Melatonin is the hormone that is primarily responsible for the feeling of sleepiness. It is released from the pineal gland in the absence of light and bathes the whole body. One of its most influential sites of action is the pituitary gland. Melatonin decreases the pituitary release of hormones responsible for activity, sexual function, and stress responses. The precursor for melatonin is the neurotransmitter serotonin. When the pineal gland is activated by lack of light, it starts converting serotonin to melatonin. The net result is a decrease in available serotonin. Because serotonin is typically responsible for our alertness during the day, this secondary effect contributes to sleepiness at night. The introduction of light in the morning causes melatonin production to decrease and for serotonin (and other hormones associated with wakefulness) to increase.

The change of seasons is sensed by organisms in a variety of ways, but one of the most influential for humans is the increase or decrease in day length. Although various factors likely contribute to variations of SAD, changes in daylight and a disruption of the melatonin/serotonin balance is key. Some of us, based on our genetic disposition, are very sensitive to the changes in daylight that occur with the change in seasons.

The most common form of SAD occurs in the fall/winter as the days get shorter (“winter blues”). People who suffer from this form of SAD simply feel like hibernating. They have trouble getting up in the morning, feel depressed, feel hopeless, have low energy, and may gain weight. One of the main theories for this type of SAD is that the decrease in sunlight shifts the melatonin/serotonin balance in such a way that there is more melatonin than serotonin. The increased exposure to melatonin results in a quieting of the pituitary gland, which results in the symptoms listed above. Because the pineal gland is creating all of the extra melatonin out of serotonin, less serotonin is available to support the efforts of happy wakefulness and concentration. Treatment for fall/winter SAD can include an increase in exposure to bright full spectrum light, exercise, and time spent outside during the day. Some medications can also beneficial.

Spring and summer SAD (“summer blues”) tends to have a slightly different effect on people but is also caused by a disruption of the serotonin/melatonin balance, although it is opposite. Symptoms include insomnia, irritability, increased libido, weight loss and anxiety.

Reverse seasonal affective disorder is not necessarily associated with the spring or fall and is defined by symptoms of elevated mood, excessive socialization, and hyperactivity. Some people think that this is a form of bipolar disorder. The fact that the change in seasons has such an uncharacteristic effect on some people is likely due to genetics, lifestyle, and stress. Their brains are hardwired to have this inverse reaction to the hormones monitoring sleepiness and wakefulness. The genetic anomaly may be in receptor subtypes or it may be in the processing of the secondary effects of serotonin.

As with all forms of SAD, if sleeping patterns can be normalized, the individual’s symptoms are likely to decrease. However, feelings of extreme hopeless or serious weight loss should be taken to a medical doctor. They will be able to best determine treatment for your specific condition based on a history of potential underlying causes.

Overall skin coloration is determined by the degree to which cells in the skin called melanocytes produce the pigment melanin. Melanin is also responsible for hair and eye coloring. The subtype pheomelanin is responsible for red hair, while the subtype eumelanin is responsible for grey, black, yellow, and brown hair. People with certain ancestries have the genetic coding to create a lot of melanin in their skin and therefore have dark skin. Albinism occurs in individuals who produce no melanin. Freckles are small bunches of melanin that are visible on individuals with fair skin. The gene for the melanocortin-1 receptor (MC1R) plays a role in the presence of freckles; individuals with the dominant variant of MC1R have freckles. The technical word for normal, flat freckles that are a shade of red or brown is ephelides. The concentrations of melanin that are responsible for freckles are much different than clusters of melanocytes, which is associated with skin cancer. People with freckles have a normal number of melanocytes; their melanocytes just create clusters of melanin.

