What do epigenetic food choices look like in our everyday lives? In this chapter I want to explore protein, fat, and cholesterol. In chapter 17 we’ll look at sugar, and in chapter 18 we’ll discuss wheat and gluten. And we’ll find that the conventional advice is not always supported by science.
Let’s begin with protein. As we saw in chapter 15, the right protein choices positively affect the environment around our cells, and thus our health. We all probably learned in school that proteins are the building blocks of our cells: protein’s vital role is to build, maintain, and repair all our bodily systems, and it is necessary for growth and development throughout our life. We may also remember that protein is broken down in the body into amino acids and fats, which both our brain and the rest of our body need to thrive.1 Amino acids are actually the building blocks of proteins. Everything from our bones to our organs, muscles, arteries and veins, skin, hair, and fingernails is made of protein.2
In fact, we have around eight billion (8 x 109) proteins per cell.3 Proteins called hemoglobins help carry the oxygen that reddens our blood.4 Enzymes that digest our food, synthesize essential substances, and break down waste products for elimination are all proteins.5 Proteins produce the energy needed for life when fats and carbohydrates are in short supply during times of starvation.6 Proteins and steroids form hormones, which regulate the delicate chemical changes that constantly take place within the body governed by the endocrine system.7 Our chromosomes have proteins in their structures. Protein is like a vehicle that “drives” fat and cholesterol throughout the body.8
To say that protein is an important nutrient is certainly an understatement. And, as with most nutrients and vitamins, too much, too little, or poor-quality protein in the diet will have detrimental effects on our physical health.9
Your Brain on Protein
Your brain thrives on good-quality protein sources. It needs protein for neurotransmitter activity, since many of your internal chemical messengers consist of amino acids, amino acid derivatives, and small proteins that are built from amino acids, known as peptides.10 Neurotransmitters enable the brain cells (neurons) to “talk” by relaying information between them.11 Adrenaline, noradrenaline, and dopamine are made from the amino acid tyrosine.12 These neurotransmitters make you feel good, stimulate you, motivate you, and help you cope with stress.13 GABA, derived from the amino acid glutamate, on the other hand, counteracts these neurotransmitters, relaxing you and calming you down after stress.14 Serotonin is another important neurotransmitter, made from the amino acid tryptophan, that keeps you emotionally balanced.15 Melatonin, also derived from the amino acid tryptophan, is crucial in establishing the sleep/wake cycle.16 Endorphins are peptides (small proteins) and act at opioid receptors and therefore modulate pain.17
Neurotransmitters carry electrical signals across synapses, the gaps between nerve cells, thereby delivering chemical messages from one cell to the next.18 This inter-cell interaction is what it means to build short-term memory.19 And once a neurotransmitter has delivered a chemical message, it is released back into the synapse, which is like a swimming pool filled with an electrical-chemical cocktail. The neurotransmitter is recycled, reabsorbed, or broken down.20
A deficiency in amino acids affects your neurotransmitters’ ability to have these meaningful conversations. It can make you feel flat, apathetic, and unable to relax; lacking in motivation, focus, and concentration; and unable to build solid memory.21 Clearly that is not a desirable situation for your brain!
On the other hand, sufficient amounts of good-quality proteins in your diet, and thus amino acids, help with mental health issues.22 These amino acids are more effective than prescription drugs—most of the latter have awful side effects.23 When Hippocrates said “let food be thy medicine,” he truly hit the mark, since a healthy, balanced diet of real foods can keep both your brain and body in shape by ensuring that you receive an adequate intake of amino acids.
