Monday, July 19, 2010

Can Staying Up Late Cause Heart Disease? by TS Wiley

Can Staying Up Late Cause Heart Disease?

What happens to the biggest clock in your body when the light never sinks into the sunset (e.g., Schwartz 1996)? When the fuel that feeds your heart never varies and the panic perceived by sleep loss never ends?
So many things you can't even imagine.

And not one of them is good.

In order to understand the magnitude of damage that can be done by staying up after the sun goes down, we need to grasp the mechanisms of the cosmic clock we call a heart.

In a Heartbeat
Bump-bump, swish, lub-dub, lub-dub, bah-boom, bah-boom . . . however the act is interpreted verbally or on the written page, we all recognize a heartbeat or the lack of one. All the cells of our hearts, like little tuning forks, resonate together to set the beat (e.g., Lakatta 1993). That beat, provided by our "heartstrings," reverberates throughout the circulatory system (e.g., Attali 1996).

Tibetan, Chinese, and Ayurvedic medicine all consider pulse sounds the major key to diagnosis. Eastern physicians study the rhythms of pulse for many years in order to qualify to practice medicine. By studying at least six different pulse points, they are able to discern many different rhythmic patterns or "songs." These human EKG machines believe that there are as many different rhythms as there are diseases. Each illness has its own song. It's possible to hear the music and the discord (e.g., Holden 1998).

The scientists at the Santa Fe Institute for Biological Complexity, in their attempt to categorize scaling, or how the various characteristics of all living things, like pulse rate and life span, change according to body size, have decided we humans all get only a billion. That's the magic number--one billion lub-dubs (e.g., West 1997).

From the smallest tree shrew to a blue whale, nobody actually gets more than a billion. But size does matter when it comes to time on this earth. The mouse uses its billion up faster than the elephant because of their respective metabolic rate. These scientists have a formula--a cat, one hundred times more massive than a mouse, lives one hundred to the quarter power, or about three times, longer than a mouse (e.g., Mackenzie 1999). Therefore, a cat's heart beats one third as fast as a mouse's. The fluctuations on all time scales, the timing of a beat being fixed from the timings of the last few before it, really means your heart is not tuned to only one frequency.

The New England Journal of Medicine reported in an article in February of 1999 that the human heart shows an electrical response to a variety of "radio" frequencies. By responding to a range of frequencies, our heart protects the brain and itself from damage that could result from an overreaction to any one stimulus at any one frequency. This information makes cell phones all the more horrifying. The heart is made of what scientists call an excitable medium, that is, one that generates and conducts electricity (e.g., Lakatta 1993).

The Consciousness Interface
Your heart and your immune system, far more than the gray matter that we think of as constituting the mind, are sentient in their own right. Evidence of your heart's active intelligent participation in your existence is found in studies of beat rhythms (e.g., Levin 1998). Your brain's growth and development are, in fact, completely maintained by immune factors called cytokines originating in your heart.

Your heart clenches and unclenches like a fist about 60 times a minute on average. The image of a constant, unwavering, orderly "ticker" beating away like clockwork is given to us as schoolchildren. We're taught that the terms "health" and "order" are synonymous. In fact, we refer to almost all diseases as dis-orders. But the truth is just the opposite. An "ordered" heart is one of slow, steady, unvarying beats (e.g., Holden 1998; Shimizu 1993).

Every first-year med student knows that this is the tempo of a sick heart. If you look at recordings of long series of heartbeats and calculate the lengths of the beat-to-beat intervals, it looks like they are spaced at longer and shorter intervals in a completely random and erratic manner.

Not erratic in the fluctuating way in which your heart responds to your body's activity level, but genuinely wild, even during sleep. There are speed ups and slowdowns, not just hourly, but minute-to-minute, too. Researchers monitored 10 healthy volunteers and ten people with congestive heart failure (e.g., Holden 1998). On first look, the heart rhythms appeared much the same in both groups, but the beat-to-beat rhythms of the healthy hearts were, in fact, far different from those of the brokenhearted.

In the healthy hearts, a sequence of two hundred steps up tends to be followed by two hundred steps down. On an EKG, this means that the period in which the heart slows down will be followed by a period in which it speeds up, sort of like a built-in mechanism that sets the beat long-range, so it fluctuates to a predetermined mathematical landscape.

The healthy heart has long-term "memory."

The timing of the next beat depends on the "beat history" of the distant past. Disease, by contrast, is really heart amnesia (e.g., Lakatta 1993). In a broken heart, if a run of 200 beats gets progressively slower, the next 200 are just as likely to get slower as they are to get faster. By measuring longer and longer intervals, the scientists can find the extra information about the "average" hidden in the fluctuations (e.g., Holden 1998).

