Inflammation and Free Radicals
Maybe five percent trans (and other mutant fats) doesn't sound that scary. The real trouble is not so much that there's bad fat in the bottles (and other products).
The real trouble has to do with the fact that after you eat these distorted, mutated fatty acids, they can reproduce inside you.
Imagine a zombie movie, filmed at the molecular level, except the mutant fattys don't stumble through your bloodstream in slow motion. Using radicals (defined in the next section),
mutated PUFAs convert normal fatty acids into fellow ghouls at the rate of billions per second. I call this conversion-on-contact the Zombie effect because, as every horror-movie connoisseur knows, when a zombie bites you, you become one of them. When a throng of molecular miscreants starts hacking away at your cells, things can really get scary. Their ability to damage normal PUFAs makes this class of oxidized PUFAs more dangerous than the trans fat we've all heard about on the news. Since they're a lot like trans, only worse, I call them MegaTrans.
There are many technical names for MegaTrans, including peroxidized lipoxygenases, oxidized fat, lipid peroxides, lipid hydroperoxides, and a others. Think of them all as different gangs of bad fats. [...]
The Reason Vegetable Oil Inflames Your Arteries
Free radicals are high-energy electrons that are involved in every known disease. They behave like molecular radiation, burning everything with which they come into contact, inside your body or out.
In the frying pan, MegaTrans reacts with oxygen to generate one free radical after another. Frying in vegetable oils doesn't so much cook you,: foods as blast them with free radicals—fusing molecules together to make the material solid. Chemists call this series of reactions a free radical cascade.
Free radical cascades damage normal PUFAs, turning them into ugly molecular ghouls (the Zombie effect). Just a little MegaTrans in the bottle of canola oil can become a lot of MegaTrans after you—or the cereal/ donut/frozen dinner manufacturers-cook with it. On the plus side, f
ree radical cascades make your food extremely crispy. (Free radical cascades also happen to play a role in the polymerization reactions that make plastic solid. This is probably the origin of the well intentioned, but not strictly scientific, assertion that
"margarine is one molecule away from plastic.") On the minus side,
free radical cascades make your arteries extremely crispy. They will also damage other bodily tissues, which can generate inflammation, a kind of chaos that interferes with normal metabolic function. [...]
Lipoproteins are designed like M&Ms: just as the candy's coating prevents the chocolate inside it from getting all over your hands, the protein coat en-ables lipoproteins to circulate throughout your body without getting their messy insides smeared on your arterial walls. Of course, lipoproteins don't carry chocolate.
If your diet is healthy, your lipoproteins are full of essential fats, vitamins—all kinds of good stuff. If you eat bad fat, your lipoproteins carry bad fat too, and that can make the whole fat circulation system break down. When the fat circulation system breaks down, people's cholesterol numbers get out of whack. HDL may go down, while LDL and triglycerides may go up. Let's take a closer look.
A lipoprotein is a particle made of fat (lipid) that's been wrapped with a protein coat (hence, lipo-protein). Some lipoproteins are big, and some are small. The big ones are generally lower in density than the small ones because they carry so much buoyant fat. Some of the big• ones are called LDL., for low-density lipo¬protein. And some of the smaller ones are called HDL, for high-density lipopro¬tein. Sound bite science has us calling HDL "good" and LDL "bad," but these terms are misleading. Both LDL and HDL help deliver vitamins and essential fatty acids to our tissues. Though it may contain bad fats, no lipoprotein is inherently bad. Furthermore, lipoproteins exist in a wide variety of densities (their particular density depending how much protein they contain), and their densi¬ties vary as they circulate throughout the body during their life cycle. The binary designations of "high" and "low" density are arbitrary and only add to the confusion. Calling LDL and HDL bad and good cholesterol doesn't make sense either, because lipoproteins aren't cholesterol. They are protein-encased parti-cles that contain cholesterol and all sorts of other kinds of fats—many of which are vitamins and other essential materials. Lipoproteins distribute all these ma¬terials to tissues in need. Without enough of these tiny nutrient couriers in circu¬lation, our tissues would starve.
Lipoproteins contain some cholesterol, but mostly they contain triglycerides, other fatty nutrients (like lecithin, choline, essential fatty acids, and phospholipids), varying amounts of fat-soluble vitamins, and retinoids—all wrapped inside a protein coat.
After your food is broken down by enzymes in the intestine, the fat and most other nutrients get absorbed into intestinal cells (called enterocytes). Here, fat and fat-soluble nutrients are prepared for circulation through the bloodstream. Since fat particles won't dissolve in blood, the intestinal cells wrap these tiny balls of fatty nutrients in a protein coat. Lipoproteins made in the intestine are called chylomicrons. Other tissues that participate in the lipid cycle make other types of lipoproteins, all with the same general design: a blob of fat wrapped in protein.
Cells that make lipoproteins don't throw just any old protein coating the fats, kick the little particle out into circulation and say, "Good luck!" The cells of our bodies must be able to recognize lipoproteins as sources of nutrients. So the protein coating (made of apoproteins) also serves as a of barcode describing the particle's origin and contents. When released into circulation, the wonderfully designed apoproteins also function like little handles, enabling hungry cells to grab the lipoprotein particle as it floats by.
As with any package delivery service, the accuracy of this labeling systern is critical to the success of the whole delivery process. I
f anything were to damage the label (we'll return to this idea soon), the lipoprotein would fail to carry out its function, and the whole system would be thrown out of whack.
{It is here where sugar and inflammatory fats create the most damage}
After the packaged lipoprotein leaves an intestinal cell, it travels through the bloodstream for several hours, completing many circuits. As it floats along, it deposits its fatty nutrients into the tissues that need them most.