Of the twenty amino acids needed for proper construction of proteins, eight (or nine, for children) are called essential amino acids, since the body cannot synthesize or make these for itself.24 These essential amino acids must come from our diet.25 Good-quality animal proteins, such as grass-fed, organically raised beef and eggs from pasture-raised hens, are excellent sources of these amino acids.26 Many of these essential amino acids are also found in plant-based proteins, such as soybeans, quinoa, seeds, nuts, beans, rice, and legumes. These plant-based proteins are incomplete sources of all the amino acids and need to be eaten in combination with other foods in order to maintain good health.27 Brown rice and lentils, for example, combine to give us a complete protein source.28
Another important point to note about meat is how much muscle meat we consume, and the impact this has on our bodies. Muscle meat has large amounts of the amino acid methionine, which produces the toxic by-product homocysteine.29 Even though meat is a good source of vitamin B12,30 our body uses up vitamin B12, as well as vitamin B6, folate, choline, and betaine, to neutralize the homocysteine. If we consume excess amounts of muscle meat, we can reduce the amount of these vitamins in our body, which are essential to the proper functioning of many biological processes.31 Indeed, high amounts of methionine can decrease the level of glycine in our body, which is another essential amino acid predominantly found in the skin, bones, cartilage, and organs of the animal. An imbalanced methionine-glycine ratio can have negative health effects on our mental and physical health, potentially increasing our risk for mortality.32
Our obsession with muscle meat is actually a recent historical phenomenon. In the past, the sections of animals we prize most today, such as muscle cuts like sirloin steak, were often thrown away or fed to the dogs, while the animal bits we have deemed less culturally pleasing, such as eyes, kidneys, bones, and feet, were treasured for their life-sustaining properties.33 Even in nature, many carnivores leave behind the muscle meat in favor of the more nutritious parts of their prey.34 Although eating these parts of the animal may sound unappealing, if you do eat meat, and want to do so in a healthy and balanced way, try slowly incorporating them into your diet in blended soups, bone broths, and stews.
The bottom line with protein: get enough high-quality protein without overdoing your servings of muscle meat. Consider plant proteins, eggs, and organ meat, and look for grass-fed beef and pasture-raised poultry.
Cholesterol: Scapegoating the Scarecrow
The subject of eggs and meat leads us inevitably to a discussion of cholesterol. It is a rather unfortunate truth that “science advances one funeral at a time.”35 Many individuals today equate the consumption of animal protein sources with cholesterol levels and a higher risk of mortality. Yet, while the cholesterol and heart disease hypothesis has gained much ground culturally, with the low cholesterol and “heart healthy” labels on food in grocery stores around the world, the science of cholesterol has regressed into a game of broken telephone. The original data in this area of nutrition, with its imprecise correlations, has been lost in a sea of interpretations and so-called facts: high cholesterol levels are bad news.36 How could anyone possibly argue otherwise?
Today the terms LDL cholesterol and HDL cholesterol are bandied about with such ferocity that it certainly is useful to stop and ask yourself what exactly they mean. LDL and HDL are lipoproteins that carry cholesterol around your body—they are not cholesterol. LDL is the “vehicle” that carries cholesterol to the cells, and HDL takes excess cholesterol away from the cells.37
Cholesterol itself is mainly synthesized by the liver. It is essential for the production of hormones, vitamin D, bile acids for food digestion, and cell membranes, to name just a few of its beneficial functions.38 It even acts as an antioxidant, combating the damage done by free radicals in the body. One of the major flaws in the cholesterol/heart disease hypothesis is the assumption that cholesterol, observed at sites of damage in the body, must somehow have caused that damage. As an antioxidant, however, cholesterol is a vital part of the healing process, not the cause of the damage!39
Of course, vitamins, antioxidants, and herbs do reduce cholesterol levels in the body. Yet these substances do not fight and destroy cholesterol as a malignant substance—they take over cholesterol’s role as an antioxidant.40 If you decided to take out the garbage at home, instead of your spouse for instance, your husband or wife is not the “bad guy” by default. It is the same with cholesterol: a decreased amount of cholesterol does not mean that cholesterol is unhealthy; it merely means someone else is taking out the trash.
In most cases, the body does a very good job all on its own of balancing cholesterol levels.41 We have all been led to believe, for example, that eating a piece of steak will raise cholesterol levels. However, this is not necessarily the case. The liver will simply reduce its cholesterol production in response to signals from the digestive system, thereby maintaining the correct cholesterol balance that the body needs.42
Similarly, neither LDL nor HDL is intrinsically unhealthy.43 The problem comes in when you upset the balance of the system. An “accident” in your body keeps LDL in your bloodstream, preventing it from reaching the cells, much like an accident during rush hour will prevent you from getting to work—you are stuck in the resulting traffic jam. During this time, the LDL oxidizes and is now seen as a threat (think of those individuals who get irritated in traffic and develop road rage), which kicks your immune system into action and can contribute to plaque buildup inside the blood vessel walls, which leads to heart disease. Essentially, the biological processes associated with cholesterol are a lot more complicated than merely good and bad cholesterol.44 Just as there is no magic bullet for health, there is no one “bad guy” to point out in terms of disease.
