determining factor of heart disease risk alone.

This graphic shows that a person can have a normal LDL (LDL-C) on today’s current lipid panel, but actually be at high risk due to particle number. This would be likely in a person with high triglycerides. That is why triglycerides are an extremely important factor in determining cardiovascular risk. Triglycerides, although being a blood fat, are not caused by fat intake, but rather by excess sugar and refined carbohydrates. This fact has been known for decades.

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Why is Particle SIZE Relevant?

Further, studies have now shown that there is more than one type of LDL. LDL that is small, dense and oxidized (pattern B) is directly related to an increased risk for heart disease. “Aside from smoking, which is an eminently modifiable risk, small dense LDL particles are by far and away the #1 cause of heart disease, “ states Dr. William Davis, Cardiologist. What raises small, dense LDL? Sugar and processed carbohydrates, including grains.

On the other hand, LDL that is large and buoyant (pattern A), is shown to cause NO increased risk for heart disease. Here is the kicker! Studies show that the consumption of saturated fat changes the pattern of LDL from small and dense (dangerous and atherogenic) to large, buoyant (benign, protective).

So, when we replace beneficial saturated fats in our diets with sugar, carbohydrates and processed grains, the pattern of our LDL changes from a beneficial pattern, to a dangerous one. Conversely, when we drop the sugar, refined carbs and processed grains, and add healthy saturated fats back to the diet, we change the pattern of our LDL from dangerous, atherogenic, small dense LDL to healthy pattern LDL.

Quotes To Consider

“One important predictor of heart disease is the relative size and number of LDL particles in the bloodstream. Two peoples can have the same overall LDL concentration, but very different levels of risk depending on whether they have a lot of small, dense LDL particles or a small number of large, fluffy particles,” states Dr. Allan Sniderman, Professor of Cardiology at McGill University in Montreal.

“Eating refined carbohydrates tends to raise the overall number of LDL particles and shift them toward the small, dense variety, which contributes to atherosclerosis. Saturated fat tends to make LDL particles large, more buoyant, and less likely to clog arteries, at least when carbohydrate intake is not high. Small, dense LDL is typically found in heart patients and in people who have high triglycerides, central obesity and other aspects of so-called metabolic syndrome,” states Dr. Ronald M. Krauss, Director of Atherosclerosis Research at Children’s Hospital Oakland Research Institute and former Chairman of the American Heart Association’s Dietary Guidelines Committee.

“The research suggests that health authorities should pivot away from fat restriction and encourage people to eat fewer processed foods, particularly those with refined carbohydrates,” states Dariush Mozaffarian, Dean of the Friedman School of Nutrition Science and Policy at Tufts University.

Note in this illustration, two people with the same LDL (LDL-C) can have very different cardiovascular risk, depending on particle size.

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This is why our current lipid panel, that only measures cholesterol WITHIN the LDL particle, inappropriately determines risk for heart disease, as the test misses BOTH particle NUMBER and particle SIZE. Therefore, many are being treated with cholesterol lowering medications who may not need it. Conversely, many who may need to improve their cholesterol profile, are being diagnosed as normal.

But without having quick access to these newer lipid tests, what are other ways to more accurately predict cardiovascular risk with the tests we have now?

According to Dr. Steven Sinatra, Board Certified Cardiologist and prominent expert in the field of natural cardiology. “The following two ratios are far better indicators of heart disease risk than total cholesterol alone:

• Your HDL/Cholesterol Ratio: Divide your HDL level by your cholesterol. This percentage should ideally be above 24%. Below 10%, it’s a significant indicator of risk for heart disease.

• Your Triglyceride/HDL Ratio: Divide your triglycerides by your HDL level. This percentage should ideally be below 2.”

A Quick Note

The Framingham Heart Study, the longest running study on nutrition and heart disease, showed only a minimal correlation between elevated LDL and heart disease. However they found a SIGNIFICANT correlation (about 4x greater predictive value) between low HDL/high triglycerides and heart disease. Increasing HDL and lowering triglycerides then should be of primary importance in heart health strategies.  Yet, often triglycerides are overlooked until they reach astronomical levels (above 500 – when optimal is WELL below 100)

Inflammation

Inflammation, a good thing, right? We cut our finger, it gets red, swells up. White blood cells rush to the site to fight infection. Special cells also go to the site of the injury, and clean up the wound. In a week, you are good as new, right? Right! Inflammation is a wonderfully protective measure. However, inflammation is always meant to serve a purpose and be a short-lived process. If you cut your finger, you wouldn’t expect inflammation to be present a year later, or ten years later. You want inflammation to do its job, and then go away. But what if, by our lifestyle practices, we have constant internal inflammation that never stops. Most medical and scientific experts now agree that inflammation is at the root of most chronic disease.

