The Paleo Solution Part 3

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Peptide YY (a.k.a. PYY) is yet another hormone trying to tell us when to stop eating. Protein and fat release a lot of PYY and are thus very satisfying. Carbohydrate, by contrast, releases relatively little PYY, which is why your breakfast of bran m.u.f.fins and juice leave you ravenous in a few hours.

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Geek-Speak PYY is a gut hormone that reduces hunger while simultaneously improving central nervous system sensitivity to leptin. PYY is released by neuroendocrine cells in the ileum and colon in response to feeding. Protein causes greater PYY secretion than fat, which causes greater PYY secretion than carbohydrate. PYY plays a synergistic role with leptin in helping us feel satisfied after a meal.

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Cortisol raises blood sugar levels, which can cause fat gain. Although many people don't know this, cortisol release from stress and a lack of sleep factors prominently in body fat gain, leading to that pesky spare tire around the midsection. Cortisol shouldn't be feared, because it is a crucial anti-inflamatory-we just don't want too much of it.

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Geek-Speak Cortisol is often referred to as a "stress hormone," given that it is released in response to stress and anxiety. Cortisol increases blood pressure and acts as an anti-inflammatory by lowering the activity of the immune system. It will trigger the breakdown of muscle ma.s.s by converting protein (amino acids) into glucose via gluconeogenesis. Cortisol decreases insulin sensitivity, lowers the rate of bone formation, and causes a loss of collagen in the skin and other connective tissues. The following increase cortisol levels: intense or prolonged physical activity, caffeine, sleep deprivation, stress, subcutaneous fat tissue, and certain contraceptives.

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Insulin-like Growth Factor-1 (IGF-1) is another hormone we want "just the right amount" of. It aids in physical recovery, but poor diet can abnormally raise IGF levels, which in turn increases both our likelihood for cancer and our rate of aging.

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Geek-Speak.

IGF-1 is critical to the growth of children and has an anabolic effect in adults. IGF-1 activates the insulin receptor but generates a response that is only 10 percent of that observed for insulin. Low IGF-1 promotes cell maintenance and stress resistance. IGF-1 levels are highest during p.u.b.escent growth spurts. Exercise, stress, and nutrition can affect IGF-1 levels. Increased levels of IGF-1 stimulates both growth and aging.

Now that you have met the players in this digestion/endocrinology orchestra, you likely understand a little about the chemistry of our food and "who" the primary hormones are that we must consider in digestion, health, and disease. Gold star for you. This is a nice start, but we have some more work to do. Next, we need to consider what actually happens to both our food and our hormones during various conditions like fasting and overeating. With this knowledge we will be in a position to understand Type 2 diabetes, various types of cancer, Alzheimer's, Parkinson's, infertility, cardiovascular disease, and osteoporosis.

FOUR.

Digestion: Where The Rubber Hits The Road.

You find the last chapter a bit overwhelming? Do you need an espresso? A hug? Don't worry, this will all make sense soon. To understand how all these different pieces fit together, we need to track a typical meal that contains some protein, carbohydrate, and fat through the digestive process. "From the lips to the hips," as it were. Let's make this a meal of baked salmon (protein), avocado (fat), and fruit salad (carbohydrate). We will track not only the digestive fate of our meal, but also the hormonal effects of: 1. Normal eating.

2. No eating at all (fasting).

3. Overeating.

We are looking at this because things like type 2 diabetes occur when the normal hormonal signals a.s.sociated with food (I'm hungry, I'm full. Where's the remote?) get "lost." It is the loss of this hormonal communication that leads to obesity, accelerated aging, many types of cancers, and the other health issues we will consider. Let's get digesting!

The Mouth: Salivary Glands, Teeth, and Garden Supplies.

For simplicity, let's a.s.sume we take a bite of our meal that contains all three ingredients-a little salmon, avocado, and fruit salad.

Big picture: From a digestive perspective, the mouth is mainly about the physical breakdown of our food. Chewing breaks large pieces of food into smaller pieces, making it ready for chemical and enzymatic digestion later in the process.

Protein: Our baked salmon is broken down into smaller pieces but remains chemically unchanged.

Carbs: The fruit salad is an interesting mix of monosaccharides (glucose and fructose), disaccharides (sucrose, which is glucose and fructose again), polysaccharides in the form of starch (many glucose molecules connected together, which we can digest), and fiber (which is important for digestive health, but we do not break it down-Unless you are a termite).