Death by Low Cholesterol?
Limiting your cholesterol intake can actually lead to physical and mental ill health, as well as early death.45 According to a growing body of research, low levels of cholesterol are associated with decreased cognitive performance,46 increased mortality risk,47 increased risk of cancer,48 less emotional stability and control,49 a greater chance of developing depression,50 an increased suicide risk for certain parts of the population,51 a higher risk factor for hemorrhagic stroke,52 and a decreased ability to fight infection.53
The brain, in particular, needs cholesterol. Despite the fact that your brain makes up just 2 percent of your body weight, it uses 25 percent of your free cholesterol.54 Cholesterol is an essential nutrient for neurons and a building block of the cell membrane.55 When cholesterol levels are low, the brain does not work very well: adequate cholesterol levels improve mental cognition.56
The Big Fat Myth?
So how exactly did cholesterol become the evil Professor Moriarty of nutrition research? One of the key figures behind the diet-heart hypothesis that dietary cholesterol can lead to cardiovascular disease was Ancel Keys.57 Building on earlier experiments carried out by Russian scientist Nikolai Anichkov, who researched the dietary patterns of rabbits and concluded that cholesterol in the blood leads to heart disease (otherwise known as the lipid hypothesis), Keys concluded from his own studies that saturated fat consumption leads to increased cholesterol levels, which in turn leads to an increased risk of cardiovascular disease and heart-related mortality.58
Keys’s research, however, was far from conclusive. The 1950s informal Six Country Analysis,59 which compared a country’s overall amount of saturated fat available for consumption and heart disease levels, began by excluding data from a number of the countries—argued by many to be a classic example of publication bias. What would his results have looked like if he had used the data from all the countries he examined at the start of his research? When he chose to exclude the other countries, what did he mean by their lack of “fully comparable dietary and vital statistics data”?60
Yet despite this missing data, Keys’s actual observations do not equal causation, regardless of how many times they are repeated in government policy, media sources, clinical offices, scholarly establishments, and academic sources. In fact, when all the data was analyzed by two of Keys’s contemporaries, an entirely different observational conclusion emerged: saturated fat consumption decreased the risk of overall mortality (in terms of death unrelated to heart disease).61
Keys’s Seven Country Study, a cohort-based research project that follows groups of individuals over time, began in the late 1950s and continues to this day. Like the Six Country Analysis, this study has its limits. It is based on observational data, and, while there has been a correlation between saturated fat intake and heart disease, it is by no means an unambiguous one. For instance, participants in Italy, Croatia, Serbia, and Japan did not experience an increased risk of heart disease with higher cholesterol levels. On the other hand, the cohorts with the highest levels of cholesterol (American railroad workers) did experience a rise in heart-related disease and mortality. Based on this study, it therefore appears that cholesterol is not always an alarm bell—it depends on the context. Instead of blacklisting cholesterol, researchers should try to determine what makes these populations particularly susceptible to heart disease.62
In fact, the cholesterol witch hunt that has taken place over the last several decades has actually hidden a number of important findings in the Seven Country Study. For instance, a 2002 paper noted that lower LDL levels were associated with an increased incidence of depression among the older groups. Moreover, like the Six Country Analysis, individuals with higher cholesterol levels actually lived longer than the cohorts with lower levels of cholesterol, who were actually at a greater risk of developing cancer. Nevertheless, Keys’s studies have become the foundation of the diet-heart hypothesis, despite the lack of conclusive clinical evidence to support it.63
Indeed, even the renowned Framingham Heart Study, another cohort-based research project that began in the mid-twentieth century to examine the causes of heart disease and continues to this day, does not support the diet-heart hypothesis.64 According to one of the lead researchers, “There is, in short, no [overall] suggestion of any relation between diet and the subsequent development of coronary heart disease.”65 Indeed, according to a pattern that began to emerge by 1997, limited saturated fat intake may in fact result in an increased risk of cognitive decline and cancer.66 These findings are similar to the overall mortality results of the Six Country Analysis and Seven Country Study discussed above and highlight the critical need for more research to be carried out on the long-term effects of decreased saturated fat consumption and the relationship between saturated fat intake and cholesterol.67
The Good, the Bad, and the Ugly Fats
Your body needs fat for all its processes, as does your brain.68 Fats protect you from disease; aid the absorption of fat-soluble nutrients such as vitamins A, D, E, and K; control inflammation; help with blood clotting; balance your mood; make you more focused; and can maximize your intelligence through improving cognitive function, to give just a few examples.69 In fact, your brain is around 60 percent fat—without fat in your diet you cannot think or build memory correctly.70
Fats come in several different forms: saturated fats, monounsaturated fats, polyunsaturated fats, and trans fats.71 Saturated fats have no double bonds in terms of their chemical makeup and are found predominantly in animal products and tropical oils (such as coconut or palm oil). Monounsaturated fats, which consist of one double bond, are found in nuts, seeds, olive oil, and avocados, for example. Polyunsaturated fats have two double bonds and can be found in animal products, nuts, seeds, and many different kinds of oils. Trans fats, or hydrogenated fats, are mainly found in highly processed and refined foods, such as margarine, fast food, and heated oils. Food sources generally have varying combinations of these types of fats.
