This is part 4 in a series. Part 3 - Entire series
The Science of Paleo - The Misunderstood Macronutrient
One of my general frustrations with the public policy and advocacy of nutritional information is that if nutritional advice can't be distilled down to a single sentence, it won't be able to reach and inform a wide audience, but if it does get distilled down to a single sentence, it loses so much accuracy it's not necessarily helpful. Nowhere is that more true than with fat.
Among popular understanding of nutrition and even among some nutritionists, fats are a pejorative, and we have an awful love/hate relationship with them. Bottom line is we need fat. It makes up the membranes and connective tissue of every cell in our body. It insulates us and keeps us warm. It provides protective cushion around our vital organs. And it is the most energy-dense nutritional molecule we can process. But when we carry too much excess body fat, or adipose tissue, it seems incredibly difficult to get rid of and it forebodes the onset of a plethora of diseases. Common sense and common dietary advice has for decades prescribed that if you eat less fat, you'll be less fat. The reality is not quite so simple.
While our understanding of carbohydrates, fiber, and insulin metabolism has grown quite mature, our understanding of fats and their role in various biomechanics is relatively elementary. We have identified specific functions of specific types of fats, but for the most part our understanding of dietary fat's impact on our health operates can only be described in "black box" statements -- we know that if you put this much of this kind of fat into your body, certain results are likely to follow, but we don't really know why or even if the dietary fat are causal or correlative. So even among nutrition scientists, wrapping our heads around fats and what they do means sifting through a lot of vague and contradictory black box studies. So let's do some sifting, but first I want to talk about two major health concerns that come along with fat - obesity and cardiovascular disease.
Does Eating Fat Make You Fat?
Body fat, or adipose tissue, is just loose connective tissue - cells that serve as warehouses for excess fat. These warehouses insulate the body from cold and store energy for when it's needed later. Humans store body fat in very specific areas called adipose depots. Body fat that collects under the skin (subcutaneous fat), around the abdomen protecting internal organs (visceral fat), in bone marrow, and around the breasts (yes, even in men). Women have additional adipose depots in the buttocks and thighs, due to sex hormone differences.
The simple relationship with caloric intake and body fat development basically holds true - if you consume more calories than you burn off or excrete, you'll store the excess as fat, and if you consume fewer calories than you burn off or excrete, you'll rely upon your stored fat to make up the difference. As with all things nutritional, it's a little more complicated than it seems.
First, the rate at which we burn off calories is not constant. Our rest metabolic rate shifts throughout the day depending on how much we've eaten, what we've eaten, and our body composition. Your metabolic rate is in fact the lowest when you simply don't eat - your body goes into a conservation mode and only expends the minimum base of energy necessary to keep vital organs functioning, which is why you may have heard people say that skipping a meal may not actually help you lose weight at all. Some foods require more energy to digest than others - fiber and protein require the highest amount of energy to process while dietary fat requires the least. Correspondingly, different types of tissue in your body require different levels of energy to maintain - more lean muscle increases your metabolic rate far more than adipose tissue does. so while exercise does increase your metabolic rate during exercise, it has not been shown to raise your base metabolic rate, however if your exercise includes resistance training that builds additional lean muscle mass, your base metabolic rate should go up.
Second, what you eat and when changes how your body processes those calories. As we discussed in the previous section, when your blood glucose levels rise, your pancreas secretes insulin to signal your cells to process that glucose, but at the same time that insulin signals your cells to take any fats you've just eaten and store them away in adipose tissue. Absent this insulin spike, fats will be metabolized and used as energy so much as they're needed. This is in part why obesity is so common in a high carbohydrate diet, even though it's relatively low in fat - all of those fats just get stored away.