Melanin has an extremely important role- it absorbs UV light and dissipates the UV rays as heat. This process protects our DNA from the damage that can be imparted by UV rays. Individuals with dark skin have more UV-dissipating capacity. This important function of melatonin is appreciated throughout nature. Melanin can be found all over nature from bacteria to humans, with the curious exception of spiders. Sunlight is therefore a stimulus for melanocytes to produce melanin because they are trying to protect the body from UV rays. The increased production of melanin that occurs after melanocytes are exposed to sunlight results in a suntan- or the darkening of freckles. Because newborn babies haven’t been exposed to sun, they not have freckles and the use of sunscreen or the clothing protection can prevent freckles. Repeated exposure to the sun throughout life can result in liver spots, which are basically permanent freckles that do not fade away. Reverse freckles, or white freckles, are simply spots of no melanin.

Some people try to get rid of freckles through a bleaching process involving an agent such as hydroquinone that slows down the process at which melanocytes produce melanin. There is an autoimmune condition called vitiligo in which melanocytes are attacked by the immune system and become too weak to produce melanin. The result is patches of white skin and eventual whitening of areas of the body. This is what happened to Michael Jackson.

Taste preferences and aversions are related to both physiology and psychology. In a physiological sense, we will crave foods that fulfill our body’s needs. For example, we will crave salt when our electrolyte balance is off and crave sweets when we feel like we need calories. The placement of the sweet receptors on the tip of the tongue is probably no accident- our brains need sugar to keep running and so we seek it out first and foremost. If you want to know how something tastes, you stick the tip of your tongue on it. A sweet sensation will likely elicit a response from your brain that the tasted object would be good to eat. Taste aversions are often associated with foods that have made us ill. Taste aversions can be stronger than our innate senses. For example, a rodent can be made to hate sweet treats if we associate them with something that makes the rodent sick.

Bitter flavors typically signify natural toxins and sour flavors signify the presence of acid. We often include these flavors in our food choices, which may in part be due to the fact that we have trained our palates to be more sophisticated than those of our evolutionary forbearers. Sour and bitter flavors can be used to balance sweet and salty flavors, bringing balance and variety to our meals. The ability to sense bitter tastes, however, is a dominant genetic trait that follows a classical Mendelian pattern; about a quarter of people hardly taste bitter at all, half of people taste bitter to a moderate degree, and about a quarter of people are very sensitive to bitter flavors. This is one way in which individuals differ in their taste preferences. This genetic component of individual taste preferences is strengthened by our sense of smell, which is based on the smell receptors that we inherit and, in turn, have a huge impact on how we taste things. In fact, up to 75% of what we perceive as taste may actually be smell!

The psychological side of taste is quite interesting, as well. I think that we all have comfort food, nostalgic food, a social drink, or childhood treat. These dishes- fried chicken, chocolate chip cookies, gin and tonic, ice cream, whatever- are attractive to us for more reasons than our physiological needs. Smelling and eating these foods tap into our memory banks and gets the attention of our reward centers. We each have our own experiences and environments that direct these unique food preferences.

As we age, both the physiological and psychological sides of taste change. Not only do we have more foods to be nostalgic or emotional about, but we lose taste buds from the top of our mouth and side of our tongue so that all of our taste sensation is focused on the center of the tongue (salty and sweet). As we age further, this section of the tongue also gets less sensitive and food seems blander. One response may be to add more sugar and salt to food. As we age, we may seek a bit more “kick” in our food through spices such as chili peppers, wasabi, or ginger. Although these elements seem to add more flavor to our food, they actually work through a system that is completely separate from our taste buds. Our sense of taste can be further reduced during life from smoking, scalding, allergies, medications that are commonly taken by older people, tooth decay, or head injury. As one’s sense of smell decreases around the age of 60, taste perception also decreases.

Unlike fish, who can taste with their fins, we humans are limited to our little tongue and nose. So, enjoy your food while you can and be responsible about how you eat in your later years. If you are bored with food, try adding a little spice.