A simple internet search of fats will inevitably come up with a list of sites noting the same warnings. Saturated fats are principally associated with trans fats in the scientific “naughty corner” because they are said to raise blood cholesterol levels and lead to heart disease, while mono- and polyunsaturated fats are “good fats” that form an essential part of a balanced diet. Yet, as I discussed above, both unoxidized LDL and HDL cholesterol play a vital homeostatic role in many of the biological functions of our brain and body. Indeed, reduced cholesterol intake has been associated with increased overall mortality, increased risk of stroke, and cognitive decline in the studies mentioned above.72 It is unclear, based on the evidence pool we currently have, if a diet high in unoxidized LDL and HDL cholesterol and low in saturated fat will achieve the same benefits or be more detrimental.
Yet even if you are especially worried about saturated fat intake, you do not have to give up animal products. Wild game meats like venison have a significantly reduced saturated fat content compared to modern, industrial-based sources of meat, eggs, and dairy, and even compared with domestic grass-fed animals. However, grass-fed domestic animals like lamb and beef have a significantly higher concentration of a particular kind of saturated fat, stearic acid, as opposed to conventionally raised beef. Stearic acid does not raise cholesterol levels (not that we should be particularly concerned with cholesterol per se, as I discussed above, but rather the context of cholesterol) compared with the two other types of saturated fat: palmitic and myristic acid.73 Animal livers and shellfish (if you are not allergic!) are also low in fat but are excellent, concentrated sources of essential fat-soluble nutrients such as vitamins A and K.74 Since all these naturally raised meat sources are nutrient dense, a little goes a long way in terms of their health benefits.75
In fact, animal foods that contain saturated fat play other important roles in human nutrition. For example, some individuals cannot effectively turn beta-carotene, found in vegetables such as sweet potatoes, for instance, to vitamin A (the two are not interchangeable, contrary to popular opinion) in the body due to their genetic makeup and other environmental factors, such as food allergies.76 Similarly, there are two types of vitamin K.77 Vitamin K1 is found in dark green leafy vegetables and other plant-based foods, while vitamin K2 is found in animal products.78 Due to genetic factors, a large number of people cannot benefit from K1 alone.79 How will the health of these individuals fare if they reduce or eliminate all animal sources that contain saturated fat from their diet? Indeed, since animal fats are one of our best sources of these essential fat-soluble nutrients, how will the health of mankind in general fare if we remove them entirely from our diets? Not only do these animal fat sources contain essential vitamins but they also increase the absorption of fat-soluble vitamins in other foods, such as vegetables and fruit.80
In terms of fat-soluble nutrients, the observations of Weston A. Price, a dentist and researcher who spent years traveling and researching the various diets of populations around the world, are particularly interesting. He noticed that it did not matter what kind of foods the different people he came across consumed, whether they ate what we consider a “low-carb,” “high-carb,” or “high-fat” diet, as long as they ate a diverse traditional diet based on their respective locations. Yet a similar characteristic of all the healthy populations he observed was the intake of fat-soluble vitamins in animal foods, such as organ meats, eggs, seafood, dairy products, and small animals and insects. Ultimately, the exact amount of animal fat the populations ate did not matter as much as the fact that they ate these types of foods, and therefore consumed concentrated sources of the essential fat-soluble vitamins needed for the maintenance of good health.81 Yet as soon as the native populations made the “nutrition transition” to the current Western diet of unvaried, processed, and refined foods, their health suffered as a result, with an increase in the incidence of chronic illnesses such as diabetes and heart disease.82
Throwing (Polyunsaturated) Fat onto the Fire?