As visceral fat buildup grows, we start to fill out around the midsection and grow a gut. Once visceral fat buildup begins, it can easily go from bad to worse very quickly - if you're slightly pudgy, it's a lot easier to get fatter than it is to get slimmer. The reason is that fatty adipose tissue also releases hormones, and visceral fat is more hormonally active than most - releasing more adipokines and resistin than other fat cells. Increased adipokines can cause glucose tolerance - glucose levels in the blood remain high despite the presence of insulin, and increased resistin can cause insulin resistance - reduced glucose uptake into cells despite high presence of insulin. High levels of glucose and insulin in turn cause you to store more fat, creating more visceral fat buildup, complicating the problem further. It's no wonder that high visceral fat amounts are very positively correlated with metabolic syndrome - cardiovascular disease, type-2 diabetes, and more.
Stress makes matters worse. When you're stressed out or panicky, your body releases a hormone called cortisol which, evolutionarily, primes your body for physical exertion anticipating the stress has a life-threatening environmental cause. If you've ever watched Star Trek, it's your body's way of calling out "red alert". Normal function shifts, and everything moves toward self-preservation. The activity of your digestive system, reproductive system, and immune system shut down. Mental acuity goes up for storage of short-term emotional events. In our modern life where stress comes from deadlines, rush hour, and bills rather than lions, tigers, and bears, these biological responses over time have sharply negative consequences. Cortisol breaks down collagen in the skin, which is why you look tired and aged when you're overstressed. And the digestive system shutdown drives your body to store energy as fat rather than consume it, which is why they say that stress can make you fat.
Cholesterol and Artery Cloggage
Another massive oversimplification comes from the dietary guidelines on cholesterol. Thirty years ago, the prescription was to simply keep your blood cholesterol level down below 200mg/dl. Around ten years ago, the prescription gained a nuance in differentiating between your HDL levels ("good" cholesterol) and your LDL levels ("bad" cholesterol).
The first problem with that is that there's really only one kind of cholesterol. Cholesterol is a kind of fat, and it's absolutely essential that your body have cholesterol. It's a critical component for making cellular membrane, bile acid, certain steroidal hormones, and certain vitamins. Cholesterol has to be transported around your body by your bloodstream, but since cholesterol is oily and your blood is water, cholesterol is not soluble in blood, so it requires a transport molecule called a lipoprotein. Lipoproteins also transport other fats around your body stored as triglycerides. The amount and makeup of the fats carried in the lipoproteins affect its density. High-density lipoproteins (HDL) are cholesterol hungry, and in the presence of excess cholesterol in cells or in the bloodstream, HDL will suck up that cholesterol and transport it to the liver and steroidal glands (like the adrenal gland, ovaries, or testes) for other uses. Low-density lipoproteins (LDL) transports cholesterol from the liver to cells around the body as they need them.
So why would having more LDL be bad? Basically, doctors and nutritionists have observed that people who have high levels of LDL and lower levels of HDL are more likely to develop atherosclerosis - the development of fatty deposits on the interior of your arteries that can cut off blood flow or release clots, causing heart attacks, aneurysms, or strokes. The fats in LDL, like many fats in the body, can become oxidized by the presence of free radicals. When oxidized LDL bounces off an arterial wall, it causes inflammation and the immune system gears up to respond. White blood cells called macrophages attack and absorb the oxidized LDL but cannot process them. The macrophages rupture, spilling oxidized cholesterol into the bloodstream. These ruptured macrophages and oxidized cholesterol are sort of "sticky", and once released they stick to the arterial wall causing further inflammation. More macrophages are summoned, and the process repeats. When these sticky foam cells accumulate in a single spot, they begin to form an atheroma. Calcium in the blood bonds to the outside of the atheroma, and a hard cap forms on the outside. The atheroma can cause sufficient inflammation to close off the artery or the atheroma can burst, releasing the hard cap into the blood stream and potentially causing a harmful clot. Since HDL is cholesterol hungry, it interrupts this cycle because it absorbs and delivers to the liver the free-floating oxidized cholesterol, reducing the risk of a cardiovascular event.