Since the whole discussion about cholesterol revolves around heart health and cardiovascular risk, what role does inflammation play in heart disease? According to Dr. Ronald Hoffman, Medical Director of the Hoffman Center of New York City, “Chronic inflammation damages the arterial wall, creating plaque and increasing the risk of blockage and blood clots.”

Dr. Gary Fettke, Orthopedic Surgeon and Nutritional Expert, American Society for Nutrition, in his speech “A Nutritional Model of Inflammation and Modern Disease,” identifies the greatest culprits in systemic inflammation. He states “Sugar, refined carbs and man-made polyunsaturated fats are the root cause of inflammation, and in a nutshell, the cause of modern day disease.” Anyone see a recurring theme here?

So, how do we measure inflammation?

Dr. Hoffman states, “C-Reactive Protein (CRP) is a protein found in the blood that is a sensitive measure of inflammation and implicated in atherosclerosis. The American Heart Association and the U.S. Centers for Disease Control and Prevention have defined risk groups as follows: Low risk: <1.0 mg/dL / Average risk: 1.0-3.0 mg/dL / High risk: above 3.0 mg/dL.”

What can we do to stop inflammation?

Dr. Hoffman suggests: “Eat an anti-inflammatory diet. A diet high in refined carbohydrates is pro-inflammatory. Cut the carbs and eat natural unprocessed foods. Minimize cheap, refined vegetable oils like cottonseed, safflower and corn oil (high in Omega 6) and shun hydrogenated oils altogether. Anti-inflammatory foods include most nuts, avocados, garlic and onions, fatty fish, berries and even red wine, coffee, tea and chocolate (dark). In addition, exercise, lose weight, quit smoking, de-stress and sleep.”

What does this mean for the majority of us?

What it means is that we should strive to achieve a diet and lifestyle that causes the lowest amount of inflammation and creates the least number of small, dense, atherogenic LDL particles.

A diet low in carbohydrates, particularly processed carbohydrates and refined sugar, will be the primary way to reduce “bad” LDL. It also means that saturated fat should replace trans fats and excess polyunsaturated fats in our diet, as saturated fats are neither inflammatory nor do they contribute to small, dense LDL. Rather, they change the pattern to protective, large LDL. Saturated fat also raises HDL (“good” cholesterol.)

It means is that we can stop vilifying fat and cholesterol and use them as part of a balanced diet as we once did. It means drop the man-made margarine and embrace real butter again. It means eat nourishing eggs for breakfast rather than muffins, danishes and waffles, loaded with sugar, or even bagels and “heart healthy whole grain” bread that quickly becomes sugar in the body. Foods that contain sugar or those that turn into sugar quickly, drive up blood sugar and insulin levels. This in itself is one of the greatest risk factors of chronic disease.

Dr. William Castelli, Director of the Framingham Heart Study (the longest running nutritional study in history) for 30 years, further explained “triglycerides are more or less related to the refined carbohydrate in your diet, the white flour, the sugar, the candies, the cookies, the cakes, the ice creams. If you can get them to get away from a lot of that refined carbohydrate stuff, you can lower those triglycerides.”

Lowering triglycerides DIRECTLY lowers our risk of heart disease. Once again, although triglycerides are fats in the blood, they are not caused by dietary fat. Rather, as noted above, triglycerides are raised by a diet high in carbohydrates.

He further stated “In Framingham, Massachusetts, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower the 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 active.”

So drop the refined sugar and processed carbs from the diet. Focus on quality carbs found in fibrous vegetables, low glycemic fruits and nuts. Drop the inflammatory polyunsaturated oils. Put balanced amounts of healthy saturated fat and cholesterol back into the diet. Get moderate exercise and adequate sleep for optimal total health.

