can I lose weight with ketosis?

If Ketosis Is Only a Fad, Why Are Our Kids in Ketosis?

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Our Kids Are in Ketosis

Some time ago, I published an article on Medium titled “Our Kids Are In Ketosis”. The article turned many heads and has been shared thousands of times on social media. It has also been cited by an MD in a YouTube video here. So what is the fuss about?

Various ways of eating are labelled as “diet fads” by many people, including many doctors, scientists, and nutritionists. A fad is defined as “an intense and widely shared enthusiasm for something, especially one that is short-lived and without basis in the object’s qualities; a craze” (Google dictionary). Some diets should be labelled fads because it is impossible to maintain them long term. Fruitarian, for example, is one such fad; it is impossible to maintain safely long-term by humans, primarily because one may die from starvation, pancreatic cancer, or as a result of insufficient nutrients in a diet that contains only fruits. In addition to the demand that is placed on the use of insulin to remove the glucose oversupply from the blood, fruitarian diets lack essential amino acids and essential fatty acids for survival.

Some may suggest that the Standard American Diet (SAD), also referred to as the Western Diet, is a fad. The majority of the US population consumes the SAD diet with dire outcome: heart disease, obesity, type 2 diabetes, non-alcoholic fatty liver disease, cancer, Alzheimer’s disease, multiple sclerosis, Parkinson’s disease, nearly all (if not all) autoimmune diseases, and a host of other non-communicable diseases are outcomes of the SAD diet. While on a human life scale we may think of the SAD diet as sustainable, it clearly is not. It has been on the menu for over 50 years, and it feels awkward calling it a fad, even though it most certainly meets “without basis in the object’s qualities”.

“Let food be thy medicine, and let medicine be thy food”

This wise sentence is attributed to Hippocrates. As ancient as this statement is, it still holds true today—if only we followed its wisdom. I am a follower of another Hippocrates saying with a slight modification: “You are not what you eat but how you metabolize what you have eaten!” You will find this sentence as my intro (mission statement) on my FB page. The distinction between what we eat and how we metabolize what we have eaten is essential; it defines who we are.

Understanding Diet and Nutrition

In order to understand how nutrition affects us and what we should be eating, much needs to be understood about the human digestive and metabolic systems. While there is a lot of discussion about the importance of carbohydrates in our diet today—particularly consuming many servings of complex carbohydrates, such as whole grains, starchy vegetables, and fruits daily—this was not always our understanding. For example, when I grew up, carbohydrates were understood to cause obesity(1). Most of my childhood was spent on a relatively low carbohydrate diet—and that was normal for Europe at that time. Cereals—whole grain or otherwise—didn’t exist, neither was I growing up drinking orange juice and eating pancakes with syrup in the morning. In those years, the role of carbohydrates in metabolic disease was clearly understood—and metabolic disease was very rare.

I grew up eating lots of animal meat: pork, bacon, beef, eggs, poultry—including duck and geese—and organ meats, including liver, kidneys, bone marrow, heart, gizzards, pork ears, snouts, hoof, chicken feet, even chicken blood, pork and beef blood in sausages, such as blood sausage—still sold in many places—cooked in pork lard, duck fat butter, or beef tallow, and lots of fatty fish. We also ate a lot of dairy, including milk and cheeses plus all other dairy forms. We had various dairy and cultured milks as well. Of course, we drank milk that could be placed in the window for a day and by next day it was kefir without any added culture and without rotting. Our staples were potatoes, beans, rice, onions, and apples that lasted through February in cold storage. Other fruits and vegetables were all only seasonal, lasting a very short time.

We didn’t have processed foods and processed oils of any kind. While some canned foods and sweetened drinks certainly existed, those were seldom consumed. There was no such as daily dessert. If I was a good girl, maybe once a month I was taken to special pastry places and I could pick one dessert. If you think my family was poor and hence I was eating this way, you are wrong. I was a privileged child. I spent several of my childhood summers in the South of France eating more seafood, but basically the same exact diet. The European diet, when I grew up, was a very cholesterol rich fat-heavy low carbohydrate diet.

It is important to note that while cholesterol levels have been consistently dropping over the past several decades(2)—as a result of the recommended SAD diet full of vegetable oils—the rates of cardiovascular and metabolic diseases have been increasing over the same period, indicating a possible inverse relationship. This is promptly ignored by medicine and there is a continual push toward the consumption of lower cholesterol foods, such as whole grains, fruits and vegetables, and vegetable oils. This, in spite of several studies showing the above mentioned inverse relationship, suggesting that higher cholesterol extends healthy lifespan(3,4). The reason I mention cholesterol is because a reduced carbohydrate diet, such as the one I grew up on, is necessarily a heavy saturated fat and cholesterol diet.

Yet, during those years in Europe, metabolic diseases (such as non-alcoholic fatty liver, cardiovascular disease (CVD), stroke, type 2 diabetes, etc.,) were rare. This article shows the confusion. In it, they discuss the rates of CVD, which was very low in France at the time, to be caused by a “lag”. The assumption being that the heavy saturated fat-filled foods will catch up with the French and they will eventually develop CVD. Interestingly, the French ate heavy saturated fat for centuries before this study, so the catching up is a silly theory aiming to explain the French Paradox. And the catching up is still going on without any success—though now that American junk food is available to the French, it may be only a matter of time.

