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Sick and Tired, the Book of the Dead

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You darkness, enfold the spirit of those who ignored your glory.

Take us now.

--Mayra Montero, a prayer to be said for the dying from You Darkness, 1999

The soft comfort rendered by the sounds of amphibians at night is as deeply buried in the human consciousness as is the silvery music of running water. The pounding of the ocean on the shore, a gurgling Roman fountain, crickets chirping, and frogs croaking all bode well for humanity. And we count on that.

Since day one we have felt secure hearing those sounds because they translated into survival: food, water and company. Now that's all changing. The frogs are too quiet.

Amphibians, frogs, and toads are dying under mysterious circumstances. In some cases, not even the bodies are found. According to New Scientist magazine, in the Causuco National Park in Honduras, more than one species of jungle frog has vanished without a trace; there are no tadpoles left, either. These creatures lived in delicate balance between water and land, air and light. So do we.

It's a chilling prospect to realize that, in the end, our disappearance, like that of the amphibians, will most probably happen from some unspecified and general collapse, not from a careening asteroid or a nuclear holocaust. Maybe it's begun already. We, those of us humans alive today, could be hurtling toward extinction.

Some of us are about to go the way of other less adaptable branches of our family, such as Homo habilis, Homo erectus or Homo neanderthalensis. Some of those hominids were out-populated or absorbed by other branches of the family. But many more of them were just less adaptable than us.

You see the rule of thumb in evolution is: when you change the environment, the environment changes you ... if your genes will allow it to. All our current genetic makeup evolved in a time before we had the ability to bring light to the blackness just because we wanted to.

Our first attempt at celestial control, firelight, changed those of us who could change. It was the acquisition and use of fire that first lengthened our day and shortened our night. Shorter nights meant: less melatonin production. Less melatonin production meant more estrogen and testosterone in circulation. More light also means more cortisol, and, of course, cortisol's mobilization of blood sugar always means more insulin follows. The firelight not only gave us the opportunity for more available protein by cooking our meat, but gave us the ability to store more fat by lengthening the days and extending the season of summer.

Those of us who could genetically adapt to live with less sleep, more carbohydrate, and the increased fertility that it brought lived on. Those who couldn't adapt - died, not fit to live, not fit to survive in the new environment of light at night and year-round carbohydrate supply. For all previous human time, although carbohydrates were available in the months from late spring to late fall, we never craved them until the hours of sunlight changed as the planet tilted our piece real estate toward the sun. By June and July, our nights were only seven or eight hours long, compared to the dead of winter, when the blackness lasted at least 13 hours each day. The short nights coincided with an abundance of carbohydrate.

For millennia upon millennia, it all stayed the same. There was climate change, for sure, and species came and went. After all, "everything, everyone, everywhere, ends." But what we've done... extending the night has not only changed our health and reproductive capacity, but changed, for better or worse, the entirety of the web of life. You see, in all things cosmic and in evolution timing is everything.

We and everything else alive, from plankton and fungus to elephants and ants, are synchronized to the orbit and rotation of the earth in and out of the sun's light to assure us a food supply. All things great and small have internal sundials that measure time with molecular clocks in every cell that switch enormous cadres of regulatory genes on and off.

The light, whether a particle or a wave, always sparks biochemical reactions in all living things...

The whole ball of dirt heats up and cools down, heats up and cools down, over and over again, day in and day out. Plants grow. We animals eat them and each other. We die and become fertilizer. Plants grow, and it starts all over again. World without end... Amen.

All of this wild chemistry is happening on a spinning, gyrating, oscillating earth that, if you could hear the song of the cosmos from outer space, rings like a bell. Even the sun metabolizes and respires. The earth heaves and sighs, and we and the earthworms make everything fertile over and over again.

The ancients were right on. There is an ever-churning circulating flow of energy driven by the light.

We and every other living thing on earth are truly beings of light.

