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It can be tempting to trade sleep for a few precious hours of wakefulness, but it is important to consider the hidden costs. Sleep is precious, too.

Numerous studies have found that insufficient sleep increases a person’s risk of developing serious medical conditions, including obesity, diabetes, and cardiovascular disease.

Lack of adequate sleep over time has also been associated with a shortened lifespan.

An analysis of data from three separate studies suggests that sleeping five or fewer hours per night may increase mortality risk by as much as 15 percent.

One of the most important benefits of sleep is that it provides cells and tissues with the opportunity to recover from the wear and tear of daily life. Major restorative functions in the body such as tissue repair, muscle growth, and protein synthesis occur almost exclusively during sleep.

Insufficient sleep may cause health problems by altering levels of the hormones involved in such processes as metabolism, appetite regulation, and stress response.

Obesity—Several studies have linked insufficient sleep and weight gain. One study found that people who slept fewer than six hours per night on a regular basis were much more likely to have excess body weight, while people who slept an average of eight hours per night had the lowest relative body fat of the study group.

Another study found that babies who are “short sleepers” are much more likely to develop obesity later in childhood than those who sleep the recommended amount.

Diabetes—Studies have shown that people who reported sleeping fewer than five hours per night had a greatly increased risk of having or developing type 2 diabetes. Fortunately, studies have also found that improved sleep can positively influence blood sugar control and reduce the effects of type 2 diabetes.

Cardiovascular disease and hypertension—A recent study found that even modestly reduced sleep (six to seven hours per night) was associated with a greatly increased the risk of coronary artery calcification, a predictor of future myocardial infarction (heart attack) and death due to heart disease.

There is also growing evidence of a connection between sleep loss caused by obstructive sleep apnea and an increased risk of cardiovascular diseases, including hypertension, stroke, coronary heart disease, and irregular heartbeat.

Immune function—Interactions between sleep and the immune system have been well documented. Sleep deprivation increases the levels of many inflammatory mediators, and infections in turn affect the amount and patterns of sleep.

While scientists are just beginning to understand these interactions, early work suggests that sleep deprivation may decrease the ability to resist infection.

In a recent study, people who averaged less than seven hours of sleep a night were about three times more likely to develop cold symptoms than study volunteers who got eight or more hours of sleep when exposed to the cold-causing rhinovirus.

In addition, those individuals who got better quality sleep were the least likely to come down with a cold. 

The epigenome is the complex machinery that determines how active each of our genes are. You can look at the epigenome as an on-off switch for genes.

The epigenome is very important for gene expression (which genes are active or inactive), and thus cellular function as a whole.

The problem is that during aging the epigenome becomes increasingly dysregulated.

Liver-specific genes are switched on in brain cells, stomach genes are switched on in muscle cells, and so on.

Genes that need to be turned off are turned on (like cancer-promoting genes), and genes that need to be turned on are switched off, such as genes that repair or protect our cells. 

Generally, we see that our DNA becomes more demethylated (there are less methyl groups sticking on the DNA which would normally prevent the DNA to be translated into protein). As a result, gene transcription is less suppressed in many areas.

This leads to specific genes becoming active that should not be active, like cancer-promoting genes.

We now know that epigenetics is the complex machinery determining how active or inactive each of our genes are. Genes are the keys on the piano- but epigenetics is the player of the piano, determining how genes are expressed or silenced.

The problem that occurs during aging is that our epigenetics become increasingly dysregulated.

Liver-specific genes are erroneously switched on in brain cells, stomach genes are switched on in muscle cells, and so on.

Genes that need to be turned off are turned on (like cancer-promoting genes), and genes that need to be turned on are switched off, such as genes that repair or protect our cells. 

Generally, we see that our DNA ages and becomes more demethylated (which we will explore more in The Big Rewind workshops). As a result, gene transcription (the process by which DNA is copied for protein synthesis),  is less suppressed in many areas.

This leads to specific genes becoming active that should not be active, like cancer and other disease-promoting genes. Combine that with the chronic inflammation that also accompanies aging and we have increased cellular dysfunction.

The epigenome is the complex machinery that determines how active each of our genes are. You can look at the epigenome as an on-off switch for genes.

The epigenome is very important for gene expression (which genes are active or inactive), and thus cellular function as a whole.

The problem is that during aging the epigenome becomes increasingly dysregulated.

Liver-specific genes are switched on in brain cells, stomach genes are switched on in muscle cells, and so on.

Genes that need to be turned off are turned on (like cancer-promoting genes), and genes that need to be turned on are switched off, such as genes that repair or protect our cells. 

Generally, we see that our DNA becomes more demethylated (there are less methyl groups sticking on the DNA which would normally prevent the DNA to be translated into protein). As a result, gene transcription is less suppressed in many areas.

This leads to specific genes becoming active that should not be active, like cancer-promoting genes.