Muscle contraction begins with a signal from your brain, which propagates through your nervous system and causes the release of the neurotransmitter acetylcholine at the neuromuscular junction. When the acetylcholine binds to its receptors a muscle, a series of intracellular events occurs and the muscle fibers contract. The energy source for this contraction is called ATP. During normal exercise, glucose (sugar) and oxygen produce a sufficient amount of ATP to fuel muscle contractions (via the Krebs Cycle). However, during extreme efforts like sprinting, our bodies require more energy and a different energy cycle is revved up to produce much greater volumes of ATP for a short amount of time. Each of these cycles of energy production produces pyruvic acid, a product of glucose breakdown. At moderate levels of exercise, moderate levels of pyruvic acid are produced and much of it goes into the Krebs Cycle to produce energy; at high levels of exercise, high levels of pyruvic acid are produced.

Pyruvic acid is converted into lactic acid and at high levels of exercise, more pyruvic acid is produced than the body can handle and a buildup of lactic acid results. At a certain point, our body can clear lactic acid at the same rate that it is being made. This is called the lactate threshold and it is a very important aspect of training for elite athletes. The higher their lactate threshold, the longer they can go at a high tempo before the build-up of lactic acid brings on burning and muscle fatigue.

A process called the lactate shuttle is important because it allows for some of the lactic acid to be oxidized and converted into additional energy for the muscles. Efficient clearance of lactate is likely an important factor in lactate threshold and it has been suggested that lactate may ultimately contribute to the prevention of fatigue.

The burning sensation associated with the build-up of lactic acid is due to the presence of hydrogen ions in the blood. The hydrogen ions released by the lactic acid may act locally to indicate fatigue, but may also act on peripheral nervous system receptors to send the signal to the brain that glucose is being utilized at a high rate and muscle fatigue is setting in. In this way, the central nervous system (which initiated the muscle contraction in the first place) regulates the physical activity.

Vitamin D is found in foods such as fatty fishes, eggs, beef liver, and UV light-exposed mushrooms. So….why is it that people head out into the sun and say, “I need to go and get some vitamin D?”

It is because UVB exposure above the UV index level of 3 is necessary to activate the vitamin D. There are several forms, or vitamers, of vitamin D and they are not all equal. The foods mentioned above contain a pro-form (7-dehydrocholesterol) that becomes active (cholecalciferol) in the skin following UV exposure. The cholecalciferol then travels from the skin to the liver, where it is hydroxylated (calcifediol/25-hydroxyvitamin D3). Finally, the modified vitamin moves to the kidney, where it undergoes another round of hydroxylation to become calcitriol (1,25-dihydroxyvitamin D3), the most active form of vitamin D3. The vitamer of vitamin D that is supplemented in foods is cholecalciferol- it has already been irradiated and is therefore active.

It is possible to ingest too much vitamin D, which makes sense since its role is to maintain normal blood calcium levels. Too much vitamin D results in hypercalcaemia, a condition that can lead to increased blood pressure, weight loss, nausea, vomiting, and even kidney damage. For pregnant women, hypercalcaemia can cause very serious fetal damage. Excessive vitamin D levels occur when people take too many supplements- not from getting too much sun exposure.

Here are the details….digestive enzymes break down ingested asparagus and produce methanethiol (or methyl mercaptan), which is believed to be the aromatic culprit in stinky asparagus urine. (However, some scientists believe that a different family of thioesters that are the byproducts of acid reacting with sulfur-containing alcohol are responsible.) The methanethiol waste product is then (somewhat mysteriously) transmitted through the kidney to the urine. Ironically, asparagus is a diuretic, which contributes to the rapidity with which the scented urine exits the body. The aromatic nature of the methanethiol is due to the fact that it is released as a gas when you urinate.

Interestingly, a similar process is employed by skunks when they make their musk. The difference with skunks is that they have specific glands for storing and concentrating sulfur-containing chemicals, which they can create from more products than asparagus. Methanethiol is also released from decaying organic matter. It is truly a wonderful aroma.