Every part of us reads the changing light intensity and spectrum. When you hold the back of your hand up to the window, cells called cryptochromes in your bloodstream pick up the blue spectrum of the light through your skin. These cryptochromes carry a piece of the sky all through you. That light energy and the carbohydrate (sugar) you eat even keep the symbiotic bacteria that live in the dark deep of your middle thriving. And in return for being a good host, they keep you thriving.

A lot of us aren't thriving anymore. It's not just aging. The aged in many parts of the world actually feel fine until one day it's just, well, lights out. It hasn't been like that for man or our pets (who share our environments) for a century or more. Think about it... depressed beavers? Infertile deer? Obese snakes? No. But, our dogs and cats have cancer, obesity, diabetes and heart disease.

To make sense of diseases such as obesity, diabetes, heart disease and cancer, all you need to understand are our physiological connections to the earth, sun and sky. Unless a microbe, virus, toxin, or tiger gets you fair and square, all other "disease states" can be explained by identifying the function that the particular "disease" could possibly have had in evolution, and then by locating the modern cultural trigger that has set in motion the ancient physiological response. Researchers have done that with obesity (1) and diabetes (2) in regard to seasonal variation in the food supply and day length and with mental illness (3), infertility (4) and sleep loss.

Once you look at eating, sleeping and reproducing, you'll discover cancer (5) and heart disease (6) also have a biophysical explanation (7). Of course dietary intervention certainly could reverse the course of some diseases. Cutting out carbohydrates out of season might actually cure obesity and most diabetes, but not necessarily all heart disease, and certainly not all cancer. Food is part of the equation, all right, but it is not the actual answer. Food is certainly, in many cases, the instrument of death, but not necessarily the cause of death.

The real answer to who holds the sword over our heads, in terms of our health, is in fact, just above our heads. The real answer lies in circadian and circannual rhythmicity, chronobiology, evolution vs. modern life. The real answer is to eat and sleep and reproduce in sync with the spin of the planet or go the way of the dinosaurs.

Your subconscious, via hormone and neurotransmitter activity, has, over the course of evolution, because of seasonality and our dependence on plant and animal foodstuffs as energy, been conditioned and fine-tuned to believe and act on the following: when the lights stay on too long (8), "Eat carbohydrates now or die later." When the light is long, your systems read summer. When your environment is temperature controlled, your systems read summer. When you want a midnight snack, it's never string cheese or a hard-boiled egg. It's cake or cereal or wine because this light-responsive instinct to put on fat in the summer to survive the winter has been the basis of our feast-or-famine metabolism for at least 3 million years. All of the effects of chronic light exposure and the carbohydrate consumption that follows that exposure would have, in another place and time, prepared us for the worst--for no food and for the shorter, darker, colder days of less sun. (9)

We have always "feasted" to endure the "famine" that always followed--until now.

Unfortunately, the truth in our time is that we eat carbohydrates now and die sooner. (10)

This is the survival formula = The Hibernation Hypothesis:

A. Long hours of artificial light = "summer" in your head

B. Summer comes always before "winter" and "winter" signifies famine to your internal controls

C. Famine on the horizon provokes instinctive carbohydrate craving to store fat for scarcity

This storage is accomplished by:

1. Increasing carbohydrate consumption until your body responds to all the insulin by becoming insulin-resistant in muscle tissue;

2. Ensuring that the carbohydrates taken in end up as an internal intra-abdominal fat pad; when that's full:

3. It prompts the liver to dump the extra sugar into cholesterol production, which will keep cell membranes from freezing at low temperatures.

If you slept at night for the number of hours it would normally be dark outside, you would only crave sugar in the summer, when the hours of light are long. It's the long hours of artificial light that confuse this ancient energy regulation system, while also destroying the lining of your heart; so the attendant excess cholesterol can obstruct blood flow. It is this "perennial adaptation," or the chronic, constant sleep loss (intent to hibernate), that causes overconsumption of carbohydrates and obesity and its attendant high blood pressure, high cholesterol, and inevitable heart failure.