Ketosis

When one consumes a low carbohydrate high fat diet, even with high protein and some beans time to time, the person will be in a state of ketosis.  In ketosis, the body can use both glucose and fat (both consumed and stored fat) as its fuel. Fat is converted to ketones, or β-Hydroxybutyrate (BHB). This state is reached by diets rich in animal fats, medium amounts of protein, and little or no carbohydrates. Rather than hindering health, ketosis supports and protects it (5), as it can be seen in the treatment of epilepsy(6). Ketosis is the basic human metabolic process. This is further discussed later.

Carbohydrates Versus Fats

When some time ago I bumped into the book Metabolic regulation: A Human Perspective by Keith N. Frayn (3rd edition), in chapter 2.1 and 2.2 I came to two very unusual sections that made me jump up.

The chapter section states the following:

“…fatty acids are usually a preferred fuel (over glucose) for skeletal muscle… Fatty acid release is very effectively switched off by insulin, so muscles no longer have the option of using fatty acids… The characteristics of individual cells or tissues ‘set the scene’ for metabolic regulation. For instance, the metabolic characteristics of the liver mean that it will inevitably be able to take up excess glucose from plasma, whereas other tissues cannot adjust their rates of utilization so readily… The brain, in contrast, has a pathway for utilizing glucose at a rate that is relatively constant whatever the utilizing glucose concentration, a very reasonable adaptation since we would not want to be super-intelligent only after eating carbohydrate, and intellectually challenged between meals.”

I was surprised. In all literature that advises healthy nutrition, we are told to consume a ton of carbohydrates. The USDA Dietary Guidelines recommend My Plate (what used to be the food pyramid, see the history of the USDA guidelines here), which is mostly carbohydrates, with a little bit of meat or fish, eggs, dairy, and some oil on top. Basically most of the diet—over 60 percent—is supposed to come from carbohydrates, such as whole grains, fresh fruits, vegetables, nuts, and seeds. Those are all carbs. The paragraph from the book was intriguing to me, because it tells us that we don’t need to eat carbs, contrary to USDA dietary recommendations.

Skeletal muscles actually prefer to use fat rather than glucose! We have a very carbohydrate-centric view of nutrition today, much more so than when I grew up, yet our muscles and some other organs too, such as the heart(7,8), actually prefer fat as fuel and not glucose! Why are we eating so many carbohydrates?

The Fuels of Our Body

Few professionals, even within the field of nutrition, realize that glucose is not our primary fuel and ketones are not our backup fuel. The human body has no primary or backup fuel: it has three fuels. Some of these fuels are toxic if they stay in the blood too long in larger amounts than needed, and so the body must remove them fast. I presume that the urgency for glucose use—meaning the urgency for the removal of glucose from the blood—is misleading and makes people think that if the body switches to using glucose the moment it is provided, it must be its primary fuel; but this is incorrect assumption. This suggests that the first task that has to be done is the preferred task, but this is seldom the case. For example, assume you trip on your way to a dinner party, hit your head into the cement, and now see double. Although your urgent task now is to head to emergency to see if you received a concussion or other serious damage, the emergency visit is not your preferred task. It just suddenly became a priority you need to tend to immediately before you join the dinner party.

It is true that when we eat carbohydrates, the body must stop everything and remove the excess glucose from the blood. The maximum comfort level for glucose in the blood is 99 mg/dL (5.5 mmol/L) and if we eat carbohydrates in such amounts that this is exceeded, it is literally an emergency and the body must remove the excess glucose. For reference, 99 mg/dL is one teaspoon of glucose in the entire 5 liters of blood. Extra glucose in the blood is toxic. However, having to remove glucose immediately does not make it into the primary fuel.

The three fuels our body can use are: alcohol, providing 7 kcal per gram, glucose, providing 4 kcal per gram, and fat, providing 9 kcal per gram. While alcohol is a viable fuel for the human body, it creates many adverse effects, causing damage, so it is not recommended to be used as fuel, though alcoholics often use it as such. Given that alcohol is the most dangerous of all the fuels(9), if our body is provided the three fuels simultaneously, alcohol will be burned first. Yet we don’t ever assume that alcohol is our primary fuel.

How the Body Prioritizes Fuels

Priority can be assigned for many reasons. One can give priority to something preferred, but if this means that something harmful has to wait to be removed, there is a risk of disease. If this was the method our body chose for prioritization, we may not have remained alive long enough to become who we are today. One can prioritize by the amount of energy each fuel gives, using up first the one that gives the most energy, and saving the rest for later. But, again, if the rest causes damage while waiting to be used, then this has to be avoided. One can also prioritize based on the removal of toxic fuel first and save the least toxic fuel to be used last.

If our body prioritizes based on preventing damage by burning the fuel in order of toxicity, then the order would be:

  1. Alcohol
  2. Glucose
  3. Fat

If priority would be given to those fuels that provide the most energy, the order would be:

  1. Fat
  2. Alcohol
  3. Glucose

If the priority is based on the USDA dietary guidelines, then the order would be (alcohol as fuel is usually not mentioned anywhere):

  1. Glucose
  2. Fat

What we actually see happening is that the body burns fuel in the order of which it causes the most damage in the blood. The most dangerous fuel in the blood is alcohol. Its side effects can even be fatal, so clearing that from the body is necessarily task #1.

The urgency with which we must respond to the situation is dependent upon its outcome.