There is also a potential health risk in replacing dietary saturated fats with polyunsaturated fats (PUFAs) for the long term. Most famously, the randomized and double-blind 1969 LA Veterans Heart Study, which followed 846 elderly veterans for up to eight years, found an increased risk of cancer over time among the group that consumed four times more PUFAs than the control group, who ate a typical American diet.83 Apparently, nutritional science now tells us it is a matter of picking our demise: Would we like a side of heart disease, or cancer, with our fat?
And if this study is not perplexing enough, the several major research projects that are predominantly used to support an increased consumption of PUFAs are subject to a number of scientific difficulties. Although the 1968 Oslo Heart Study found a reduced rate of cholesterol and heart disease in the experimental group, which consumed more PUFAs, they gave this group far more attention compared to the control. For example, the experimental group, unlike the control group, were handed more than just a general multivitamin: they had to decrease their added sugar consumption, decrease their trans fat intake, increase their fish consumption (and therefore omega-3 intake), and exchange white bread for brown bread, among other requirements. 84 All of these changes can have positive health effects! How much of the reduction in cholesterol levels and mortality rates from heart disease in the experimental group can be attributed to saturated fat alone? We don’t know; all the other changes made in their lifestyle habits could be equally important.85 At best, this study shows that lifestyle factors can play an important role in the risk of heart disease, as does the St. Thomas’s Atherosclerosis Regression Study (STARS) trial and the Diet and Reinfarction Trial (DART 1), both of which made a number of other changes unrelated to dietary fat (such as an increased consumption of fruit and vegetables) to their participants’ diets.86 The “background noise” of these variables makes it impossible to draw the conclusion that reduced saturated fat intake is healthy.
The 1972 Finnish Mental Hospital Study (1972), however, was particularly shocking for its lack of control.87 For instance, a number of the participants in the trial were on thorazine, an antipsychotic drug that can cause heart problems such as arrhythmia. Considering the study was attempting to find out if PUFAs were a suitable alternative to saturated fats in terms of heart disease, the presence of an uncontrolled variable with the potential to increase cardiovascular disease and heart-related death is not really a clever idea, to say the least.88
What is more, several meta-analyses that have examined the relationship between dietary fat in general and heart disease highlight the lack of certainty in this area of nutrition. A 2009 systematic review of randomized control trials (RCTs), the most rigorous and reliable form of trials in medicine, for instance, noted that there was “insufficient evidence” for a link between saturated fat consumption and cardiovascular disease.89 Likewise, in 2012 the Cochrane Collaboration, an independent and not-for-profit scientific research organization whose reputation for high-quality and unbiased data is exceptional, noted that there are “no clear effects of dietary fat changes on total mortality . . . or cardiovascular mortality.”90 The 2010 systematic analysis on dietary fat and heart health that did favor a reduced saturated fat intake strangely included trials like STARS, DART 1, the Oslo Heart Study, and the Finnish Mental Hospital Study discussed above, which in all likelihood skewed their data in favor of PUFAs.91
Anthropological data also suggests that keeping your PUFA intake to a minimum can be beneficial in terms of heart disease. For example, three Pacific island populations (the Pukapuka, Tokelau, and Kitava) with varying carbohydrate, fat, and protein intakes all had almost no incidence of heart disease, despite the fact that they did not eat the same kinds of diets. Yet regardless of the culinary diversity among these three populations, all of them maintained a fat ratio that predominantly kept PUFA intake to around 2 percent of their fat intake, while saturated fatty acids were their main source of fat. From this observational data, it appears that the amount of fat you consume is not as important (in terms of heart disease) as the ratio of your saturated fat to PUFA intake.92
This Is Your Brain on Saturated Fat?
It is not any more “certain” that saturated fat intake causes cognitive decline. In 2012, the media were quick to sensationalize a study that linked saturated fat to mental issues. The researchers, after examining the dietary fat intake of more than six thousand elderly women over a period of time, noted that higher saturated fat intake was “associated with worse global cognitive and verbal memory trajectories.” Yet, once again, this study was observational, and only examined one population group: mature women. Its conclusions cannot be applied to the population in general.93 Most significantly, the results are correlational in nature—this study does not indicate cause and effect.94 You cannot say that it is now a proven fact that eating a steak will give you heart disease and brain damage to boot. It would be nice and simple if science worked this way, but it does not.