Salivary amylase begins the process of breaking down starch in the mouth. This has very little activity due to the relatively short time in the mouth, especially if you are like my wife and take your food down like a boa constrictor.

The sweet taste from the fruit "primes the pump" for the rest of the digestive process. This is an electrochemical communication between the taste buds and the brain, and the rest of the digestive system. As we will see later, this system can be fooled by artificial sweeteners with truly catastrophic effects.

Fat: The avocado is reduced to a paste in the mouth but is chemically unaltered.

The Stomach: Hydrochloric Acid, Pepsin, Parietal Cells, and Ladies' Wear.

Big picture: The stomach is an acid environment that plays host to a small amount of protein digestion by the action of acid and the enzyme pepsin. The stomach is really just staging the food for the serious digestion a few stops down the line. Cells that line the stomach sense food and release leptin into the circulation. Leptin pa.s.ses into the brain, signaling the appet.i.te centers that we are "fed," thus decreasing appet.i.te, while increasing our metabolic rate in response to food.

This increase in metabolic rate is manifested mainly as an increase in fat "burning" for energy. The stomach releases several hormones to stimulate downstream digestion. One of these is cholecystokinin (CCK), which is another hormone that sends a satiety ("I'm full") signal to the brain while also stimulating the release of bile salts and pancreatic enzymes in the next step. Although this is still very early in the digestive process, communication with the brain is already occurring that we are "fed." What might happen if this signal is sluggish or absent?

Protein: A small amount of chemical and enzymatic digestion occurs in the stomach. Imagine thousands, perhaps tens of thousands, of amino acids strung together. The digestion in the stomach breaks them down, but the pieces are still large. Our salmon still looks like salmon for the most part.

Carbs: No digestion occurs in the stomach.

Fats: Virtually no fat digestion occurs in the stomach. In the stomach, fat and carbs are just hanging out, drinking coffee, and playing cards to pa.s.s the time.

Small Intestines: Pancreatic Enzymes, Bile Salts, and Home Appliances.

Big picture: The acidic contents of the stomach (now called chyme) are emptied into the first portion of the small intestine called the duodenum. Bicarbonate is injected into the chyme to change the mixture from an acidic to a basic environment. The enzymes that break down protein, carbohydrate, and fat work best within narrow pH (acid/base) ranges. The stomach is acidic enough to dissolve a penny, but the main digestion, which happens in the small intestine, is an alkaline or "basic" environment. Baking soda is an example of a common base.

As the chyme enters the small intestines, it is mixed with pancreatic enzymes (not surprisingly, from the pancreas!) and bile salts released by the gall bladder. Folks, the real fun is about to begin!

Protein: The proteins, which are now hundreds or thousands of amino acids long, are rapidly reduced to tri- and dipeptides (three and twoamino acid proteins) by the action of pancreatic enzymes. These small peptides are finally cleaved into single amino acids as the peptides interact with the brush border of the small intestines. The brush border has enzymes that catalyze this reaction of small peptides into free, single amino acids. The free amino acids enter the blood stream and are transported to the liver, and then the rest of the body for use in growth and maintenance.

Carbs: Monosaccharides can enter the blood stream directly, just like amino acids. However, disaccharides like sucrose must be cleaved into monosaccharides at the brush border of the intestines. And polysaccharides such as starch must be broken all the way down into free glucose. The bottom line is that carbohydrates must be reduced to single molecules to be absorbed through the intestinal wall and transported into the circulation. So folks, this is an opportunity to see "complex carbohydrates" for exactly what they are: Lots of sugar. No matter what type of carbohydrate we absorb, it all goes into the system as either glucose or fructose, aka sugar.

Fats: If you recall, when the chyme enters the small intestines from the stomach, pancreatic enzymes and bile salts are mixed into the party. The bile salts are vitally important in the digestion of fats. As I'm sure you are aware, fats and water do not mix, and if we want to digest fat (and yes, we do want that, my fat-phobic-friends), then we need fat to be dissolved in the bile salts. Bile is virtually identical to soap in that it has a piece that likes to a.s.sociate with water, and another piece that likes to a.s.sociate with fats. This is why soap is so effective in cleaning dirty dishes.

This process of dissolving the fats in the bile salts is called emulsification. Once emulsified, the pancreatic enzyme lipase* can break apart the fat, which as you learned earlier, is made up of glycerol and fatty acid molecules. With the glycerol and fatty acids free of one another, they can be transported through the intestinal wall, and are then rea.s.sembled on the other side.

