The Primal Blueprint (18 page)

The
Primal Blueprint
eating philosophy might seem a little unusual at first for those trying to do the right thing by Conventional Wisdom. After all, here’s a plan that suggests that most fats are not bad at all. In fact, pundits might describe the
Primal Blueprint
as a high-fat, moderate protein, fairly low-carb diet—particularly in comparison to the exceedingly high-carb diet that has been recommended for years by the USDA Food Pyramid, American Heart Association, and American Medical Association.

We now know that these and other experts’ outdated and never proven suggestion to essentially eat 300 or more grams of carbohydrates each day has contributed greatly to the destruction of human health. It’s not unusual for an average American to consume 500 or 600 grams of insulin-generating, fat-storing carbohydrates daily. Keep in mind that Grok and his clan probably worked hard to gather an average daily intake of
only 80 to 100 grams of carbs, most of which came from fibrous natural vegetables and fruits. By averaging between 100 and 150 daily grams (certain extremely active folks may adjust this upward, which I’ll discuss later) of vegetable- or fruit-sourced carbs, you can achieve optimally low levels of insulin, enjoy stable energy levels, and easily reduce excess body fat and keep it off. If you want to accelerate your fat loss for a period of time, lowering your average carb intake to 50 to 100 grams or less per day will allow you to easily drop an average of one to two pounds of body fat per week. We will discuss this strategy in detail in
Chapter 8
.

Sitting down again? Here’s another zinger that will blow your mind and set you straight from all the confusion and conflicting information about what the secret to weight loss and long-term body composition success really is.…

Eighty percent of your ability to reduce excess body fat is determined by how you eat, with the other 20 percent depending on proper exercise, other healthy lifestyle habits, and genetic factors
.

It’s as simple as this: if you have excess body fat, it’s directly reflective of the amount of insulin you produce from your diet combined with your familial genetic predisposition to store fat. In plain-speak, if you eat like crap and have bad (genetic) luck, you’ll get fat and sick and you’ll probably die early. On the other hand, bad diet and good luck (having the “skinny gene”) might allow you to avoid a plump figure but also might result in a physique that I call “skinny fat”—having minimal subcutaneous fat, minimal lean body mass, and poor muscle definition but still having dangerous amounts of visceral fat surrounding the organs.

Furthermore, skinny fat folks can and do get heart disease, hypoglycemia, arthritis, sarcopenia (loss of muscle mass), chronic fatigue, compromised immune function, and a host of other adverse health consequences heavily attributed to diet. A slender type 2 diabetic can experience an even greater risk for serious disease, because he or she is less able to activate the so-called thrifty genes that efficiently store excess dietary glucose in fat cells (sort of a “toxic waist site” where it’s relatively harmless in comparison with glucose that floats around in the bloodstream causing intense cellular damage). While the outward visibility and overall impact severity of poor lifestyle habits vary widely due to luck of the draw, we all share an evolutionary genetic predisposition to suffer chronic disease when we eat foods that are misaligned with our genes.

On the positive side, your ability to reduce excess body fat and maintain desirable body composition is directly reflective of your ability to moderate insulin production with healthy dietary habits and, to a lesser extent, your willingness to follow a sensible exercise program that combines extensive low-level cardio; frequent short, intense
strength-training sessions; and occasional all-out sprints. Even if you have struggled with excess body fat for your entire life, you can quickly and dramatically alter your destiny by following the simple laws of the
Primal Blueprint
.

I’m not talking about achieving “success” with a short-term crash program. The
Primal Blueprint
is based on eating as much as you want, whenever you want, from a long list of delicious foods—and simply avoiding eating from a different list. When I say you will notice results quickly and dramatically, I’m referring primarily to the immediate increase and stabilization of energy levels, less hunger and mood swings related to “bonking” (running low on blood glucose), improved immune function, and a reduction in the symptoms of allergies, arthritis, and other inflammatory conditions.