Higher fat intake has actually been associated with increased mental wellbeing. For instance, in a recent study carried out by the Mayo Clinic, there was a reduction in the risk of developing dementia among the group that consumed a diet high in saturated fat.95 And, as I discussed above, lower cholesterol levels have been associated with decreased cognitive performance. Adequate amounts of “good” cholesterol are incredibly important for healthy nerve transmission.96 Your brain cannot communicate very well without this nutrient, a finding supported by a recent paper published in the Journal of Biological Chemistry. In this study, dietary cholesterol intake was an important factor in the prevention of amyloid plaque buildup, which can contribute to the development of Alzheimer’s disease.97 Considering how saturated fat is actually one of the main components of brain cells and how significant cholesterol is in terms of brain health as demonstrated by the studies examined above, cutting them out of your diet may have deleterious effects on your overall health.
It is also important to remember that eating foods high in saturated fat does not equal skyrocketing saturated fat levels in the blood. In a 2014 study published by Ohio State University, for example, participants who remained on a diet high in saturated fat did not necessarily have higher levels of saturated fatty acids in their blood. Rather, it was an increased intake of carbohydrates that increased the level of saturated fat found in the blood, potentially increasing the risk of heart disease and diabetes.98
Of course, the fact that this study was financially supported by the meat and dairy industries does highlight a potential publication bias, yet the urgent need to change our overly simplified understanding of saturated fat and cholesterol is corroborated by several other papers.99 According to one recent Finnish study that examined the dietary habits of children, the quality of carbohydrates consumed appears to be as important as saturated fat intake in terms of the fatty acid composition in our blood.100 In another study, elderly subjects were assigned to one of two dietary groups: one group ate three eggs per day and the other ate the same amount in egg substitutes for a one-month period. There was a significant increase in both LDL and HDL cholesterol for those who ate eggs, but the ratio between the two was not affected significantly. In other words, if the LDL cholesterol went up, the HDL cholesterol did too, thereby counteracting the effect of higher LDL levels.101 Indeed, in an eight- to fourteen-year follow-up study of around thirty-eight thousand men and eighty thousand women at Harvard University, there was no statistically significant difference in risk for heart attacks and strokes among people who ate eggs less than once a week compared with those who ate more than one egg per day.102
Along with organ meats, eggs contain high-quality protein and are the richest source of phospholipids in average diets, have all the essential amino acids in the closest thing to a perfect ratio, and are a great source of choline (a B-complex vitamin needed for transmission of electrical charges across synapses, thereby improving memory), while the egg’s lecithin is a good “bad cholesterol” lowering agent.103 Eggs, as long as they are treated the way God intended (that is, the laying hens are pasture-raised without the use of synthetic chemicals or hormones), are literally a superfood that can lower cholesterol!
Too Many Researchers Spoil the Broth?
What do all these studies on fat and cholesterol ultimately tell us? Eating saturated fat–containing foods like eggs can potentially raise your cholesterol, but can do so in a way that maintains a healthy cholesterol balance in your body. Cholesterol acts as a nutrient in the body, as does saturated fat. Eating saturated fat, however, does not always raise your cholesterol levels. Even if saturated fats may raise your cholesterol levels, they can do so in a way that maintains a healthy balance of LDL and HDL cholesterol in the body. Carbohydrates can also increase the level of fatty acids in your blood.
As Dr. Fred A. Kummerow, a leading researcher on cholesterol, notes, “You do not need a source of cholesterol to develop heart disease.”104 Your cholesterol levels will even change according to the amount and types of protein you consume, and the amount of calories you consume in general—from any food source.105 I think it is quite safe to say that we need to reexamine the overly simplified understanding that saturated fat will raise your cholesterol and potentially kill you.
What Is the “Fat” of the Matter?
Ultimately, Keys’s diet-heart hypothesis, much like Norman Borlaug’s wheat-breeding experiments discussed in chapter 6, was a notable, if imperfect, achievement for its time.106 Yet it should be the start of our expeditions into the world of nutrition, not the end of them. It should be transformed by our growing understanding of nutritional information; it should not constrain the way we carry out nutritional science.
