carbohydrates are not essential

Carbohydrate Addiction

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With the nutrition wars going on (explained well here), recommending the key macronutrients and their proper proportions for our health, the two dominant camps that have emerged are the carbohydrate proponents and those that oppose the consumption of carbohydrates—some oppose only in “excess” (low carbs, ketogenic, Atkins, etc.,) and others “completely” (zero carbs). Between the members of these groups, angry words are exchanged, and competencies, educations, and other personal nonscientific arguments are bandied around. I call this nutrition bullying. And then there are the substantive conflicts and inconsistencies. Like the following confusing statements – 10 pages apart in the National Academies of Sciences Dietary Reference Intake (DRI) guideline book.

In the chapter titled Clinical Effects of Inadequate Intake on page 265 the opening statement is as follows:

“The Recommended Dietary Allowance (RDA) for carbohydrate is set at 130 g/d for adults and children based on the average minimum amount of glucose utilized by the brain.”

Going to page 275 in the same chapter, we read:

“The lower limit of dietary carbohydrate compatible with life apparently is zero, provided that adequate amount of protein and fat are consumed”.  

As you can see: on the one hand, dietary carbohydrate is needed for the brain, and on the other hand, the carbohydrate need is zero for life (thus, zero for the brain). If we had a third hand, I would like to hold in it the USDA recommendations passed on to all nutritionists, suggesting that the ideal carbohydrate intake is 45-65% of the daily Calories. For a typical 2000 Calorie diet (as it is on all food labels) this comes to 225 – 325 gr carbohydrates a day. Thus, we are told that the human body needs zero carbohydrates to stay alive, provided that fats and proteins are consumed in adequate amounts, and also that the RDA is 130 gr carbohydrates for the use of the brain that needs no carbohydrates, while the USDA recommends 225 – 325 gr carbohydrates. Major confusion! Even worse, this confusion is not well known; it goes unnoticed by almost all scientists, dietitians, and nutritionists—not to mention the general public. I would like to shed some light to the sources of this confusion, hopefully providing you with much needed clarity on this hot subject.

Let the Carbohydate War Commence

From an academic perspective the war makes a lot of sense. After all, those who have supported the high carbohydrate paradigm of the Standard American Diet (SAD) have built their careers on its credibility. Whether they themselves follow the recommendations of the SAD or not, they have a vested interest in maintaining their stand in the high carbohydrate field. Similarly, those whose lifelong research has been in the low or zero carbohydrate fields have a vested interest in sticking to their guns.

Those not members of either camp (many scientists, nutritionists, and almost all people in general) can be forgiven for feeling like spectators on the sidelines of a tennis match, during which one’s head ends up spinning from looking left and right nonstop. Many people decide to just jump head first in and test the waters to see where they end up. This causes a lot of problems because macronutrients represent life sustainment and are not up for games and self-experimentation—people can get hurt. Each macronutrient has its very specific quality. Some are necessary for the body to keep it healthy and others are not needed at all or can even be harmful. An educated choice is a better approach but beyond the above described controversy, there is much misinformation on the internet, creating further confusion.

Macronutrient Choices: What They Do and Do Not Do

There are three macronutrients: carbohydrates, proteins, and fats.

Carbohydrates

Carbohydrates are all plant matter: all fruits, vegetables, nuts, seeds, and grains. While many people think that vegetables, fruits, and whole grains are “not carbohydrates”, only sugar and desserts are “carbs”, in reality, all carbohydrates turn into sugar in our bodies. In this sense, there is very little difference between eating 4 grams of sugar from a teaspoon or 4 grs sugar equivalent from an apple or a slice of bread.

Carbohydrates can be “free glucose”, such as the teaspoon of glucose or the amount of glucose in a fruit, or they can be attached to fiber and need separation, or to other carbohydrate forms that need to convert to glucose, such as fructose, starches, galactose, or lactose. Those carbohydrates that need any type of conversion by the body into glucose are not listed as “sugar” on product labels. In general, on every food label you find sugar (free glucose), fiber, and carbohydrates. Since fibers don’t convert to sugar, to find out the total amount of sugar that will become active sugar in the body, we need to subtract fiber from total carbohydrates.