This information is enough to illuminate the rhythmic differences between healthy and sick hearts. Over the last 20 years, mathematicians and physicists have realized that what looks random is not random at all. It's chaotic, and unpredictability is a hallmark of a chaotic system. Chaos differs from randomness in that chaotic behavior always arises from simple underlying causes. Irregular rhythms like sunspots or the oscillations of El Nino are examples of chaotic rhythms rather than random single occurrences. Healthy heartbeats are highly chaotic, just like cosmic activity or the weather, because a chaotic system is more adaptable (e.g., Storey 1997; Wehr 1997). When you don't sleep or cut sleep short, patterns can't be adapted. A chaotic system is highly dynamic, always changing and fluctuating to maintain homeostasis. A chaotic system is always poised in a state that is incredibly sensitive to small influences.

How the Beat Goes On

The oppositely polarized inside and outside of your heart cells always have an unequal distribution of ions inside and outside of the cell. The systemic sympathetic nervous system communicates with the nerves all over your body and brain by initiating waves of change in the polarity inside and outside the membrane of neuronal cells like those in the heart. The pouring of positive and negative ions in and out through gates in your heart cells' membranes produces a "current" of electricity (e.g., Lakatta 1993).

The muscle cells of the heart are thrown into play by an electrical current that comes in polarized waves and contracts and squeezes blood through two adjacent pumping chambers called the left and right ventricles. There's a special colony of cells at the top of the right side. These cells electrically "keep the beat." This rush of electricity sweeps in a spiral around the entire heart, from the double-humped top to the pointy little bottom, making a complete circuit top to bottom -- bottom to top.

As this happens, your arteries actually "feel" the blood flowing through them. The sensors that read how hard your blood pushes and pulls as it rushes through you are called endothelial cells. These cells are alive in their own right (e.g., Shimizu 1993).

They change shape, move around, and switch a myriad of genes on or off in response to blood pressure and velocity, hormones and cytokines that they detect in the blood, and (here's the big problem with not sleeping) photons of light brought into the blood by cells called cryptochromes. Endothelial cells control through changing blood pressure the flow dynamics moment to moment.

Endothelial cells also control how fatty acids floating in your blood are metabolized. Fatty acids are what the doctor measures when he threatens you about your high cholesterol. The blood tests they take to measure your cholesterol look at different components of fatty acids in your blood, components with acronyms like VLDL, HDL, and LDL. Whether the LDLs (low density lipoproteins) are split from the VLDLs (very low density lipoproteins) that were made in your liver from the carbohydrates that you've eaten and become heavy, oxidized, smaller LDL particles is at the discretion of your endothelial cells (e.g., Pinkney 1997).

Doctors tell you to fast before the test, not because a high-fat meal will skew the results but because a high-carbohydrate one will. Carbohydrates turn into triglycerides (body fat) to insulate and nourish you when there's no sugar left to eat. Carbohydrates simultaneously turn into these fatty acids, too, to patch your heart cells against leaks if you freeze and as nourishment for your heart muscle cells as the planet turns in and out of the light of and spins around the sun. (e.g., Bjorntorp 1991; Hearse 1997; Yudkin 1988; Wiley 2001). Days are not all the same length all year long and your heart has evolved to "know" that.

Your heart has a seasonal metabolism.

Your summer heart runs on straight sugar (glucose) and your winter heart runs on free fatty acids. Because it's always summer (long light/high carbohydrates) in our hearts now thanks to temperature and light control, our arteries never get a chance to use up all the cholesterol (e.g., Howell 1997). In addition, your serotonin, which goes up with your insulin, keeps building, leading to ultimate serotonin resistance, which gives you high blood pressure on the way to blood clots, and--as long as the lights shine and you stay up--your cortisol (W) stays up. And chronic high anything means compensatory resistance (e.g., Bergendahl 1996).

Cortisol production is, in the first place, a coping mechanism in place to deal with episodic stress. Your heart lining loves cortisol, in small doses. The endothelial cells in your heart lining can't do all the jobs they do without small, usable measures of cortisol. Big hits, however, signal big danger to your endothelial cells. Big hits all day long, all week long, all year long for decades can mean cortisol resistance and a bad temper, and no patience, and skewed time perception, and pervasive panic (e.g., Bergendahl 1996; Fimognari 1996).