Glucose is the second most dangerous fuel in the human body after alcohol. Fructose, a sugar that is part of table sugar, honey, and most fruits, turns into ethanol (an alcohol) causing damage, and glucose—referred to as blood sugar—is toxic to our nerves, may cause eye damage and type 2 diabetes, and cardiovascular disease (including stroke) as well.

By contrast, fat is a safe fuel to the point that it is usually stored in our body—something many of us wish to have less of. It is not a toxic substance and at 9 kcal per gram, it provides the most energy. Alcohol inhibits the burning of glucose and fats, making it the mandatory first fuel to burn. So the actual order of fuel priority is:

  1. Alcohol
  2. Glucose
  3. Fat

So why was I so surprised reading that some organs prefer to use fat for fuel? We read and hear so much about carbohydrates as the most important fuel, the kinds of carbohydrates we should be eating, and how much. We can learn very little about the other important fuels: alcohol and fats. Yet, as the surprising paragraph suggests above, often the other fuels are more important. In particular, if we look at the human lifespan, other fuel needs become stunningly obvious. I think we have forgotten that babies are born in ketosis and their primary fuel is ketones.

Human Fuel from Conception

Indeed, babies are born in ketosis(10) and mother’s milk is low in carbohydrate and high in fat (LCHF), which keeps the newborn in ketosis all through nursing. Breast milk contains more glucose across time, as the child matures.  At full maturation (about one month), its nutritional content per cup (8 oz) is 10.8 gr fat, 2.53 gr protein, 16.9 gr carbohydrates (in the form of lactose) and total energy of 174.92 kcal. It also contains 87.5 gr water. Subtracting the water and looking at the macronutrient ratios only, this glass of mature nursing milk is 55.57% fat, 5.79% protein, and 38.65% carbohydrates (in lactose, so not free sugar). In terms of fatty acid composition: 4.942 gr saturated fat, 4.079 gr monounsaturated fat, and 1.223 gr polyunsaturated fat, which in percentages: 48.24% saturated fat, 39.82% monounsaturated fat, and 11.94% polyunsaturated fat. One must agree that babies are not fed poison by their mothers and that Nature didn’t provide toxic nursing milk such. In fact, we can see that babies grow very rapidly while nursing milk and we know from studies that babies who are nursed, have a better chance for survival, grow healthier, faster, and their brain develops better (see here and here).

As babies grow, they retain metabolic flexibility, meaning they stay in ketosis for periods time, which changes by age and how often they are fed, and they do enter the carbohydrate metabolic process as they eat(10-12).

The below figure is very telling. On the vertical axis you find β-hydroxybutyrate [BHB], which is the level of ketones measured in blood, and on the horizontal axis, time passing in hours and days between feeding times. The graph inside contains people of all age groups and both genders. Officially, a fed person (with carbohydrate containing food) has zero amount of BHB in her/his blood. As time passes, and if the person fasts for a blood test or a medical procedure, slowly BHB increases in the blood. The clinically accepted level of BHB in the blood that is not considered ketosis is 0.3 mmol/L, which can easily be reached by healthy individuals as a result of such fasting. Anything above 0.3 mmol/L and chronically maintained 0.3 mmol/L means the person is in ketosis.

From Annu. Rev. Nutr. 2006. 26:1–22; doi: 10.1146/annurev.nutr.26.061505.111258

Figure 1. George F. Cahill Jr. showing time passing without food and ketosis level by age and gender

Note that babies are born with 0.5 mmol/L or higher level of BHB and remain in ketosis until they are fed, which immediately after birth cannot happen since the mother has no milk yet—this means the baby remains in ketosis until the time comes that milk is released by the breast of the mom. It is suggested that the baby is in ketosis because it is not being fed(10), meaning starvation, but this is questionable, since babies remain in ketosis even after being fed—more on this later. The human brain uses 20% of the energy the body generates. In the case of infants, the need for energy arises very quickly, as shown in Figure 1, approximately in 20 minutes. There are other factors as well, such as the brain is over 80% fat and cholesterol(13), with the cholesterol alone representing 20-25% of the total cholesterol of the body (here).

Thus ketosis, in one scenario, is a state into which our metabolism reverts to when food is not immediately available on demand (starvation). On the other hand, studies on the fetus in utero show that the fetus is in ketosis even though it is never under nutritional duress(14,15) and there are ketones in the placenta(16) as well. Therefore, it is very difficult to suggest that ketones are a backup fuel used only in starvation if the fetus is in ketosis time to time even without starvation. Clearly, being in ketosis provides some benefits that are not possible to achieve using the glucose metabolic process. I venture to suggest that the ketogenic and the glucogenic metabolic processes have distinct functions, each to benefit us on its own way.

Concluding Thoughts

To conclude the importance of ketosis, let me offer some anecdotal evidence. In the Facebook migraine groups I manage (see here and here), all migraineurs are asked to run a special blood glucose/blood ketone test that starts with fasting and premeal tests and continues for 5 hours postprandial. There are many children with migraines whose parents are in the groups—the children are from ages 2-18, so for them parental help is required. Thus, over time, I have had the opportunity to evaluate the 5-hour blood test results of children of all ages—I think the youngest was 5 years old and the oldest 16, so far. I have yet to see a blood ketone test of a child anywhere in this age group that is not showing ketosis both before and after a meal—even if the meal has fruits and dairy in it.

I suppose ignorance is bliss. Few doctors or researchers have the same opportunity I have in being able to measure the blood ketones of various ages of children for five hours postprandial plus fasting and premeal measures, therefore, most don’t realize just how much our kids are in ketosis.