The fats (triglycerides/TAGs) must be transported to the liver just like protein and carbohydrates, but as I mentioned before, fats and water do not mix well. This problem is solved by packaging the TAGs with special proteins that carry them to the liver. This whole complex is called a chylomicron, and it plays a central role in cholesterol, which we will consider later. Unlike protein and carbohydrates, fats are transported in the lymph vessels first, then once they enter the general circulation, they make their way to the liver or are used by tissues of the body.

My Liver! My Liver!

Detour! Although digestion in the GI tract is not complete, we have learned as much from that as we need to. Everything beyond this point is just p.o.o.p anyway! We now need to look at the fate of our macronutrients (protein, carbs, and fat) as they interact with the liver.

Big picture: When nutrients are absorbed through the intestinal lining into circulation, the hormone peptide YY (PYY) is released. It is another player in satiety both directly and because it improves leptin sensitivity. Protein releases a relatively large amount of PYY and is therefore very satiating. Fat releases a significant amount, but less than protein, while carbohydrate releases the least PYY. This should give you a hint of how to construct a meal to improve your sense of satiety (Protein + Fat = Where it's at). Also, you might have noticed that we have met several hormones involved in communication between the digestive system and the brain. When things are working properly, we have excellent appet.i.te control and tend to eat just the right amount of food for our activity and maintenance needs. When this communication breaks down, chaos ensues.

The Fed, the Underfed, and the Ugly.

The next section is somewhat like a "choose your own adventure" story in that we will look at three alternate endings with our food. A "normal" fed state in which we take in about as many calories as we need (in geek speak that's isocaloric), the fasted state (hypocaloric), and the overfed state (hypercaloric). Keep in mind, we need to understand all this to make sense of how obesity, cancer, and neurodegeneration can happen when our food no longer sends the hormonal signals that keep us slim and healthy.

Normal Feeding.

Protein: Really, we are talking amino acids now, as the protein (salmon) that initiated this meal is now broken into individual amino acids. The fate of amino acids can now go one of a few ways. The liver can absorb amino acids and either use them for its own functioning, convert one amino acid into another form (changing one tinker toy into a different kind), or convert that amino acid into sugar via a process called gluconeogenesis (gluco-glucose, neo-new, genesis-birth or creation).

If amino acids are not used in the liver, they are circulated to the body and used to grow new cells, repair damaged cells, grow hair and skin, make hormones, and a host of other functions. The pool of amino acids in our bodies is considered "labile" or flexible, as we can use proteins from our muscles and other tissues in times of scarcity to make glucose via gluconeogenesis. Many doctors and health authorities want you to believe that you'll keel over and die without carbohydrates. Not true-we have several ways of making carbohydrates from proteins and fats. You will understand this process much better before the end of this chapter.

Carbs: Once carbohydrates are broken down into free glucose by the digestive process, the glucose makes its way from the intestines to the liver quite quickly, but its fate is not yet decided. Free glucose causes the release of insulin from the pancreas as it enters the blood stream. Insulin activates GLUT4, one of several glucose transport molecules found in our cell membranes. Under normal circ.u.mstances, these transport molecules facilitate blood glucose absorption by the liver. The glucose is then stored as a form of starch called glycogen. This stored glucose is critically important for maintaining blood glucose between meals. The glucose that is not used by the liver pa.s.ses to the systemic circulation and is used by the brain, red blood cells, and other tissues as a fuel source. A primary example of this is glycogen being stored in the muscles, which can then be used as energy when performing explosive, short activity. If the carbohydrate amount is relatively small, this is the end of the story. However, we still need to consider fructose.

Fructose must be handled by the liver, as none of the other tissues in the body can utilize fructose directly. Fructose is converted to glucose by the liver and then stored as glycogen. If our fructose intake is low and our total calorie intake is not excessive, things are "OK." But keep your eyes open-excessive fructose is a player in the development of obesity, depression, diabetes, and the a.s.sociated diseases of metabolic derangement.

Fat: Triglycerides/TAGs are transported to the liver in lipid/protein packages called chylomicrons. The chylomicron can drop off TAGs at the liver or it can carry the TAGs around the body to be dropped off at muscle, organs, or fat cells to be used as fuel. Once a chylomicron has dropped off most of its TAGs, it will make its way back to the liver and be reused in the important cholesterol story, which we will cover in just a bit.

Fasted State.