If we look at this logically though, we see there isn't a causal relationship that can be established. People who have higher levels of LDL and lower levels of HDL tend to be at higher risk for atherosclerosis. But that doesn't mean having high LDL and low HDL causes atherosclerosis, and it seems like it's the oxidation of LDL by free radicals and the inflammation of the arterial wall that is a necessary condition for atherogenesis - the creation of an atheroma. And while it may seem like common sense that increasing your dietary cholesterol increases your blood cholesterol, there has not been a clearly established causal link - and in fact in some studies raising dietary cholesterol decreased blood cholesterol.
So if we're aiming to minimize our risk of atherosclerosis, we ought to:
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... eat foods that optimize our blood cholesterol profile - higher HDL and lower LDL.
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... make sure our diet is rich in antioxidants to counter the harmful effects of free radicals.
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... make sure our diet has anti-inflammatory properties, not inflammatory ones.
Know Your Fats
Almost fats we eat are composed of three fatty acids joined by a module of glycerol to form a triglyceride molecule. But not all fatty acids are the same, and they have wildly different properties. There are seven main kinds of fatty acids, and nutrition scientists have been able to make black-box observations about their effects on blood cholesterol profile, susceptibility of LDL to oxidation and macrophage uptake, inflammatory/anti-inflammatory properties, and general risk of cardiovascular disease, and since they're black-box and subject to interpretation, I'm actually going to cite studies for your own edification.
Trans-isomer Fatty Acids
While some trans-isomer fatty acids appear in nature, the vast majority of the ones in a human diet are manufactured. An unsaturated fat (a fat not fully stocked with hydrogen atoms but instead with some double bonds remaining) is chemically processed with additional hydrogen atoms to increase its saturation to partially or fully hydrogenation. The structure of the resultant trans-isomer fatty acid, or "trans fat" for short, is more resistant to rancidification so it lasts longer without spoiling and is solid at room temperature. Trans fats were first introduced into the market in 1911, as the Procter and Gamble Company brought to market its crystallized cottonseed oil, or Crisco. The predominant cooking fat at the time was lard, beef tallow, or butter, but Crisco's inexpensive cost and longer shelf-life quickly made it a popular commodity.
However, trans fats cannot be processed by the enzymes in the body due to their unique structure. The enzyme lipase, which is essential in digestion and transportation of fats in lipoproteins, is ineffective on trans-isomer fatty acids, and so lipoproteins containing trans fats remain in the blood stream for longer periods of time, rendering them more likely to be oxidized, to deposit themselves in the arterial walls, and contribute to plaque formation. Concentrations of LDL increase with dietary trans fat intake and concentrations of HDL in the blood decrease.
It is because of the clearly and unambiguously deleterious effects of trans fats on your health that there has been such a backlash against their presence in foods. Trans fats are found in shortening and margarine - the best way to tell is to look at ingredients. If you see "hydrogenated vegetable oil", partially or fully, there are trans fats lurking within. Your diet should be free of trans-fat, if possible. There are no redeeming nutritional effects to consuming them.
Saturated Fatty Acids
Next to trans fats, saturated fats receive the most disdain from nutrition scientists, and for good reason. But it depends on what kind of saturated fatty acid. There are four we find in our diet: stearate, laureate, myristate, and palmitate. They operate on our bodies with different effects.
Palmitate is why saturated fats get such a bad reputation - seldom do you see the term "saturated fat" without the descriptor "artery clogging". Palmitate lowers HDL and raises LDL. There are many hundreds of studies all indicating the link between saturated fat and poor blood cholesterol profiles, however in the western diet, this means palmitate. Palmitate is the primary saturated fatty acid in grain-fed animals, both their meat and their dairy products. A number of studies that focused on populations with rich saturated fat content in their diet but low palmitate content found low incidences of cardiovascular disease. Palmitate is the culprit.
Stearate seems to be neutral with regard to blood cholesterol profile and beneficial at reducing unhealthy clotting. Laureate and myristate, which consists of up to 60% of the energy in the diets of certain Polynesian populations have no harmful cardiovascular effects from so much saturated fat.
So the saturated fats found in the tropics in coconut, palm, and palm kernel oil seem to be fairly neutral for consumption. The saturated fat in grain-fed meat and dairy seem to be problematic in increasing our risk for cardiovascular disease.