It doesn't matter if you eat saturated or unsaturated fat, good fats or bad fats; if the endothelial cells lining your heart are dead, so are you. Endothelial cells lining every blood vessel in your body is a player in the larger scheme of the sensory organ known as your heart. The rush of your blood, the push and the pull, is called "shear stress" on the walls of your arteries (e.g., Hademenos 1997).

Shear stress action over a smooth patch of endothelial cells activates three very important genes: one that produces nitric oxide, which controls the clamping down of your blood vessels, which, in turn, controls the speed and volume of your blood pressure, and two other genes that inhibit blood clotting and smooth any muscle overgrowth (lumpy bumps). Endothelial cells that read too much turbulence or, on the other hand, none at all, produce very little activation of these genes (e.g., Shimizu 1993).

This is a bad thing.

That means that while constant chronic running on a treadmill produces too much turbulence, never moving away from the television or computer screen at all from day to day is just as bad. A little stress, episodically, is a very good thing. Just like a little cortisol, episodically, keeps the rhythm and proves you're alive. A lot of chronic stress, of course, means you're a loser to nature and should go away permanently. Just a little cortisol bath makes endothelial cells very happy. A lot of cortisol will drown them. Since cortisol stays up as long as the lights are on, we're probably drowning. So just keeping the lights on late, year-round, can cause endothelial cell death (e.g., Hearse 1997; Miguez 1995; Pinkney 1997).

Any increase in blood pressure from your sympathetic nervous system or heavy carbohydrate intake in the wrong season can change blood pressure to create even more shear stress and hurt your endothelial cells two ways. The ten to fifteen pounds of water weight we carry on a high carbohydrate diet is enough of a volume increase to account for the chronic subclinical high blood pressure seen in the majority of men more than 35 years old (e.g., Hearse 1997; Yudkin 1988).

Any high blood pressure, no matter how slight, always means shear stress.

The other major killer of the endothelial cells in the lining of your heart is chronically high levels of endotoxin LPS. Endotoxin LPS is the bacterial "sweat" coming from the four pounds of symbiotic bacteria living in your gut. Endotoxin LPS, as it accumulates all day long from reproducing symbiotic bacteria, activates your immune system and interleukin-2. Interleukin 2 puts you to sleep and melatonin drops your temperature to lower the number of bacteria reproducing again. They get a chance, you get a chance. When you fight sleep instead of surrendering, those levels rise and stay high (Brugger 1995; Schwartz 1996; Sensi 1993; Storey 1997; Tamura 1997).

That can kill your heart. One of the most obscure ways to kill your endothelial cells by not sleeping is through high homocysteine.

A man named Kilmer McCully realized about thirty years ago that children with a genetic disease called homocysteinuria always died of heart attacks from clogged arteries by the age of ten or eleven (e.g., McCully 1996).

Children with homocysteinuria genetically fail to make an enzyme that metabolizes homocysteine to remove it from the bloodstream. McCully was smart enough to realize that high levels of building homocysteine must be associated with coronary artery disease in adults, too. He was right.

Of course, no one took him seriously until scientists found that an increase in folic acid supplements would compensate for the missing enzyme in the elimination pathway for homocysteine. Once there was a treatment, suddenly there was a disease--a genetic folic acid deficiency. A widespread genetic folic acid deficiency in the majority of the aging male population is a virtual impossibility, so the pathways of homocysteine manufacture and metabolism must be being affected by something in the environment (e.g., Clark 1998).

Sure enough, only a few feedback loops and cascades backward, a crucial enzyme for metabolizing methionine, the precursor to homocysteine, is knocked out by a cryptochrome carrying blue light (e.g., Hsu 1996). To get the right answer, you have to ask the right question.

The amount of daylight you are exposed to, compounded by the amount of artificial light, controls the production of a minuscule, seemingly esoteric, high-up-in-the-cascade-of-other-hormones-and-functions thing that can kill your endothelial cells--which line your heart--which control clotting, overgrowth, fat metabolism, and blood pressure.

The four most obvious ways that you can kill your endothelial cells are:

1. Chronic high cortisol (never-ending light and stress)
2. High levels chronic levels of endotoxin LPS (no sleep)
3. High homocysteine (too much light)
4. Shear stress created by what would be seasonal high blood pressure (carbohydrate "water-weight," and serotonin resistance and insulin resistance that have no natural end because winter, cold and darkness never come) (e.g., Wiley 2001).

Since numbers 1, 2, and 3 are all the result of modern life, and 4--the all-sugar, all-the-time diet--is the direct result of 1, 2, and 3 also, it's probably safe to say that heart disease, which is a state of endothelial cell demise, is caused by no sleep and too much light, right?