Here is an example to help you understand what I mean: take a slice of unsweetened whole wheat bread from the USDA database. You will see the following on the label and in [] are my explanations:

Carbohydrates by difference: 12.11 gr [total carbohydrates]
Fiber: 1.7 gr [both soluble and insoluble]
Sugar, total: 1.23 gr [free sugar].

We know that a slice of unsweetened wheat bread like this doesn’t taste sweet, yet, if you subtract the fiber from the total carbohydrates, the actual sugar amount in the slice of whole wheat bread is 12.11 – 1.7 = 10.41 gr. This amount truly represents everything that is either glucose or that converts to glucose in the body and not only the sweetness value the slice of bread has by its free sugar content. The actual sugar amount for the bread is 10.41 gr, or almost 3 teaspoons of sugar, in a food item that nobody considers sweet.

Every single carbohydrate item you can think of provides mostly sugar to the body in terms of macronutrients—very little protein and fat. Carbohydrates can also provide micronutrients, such as vitamins, minerals, and various antioxidants, plus fiber. However, we must remember that, according to one of the above quotes, supported by the real-life experiences of many ethnic/tribal societies and those individuals who have followed a carb free diet, carbohydrates are not essential for life at all. We can completely live a healthy life without a single slice of bread, without a single apple, or any other carbohydrates. How about the micronutrients in carbs and fiber: do we need those? The answer must be “no” if we have zero need for carbohydrates—therefore, carbohydrates are not an essential macronutrient.

Proteins

Proteins are mostly in animals and seafood. I created a table listing all amino acids—proteins are made from amino acids.

Amino Acids
Amino Acids

We have two types of amino acids: essential and non-essential. Within the non-essentials, most are glucogenic (meaning they convert to glucose), and one can be converted either to glucose or to ketones. Among the essential amino acids, three can only convert to glucose, two only to ketones, and four to either. Two questions should pop into your mind immediately: 1) Is there a reason why some of the amino acids convert to glucose and others to ketones and 2) why do we have amino acids that only convert to ketones? The answer is quite simple: the body can use two fuels for energy: glucose and ketones and it needs to have the ability to move between these two metabolic processes seamlessly. Thus, amino acids that can only be used as ketones, can be used by our body very well. The reason for some to only convert to ketones is that some cells in the body (including the brain that controls Parkinson’s disease1 and Alzheimer’s disease) work better and improve while using ketones.

Lastly, plants contain little protein compared to animal/seafood sources, therefore, those with a mostly vegetarian or vegan diet are greatly disadvantaged in the essential amino acid category.

Fats

The third macronutrient class is fats (fatty acids). Fatty acids are found is all animal sourced foods, including seafood and, in some carbohydrates—not all. Unlike carbs or proteins, all fats are essential. We typically discuss fats as saturated, monounsaturated, and polyunsaturated fats, but in reality, these three fat types are always found together in nature, so it is best to discuss fats from the perspective of what type of omega fats they are. There are several but the most well-known are omega 6 and 3. Omega 6 can be found mostly in plant-based foods and some in animal fatty acids, and omega 3 is in mostly animal/seafood sourced foods. There are three types of omega 3 fatty acids: ALA (from plants only), EPA and DHA (from animal and seafood only). The human brain is over 60% fat, much of it is DHA (EPA is a precursor to DHA) and since that is only found in animal/seafood sources, eating meats and seafood is essential. Those who get their omega 3s as ALA from carbs are in trouble, because the human body is not capable for quantity conversion of ALA to EPA or DHA. This causes some major problems for vegetarians and vegans—males and females differ slightly in conversion rates2,3.

Are We Eating Foods or Drugs?