Big picture: The fasted state can mean going completely without food for a period of time or simply a reduced calorie level relative to energy expenditure. As we will see, how our body responds to a calorie deficit is largely dependent on our hormonal state. It may seem odd to consider fasting when we are talking about eating food, but a significant breakdown occurs in the overfed state in which parts of our body "think" it is starving. It's ugly, and we need to understand the mechanisms of fasting to understand how overeating goes so terribly wrong.

Protein: Although protein is critical as a structural element and in maintaining fluid balance with proteins in our blood called alb.u.min, proteins are also fairly expendable. Your body is more concerned about avoiding a blood sugar crash than it is about maintaining muscle ma.s.s. That's why during fasting we tend to convert large amounts of amino acids into glucose, which is stored in the liver as glycogen and then released to maintain blood glucose levels. In other words, in a fasted state, your hard-earned muscles might be converted into glucose. As we will see, hormone status and the presence of ketones (you'll meet them in a bit, I promise) can change how much protein we convert to glucose. This is really important if our fast is unintentional and we are facing a long period of starvation.

Carbs: In the fasted state, virtually all dietary carbohydrate is initially sequestered in the liver. Although the muscles and organs like glucose just fine as a fuel, there are other tissues like red blood cells and certain parts of the brain that can run on nothing but glucose. For this reason, the body becomes quite stingy with how it spends its glucose. The adaptable tissues s.h.i.+ft to fat and ketone metabolism, saving the glucose for the vital tissues.

Fats: During fasting, the body uses stored body fat as a fuel. As the body s.h.i.+fts to fat as a primary fuel source, a by-product of fat metabolism begins to acc.u.mulate: ketones. Now, ketosis is not a reason for panic! Your doctor and dietician should not confuse ketosis with ketoacidosis (a potentially life-threatening metabolic state). These two states are as different as night and day, and I'll pay good money to hear a doctor or dietician accurately describe the biological distinctions, as most cannot.

The metabolic state of ketosis is normal and almost as old as time. Ketones are like small pieces of fat that are water soluble, and given a few days or weeks, most of our tissues can s.h.i.+ft their metabolism to burn ketones. Interestingly, many tissues such as the heart, kidneys, and intestines function better on ketones than on glucose.

A metabolic s.h.i.+ft to ketosis solves two very important problems: 1. It protects scarce blood glucose by s.h.i.+fting as much of our metabolic machinery as possible to a nearly limitless fuel supply. We have a day or two of liver glycogen, but even if we are relatively lean, we have literally months of stored body fat. A s.h.i.+ft to ketosis saves scarce glycogen to be used to maintain minimal blood glucose levels.

2. Ketosis halts gluconeogenesis. The by-products of ketosis block the conversion of amino acids into glucose. This spares muscle ma.s.s that would be very valuable in a state of prolonged starvation. In addition to blocking gluconeogenesis from amino acids, ketosis provides a sneaky, alternative way to make glucose using the glycerol backbone of fats. All in all, it's a very efficient system for protecting blood glucose and muscle ma.s.s under the stress of starvation.

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Geek Rant.

Now, this may sound like heresy, but there are no "essential carbohydrates." Our bodies can make all the carbohydrates it needs from protein and fat. Although glucose is critical for many of our tissues, the redundant mechanisms in our bodies for producing glucose indicate it was a fuel that was transient in our past. We are not genetically wired for a 50 percent carbohydrate, bran m.u.f.fin diet, despite what the USDA, AMA, and FDA have to say on the topic. Capisce?

With that clear in your mind, we need to look at one more piece to this puzzle, the "overfed state." This will help us make sense of how eating too much of the wrong food can cause serious problems.

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Overfed State.

Big picture: Overfeeding is a problem. I know, shocking, right? Well, here's the thing: our physiology is actually wired to exist at a caloric excess. Goofy dieticians and some "nutritional scientists" will tell you we need to maintain a caloric "balance" to remain slim and healthy. This is baloney. Figuring out a caloric balance is virtually impossible if it's left up to "us." Metabolic studies have shown an enormous variance between people and how they handle calories. One person can overeat several hundred calories every day for years and never gain a kilo. Other people seem to gain weight by looking at food. What gives? What's the difference? Hormones and the signals a.s.sociated with hormones.

It should not come as a surprise that our bodies have complex sensors that tell us not only if our blood glucose is high or low, but also how much total energy we have in storage. Leptin, which tells the brain we are "full," is not only released in response to food, but it is also released from our body fat. This should make sense on a mechanistic level: A relatively large amount of fat will release a relatively large amount of leptin, which sends the signal "I'm full, no need for more food." Conversely, if we are getting very lean and our energy reserves become low, our leptin signal will be low and we experience hunger.