Thus, while today in most countries around the world any type of food is just a short walk/drive away 24/7, and we need not experience hunger and starvation, our children are still in ketosis 24/7. Shouldn’t that tell us something about the importance of ketosis?

References

  1. Dawkins, M. Carbohydrates and Adiposity. British medical journal 1, 719-720, doi:10.1136/bmj.1.5385.719 (1964).
  2. Farzadfar, F. et al. National, regional, and global trends in serum total cholesterol since 1980: systematic analysis of health examination surveys and epidemiological studies with 321 country-years and 3.0 million participants. The Lancet 377, 578-586, doi:10.1016/S0140-6736(10)62038-7 (2011).
  3. Ravnskov, U. High cholesterol may protect against infections and atherosclerosis. QJM: An International Journal of Medicine 96, 927-934, doi:10.1093/qjmed/hcg150 (2003).
  4. Kaysen, G. A. et al. Lipid levels are inversely associated with infectious and all-cause mortality: international MONDO study results. Journal of lipid research 59, 1519-1528, doi:10.1194/jlr.P084277 (2018).
  5. DuBroff, R. & de Lorgeril, M. Fat or fiction: the diet-heart hypothesis. BMJ Evidence-Based Medicine, bmjebm-2019-111180, doi:10.1136/bmjebm-2019-111180 (2019).
  6. Berghoff, S. A. et al. Dietary cholesterol promotes repair of demyelinated lesions in the adult brain. Nature communications 8, 14241-14241, doi:10.1038/ncomms14241 (2017).
  7. Park, T.S., Yamashita, H., Blaner, W. S. & Goldberg, I. J. Lipids in the heart: a source of fuel and a source of toxins. Current Opinion in Lipidology 18, 277-282, doi:10.1097/MOL.0b013e32814a57db (2007).
  8. Noh, H.-L., Yamashita, H. & Goldberg, I. J. Cardiac Metabolism and Mechanics are Altered by Genetic Loss of Lipoprotein Triglyceride Lipolysis. Cardiovascular Drugs and Therapy 20, 441-444, doi:10.1007/s10557-006-0633-1 (2006).
  9. Van de Wiel, A. Diabetes mellitus and alcohol. Diabetes/Metabolism Research and Reviews 20, 263-267, doi:10.1002/dmrr.492 (2004).
  10. Cahill, G. F. Starvation in man. N Engl J Med 282, doi:10.1056/nejm197003052821026 (1970).
  11. Storlien, L., Oakes, N. D. & Kelley, D. E. Metabolic flexibility. Proceedings of the Nutrition Society 63, 363-368, doi:10.1079/PNS2004349 (2007).
  12. George F. Cahill, J. Fuel Metabolism in Starvation. Annual Review of Nutrition 26, 1-22, doi:10.1146/annurev.nutr.26.061505.111258 (2006).
  13. Chang, C. K., DS; Chen, JY;. Essential fatty acids and human brain. Acta Neurologica Taiwanica 18, 10 (2009).
  14. Herrera, E. & Amusquivar, E. Lipid metabolism in the fetus and the newborn. Diabetes/Metabolism Research and Reviews 16, 202-210, doi:doi:10.1002/1520-7560(200005/06)16:3<202::AID-DMRR116>3.0.CO;2-# (2000).
  15. Herrera, E. Lipid metabolism in pregnancy and its consequences in the fetus and newborn. Endocrine 19, 43-55, doi:10.1385/endo:19:1:43 (2002).
  16. Orczyk-Pawilowicz, M. et al. Metabolomics of Human Amniotic Fluid and Maternal Plasma during Normal Pregnancy. PloS one 11, e0152740-e0152740, doi:10.1371/journal.pone.0152740 (2016).

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Health and the Nutrition Connection: Focus on Fats and Cholesterol

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I am a migraine specialist, but recently, I have had more opportunities to work with non-migraineurs to improve their general health. Patient by patient, I have learned that most of the steps I use in my migraine-prevention protocol result in significant improvements for many health conditions. With the use of proper nutrition alone, patients reverse their pre-diabetes, insulin resistance, prostate issues (PSA number), cholesterol issues (high triglycerides, high LDL, and low HDL), arthritis, migraines, and even fibromyalgia flareups. Here, I would like to summarize what I found is wrong with our current nutrition paradigm and how to correct it.

The Cholesterol Problem: A Convoluted History

In the mid-20th Century, a charismatic and highly influential researcher (Ancel Keys), based on somewhat fraudulent data selection, “proved” that saturated fat causes cardiovascular disease (CVD). Keys came to this conclusion based on what has come to be known as the 7 countries study even though he originally studied the data from 22 countries. The data of 15 countries (including France) were not included because they didn’t line up with the original hypothesis that “saturated fat, particularly LDL cholesterol, causes CVD”.  This created later what was referred to as the French Paradox: how is it that the French have the fewest number of CVD and yet eat the most saturated fat?

Based on Keys’ “findings”, further research aimed at describing the connection of saturated fat and CVD. What they discovered was that for every person with a fatal heart attack, cholesterol (LDL in particular) filled the artery. Without further ado, they decided that cholesterol, particularly LDL (low density lipoprotein), must be the reason for CVD. Since cholesterol in the arteries seemed like it was made from fat, highly saturated fat is a solid lipid at room temperature, saturated fat was held responsible. This theory became the dogma and was subsequently taught to generations of medical professionals.