You are thinking “how silly is this question? Of course, we are eating foods.” Hold that thought. We need to understand the hormonal connection to be able to answer the question if certain foods can be drugs. If we eat something that is not needed for our life and survival, such as a carbohydrate, what role will it play? There is a battle going on inside your body as you eat; the battle of hormones, how macronutrients affect them, and how your brain reacts to what you eat. This is currently a highly controversial topic between the two warring camps of scientists. I want to present here some of the arguments in this debate.

Let’s talk about hunger and what drives hunger considering the macronutrients we discussed—focusing on carbohydrates, the subject of the most heated debates.

A scientist colleague, Dr. David Pendergrass, describes what food is and what it does in terms of our metabolic and endocrine (hormonal) system very eloquently on his blog:

“Clearly carbohydrates are not drugs in the same way that heroin is. They are indeed nutrients. Yet they activate the dopaminergic mesolimbic pathway (so called rewards or saliency pathway depending upon the neurobiologist you happen to be talking to…), in the same way heroin, nicotine, and alcohol do. To that end…, it has drug-like capacity. The neurobiologist perspective to addiction is that down-regulation of receptors MUST occur and that withdrawal syndromes occur. Heroin and opiates are addictive under that qualification as the opiate receptors downregulate via intracellular Ca++/phosphorylation events, decreased receptor expression and receptor withdrawal mechanisms…So by this definition, carbohydrates may indeed be considered addictive because of the insulin receptor down regulation (AKA insulin resistance) that occurs with chronic hyperinsulinemia. Since insulin is considered an anorexogenic peptide, then you would need progressively more carbohydrate to induce satiety as more and more insulin is needed to bind to insulin receptors to achieve the same results. This particular description might well merit the term addiction in the down-regulation sense.

Addiction by a behavioral definition is different. It suggests that anything drugs (carbs, alcohol, sex, gambling, food) that is patently ‘bad-in-excess’ or to the point that it affects health or work or relationships and is difficult to stop, would be an addiction by psychologists. In these cases, there is neuronal reinforcement of the behavior by the compulsion. This neural plasticity is accompanied by specific changes in neurotransmitter release and receptor organization across the synapse. Indeed, increased numbers of synapses occur with such compulsions. Again, this is a function of the behavior-causing neuronal rewiring in the dopaminergic mesolimbic pathway that supports the compulsion. In this manner and definition, carbohydrates by a psychological definition would also be considered addictive.”

It is important to recognize the differences between – let’s say – opioids and carbs. The process of down-regulation, the reduction in receptors in numbers and sensitivity, takes significantly longer for carbs, allowing for the development of a chronic condition we know as type 2 diabetes, considered to be a terminal chronic disease if left untreated. Actually, type 2 diabetes can be reversed in most cases—this is a subject for another article in the future. Studies show that some foods—those with high glycemic index (GI)—seem to activate those reward pathways in the brain that are also activated by street drugs. Furthermore, ghrelin, a hormone involved with hunger and satiety is also involved with the reward brain circuit in both food and drug-induced reward mechanisms.

In any case, both with street drugs and carbs, the receiving hormone or neurotransmitter (in the brain) loses its receptors or their sensitivity to deliver the drug or carbs to the target cells4. With such identical mechanisms and ultimate consequences, eating carbohydrates suspiciously looks like an addiction. Furthermore, we must ask what makes quitting carbohydrates so difficult. Many people struggle to quit—often quitting for some time and then returning, unable to hold sweet-free life. This table, “relative sweetness value”, shows some really scary numbers. Natural sugars, such as sucrose and fructose, are significantly sweeter than glucose by taste—is sweetness the driving factor? Apparently, it may just be so5. It is worthy to note that while fructose is the sweetest of all natural sugars at 110 in relative sweetness factor, glucose is only 74, so there is a significant difference between them—compare this to lactose in milk at 16. Aspartame, a very common sugar substitute has a relative sweetness factor of 18,000! Wow! If relative sweetness value alone drove sugar addiction, then sugar substitutes would elicit an addiction as well—and indeed they do. “Intense Sweetness Surpasses Cocaine Reward.” And while my initial hunch was that since fructose has a higher relative sweetness value than glucose, it would elicit a higher reaction in terms of addiction, this is not the case. A specific scale, the Yale Food Addiction Scale (YFAS) was developed to assess food addiction.