Regarding weight loss, we must recognize that our minds are so messed up on this topic that it’s hard even to have a sensible conversation about it. The stories of losing massive amounts of weight in a short time are so commonplace that we seem to expect nothing less when we pursue weight-loss goals. First, the
Primal Blueprint
is really about improving body composition, not about weight loss. For most, a reduction in body fat percentage and an increase or maintenance of muscle or lean body mass.

Clearly, altering your body composition by just a few net pounds by losing fat weight and gaining a little muscle weight produces more impressive appearance changes than someone who drops 20 quick pounds on a crash diet that depletes muscle mass and water. Lean body mass (muscle, skeleton, and all the rest of you that is not fat) is also directly correlated with “organ reserve”—the highly desirable ability of all your vital organs to function optimally beyond basal level (e.g., elevating your heart rate during exercise). We’ll discuss this critical longevity component further in
Chapter 6
.

When you trigger your genes to stop storing body fat and start burning it, as well as to build or maintain muscle mass, you can sensibly and realistically lose a pound or two of body fat per week. You can even do this with minimal exercise, but the rate of fat loss (and the gaining, sculpting, or toning of lean muscle) can be accelerated significantly when you choose the right exercise regimen. Mostly, your success depends on how aggressive you are in keeping dietary insulin levels moderated, thereby extracting more of your caloric needs from fat stores.

Not a day goes by without a friend, client, or
MarksDailyApple.com
commenter relating to me how he or she notices improvements within days of switching to the
Primal Blueprint
eating style. As I will detail in this chapter, you have the chance to alter your biochemistry at each meal—to stimulate an efficient fat-burning metabolism and consistent energy levels or to do the opposite with poor food (and exercise) choices. The momentum you build with good choices will make it easier to discard old habits in favor of both instant gratification (from filling meals and stable energy levels) and positive long-term health and metabolic consequences.

The insulin story is perhaps the most health-critical concept in the book, so I want you to fully understand it on both a practical and a biochemical level. Like so many things in life, a moderate amount of insulin is good and a lot can be bad—very bad. By now you understand insulin’s role as a storage hormone and that eating more carbs results in more insulin production. Insulin delivers nutrients to all cells, but for our purposes, we’ll focus on insulin’s role delivering nutrients to liver, muscle, and fat cells. When the system works as designed by evolution, cell receptors use insulin as a key to unlock pores within the membrane of each cell. With the cell door open, nutrients can then be stored inside the cell. It’s an elegant way for cells to gather the nutrients they need and also to eliminate excess glucose from the bloodstream (remember, excess glucose is highly toxic) and store it as fuel for a later date.

Unfortunately, when we produce too much insulin over time, as happens when our modern diet is high processed carbohydrates, several things go wrong. First, muscle and liver cells aren’t able to store a whole lot of glycogen (the stored form of glucose), so it’s easy to exceed storage capacity with a typical moderate-to-high–carb modern diet. The average person can only store about 400 grams of glycogen in liver and muscle tissue (even a highly trained athlete can only store perhaps 600 grams). When your liver and muscles become filled with glycogen, any glucose remaining in the bloodstream that isn’t used in “real time” by your brain or muscles (such as during an intense workout) gets converted into triglycerides in the liver and sent to fat cells for storage.

When blood insulin levels are high, those same fat cells store not only the excess glucose but the fat you ate at your last meal. Moreover, high insulin signals the fat cells to hold on to the fat and not release it for energy. If the pattern of high insulin-generating meals continues, fat cells swell up and we gain weight. Eventually, especially among people who don’t exercise much, muscle and liver cells start to become
insulin resistant
—their receptors become desensitized to insulin’s storage signals (the aforementioned insulin key doesn’t unlock the cell membrane to allow nutrients in). Inactive folks generally have plenty of muscle and liver glycogen stored at all times. Because they are unpracticed at burning and inefficient at restocking energy from dietary nutrients, insulin takes ingested carbohydrates and fats on an express train, passing right through the liver, to their ultimate destination in fat cells.