Steps one, two, and three also correspond to the hormonal portrait of Type II diabetes--a disease that, in truth, is the end result of excruciating fatigue from light "toxicity." On the way to the end, you may well encounter one of the following--obesity, heart disease, stroke, mental illness, or cancer. The medical community, the FDA, the National Institutes of Health, and your TV will tell you that these PUO (Plagues of Unknown Origin) can only be cured by an even lower fat diet, at least three to six hours of exercise a week, and a cadre of supplements and vitamins.

Who are you going to believe?

Next time: Meet the Neighbors -- what sleep loss does to your immune system...

References:

(1) Van Cauter, Eve, et al. Sleep and the Epidemic of Obesity in Children and Adults. European Journal of Endocrinology 2008; 159: S59-S66.

Nedeltcheva, Arlet, et al. Sleep Curtailment is Accompanied by Increased intake of calories from snacks. American Journal of Clinical Nutrition 2009 Dec 3; 89: 126-133.


Lamberg, et al. Rx for Obesity: Eat Less, Exercise More, and--Maybe--Get More Sleep. JAMA 2006; 95: 2341-2344.

Leproult, Rachel, et al. Role of Sleep and Sleep Loss in Hormonal Release and Metabolism. Karger 2010; 17: 11-21.

Petrucci, Gina. Sleep Loss as a Risk Factor for Obesity. Bariatric Nursing and Surgical Patient Care 2007; 2(3): 185-188.

Van Cauter, Eve, et al. Impact of Sleep and Sleep Loss on Neuroendocrine and Metabolic Function. Hormone Research 2007; 67: 2-9.

Taskar, Varsha, et al. Metabolic Causes and Consequences of Sleep Disorders. Clinical Pulmonary Medicine 2008 Jan; 15(1): 40-44.

(2) Trento, Maria, et al. Sleep Abnormalities in Type 2 Diabetes may be Associated with Glycemic Control. Acta Diabetologica 2008 Dec; 45(4): 225-229.

Van Cauter, Eve. Decreased sleep duration and quality: novel risk factors for obesity and diabetes. Presented at European Society of Endocrinology 2008. Berlin, Germany. Endocrine Abstracts 16 PL7.

Spiegel, Karine, et al. Sleep loss: a novel risk factor for insulin resistance and Type 2 diabetes. Journal of Applied Physiology 2005; 99: 2008-2019.

Leproult, Rachel et al. Slow-wave Sleep and the Risk of Type 2 Diabetes in Humans. PNAS 2008 Jan; 105(3): 1044-1049.

Ayas, Najib, et al. A Prospective Study of Self-Reported Sleep Duration and Incident Diabetes in Women. Diabetes Care 2003 Feb; 26(2): 380-384.

(3) Wehr, Thomas, et al. 48-Hour Sleep-Wake Cycles in Manic-Depressive Illness: Naturalistic Observations and Sleep Deprivation Experiments. Archives of General Psychiatry 1982; 39(5):559-565.


Wehr, Thomas, et al. Treatment of a Rapidly Cycling Bipolar Patient by Using Extended Bed Rest and Darkness to Stabilize the Timing and Duration of Sleep. Biological Psychiatry 1998 Jun; 3(11):822-8.

Leibenluft, Ellen, et al. Relationship Between Sleep and Mood in Patients with Rapid-Cycling Bipolar Disorder. Psychiatry Research 1996 Jul; 63: 161-168.


Mendlewicz, Julien, et al. Diurnal Hypersecretion of Growth Hormone in Depression. Journal of Clinical Endocrinology & Metabolism 1985; 60(3): 505-512.


Van Cauter, Eve. Circadian and Sleep-Related Endocrine Rhythms in Schizophrenia. Archives of General Psychiatry 1991; 48(4):348-356.

P Linkowski, Paul, et al. The 24-Hour Profile of Plasma Prolactin in Men with Major Endogenous Depressive Illness. Archives of General Psychiatry 1989; 46(9): 813-819.

Wehr, Thomas, et al. Sleep and Biological Rhythms in Bipolar Illness. American Psychiatric Association Annual Review 1987; 6:61-80.