From an evolutionary standpoint, getting addicted to something is not a good thing as withdrawal (withdrawal is a necessary component of addiction) produces weakness and works against the survival of the fittest. In the long history of human evolution, glucose/fructose were not available in big quantities, and so addiction danger was never present. This also immediately implies that because of the short/seasonal availability of glucose and fructose, it would have created an evolutionary advantage to those whose carbs cravings was strong and could gobble up all that was available when it was available. Therefore, what we now label as addiction, at one time may have had a different role and vastly different manifestation—without withdrawal—serving as a benefit to human kind. Research also found that reactive hypoglycemia (RH), a form of insulin resistance where glucose levels drop drastically after eating, initiate a different brain response from those subjects without RH. RH subjects seek higher carbohydrate and caloric content foods. In addition, there are “brakes” in the intestines and the gut area of human. Such brakes serve to cause satiety or hunger, which is based on factors of BMI, age, and gender.

Only in the very recent past have been high glucose/fructose containing foods and drinks readily available. Over-consumption of highly sweet carbohydrates don’t activate our satiety hormone (ghrelin) the same way as protein or fat does. “[G]hrelin activates an important reward circuit involved in natural- as well as drug-induced reward, the cholinergic-dopaminergic reward link”. It also appears that co-factors are involved: people with higher level of alcohol consumption may crave more sweets and those with higher consumption of sweets may crave more alcohol.

There is much more research needed to understand the exact mechanism of sugar and sweet carbohydrates cravings, though it seems clear that highly processed, fast-absorbing carbohydrates share pharmacokinetic properties with drugs of abuse. While sugar or processed carbohydrates are not likely to be classified as drugs in the near future, further evaluation for what they do to the human body is warranted, particularly given the obesity and metabolic syndrome crisis we are facing. As stated all through, carbohydrates—including both highly processed and non-processed types—are not essential for us to eat.

The biggest question we need to ask is how can something that takes up such a large percent of our caloric intake – and does so unnecessarily – be ever eliminated from our diets. Should carbohydrates be regulated by taxation and advertisement controls similarly to tobacco and alcohol? Or are we ready to continue long-term chronic disease treatments at astronomical costs because eating carbohydrates is so culturally ingrained?

Sources

1             VanItallie, T. B. et al. Treatment of Parkinson disease with diet-induced hyperketonemia: A feasibility study. Neurology 64, 728-730, doi:10.1212/01.Wnl.0000152046.11390.45 (2005).
2             Burdge, G. C., Jones, A. E. & Wootton, S. A. Eicosapentaenoic and docosapentaenoic acids are the principal products of α-linolenic acid metabolism in young men. British Journal of Nutrition 88, 355-363, doi:10.1079/BJN2002662 (2002).
3             Burdge, G. C. & Wootton, S. A. Conversion of α-linolenic acid to eicosapentaenoic, docosapentaenoic and docosahexaenoic acids in young women. British Journal of Nutrition 88, 411-420, doi:10.1079/BJN2002689 (2002).
4             Figlewicz, D. P., Bennett, J. L., Aliakbari, S., Zavosh, A. & Sipols, A. J. Insulin acts at different CNS sites to decrease acute sucrose intake and sucrose self-administration in rats. American Journal of Physiology – Regulatory, Integrative and Comparative Physiology 295, R388-R394, doi:10.1152/ajpregu.90334.2008 (2008).
5             Murray, S. M., Tulloch, A. J., Chen, E. Y. & Avena, N. M. Insights revealed by rodent models of sugar binge eating. CNS Spectrums 20, 530-536, doi:10.1017/S1092852915000656 (2015).

 

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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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