Top 8 Effects and Maladies Caused by Sleep Deprivation

In this entry, I would like to focus a little bit on proper rest and recovery but, I don't just mean from exercise training but also from life. Many of my clients are hardworking, self-employed, career-driven individuals. Because there are too many tasks that need to be handled on a daily basis, the hours of sleep needed are being compromised. Ask yourself, "Is it really worth it?" or do you need to start learning to establish boundaries to better focus on YOU. Here is an article that I want to share and hope that everyone will learn from.

By Hugo Rivera

Millions of Americans suffer from sleep deprivation. If you can lie down in the middle of the day and fall asleep within 10 minutes, then you too are sleep deprived. There are many reasons for this ranging from too much work to simply staying up watching TV. In this article we will explore what the detrimental effects of sleep deprivation are and the maladies that it can cause.

1. Impaired glucose tolerance.

Without sleep, the central nervous system becomes more active, something that inhibits the pancreas from producing adequate insulin, the hormone the body needs to digest glucose. "In healthy young men with no risk factor, in one week, we had them in a pre-diabetic state," says researcher Van Cauter when referring to a study that he conducted on the effects of sleep deprivation.

2. Possible link to obesity.

Growth hormone (GH) is secreted during the first round of deep sleep. As both men and women age, they naturally spend less time in deep sleep, which lowers GH secretion. Lack of sleep at a younger age, however, could drive down GH prematurely, accelerating as a result the fat-gaining process. In addition, there is also research that indicates a lowering of the hormone testosterone as well, something that would also make the gaining of fat and the loss of muscle and easy thing for the body to do.

3. Increased carbohydrate cravings.

This is due to the fact that sleep deprivation negatively affects the production of a hormone called Leptin. This hormone is responsible for telling the body when it is full. However, with decreased production of this hormone, your body will crave calories (especially in the forms of carbs) even though its requirements have been met. Not a good situation to be in for a dieter.

4. Weakened immune system.

Research indicates that sleep deprivation affects adversely the white blood cell count in humans as well as the body’s ability to fight infections.

5. Increased risk of getting breast cancer.

Richard Stevens, a cancer researcher at the University of Connecticut, has speculated that there might be a connection between breast cancer and hormone cycles disrupted by late-night light. Melatonin, primarily secreted at night, may trigger a reduction in the body's production of estrogen. But light interferes with melatonin release (since melatonin is secreted in response to a lack of light), allowing estrogen levels to rise. Too much estrogen is known to promote the growth of breast cancers.

6. Decreased alertness and ability to focus.

A recent study showed that people who were awake for up to 19 hours scored worse on performance tests and alertness scales than those with a blood-alcohol level of .08 percent–legally drunk in some states. Also, this can lead to injury in the weight room since lack of alertness can cause you to neglect securing a machine correctly or even lose balance as you perform an exercise.

7. Hardening of the arteries.

Stress imposed on the body due to lack of sleep causes such a very sharp rise in cortisol levels. Such an imbalance can lead to hardening of the arteries, something that can cause a heart attack. In addition, we also know that very high cortisol levels lead to muscle loss, increased fat storage, loss of bone mass, cause depression, cause hypertension, cause insulin resistance (the cells in the body lose the ability to accept insulin), and lower growth hormone and testosterone production.

8. Depression and irritability.

Lack of sleep also causes depletion of neurotransmitters in the brain that are in charge of regulating mood. Because of this, sleep deprived people have a “shorter fuse” and also tend to get depressed more easily.

Shielding The Brain From Too Much Insulin Can Prolong Life

ScienceDaily (Jul. 20, 2007) — One route to a long and healthy life may be establishing the right balance in insulin signaling in the body and brain, according to new research from Children's Hospital Boston. The study, published in the July 20 issue of Science, not only reinforces the value of exercising and eating in moderation, but also helps explain a paradox in longevity research.

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Insulin sends a vital signal in the body, telling cells to use sugar from the blood. When cells become less sensitive to insulin, which often happens as we age and gain weight, the body makes more insulin to compensate. For a long time, researchers thought that "more insulin signaling was good," says Morris White, PhD, a Howard Hughes Medical Institute investigator in Children's Division of Endocrinology, who led the new study. "But this insulin is also hammering the brain, and we now think that's probably a bad thing."

Recent studies in the worm C. elegans and in fruit flies have shown that reducing insulin signaling lengthens lifespan. But in mammals, reducing insulin signaling can lead to fatal diabetes. White suspected that the key to explaining this paradox -- and to maximizing both health and longevity -- is to reduce insulin signaling only in the brain.

To test this hypothesis, White's team measured longevity and other characteristics in three types of mice. One group had normal insulin signaling in their brains. The other two groups were genetically engineered to have reduced brain insulin signaling, having less of a protein called Irs2 that carries insulin's message inside cells.

As the mice aged and gained weight, their sensitivity to insulin decreased, and higher insulin levels began to bombard their brains. The mice with reduced brain insulin signaling lived 18 percent longer than the normal mice. They were more active in old age, retained youthful metabolic cycles (burning sugar by day and fat by night) and retained protective levels of anti-oxidant enzymes such as superoxide dismutase, which protect against oxidative stress, or "biological rusting," in the brain and body.

In contrast, the mice with normal insulin signaling had become more sedentary, had lost the metabolic rhythms of youth and had reduced anti-oxidant enzymes, leaving them vulnerable to cellular damage. Such damage correlates with a host of age-related diseases such as atherosclerosis, Alzheimer's disease and cancer, notes White.

White believes his findings suggest a new approach to preventing diseases that shorten lifespan. "If we could hit cancer and cardiovascular disease by attenuating how much insulin that gets to the brain, or the amount of insulin signaling that happens deep within the brain," he says, "that's going to be much easier than trying to cut every cancer out."

Drugs that regulate Irs2 signaling in the brain (but not elsewhere in the body) are one possible strategy, but no such drug has yet been found.

The easiest method, White says, is old-fashioned diet and exercise. Although obesity and sedentary lifestyles tune down the body's sensitivity to insulin, exercise tunes it back up. Furthermore, eating smaller meals keeps insulin low in the bloodstream, ensuring that less reaches the brain.

"This study gives a molecular explanation of why it's good to exercise and not eat too much," says White. "If we can put a sound scientific basis behind the idea that diet and exercise are good, maybe we'll convince some more people to do it."

The study also calls into question the long-term effects of insulin therapy for diabetes, White adds. "Too much insulin might be fine to keep glucose levels under control. But it's probably damaging your brain in the long run," he says. Better treatments for diabetes, he suggests, would concentrate on sensitizing the body's cells to low amounts of insulin.

The work was supported by the Howard Hughes Medical Institute, the National Institutes of Health, the Japan Society for the Promotion of Science, and the Yamada Science Foundation.

Adapted from Science Daily
http://www.sciencedaily.com/releases/2007/07/070719141139.htm