Monounsaturated Fatty Acids
Monounsaturated fats are healthful. Monounsaturated fats have been found to reduce LDL oxidation and inhibit macrophage uptake, which helps prevent atheroma formation. When substituted for saturated fats or carbohydrates in the diet, monounsaturated fats can combat insulin resistance and improve blood cholesterol profile. It also can reduce the risk of harmful blood clots. Numerous studies of Mediterranean diets that differ from the macronutrient makeup of the standard Western diet note that with higher fiber and antioxidant intake and with much higher consumption of monounsaturated fatty acids, incidences of cardiovascular disease are far more rare than the rest of the Western world.
I'll say again though that these are all black-box studies - they look at what goes in and what comes out with no comprehension of mechanisms or causal relationships. Most of the studies cited above substitute monounsaturated fats for carbohydrates, omega-6 polyunsaturated fats, or the saturated fatty acid palmitate. That being said, monounsaturated fats have no harmful effects and even if they themselves are not cardioprotective, they appear to be very healthful in the place of omega-6 or palmitate.
Cooking oils rich in monounsaturated fats include olive oil and to a lesser extent canola oil. Avocados and some nuts, particularly macadamia nuts, almonds, and pecans, are rich in monounsaturated fats as well. Grass-fed meats and wild game contain far more monounsaturated fats and far less palmitate than grain-fed meats.
Omega-3 Polyunsaturated Fatty Acids
There are two families of omega-3 fatty acids - the awesome kind and the rock star kind. I can't really emphasize how unequivocally good for you omega-3 fatty acids are, yet 25% of Americans get zero measurable rock star omega-3 fatty acids in their diet. Zero.
The awesome kind is alpha linolenic acid, or ALA. Alpha linolenic acid has been shown to reduce heartbeat irregularities, and heart arrhythmias are very strong predictors of cardiovascular disease. It's been positively correlated with lower risk of heart attack and heart disease. And it can be used to synthesize a limited amount of eicosapentaenoic acid, or EPA.
Eicosapentaenoic acid along with docosahexaenoic acid, or DHA (challenge: say those five times fast!) are the rock stars. They are the principal fatty acids in brain tissue, so they're great brain food. EPA and DHA are anti-inflammatory, reducing arterial inflammation and free radical action. They reduce blood triglycerides and LDL. They help prevent the formation of atheroma. There's some indication they may reduce cancer risk and neurodegenerative disease risk. I'm sure given enough time they'll be shown to create world peace and balance the federal deficit.
EPA and DHA are found in cold-water seafood like salmon, mackerel, trout, sardines, and oysters. They're also found in the muscle tissue of grass-fed animals and wild game, however grain-fed animals are nearly devoid of EPA and DHA. Depending on the chickens' diet, some eggs can be decent sources of DHA and EPA.
Omega-6 Polyunsaturated Fatty Acids
Omega-6 polyunsaturated fats are primarily two different acids - linoleic acid, or LA, which is the shorter chain and arachidonic acid (AA) which is the longer chain. The modern Western diet is far richer in omega-6 fatty acids than our paleolithic ancestors' diet - whereas it is believed our ancestors had an omega-6 to omega-3 ratio of about 4:1, some Americans' omega-6 to omega-3 intake ratio is as high as 30:1.
The evidence on the impact of LA is mixed. In a study where monounsaturated fat and alpha-linoleic acid was substituted for LA and palmitate, incidents of cardiovascular disease went down sharply. One study suggested that LA reduced the frequency of atherosclerosis but there is some question regarding the accuracy of its methods. But a definite drawback to linoleic acid is that it interrupts EPA synthesis from ALA. All in all, you're probably better off limiting your LA intake. Arachidonic acid, while necessary for cell membrane manufacture and repair, has been demonstrated to promote inflammation - its effects are reduced with greater EPA concentrations in the diet.