There has been some controversy as to whether everyone has stinky urine after eating asparagus. I am aware of no recent, controlled clinical study on this topic, but there is an alternative hypothesis. It is quite possible that, while we all conduct this digestive process, we do not all have smell receptors that are sensitive tor methanethiol. We all have a very unique array of olfactory receptors and it turns out that the ability to smell asparagus is a dominant genetic trait and is therefore not universal. We are born with about 400 olfactory receptors out of a possible 1000. This does not mean that we can only smell 400 different aromas; a single odorant binds with varying affinities to different olfactory receptors, creating a distinct pattern of nerve impulses to the brain that define the scent. Another odorant may bind similar olfactory receptors with different affinities, creating a unique pattern of nerve impulses to the brain and a completely unique sensory representation. The brain then interprets that scent and associates it with the object. We can smell thousands of different smells, based on the unique combination of smell receptors rendered active by a particular odorant.

Our olfactory systems are a very primitive part of our brain and tightly linked with the hippocampus and our memories. This is why certain smells evoke strong memories. Perhaps you can conduct a controlled trial of the genetic patterns of methanethiol sensing in your family at the next family gathering. That will certainly create some smell-associated memories!

The more traditional IUD is made of copper, while a newer iteration of the IUD is made of plastic and has a small compartment in it that is filled with a derivative of the hormone progesterone. This type of IUD is sometimes referred to as an intrauterine system (IUS). An IUD/IUS is T-shaped and about the size of a quarter; it is placed inside the uterus by a doctor or nurse. (The average uterus is the size of a clenched fist.) They are recognized as a form of “long-acting reversible contraception” because they can be left in the uterus and prevent pregnancy for 5-10 years. An IUD/IUS is one of the most cost efficient and effective types of contraception available [1]. They are the most common form of birth control in the world (45% of married women in China use it), although they are used by only about 1% of women United States. Americans tend to use birth control pills more than IUDs/IUSs.

The IUD and IUS are similar in size and shape and both devices cause a low-grade local inflammatory response that makes the uterine environment less hospitable to sperm or a fertilized egg. The IUD and IUS have additional mechanisms for preventing pregnancy that are unique. Copper ions released from the IUD enhance the inflammatory response and the presence of the copper ions is toxic to sperm. It is like a spermicide. In addition, the mucous in the uterus can become thicker, making it more difficult for sperm to make their way up to an egg. Finally, the copper-laden fluids of the uterus make the environment hostile to an embryo should an egg become fertilized.

The IUS, on the other hand, functions more like conventional contraceptive methods because it constantly releases levonorgestrel, a progesterone derivative. The constant level of progesterone prevents the uterine wall from becoming full of nutrients and thereby inhibits implantation. As with birth control pills, an IUS maintains a non-pregnant hormonal state so that the body cannot foster an embryo. Over time, there is some glandular atrophy and ovulation is prevented. Once it is removed, however, most women have no trouble getting pregnant if they want to.

[1] Mavranezouli I, Wilkinson C, Glasier A. The cost-effectiveness of long-acting reversible contraceptive methods in the UK: analysis based on a decision-analytic model developed for a National Institute for Health and Clinical Excellence (NICE) clinical practice guideline. Hum Reprod. 2008;23(6):1338-1345.

Hair can be considered in two separate sections, the root and the shaft. The hair root is located inside of the follicle and exists below the portion of the skin while the shaft is the portion of hair that extends out from the skin. The root of the hair receives nutrients from the blood through the dermal papilla. The nutrients that are supplied to the root of the hair through the dermal papilla, combined with oil from the sebaceous gland, can contribute to hair’s strength. This strength of the hair shaft can contribute to how long it grows before it breaks. Also, keeping it from drying out can prevent it from breaking. As such, a dry environment or treating hair with a lot of chemicals can limit its length.

The hair that grows out of the hair follicle can be course or fine. Coarse hair is thicker because it has a thick central core of cells (called the medulla) that make it stronger and less likely to break due to environmental factors. This is a genetic trait and blonde or fine hair often lacks this dense core. It is thus easier for someone with thick (likely dark) hair to grow it very long. Although the average rate of hair growth is apparently half an inch per month, the rate at which hair grows is also genetically determined.