Context is Everything

I emphasize in this booklet that just because we know where the flaws are in our current understanding about cholesterol, doesn’t mean we magically now have all the answers. For instance, we know with a relative degree of certainty that a high particle count in the presence of accompanying uncontrolled metabolic syndrome is bad. But what about the occasional individual who eats an extremely healthy, nutrient dense, low carb lifestyle and otherwise has excellent health habits (exercises regularly, doesn’t smoke, controls stress, etc), and yet still has a higher particle count? Does it matter as much? Would it be as harmful? Great question. Unfortunately, we don’t know. For the majority of people, a lifestyle that is low in carbohydrates and higher in healthy fats, almost all cholesterol markets improve. But for some that have an exaggerated response to this type of lifestyle, it is suggested that possibly “eating fat” but not “adding fat” is a better course. (Great video HERE).

Some mistaken LCHF to mean that it is a fat feast. It should never be viewed as that for the majority of metabolically damaged people. If you are normal weight and very athletic, particularly muscular, then yes, you may need more fat, just as you will need more intake in general. But for the majority of us with cholesterol concerns to begin with, we don’t need excessive amounts of fat, especially to meet some pre-conceived macro-nutrient numbers. (Please see my articles HERE and HERE.)  So when I say “eating fat” but not so much “adding fat” it means eating foods that already contain fat, such as fattier proteins, avocados and nuts, versus “adding” fats in the form of excess butter or oils (such as by adding these to your coffee, or consuming “fat bombs”). It has also been suggested by Dr. Sarah Hallberg that if one has an exaggerated response to saturated fat, that using more monounsaturated (NOT polyunsaturated) fats might help. These are found in greater quantity in olive oil, nuts and avocados (and to a lesser degree in chicken skin and lard.).

The Definitive Measure of Heart Disease

To truly assess your cardiovascular risk profile, a simple test can be performed. Please watch a very powerful video on this extremely important diagnostic tool.

In closing, once again, there is so much still unknown about the role of diet in the development of heart disease. Beliefs we have had for decades that we thought were scientifically-based are being overturned every day. This booklet is by no means a complete guide. The field of nutrition science is exploding and new discoveries are being made every day. But there are some things we DO know for certain. Let’s summarize some of them:

  • Cholesterol is an extremely important substance in the body that performs many vital tasks. No cholesterol = no life.
  • Dietary cholesterol plays very little if any role in blood cholesterol. The dietary cholesterol restriction guidelines therefore, are unfounded.
  • Low HDL and high triglycerides are a far greater predictor of heart disease than elevated LDL.
  • Saturated fat raises HDL (“good” cholesterol).
  • Carbohydrates lower HDL.
  • Carbohydrates elevate triglycerides.
  • Carbohydrates contribute to small, dense, atherogenic LDL.
  • Saturated fat contributes to larger pattern, benign LDL.
  • Inflammation is a huge risk factor in heart disease and all chronic disease.
  • Sugar, processed foods, processed grains and processed polyunsaturated fats are highly inflammatory and are a primary source of chronic inflammation.
  • Sugar, processed foods, and processed grains are also the primary drivers of high blood sugars and high insulin levels, a root cause of most chronic disease.
  • A low fat diet, with “heart healthy” grains and fruit does NOT improve your heart disease risk.
  • A low carbohydrate diet generous in healthy fats has consistently been shown to out-perform the low fat diet in regards to heart health.

Remember, though, that no one dietary program works for every person. These guidelines will help to protect the majority of people, particularly the ones at risk for the major epidemics of type 2 diabetes and metabolic syndrome (hypertension {high blood pressure} and dyslipidemia {low “good” cholesterol and high triglycerides}, obesity, insulin resistance and, once again, type 2 diabetes).

Each person should conduct their own nutritional “experiment” on themselves to determine how they feel best and what program brings their risk factors to the lowest level possible for them, considering their other non-modifiable risk factors (age, gender, race, family history, etc.).

As a final note, remember that if dietary cholesterol is restricted, your body will just make more cholesterol. In his book “Grain Brain”, Dr. David Perlmutter states “We all make up to 2,000mg of cholesterol daily because we desperately need it, and this is several times the amount found in our diets. But despite this amazing ability, it is critical to obtain cholesterol from dietary sources. Our bodies much prefer that we “spoon feed” our cholesterol from the foods we eat rather than manufacture it internally, which is a complex, multipstep biological process that taxes the liver. Dietary cholesterol is so important that your body absorbs as much as it can for use.” So do your body a favor. Eat the yolks!

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