Omega-6 fats are very highly concentrated in vegetable cooking oils, like safflower, sunflower, corn oil, cottonseed oil, and soybean oil, however there's another major concern with cooking with these oils besides omega-6 intake. Part of the reason polyunsaturated fats can be so inflammatory is they're especially prone to oxidation by free radicals. Polyunsaturated cooking oils, when old, exposed to sunlight, or heated at high temperatures, oxidize much more rapidly, and so consuming them basically begs them to do destructive damage to your body. Saturated fats like palm kernel oil or coconut oil are much more stable, even at high heats, and so are ideal for high heat cooking and deep frying. Polyunsaturated and monounsaturated fats like olive oil or walnut oil should only be used for medium temperature cooking -- no more than about 375 degrees.
Fat Selection by Food Selection
In summary, it seems like we want to ensure we get plenty of EPA and DHA in our diet, some measure of ALA, and fill the rest with monounsaturated fats and non-palmitate saturated fats. We want to limit our omega-6 intake and come as close as we can to eliminating trans fats and palmitate from our diet. Doing that should maximize our cardiovascular health and minimize our body's inflammatory responses. So what should we eat?
It sounds like we should avoid grain-fed meats, grain derived oils, and certain seed oils. Other oils offer more tangible benefits like olive oil, avocado oil, coconut oil, palm kernel oil, or grass-fed animal fats. We want to include cold-water seafood without incurring risk of mercury poisoning and pastured, grass-fed meats. Eating the right seeds and nuts also seems like good ways to balance out our fat profile.
Surprise, surprise - it's what our paleolithic ancestors would have done. And to reiterate once more, you can optimize your body's metabolism of fats by defending against harmful insulin spikes caused by too high of a glycemic load - doing that will ensure that your body burns the fats you eat instead of storing them.
Ketosis
Following the general prescription closely - minimizing foods rich in carbohydrates, maximizing foods rich in fiber, protein, and fat - will shift the very basis of your body's metabolism. Your body will switch from glycolysis (use of stored carbohydrate derivatives as its primary energy source) to ketosis (use of fatty acids as its primary energy source). Ketosis is not uncontroversial. Mainstream nutritional dogma believes ketosis to be the body's "starvation" mode as it turns to fat in the diet and in adipose tissue to find the energy it is not getting through carbohydrates in the diet. It is often argued that long-term operation in ketosis is unhealthful, but there has been no laboratory evidence of that. Furthermore, some hunter-gatherer cultures have existed almost entirely on ketosis with no noticable impairment of health or function.
The Paleo Challenge we underwent these last five weeks had the goal of inducing a ketogenic state. We deplete our bodies of glycogen and function primarily off of fat.
When the cells in the body have stored sugars (glycogen), the energy production system (Krebs cycle) burns that stored glycogen. Absent carbohydrate influx into the diet, those glycogen stores will be used up. The body then cleaves fat, both ingested and stored as triglycerides, into acetyl-coenzyme A which can also be fed into the Krebs cycle bound to oxaloacetate. In the presence of excess acetyl-CoA, the liver morphs them into chemicals called ketones. The brain cannot use fatty acids directly for energy, but it can use ketones. The brain converts the ketones back into acetyl-CoA for the brain to use for energy.
What this means is that the first two weeks aiming for ketosis suck. The brain takes awhile to adapt to using the ketones for energy as opposed to using them for fat synthesis, and during that time it runs as if it's low on fuel. We felt sluggish, spacey, grumpy, and less mentally acute. Our bodies had a tough time too - we had a harder time with strenuous exercise and we had a few rough nights of poor sleep. After those first two weeks, however, we felt perfectly fine on ketosis. Our mental acuity returned, our energy levels returned to normal, and our bodies functioned at a more regular, constant metabolism throughout the day.
That's not to say I recommend ketosis for everybody. It has its benefits, and from looking at my peers who also took the Challenge, ketosis led to some impressive instances of weight loss. But I fully recommend you do your own research and talk to a physician or dietician before considering aiming for a ketogenic state.
Continued in part 5: So what the hell do I do?