Continuing this process can lead to severe obesity. Eventually, even fat cells become resistant to further storage, because we only have a fixed amount of fat cells. At that point, the body’s last line of defense against glucose (the complete gorging of a finite number of fat cells) has maxed out. Consequently, all hell breaks loose in terms of blood glucose toxicity and insulin damage—leading to even greater risk for diabetes, heart attack, blindness, the need for limb amputation, and other disasters.

Unless you are exercising incessantly to burn stored glycogen and fat, the more insulin your pancreas produces, the more resistant your muscle and liver cells can get. This happens because the genes responsible for these receptor sites turn themselves off or “down-regulate” in response to—and defense against—the excessive insulin in your bloodstream. This is all part of the body’s quest for homeostasis and balance and your genetic response to environmental signals. It is now becoming clearer how the shocking statistic of the average American gaining one and a half pounds of fat a year for 30 years is achieved. Conversely, when insulin levels are moderated (as happens with low carbohydrate eating and/or frequent exercise), your liver and muscle cell receptor sites become
insulin sensitive
—more effective at absorbing ingested nutrients transported by insulin. Furthermore, moderated insulin levels signal genes to make more receptor sites.

An insulin-resistant liver exacerbates the situation. The “No Vacancy” sign hanging on the liver (glucose is turned away due to insulin resistance) tricks some cells in your liver into believing they are starved for glucose. In response, genes in other liver cells get the signal to commence gluconeogenesis and dump more glucose into the bloodstream-despite the fact that there’s already plenty in the bloodstream (talk about a communication breakdown!). Of course, your resistant muscle cells are deaf to insulin signaling as well, so the new, extra glucose your liver just made is also diverted to the eager fat cells – unless they too are resistant. Here is a quick summary of some of the unpleasant consequences of becoming insulin resistant:

Fat cells can’t release their stored energy into the bloodstream
, where the fatty acids could be used as fuel, because insulin keeps the fat locked inside.

Fat cells get bigger
(and fatter), so you gain weight.

More glucose stays in your bloodstream longer
, causing damaging AGEs (advanced glycation end products), chemical reactions that occur when blood-borne glucose molecules bind randomly with important proteins, rendering them useless. This can result in increased inflammation and risk of heart disease as well as the circulation problems and neuropathies (nerve damage) that characterize type 2 diabetes.

Pancreatic beta cells
, continually sensing high levels of glucose in the bloodstream, keep working harder and harder to pump out more and more insulin. Eventually, the beta cells can become exhausted and stop working entirely—similar to the plight of insulin-dependent type 1 diabetics. All of this can happen as a result of eating too many carbohydrates for too long and/or not exercising enough to maintain insulin sensitivity.

But wait, there’s more! As bad as all that glucose remaining in the bloodstream is, chronically high levels of insulin are almost worse. Insulin is very pro-inflammatory and can wreak havoc throughout the body. Scientists know that within any species, those that produce the least amount of insulin over a lifetime generally live the longest and remain healthiest (except type 1 diabetics, who might die but for supplemental insulin injections).

Excessive insulin is also now believed to be a central catalyst in the development of atherosclerosis. Insulin promotes platelet adhesiveness (sticky platelets clot more readily) and the conversion of macrophages (a type of white blood cell) into foam cells, which are the cells that fill with cholesterol and accumulate in arterial walls. Eventually, a cholesterol and fat-filled “tumor” blocks circulation in the artery, a situation further aggravated by increased platelet adhesiveness and thickness of the blood. In addition, insulin reduces blood levels of nitric oxide (a compound that relaxes the endothelium, the lining of your arteries), causing your artery walls to become more rigid. This drives up blood pressure and increases the sheer force of blood against the arterial wall, further exacerbating the atherosclerotic condition. I will further detail the chain of events causing atherosclerosis, and what you can do to prevent it, in the cholesterol section later in this chapter.