For many years, and to a great extent even today, it has been difficult to publish any result of studies in disagreement with the dogma. Information about unpublished data (by the NIH among others) has only recently surfaced. Read “The Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy Diet” by Nina Teicholz for a great explanation. The newly revealed data show that not only is saturated fat not responsible for CVD, but that it can, in fact, help reduce its occurrence.

Problems with Current Measures of Cholesterol

Although the original confusion about cholesterol and CVD stemmed from Ancel Keys, it was reinforced with laboratory testing methods that don’t quite measure what we think they measure (here). Briefly, although the original confusion about cholesterol and CVD stemmed from Ancel Keys, it was reinforced with problematic laboratory testing methods based upon incorrect assumptions.  Namely,

  • LDL is not cholesterol but a lipoprotein ball that contains cholesterol as well as fat soluble vitamins and minerals.
  • LDL is not measurable in the blood by conventional blood tests. It is calculated.
  • Triglycerides are not measurable in the blood by conventional blood tests. They are estimated.
  • VLDL is measured and an assumption is made that triglycerides/5 = VLDL, which is likely incorrect—see explanation later.
  • The equation used (with the listed assumptions) to calculate LDL: 

LDL = Total cholesterol – HDL – (triglycerides/5)

The equation above has two unknowns, and thus, it is impossible to solve mathematically. The two items we can measure with conventional blood tests are total cholesterol and HDL. An assumption is then made that everything else they measure is VLDL. It is unclear how they can separate VLDL from the remaining “cholesterol” since the blood test doesn’t measure what are called chylomicron or remnant pieces of lipoproteins. It simply assumes that chylomicrons don’t exist if fasting preceded the blood test. Below is a picture of lipoprotein formations, within which there are cholesterol and fat-soluble vitamins and minerals.

Cholesterol--Lipoprotein Balls
Cholesterol–Lipoprotein Ball

Image used from Medscape

Fasting is required for a cholesterol blood test and is assumed that after 12 hours of fasting chylomicrons don’t exist, thus the above equation is valid; see Friedewald et al 1972. If chylomicrons do exist during blood test, it invalidates the equation. Healthy individuals’ liver releases glycogen when fasting. Glycogen is stored energy in the liver that is converted to glucose and released in the blood; the lack of existence of chylomicrons may not be true.

Therefore, the above equation doesn’t really give us reliable quantitative information about LDL and definitely no information about the amount of cholesterol in LDL. Even if we could measure LDL, it is still just a lipoprotein ball, as is HDL. In effect, with the current tests, we are counting cars on the freeway to determine how many people travel on that freeway; a very rough estimate at best, but more likely, just a misleading guess.

There is one test, however, that can assess cholesterol inside lipoprotein, but it is infrequently used. It is called the nuclear magnetic resonance (NMR) imaging and is based on atomic weight and motion.

Even if the Cholesterol Tests Were Accurate, Do They Tell Us Anything About CVD?

Let us assume that despite everything we have detailed so far, we can measure cholesterol from the conventional blood test or any other test accurately and that we know the precise amount of cholesterol that is carried in LDL; we still have to ask:

  1. Does our cholesterol knowledge tell us anything about CVD?
  2. Does saturated fat (or any fat) have anything to do with cholesterol?

To understand these two questions, we need to look at what cholesterol and fat are, how they are made, and from what raw materials.

What is Cholesterol?

Cholesterol is so important for the body that, unlike other nutrients, such as glucose with a very short presence in the body, cholesterol is kept for days and is reused. Twenty five percent of all cholesterol is in the brain, forming the white matter necessary for the insulation of axons to protect against voltage leaks. Voltage leaks occur in many diseases, such as seizures, migraines, multiple sclerosis, Alzheimer’s, Parkinson’s, and alike. In the brain, a cholesterol molecule stays functional much longer than days, often for weeks, months, sometimes for years. So what exactly is cholesterol?

Good and Bad Cholesterol

There is no such thing as good or bad cholesterol; we only have one type of cholesterol with the chemical formula: C27H46O. We have some differentiation within cholesterol in terms of size and the size variation is a representation of oxidative damage1,2  but it is still the same exact cholesterol. It may have shrunk and folded on itself, became dense and sticky, caramelized. Indeed, the cholesterol inside LDL is found in 2 particle sizes: large fluffy (healthy) and small dense (damaged). The latter small, dense, damaged, caramelized ones are created by the pyruvate process by oxidation, and this cholesterol indeed participates in CVD. One should ask then why some cholesterol molecules become damaged and why some don’t. And also, is cholesterol and saturated fat connected? This is the heart of the matter, pun intended.

What is Fat?

Fat is made from fatty acids. All fatty acids are essential, meaning we must eat them. Our body cannot make them. There are two types of essential fatty acids: Omega 3 and Omega 6, within each of which there are three types: monounsaturated, polyunsaturated, and saturated fats.  Here is an example of a typical monounsaturated fat molecule: CH(CH2)7COOH (oleic acid, making up about 83% of olive oil, a mostly monounsaturated fat). Here are two types of typical saturated fatty acids: CH3(CH2)6COOH a short chain and CH3(CH2)24COOH a long chain fatty acid, and a typical polyunsaturated fatty acid is Linoleic acid C18H32O2.