Lewy, Alfred. Circadian Phase Sleep and Mood Disorders. Neuropsychopharmacology: The Fifth Generation of Progress 2002; 1879-1893.
B Clock, P Effects, SCNE Pathways 


(4) Hakim, Rosemarie, et al. Infertility and Early Pregnancy Loss. American Journal of Obstetrics and Gynecology 1995; 172(5): 1510-1517.

Board, J, et al. Nocturnal Prolactin Levels in Infertility. Fertility and Sterility 1981 Dec; 36(6):720-4.

Kovanen, Leena, et al. ARNTL (BMAL1) and NPAS2 Gene Variants Contribute to Fertility and Seasonality. PLoS ONE 2009 Dec; 5(4): e10007.

Goldman, Bruce. The circadian timing system and reproduction in mammals. Steroids 1999 Sept; 64(9): 679-685.

(5) Vena, Catherine, et al. Sleep-wake disturbances in people with cancer part I: An overview of sleep, sleep regulation, and effects of disease and treatment. Oncology Nursing 2004 Jul; 31(4): 735-736.

Blask, David, et al. Putting cancer to sleep at night. Endocrine 2005 Jul; 27(2): 179-188.

Mercadante, Sebastiano, et al. Sleep disorders in advanced cancer patients: prevalence and factors associated. Supportive Care in Cancer 2004 May; 12(5): 355-359
.

Pinheiro, Simone, et al. A prospective study on habitual duration of sleep and incidence of breast cancer in a large cohort of women. Cancer Research 2006; 66: 5521-5525.

(6) Qureshi, Adnan, et al. Habitual sleep patterns and risk for stroke and coronary heart disease: a 10-year follow-up from NHANES I. Neurology 1997; 48:904-910.

Partinen, M, et al. Sleep disorders in relation to coronary heart disease. Acta Medica Scandinavica 2009 Apr; 211(S660): 69-80.

(7) Wehr, Thomas. In short photoperiods, human sleep is biphasic. Journal of Sleep Research 2009; 1(2): 103-107.

Lin, C. Photoreceptors and Regulation of Flowering Time. Plant Physiology 2000; 123: 39-50.
Arzt, Eduardo, et al. Immunomodulation by indoleamines: Serotonin and melatonin action on DNA and interferon-y synthesis by human peripheral blood mononuclear cells. Journal of Clinical Immunology 1988 Nov; 8(6): 513-520.

Konakchieva, R, et al. Selective effect of methoxyindoles on the lymphocyte proliferation and melatonin binding to activated human lymphoid cells. Journal of Neuroimmunology 1995 Dec; 63(2): 125-132.

Maestroni, Georges. The photoperiod transducer melatonin and the immune-hematopoietic system. Journal of Photochemistry and Photobiology B: Biology 1998 Jun; 43(3): 186-192.
Clarke, Iain, et al. Photoperiod effects on gene expression for hypothalamic appetite-regulating peptides and food intake in the ram. American Journal of Physiology. Regulatory, Integrative and Comparitive Physiology 2002 Sept; 284(1): 101-115.

(8) Van Cauter, Eve, et al. Sleep and the Epidemic of Obesity in Children and Adults. European Journal of Endocrinology 2008; 159: S59-S66.

Pearson, Helen. Medicine: sleep it off. Nature 2006 Sept; 443: 261-263.

Trento, Maria, et al. Sleep Abnormalities in Type 2 Diabetes may be Associated with Glycemic Control. Acta Diabetologica 2008 Dec; 45(4): 225-229.

Spiegel, K, et al. Sleep Duration and Levels of Hormones That Influence Hunger. Annals of Internal Medicine 2004 Dec; 141(11):1-52.

(9) Van Cauter, Eve. Phase-Shifting Effects of Light and Activity on the Human Circadian Clock. Chicago Univ Il Dept of Medicine 1994.

Lamberg, et al. Rx for Obesity: Eat Less, Exercise More, and--Maybe--Get More Sleep. JAMA 2006; 95: 2341-2344.

10O'Malley, Mary. Exploring the True Morbidity of Insomnia. Presented on MedScapeCME 2004.

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