What does all this have to do with overfeeding, health, and disease? As I was saying before, we are wired to live at a caloric excess. Certain foods affect our sense of satiety and the ultimate fate of our food in very different ways. Think about the difference between the satiety signals produced by protein (very satiating) and carbohydrate (in many people low satiety actually acts as an appet.i.te stimulant). What if we are overfed, but for some reason our brain no longer "hears" the "I'm full" signal from the leptin? What if, despite significant overfeeding, we still think we are hungry? That situation creates one h.e.l.l of a problem, as you will see.

Protein: In the initial stages of protein overfeeding things run as you might expect: Some amino acids are used for structural repair, but any amino acids beyond this are converted to glucose via gluconeogenesis, or burned directly as a fuel. Protein can add to overall caloric excess, but as a stand-alone item, it is virtually impossible to overeat protein due to the potent satiety signal sent to the brain. Part of the reason for this signal is due to a maximal ability of the liver to process protein set at 3035 percent of total calories. Protein consumption beyond this point for extended periods of time results in a condition called "rabbit starvation," so named by early pioneers of the American West who would succ.u.mb to a disease characterized by muscle wasting, lethargy, diarrhea, and eventually death if one relied too heavily on lean game animals such as rabbits. We will take advantage of the satiating effects of protein to help us remain lean and strong, while rounding out our meals with nutritious fruits, vegetables, and good fats to avoid the potential of too much protein.

Carbs: This next piece is going to be longish but wickedly important. Drink some espresso, stick your head out the window, and yell "I've got to get my head back in the game!"

So, you are now familiar with the fate of glucose (and fructose) as it enters the body and is stored as glycogen in either the muscles or liver. What we have not considered is what happens if liver glycogen is completely full but there is still excess free glucose in circulation (high blood glucose levels). Once liver glycogen is full, excess carbohydrates are converted to fat in the form of a short-chain saturated fat called palmitic acid. This palmitic acid (PA) is st.i.tched to a glycerol molecule and packaged with proteins and cholesterol, and the resultant molecule is called a VLDL (very low-density lipoprotein). This PA-rich VLDL molecule is released from the liver and heads out to the body so the fat may be used as a fuel or get stored on our fannies.

DEFCON 1.

Although VLDL's move all about the body, one location they interact with is the brain. PA has a very potent effect on our metabolism and our hormonal environment in that it decreases our sensitivity to leptin. When the brain, specifically the hypothalamus (the area of the brain responsible for energy regulation), becomes leptin resistant, the satiety signal that is normally sensed from ingested food is lost. We remain hungry, despite elevated blood glucose levels, and continue to eat beyond our needs. We develop a "sweet tooth" because we cannot sense the normal signal sent by leptin that we are "full." Keep in mind, this Palmitic acid (PA) that causes the leptin resistance in the brain leads to our inability to feel full, and is made from excess dietary carbohydrate.

DEFCON 2.

This process happens in waves. Like the ocean eroding a sand castle, our insulin sensitivity is degraded and we lose the ability to respond properly to the signal. The liver becomes insulin resistant and blood glucose levels drive higher and higher. Insulin sensitivity in our muscle tissue is lost when they can physically store no more glycogen. The gene expression for the GLUT4 transport molecule is down-regulated because the muscles are literally drowning in glucose. This drives blood sugar higher, which drives insulin higher. Eventually, even the fat cells become resistant to insulin. Things are about to get bad rather quickly.

DEFCON 3.

Once systemic, full-body, insulin resistance occurs, inhibitory systems in the liver are overwhelmed and blood glucose is converted into fats and VLDLs at such a high rate that fat cannot escape into circulation, and it begins to acc.u.mulate in the liver. This is the beginning of nonalcoholic fatty liver disease. The wheels are seriously falling off the wagon by this point, as is evidenced by the next malfunction that occurs: Despite the fact the liver (in fact, the whole body) is swimming in glucose, the liver is insulin resistant and certain cells perceive the "lack of insulin" as low blood sugar. Your body does not like low blood sugar. Low blood sugar can kill you, so your body brings the stress hormone cortisol to the "rescue," and it's like throwing gasoline on a fire.

China Syndrome: Full System Meltdown.