As you can see, all fatty acids have hydrogen tying down (bonding to) at least some of the oxygen. Whether the fatty acid is unsaturated or saturated depends on the number of hydrogen bonds. Monounsaturated has a single hydrogen bond, polyunsaturated more than one, and saturated has all oxygen tied down by hydrogen. The more saturated a fat is, the more stable are its bonds. Saturated fats last longer without going rancid, can be used at higher temperatures, and are solid at room temperature.

An important point about omega 3 and omega 6 is that humans are not able to convert the vegetable form of omega 3 (ALA), found in fruits, vegetables, nuts, grains, and seeds, into the animal form that the human body can use (DHA/EPA) efficiently. Therefore, the consumption of animal products and seafood is essential for all humans to meet the necessary omega 3 requirement of our brain, which is mostly made from DHA.

How Cholesterol is Created

The chemical formula for cholesterol is not the same as for any of the fat types; in the cholesterol molecule there is no opening for saturation with hydrogen anywhere. No fat of any type has the same configuration in carbon, oxygen, or hydrogen as cholesterol. Fats are fatty acids, whereas cholesterol is a waxy substance. Cholesterol has not much to do with fat. It is not created from fat. The body can acquire cholesterol two ways:

  • Directly from cholesterol containing foods
  • Making it from carbohydrates.

If we eat enough cholesterol, the liver doesn’t make more. In other words, the liver only makes as much cholesterol from carbohydrates as the body needs. Cholesterol is essential in cell functioning and, as a result, is closely regulated by the liver. Cholesterol also serves as a precursor for the biosynthesis of steroid hormones, bile acid, and vitamin D. The cholesterol-making pathway is 37 steps long. The first step is Acetyl-CoA, a molecule generated by cellular respiration. It is produced in the second step of aerobic respiration after glycolysis and carries the carbon atoms of the acetyl group to the TCA cycle to be oxidized for energy production. Cholesterol is a byproduct of glycolysis. Glycolysis breaks down glucose and forms pyruvate with the production of two molecules of ATP. Cholesterol is not only integral to cellular respiration and the formation of ATP,  it is a product of that very function. Cholesterol is a result of glucose metabolism. This is crucially important knowledge. It goes against the dogma of “cholesterol is made from fat, therefore fat is bad”.

Cholesterol regulation is a key component of metabolic processes. When we don’t eat enough cholesterol from meats and eggs, more is made by the liver from carbohydrates. Glucose oversupply, starches, and fructose either convert to cholesterol—as noted earlier—or excess carbohydrates get packed away as future storage (visceral and ectopic fat) in and around our organs. This fat storage is initiated by insulin and is completed by our liver.

Triglycerides form visceral and ectopic fat, which are our energy reserves converted from the unused glucose and fructose. The liver’s capacity for this storage is limited and so it needs to expand in size to accept more. This is the cause of non-alcoholic fatty liver diseases, and then later, the need for more and more fat storage is what becomes insulin resistance,  that may lead to type 2 diabetes. So, by avoiding excess consumption of carbohydrates, the creation of dense, sticky, caramelized cholesterol particles can be prevented. From the cholesterol in LDL, these low-density, sticky, caramelized, damaged cholesterol particles are the only ones that contribute to CVD. However, when we reduce carbohydrates in our diet, we need to increase the consumption of fats.

There is no food that is pure saturated fat. All fats, no matter if it is in a leaf of lettuce or a pork belly, is a combination of saturated fat, monounsaturated fat, and polyunsaturated fat. They are not found separately in nature. What we can say is that some foods have less saturated fat than others. Some of the foods that have been excluded from recommended diets based on the fear of saturated fat are pork and beef:

Fat types
Table 1. Fat types

Note in the above table that pork lard has more monounsaturated fat than saturated fat, so can we say that pork lard is saturated fat? It is important to see which fat type is closest to human fat because that is what we need to eat. If we look at the human body’s fat composition (this is very hard to find, so I put this together from several research papers), it is very similar to that of pigs, meaning that to maintain our health, we should consume the type of fats our body is made from, and thus, needs.

Carbohydrates and the Insulin Connection

At this point, your head is probably spinning from too much chemistry, but bear with me. If we don’t understand the chemistry, all sorts of errant assumptions about health and disease can be made and have been made. Most importantly, for generations we have failed to recognize that cholesterol comes from carbohydrates, not fats, and as result, millions of us have developed type two diabetes by following the accepted medical advice. Just how bad is it?

When Carbohydrates Dominate the Diet

Carbohydrates were elevated to primary consumption status at the same time fats were demoted. Of the three macronutrients: fat, protein, and carbohydrates, carbohydrates are the only non-essential macronutrients. There is not a single essential element in carbohydrates. Carbohydrates provide glucose (the body can make glucose from protein and fat), fructose (44% of fructose converts to glucose and the rest to triglycerides), vitamins (all vitamins in plants are also available in animals—including vitamin C if certain parts are eaten raw—and many vitamin in animal products are not found in plants).

Another note on vitamins: we consume most vitamins in order to help our immune system fight free radicals. Free radicals are only created in the pyruvate (glycolysis) step, which is participant only in the glucose metabolic process. If we stop eating exogenous glucose (carbohydrates), our need for antioxidants is greatly reduced. Fat-burning bypasses the pyruvate process and doesn’t generate free radicals3. Over 50% of protein converts to glucose4. However, the amount of free radicals generated from protein-converting is so small that only minimal free radicals are generated.