No Escape

Oh, and here's the heart attack mechanism... it's also the endothelial lining that controls the overgrowth of smooth muscle tissue. Those bumpy lumps are the major factor, along with cholesterol plaqueing, in arteriosclerosis (clogged arteries). A disturbed blood flow over bumpy terrain activates an altogether different set of genes in the endothelial cells. These other genes are set in motion to "correct" what the endothelial cells perceive to be a "flow" problem mimicked by the lumpy bumps.

Cholesterol plaque, in and of itself, does not make for bumpy terrain.

It's the immune "factors" released from the endothelial cells themselves, in a protective attempt to restore homeostasis and distribute the shear stress of the flow of blood, that cause the problem (e.g., Johnson 1997; King 1996).

A disturbed flow actually causes the shutdown of protective genes and provokes panic in the endothelial cells. After releasing the immune factors that clamp down, increasing your blood pressure by mistake, they begin to crawl around by extending pseudopodia (little feet) in an effort to escape from areas where shear stress has changed abruptly. The migration of these cells lining your arteries leads to thinning of the artery wall.

The gaps are filled by immune cells called leukocytes (white blood cell) that make a scab sticky enough to attract cholesterol floating in your bloodstream, which makes a fat-constructed Band-Aid to strengthen the thinning artery wall. Now you have cholesterol plaque and overgrown smooth muscle and immune cells making what's known in medicine as foam cells. Foam cells constitute a "lesion" (e.g., Woolf 1994; Wiley 2001).

This new mess creates an excessively bumpy terrain and a remarkably disturbed flow, which panics your poor endothelial cells further. They, literally, run away and the artery wall thins and then your immune system tries to repair it, and it gets bumpier and bumpier and then, of course, your endothelial cells run away again, and the whole shooting match starts all over again; and again and again (e.g., Brugger 1995; Wiley 2001).

But, because you're not dead yet, you probably just have the occasional chest pain or pressure when you exercise. No doubt you're also finding it harder and harder to fight off the depression caused by the chronic high serotonin from all of the carbohydrates you've eaten.
When you never turn off the lights, the serotonin has no way to metabolize into melatonin. In fact, exposure to blue and green light actually knocks out the enzyme that would convert serotonin to melatonin -n-acetyltransferase (e.g., Wehr 1997). So, in addition to making you blue, these sky-high serotonin levels create serotonin resistance in blood platelets (e.g., Modai 1992; Nakata 1999), which makes them even stickier than usual.

That's important, because it's hard to have a heart attack without a blood clot, and it's hard to have a blood clot without sticky platelets. Sleep loss makes most of us tired, freaked out, miserable, addicted to either sugar or alcohol, maybe living on anti-depressants, and walking around with a very damaged heart lining held together by cholesterol supports.

That's heart disease.

But we don't think about it very often unless a knocking comes from within--or worse, pain. Palpitations are absurdly alarming, pain is downright incapacitating emotionally and intellectually. Any physician reading the description above would tell you that you're going to have that heart attack and you're going to have it from the cholesterol plaque clogging your arteries, but no one ever tells you to get some sleep (e.g., Brugger 1995; Hademenos 1997; Hearse 1997; Schwartz 1996; Tamura 1997; Wiley 2001).

As if that's not tragic enough, modern medicine adds to the fear (e.g., Blumenthal 1995; Nilsson 1996), making it palpable. TV and print ads and the internet bombard us with news from the front about the "war on heart disease"--just in case you didn't realize your heart was trying to kill you. We are taught to hate our hearts. It's true that human beings have always been obsessed with their hearts in life, art, and literature. Now we are obsessed with the "health" of our hearts. We seem to be locked in codependent relationships with cardiologists, researchers, and exercise physiologists and in a food fight to the death against the whimsical independence of our hearts.

In a remarkable paper published more than forty years ago in American Anthropology Walter Bradford Cannon, a Harvard Medical School physiologist, described how, in many primitive cultures, a curse from an all-powerful wizard or medicine man was enough to kill a believer.

Their hearts stopped dead.

Thanks to the media in particular, and American paranoia in general, we are far more panicked, minute to minute, about our health than we've ever been before in history, that includes in that assessment the 1914 influenza epidemic that killed twenty million people worldwide. People are far more worried about heart disease now than they were worried about catching the flu then.

We live in truly strange times. Oh yeah, and add to that free-floating terror the twice yearly visit to the cardiologist, or a trip to the grocery store, for that matter, to buy "fat-free" juice, defatted turkey burgers, and low-fat freezer-burned pasta concoctions under overhead fluorescent lights that shine with the glare of ten thousand artificial suns. It's exhausting.

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