Hungry tissues get fed by signaling endothelial cells lining their smallest blood vessels to place special proteins on their surface, which act like tiny fishing rods set to snag lipoproteins as they float by. Once snagged, the parti- cle may unload some of its payload into the endothelial cell or, alternatively, the endothelial cell may open up a tunnel-like structure right through its center to allow the lipoprotein to pass from the bloodstream, through the endothelial cell, and directly into the hungry tissues.
Hours after a meal, the amount of fat in circulation drops as lipoproteins either exit the circulation or give up their fat and shrink (gradually increas¬ing in density as they travel). Eventually, the liver picks up the shrunken, high-density remnants and sorts through the contents to recycle anything discarding any waste. Unwanted or damaged fats exit by way of the bile system back into the intestinal tract for disposal.
The lipid cycle can take any of several different routes. Fats can enter the circulation by way of the intestine (as chylomicrons) or by way of the liver, or even by way of the skin. There are actually multiple points of entry. Even the brain may participate. Fats can exit the cycle by being transported into a hungry cell, or by being exported out of the body through the liver's bile system.
The liver is like a transfer station. It sorts through the incoming lipopro¬teins to separate the good fats from the bad. When it has collected enough good fats, the liver fashions its own lipoproteins (called VLDL, for Very LDL), complete with new identifying labels, and sends them back into the bloodstream again. These particles go through another arm of the cycle, fol-lowing the same series of steps, delivering cargo piecemeal or transporting to a final destination intact. Those particles that deliver cargo piecemeal eventually get small enough to be picked up by the liver again, where they will be disassembled and their fats either discarded or recycled once more.
One loop of the lipid cycle starts in the intestine and distributes lipids you just ate. Another starts in the liver and distributes lipoproteins your liver made. And a third loop starts in the periphery—that is, the rest of the body—and distributes lipoproteins made by the skin, brain, and other organs. Each of the three sources (intestine, liver, and periphery) manufactures its own brand of lipoproteins complete with its own proprietary labels.
When everything works properly, your arteries stay wide-open, pretty pink, and clean. But when fats don't get delivered properly, they pile up in the bloodstream, damaging epithelial cells and giving arteries a yellowish, irregular, lumpy appearance that is conspicuously unhealthy . [...]
How Bad Diet Damages Lipoproteins and Causes Arterial Disease
What damages lipoprotein labels?
One of the most important factors, appears to be sugar. As I'll discuss in the next chapter, sugar adheres to things
by a process called glycation. Over time,
this stiffens cell membranes, leading to prediabetes and consistently elevated blood sugar levels. When-ever blood sugar levels are high, it creates an opportunity for sugar to gum up the protein labels on your lipoprotein particles. And that's a problem.
In 1988, researchers working in Lyon, France discovered that
when the labels on HDL particles got jammed up with sugar, they simply fell off.227 The study was done in a test tube, where the denuded HDL particles ad¬hered to the glass. In your body, the naked fat would be exposed to blood. That's no good, and I'll explain why below. Let me first point out that one of the common findings in diabetic patients is a low HDL level. One possible explanation is that the excessive sugar in their blood has knocked the coats off their HDL, and the naked particles have fallen out of circulation.
And what about LDL? In 1990, another experiment investigated what sugar does to LDL. This time, the labels didn't fall off, but rather became so deranged as to be illegible and unrecognizable to hungry cells.228 As a result, g
lycated LDL particles stay in circulation too long, which would explain why some diabetics have high LDL levels:
With so many undeliverable LDL packages floating around, they just start adding up.229,23° (When LDL levels are high because of glycation, then high LDL is a problem, as we'll see.)
Most diabetics have high triglyceride levels. Triglyceride is not a lipo-protein. Like cholesterol, it is a component of all lipoproteins. Triglycerides are carried in both LDL and HDL particles.
But the vast majority of triglyc¬eride is carried by chylomicrons (the lipoprotein particles your gut makes right after a meal) and very low-density lipoproteins (VLDL), which your liver makes from recycled fats. These plump nutrient carriers want to deliver their cargo into your hungry cells. But, like all lipoproteins, they can't do the job all alone.
They need a special enzyme—think of it as a dock-worker—to pick 'the fatty acids up and carry them into the cell. A study done in 1990 showed that sugar interferes with this process.231
So if you have high blood sugar, that sugar may shred the lipoprotein coats beyond recognition, or simply rip them off the particles' backs. If the particles ever do make it to a cellular dock, sugar keeps them from completing the delivery. [...]
In your body, one of the most dangerous things a lipoprotein can carry is oxidized, pro-inflammatory fat—MegaTrans. When that gets spilled inside your arteries, your body calls on its own HazMat unit.232 But in pre-diabetics and diabetics, so much bad fat is released (either all at once or over time) that the cleanup crews can't keep up and arteries wind up getting in¬jured by free radical cascades and, literally, fried .
Sugar and vegetable oil combine forces to destroy arteries. First, sugar blocks lipoproteins from getting to their destination, forcing them to dump their cargo into your arteries. Second, the explosive, MegaTrans-rich vegeta¬ble oil cargo coats arteries with a toxic goo. If you want to keep your arteries healthy, you'll want to know what that toxic goo does.
I'm taking lots of magnesium and potassium, have recently increased the amount of salt I'm eating, including it in my water. I also rubbed magnesium oil on both calves yesterday morning and this morning. I can't figure out why this happened to me. Anyone have any ideas? Can leg cramps happen from low calcium? I haven't been taking any calcium, although I did powder some egg shells recently and started putting a pinch in my water. Maybe it's time to start supplementing it more earnestly?