Cortisol is released to combat the perceived low blood glucose levels with gluconeogenesis. Yes, despite high levels of blood glucose from excess carbohydrate, the body now makes more glucose by cannibalizing its own tissues. In this case, muscle and organs are "burned" to make more glucose. Keep in mind, the muscles are a primary site of dealing with elevated blood glucose in the first place! So, not only is the situation made worse by adding more glucose to the blood from gluconeogenesis, we have less muscle with which to dispose of all that glucose.

This is why type 2 diabetes and insulin resistance is effectively a wasting disease of the muscles, all the while the fat cells experience record growth. Because of the high insulin, blood sugar, and triglycerides, a significant portion of the fat is stored in the abdominal region. This is the telltale sign of insulin resistance: fat stored at the waistline, creating the very s.e.xy "Apple Shape." We have now set the stage for chronically elevated insulin levels and all the fun that brings: Increased rates of cancer, accelerated aging, and neurodegenerative diseases such as Parkinson's and Alzheimer's, obesity and, ultimately, type 2 diabetes, which is characterized by insulin resistance and chronically elevated blood glucose levels.

AGEs: Yes, It Gets Worse!

Although glucose is a critically important fuel for the body, it is also a toxic substance. Sugars have a nasty habit of reacting with proteins in our bodies. These complexes become oxidized and form "advanced glycation end products" (AGEs). They damage proteins, enzymes, DNA, and hormonal receptor sites on the surface of our cells. AGEs are a major cause of the symptoms we take to be normal aging.

When we look at the pathology of several diseases, we will see that they have AGEs as a major causative factor. Our bodies DO produce enzymes to undo AGEs, but they can only undo a certain amount of damage. If our diet is too heavy in carbohydrate, the damage acc.u.mulates faster than we can fix it. Some of the worst damage happens in the pancreatic beta cells, which have already taken a beating from overproduction of insulin. The additional oxidative stress can kill the beta cells and, unlike the liver, once these cells are gone, that's it. This situation produces a hybrid form of diabetes characterized by not only insulin resistance, but also an eventual inability to produce insulin. People in this situation look like both a type 1 and type 2 diabetic.

The other effect in the insulin management story is damage directly to the GLUT4 molecules on our cell membranes caused by AGEs and oxidative damage. This further impairs the ability of muscles to absorb and store glucose.

The take-home of AGEs: 1. They accelerate your aging.

2. They damage already precarious insulin and leptin receptors, worsening insulin resistance.

3. They are key players in several degenerative diseases.

I know this is some heavy, complex material. In the next chapter we'll look at an a.n.a.logy to make some sense of all this. Remember, if you understand how these diseases manifest, you can take appropriate steps to avoid some nasty characters like cancer, diabetes, cardiovascular disease, and premature aging.

* Lipase is a term derived from the Greek "lipos," which means "fat," and "-ase," which means to cut. Quite literally, it means to "cut the fat." Whenever you see "-ase," you know it's an enzyme that's involved in a reaction. The world is a never-ending source of amus.e.m.e.nts when you master a few Greek and Latin suffixes. For example, "kattase" means "cut the cat," while teereease means to, well, "cut the cheese."

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Fructose Side Show.

Sorry, I need to take a little detour to the insanity of the fructose story. Have you seen the commercials where high-fructose corn syrup is described as "healthy" because chemically it's almost identical to table sugar (sucrose)? The irony is so thick you'd think it was a Daily Show parody (It's just as healthy as sugar!), but it's just another public relations attempt on the part of agribusiness to sell us an early grave.

Fructose preferentially fills liver glycogen. That means fructose accelerates the process described above in which liver function is destroyed due to carbohydrate overfeeding. This happens directly because the liver is the only tissue that can handle fructose, but it also happens indirectly because eating fructose increases the amount of glucose the liver absorbs. Fructose up-regulates the glucose transport molecules in the liver, making the liver "hungry" for sugar. This leads to increased Palmitic Acid production, which leads to leptin resistance. Oh, yeah, since we were talking about AGEs, fructose is seven times more reactive than glucose in forming AGEs. Funny, they do not mention that fact in all the "high-fructose corn syrup is good for you" commercials!

It's the d.a.m.ndest thing-the United States is in a health care crisis, the economy is shaky, and the government subsidizes the production of corn, making high-fructose corn syrup cheaper than dirt. Processed food manufacturers make c.r.a.p foods that are making us sick, diabetic, and dead too early. The government subsidizes the development of statins and a host of drugs to manage the diseases that are a direct outgrowth of the processed foods they are subsidizing! A h.e.l.l of a racket, am I right?

OK, back to our regular program: ____________________________.