When the USDA removed “saturated fats” and everything that contained them from our diets, it replaced all that with vegetable oils (Omega 6 oils), transfats (artificially hydrogenated vegetable oils), and carbohydrates. Diabesity (diabetic obesity), increase in CVD, Alzheimer’s disease, cancer, arthritis, incontinence, PCOS, prostate problem, neurophathy, fibromyalgia, etc., followed.

The Problem with Grains

According to the celiac.org, 1% of the global population has celiac disease and 0.4% has been diagnosed to have wheat allergy—a large percent remain undiagnosed. The wheat allergy or sensitivity of those not yet diagnosed show up like arthritis, prostate concerns, PCOS, allergies, asthma, Crohn’s disease, IBS, etc. How can we tell? When they stop eating all grains (wheat, rice, corn, rye, oats, etc.,) for at least 2-6 months, their inflammatory markers improve and they reverse their health conditions. Grains are also responsible, in a large part, for CVD and potentially cancer, because grains are inflammatory, increase blood pressure, and narrow the arteries. It was a human genetic variant that allowed some of the damaging factors of grains to be mitigated: ACE and apolipoprotein B genes, because they relate to blood pressure and the cholesterol in LDL. Blood pressure and cholesterol are both factors that respond well to low-carbohydrate, and thus, low-grain diets, suggesting that the polymorphisms may be a protective adaptation against the cardiovascular effects of grains5.

In spite of all this knowledge, grains are considered to be the most vital nutrient on “My Plate” by the USDA. Furthermore, grains are indigestible and reduce nutrition absorption.  They also need to be fortified to get any nutrition while eating them. They are the most frequent carbohydrate items on our plate that have no nutrition, only glucose from starch.

Fruits, Vegetables, Nuts, and Seeds

Other carbohydrates are fruits, vegetables, seeds, and nuts. The ideal maximum blood glucose level is 99 mg/gL (equivalent to about 1 teaspoon, a little over 4 gr of glucose for an average person. By eating a medium size sour Granny Smith apple, we take in almost 23 gr carbohydrates, of which 10.225 gr is pure glucose. This is 2.5 times as much glucose as what the entire blood supply prefers to have, so eating a medium sized sour Granny Smith apple challenges the body to remove all that glucose from the blood very fast, a large amount of glucose staying in the blood is toxic. Mind you, this one apple, with all the trouble it caused, gives nearly no vitamins at all; no vitamin C noted in the USDA table, very few amino acids and no fatty acids, those would be the essential macronutrients. An apple offers nothing but glucose and fructose. Therefore, from what we now know about the connection of carbohydrates to cholesterol, part of that apple will become cholesterol, and since it is a carbohydrate and is converted to energy using the pyruvate process, it also creates more free radicals than if you, instead, ate a steak. And lastly, since this apple has much more glucose than what the body can use, and also a lot of fructose, whatever energy from this apple is not used, gets stored as body fat.

Diet and Insulin Resistance

Insulin resistance is not a disease. It is nature’s way of helping creatures pile up fat-reserves for times of scarce resources, like winter. The trick is the seasonality of insulin resistance; it is nature’s way of remaining alive in winter but returning to normal insulin levels during the lean times, normally hibernation or starvation, thereby, when spring appears with fresh food resources, the liver will have reversed all its fattiness and by then the visceral and ectopic fat would have shrunken by fueling the body all through the winter. This is an equivalent process to the ketogenic diet – see below.

Lack of seasonality in energy storage necessarily leads to chronic insulin resistance. Chronic insulin resistance is unhealthy, leads to type 2 diabetes, and/or obesity. While this would need a lot of explanation, in short: obesity and insulin resistance need not go hand in hand. Sumo Wrestlers are extremely obese but are completely healthy without any insulin resistance while very thin people may have insulin resistance (TOFI—thin outside fat inside). Thus, insulin resistance is strictly associated with extensive visceral and ectopic fat and not with “being fat.”

One can prevent chronic insulin resistance by either following in the footsteps of our evolutionary past with seasonality, or by permanently preventing fat accumulation when not observing any seasonality. This requires cutting back on carbohydrates. When we cut back carbohydrates, depending on the depth to which we reduce carbohydrates in our diet, the body may move to burn visceral/ectopic fat by entering the state of ketosis. Ketosis is not equivalent to keto acidosis. Ketosis merely means that the body switched from burning glucose to burning fat in the form of ketones—or to be more precise, burning β-Hydroxybutyrate (βHB)6. Just like any fire needs some kindle to be started, a proper fat-burning diet is started by eating fat—and plenty of saturated fat. The ketogenic diet doesn’t use glucose for fuel, but this doesn’t mean the body has no access to glucose. A large percent of protein converts to glucose, so those organs that need glucose, still receive it, but the body’s main fuel is fat.

As noted earlier, cholesterol is made from carbohydrates, and deformed cholesterol is a consequence of the pyruvate/glycolysis process (a carbohydrate metabolic process). Since fat doesn’t convert to cholesterol and doesn’t use the pyruvate process, the ketogenic diet reduces the chance for the creation of any damaged cholesterol within LDL.

The Ketogenic Diet

The ketogenic diet is really not a diet but a metabolic process, in which the main fuel of the body is fat. While glucose is also used, it is only used for those organs that must have glucose, such as red blood cells and the brain. The ketogenic diet burns ketone bodies—fat converted to body fuel. The ketogenic diet induces nutritional ketosis—not to be confused by diabetic keto acidosis, which is the outcome of type 2 diabetes. During nutritional ketosis, the body burns stored energy for fuel (visceral and ectopic fat). As a result, it is often used for weight loss. It is an ideal nutritional method to reverse insulin resistance, since it reverses non-alcoholic fatty liver disease by reducing fat storage.