The diet-heart hypothesis is not infallible. It was built on a foundation of animal experiments, the results of which cannot be relied on as conclusive evidence in terms of human health, and observational studies with correlations that are often interpreted, dangerously, as cause and effect, which were supported by physicians with little or no training in biochemistry at the time.107 In fact, the lipid hypothesis discussed briefly above originated from an experiment that fed animal fat to rabbits, which should also strike our logical alarm bells, so to speak. God never created rabbits to eat meat or dairy or any other animal products; of course they will have an adverse reaction to eating such foods.108 Needless to say, humans are not rabbits. We cannot merely copy and paste the results of this experiment onto humans. Just as the absence of harm does not equal the presence of safety (in terms of what we consume), the presence of safety does not always equal the absence of harm in terms of real life, such as the differences between species and types of saturated fat.109 Research is a little bit more complicated than that.110
We essentially have to remember that nutritional science is almost “impossible to do,”111 as we saw in part 1. By singling out lone entities like saturated fat, we forget the context of real-life food consumption.112 Saturated fat in real, whole foods plays an important part in a healthy, balanced diet, as the studies above indicate, not to mention the other health benefits of these saturated fat–containing foods.113 On the other hand, even a small increase in saturated fat intake may be the straw that broke the camel’s back (or heart, in this particular context) if we have grown up on the MAD diet or eat a diet that is dominated by refined and processed foods, as one recent review indicates. In these cases, it could possibly be wise to decrease saturated fat intake while transitioning to an unprocessed, whole food diet, or it could do more harm than good.114
The key is not to focus solely on individual pieces of the puzzle like saturated fat or cholesterol. We need to look at the bigger picture: Are you eating real food? As a 2015 meta-analysis by the BMJ noted, official US and UK low-fat guidelines were not supported by strong randomized control trial evidence in the 1970s and the 1980s, and the subsequent vilification of saturated fat has obscured the complex interplay between the human diet and disease, including the role carbohydrates play in health.115 Ultimately, fearing fat, just like fearing carbohydrates or gluten or sugar, is not the right way to approach a healthy diet.116 Instead, we should fear the way our current industrial food system has transformed our foods into food-like products.
Artificial Trans Fats: The Real Public Enemy
By avoiding the MAD diet, we actually avoid the one fat that we cannot tolerate as human beings: the artificial trans fatty acids found in foods such as margarine and processed vegetable oils like canola and soybean oil.117 These trans fats are hydrogenated fats produced by the overheating and refining of oils, and are abundant in heavily refined and processed food-like products such as fried and industrially prepared pastries, pizza, pies, cookies, chips, crackers, cereals, breads, and drinks.118 In fact, they are present in an estimated three thousand products in food establishments today, even products with the “0g Trans Fat” label. Government regulators allow the food industry to put minimal amounts of trans fats in their products, and thus “0g Trans Fat” can contain up to 0.5g of trans fats.119 However, as many health authorities note, the only safe amount of trans fats in the diet is no trans fats.120
On the other hand, many of these same health authorities note that we need to avoid butter, since butter contains not only saturated fat but also trans fats. However, this is an oversimplification of the biochemistry of natural versus artificial trans fats. Unlike the naturally occurring trans fats in butter, these commercial fats have migrated double bonds, which have created fourteen artificial types of trans fats.121 As a result, they do not provide any nutritional benefit and are stored in the body, inhibiting the creation of prostacyclin, which is necessary for blood flow and the prevention of cardiovascular disease.122 In fact, trans fats increase the amount of oxidized LDL in the blood, which can lead to heart disease and can cause memory problems.123 And these are just a few of the major health dangers associated with the consumption of artificial trans fats. Again, it is not the food per se; it is what we have done to the food. God created fat; we have changed the wired-for-love form of God’s creation.
Research on the dangers of industrial trans fatty acids, in particular their link to heart disease, began appearing in the scientific literature in the 1950s, pioneered by the aforementioned biochemist Dr. Kummerow.124 However, only recently has the FDA decided to take notable, if slow, measures against the use of trans fats in food products—predominantly due to the activist efforts of the remarkable Kummerow, who is a hundred years old and still doing research as I write this.125 The FDA’s hesitation was in many ways a result of the food industry, which needs trans fats to make its products taste good and store well.126 Needless to say, it does us good to remember that official dietary recommendations are not always reliable, based on the latest scientific research, or bias-free—and should never just be taken at face value.127
The bottom line: avoid trans fats by avoiding fast foods and prepackaged foods, including margarine and shortening. Now let’s apply this same type of research-based reasoning to a big problem in the MAD diet: sugar.