The ketogenic diet is a strict version of the low carbs high fat diet with moderate protein consumption. A typical ketogenic diet is 80% calories from fat, 16% calories from protein, and 4% from carbs. The type of carbs that are permitted are mostly green leafy salads, spinach, broccoli and cauliflower, fruits like avocado, zucchini, etc., and some minimal raspberries and blackberries. The fats contain olive oil and animal fats. Some people in ketogenic diet also consume coconut oil. Coconut oil can only burn as ketones and so eating coconut oil prevents the burning of stored fat for fuel. Thus, coconut oil should not be consumed by those wishing to lose weight.

The strictest form of the ketogenic diet is used therapeutically for seizure cures. It appears that the ketogenic diet rebuilds the myelin (mechanism not yet understood), the layer made from fat and cholesterol (white matter in the brain) that coats neurons to insulate them from possible voltage leak. This more extreme form is also used to help other diseases where the white matter is damaged, such as Alzheimer’s disease, Parkinson’s disease, and Multiple Sclerosis, among others.

Since cancer cells feed on glucose—called the Warburg Effect, the ketogenic diet is also being tested for cancer treatment, so far with great success. For an example, see Andrew Scarborough and his recovery from Anaplastic Astrocytoma that was diagnosed in 2013.

LCHF Diet

There are nutritional concepts, other than the ketogenesis, that can help reverse some metabolic damage, such as the LCHF (low carbs high fat) diet. It is a comfortable alternative to the ketogenic diet for those who don’t wish to become fat burners, only want to reduce their chances for insulin resistance, obesity, and metabolic diseases that include non-alcoholic fatty liver disease as well as CVD.

The LCHF diet is still a carbohydrate burning diet, and as such, antioxidants are necessary, and fat is not burned. However, it removes most of those foods from the diet that appear to cause problems for many people, such as refined carbohydrates (all sweeteners, prepared, canned, and processed foods, juices, shakes, and smoothies. Some LCHF diets permit the use of some sugar substitutes), all grains (even gluten free grains are grains, so they are not part of the LCHF diet), all starchy vegetables (potatoes, yams, carrots), and the majority of fruits, with the exception of raspberries, strawberries, and blackberries.

LCHF diet encourages olive oil, coconut oil, and animal fats, lots of fish, all meat types, and dairy. The focus is on reduced carbohydrates, typically to around 100 net carb grams a day.

Individualized Nutrition

No single diet works for everyone. Genetic (heritable) and epigenetic (environmental) factors mostly determine what is healthy for a person and what is not. People whose ancestry is from Nordic environments will likely have trouble metabolizing foods that were not readily available in their location prior to commercialization, such as tropical fruits. Others, whose ancestry is more tropical, may end up with metabolic health issues from eating too much fat.

It is important to understand that the goal is not to just follow a nutritional regimen but to recognize the reaction of an individual to the food consumed.

What we see in the US, and increasingly around the world, is an epidemic created by the Standard American Diet (SAD) that assumes that all humans have identical metabolic processes. That this is not true should have been realized when Native Americans were changed to the SAD (sugar, soft drinks, grains) diet and they all became unhealthy. While the experts at that time perhaps didn’t understand what was happening, we understand it now. We need to maintain flexibility! Those suffering from metabolic disorders such as obesity, insulin resistance, type 2 diabetes, CVD, etc., should consider it a sign, a warning, and change their eating habits, change to a different nutritional base for health. Those who do well on SAD can carry on. The important point is to pay attention and be willing to change.

Sources

  1. Gesquière L, Loreau N, Minnich A, Davignon J, Blache D. Oxidative stress leads to cholesterol accumulation in vascular smooth muscle cells. Free Radical Biology and Medicine 1999; 27(1): 134-45.
  2. Al-Benna S, Hamilton CA, McClure JD, et al. Low-Density Lipoprotein Cholesterol Determines Oxidative Stress and Endothelial Dysfunction in Saphenous Veins From Patients With Coronary Artery Disease. Arteriosclerosis, Thrombosis, and Vascular Biology 2006; 26(1): 218-23.
  3. Pigozzi F, Giombini A, Fagnani F, Parisi A. CHAPTER 3 – The Role of Diet and Nutritional Supplements A2 – Frontera, Walter R. In: Herring SA, Micheli LJ, Silver JK, Cd AEft, Young TP, eds. Clinical Sports Medicine. Edinburgh: W.B. Saunders; 2007: 23-36.
  4. Coulston AM, Liu GC, Reaven GM. Plasma glucose, insulin and lipid responses to high-carbohydrate low-fat diets in normal humans. Metabolism 1983; 32(1): 52-6.
  5. Salomón T, Sibbersen C, Hansen J, et al. Ketone Body Acetoacetate Buffers Methylglyoxal via a Non-enzymatic Conversion during Diabetic and Dietary Ketosis. Cell Chemical Biology; 24(8): 935-43.e7.
  6. Reger MA, Henderson ST, Hale C, et al. Effects of Beta-hydroxybutyrate on cognition in memory-impaired adults. Neurobiology of Aging; 25(3): 311-4.

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