Hair also sheds, naturally. The normal cycle of a hair follicle lasts from 2-8 years. The first phase, also called anagen, is when the hair shaft grows out of the root. The second phase in the cycle is called catagen and is the period during which the hair follicle shrinks and the root detaches from the blood supply. Catagen lasts for a couple of weeks. The final phase, telogen, is when the hair does not grow, but is still attached. This phase lasts for several weeks. After telogen, the hair follicle moves back into anagen and begins to grow a new hair. It is the pushing out of the old hair that leads to shedding. A normal rate of shedding is 50-100 hairs a day. It is thus the length of this cycle that partially determines how long a hair can get. If one has inherited a shorter hair growth cycle of 2 years, and hair grows at an saverage of half an inch a month, the longest it could grow if it were strong is 12 inches. However, if someone had a very long hair growth cycle of 8 years and their hair were strong, it could grow 4 feet or more!

Super-long hair thus occurs only when there is a combination of several factors: a decent rate of growth, coarse hair, a non-drying environment, a long hair follicle shedding cycle, and, of course, the choice to not visit a barber.

Your dog can actually eat a little bit of chocolate, but if they eat about an ounce of milk chocolate per kilogram of body weight or as little as a couple of mouthfuls of cocoa mulch, there will be trouble. At that quantity, dogs may experience seizures. These effects are due to the caffeine and theobromine that are in chocolate. In the case of chocolate, the theobromine is more of a factor. Theobromine (which is also called xantheose) is a water soluble alkaloid that is metabolized in the liver. The byproducts of its metabolism are methylxanthine and then methyluric acid. Theobromine blocks the breakdown of cyclic AMP, thus acting as a stimulant through a mechanism much like caffeine. In humans, theobromine has less of an impact on the central nervous system than does caffeine and may also be responsible for the aphrodisiac qualities attributed to chocolate.

In dogs, however, theobromine is metabolized much more slowly than in humans, prolonging its effects on the central nervous system and smooth muscle. The first symptoms experienced by animals with theobromine poisoning may be a result of vagal nerve blockade and include increased of heart rate as well as disruption of the smooth muscles in the digestive tract. Later on, dogs can suffer from seizures due to loss of vagal nerve activity and the stimulatory effects of accumulated cyclic AMP. These symptoms can lead to death in serious cases, although early treatment is usually successful.

Interestingly, cats would also suffer from the negative effects of theobromine poisoning, but they do not have sweet taste receptors and are rarely drawn to ingest chocolate.

This nicotinic acetylcholine receptor (nAChR) is endogenously activated by acetylcholine, but is also highly responsive to the drug nicotine. When activated by either acetylcholine or nicotine, the ligand-gated nAChR opens and elicits an immediate response from the effector cells. Cells that have nAChR are found throughout the body, particularly at neuromuscular junctions and in the brain. The immediate effect of nicotine on the cholinergic system is actually a release of epinephrine (which is also known as adrenaline) and a speeding up of the heart. That sensation, however, rapidly subsides and the tobacco user then experiences a state of calm. In addition to activating the body’s cholinergic system, nicotine blocks the release of insulin from the pancreas and causes a brief period of elevated blood sugar and suppressed appetite. Because nAChRs can become less sensitive to the effects of nicotine, repeated use makes the body less responsive to the same dose and people who use nicotine need to use more to get the same effects. In addition, withdrawal from nicotine makes the user feel edgy and agitated, often leading to chain use in order to avoid these negative feelings.

The peripheral effects of nicotine may cause some of the feelings of physical relaxation, but it is the effects on the brain that are responsible for its addictive properties. When nicotine activates nAChrs in the brain, it causes the release of dopamine, the neurotransmitter associated with feelings of comfort and well-being. This pathway of dopamine release has also been called the “reward system” and is activated similarly, but to a greater degree, with other drugs such as cocaine, amphetamines, and alcohol. In addition, the reward system responds to pleasurable activities such as having sex, eating food, or receiving a lot of money. Activation of the reward system involves dopamine release from an area of the brain called the nucleus accumbens and activation of D2 dopamine receptors at target brain regions, resulting in inhibition of cAMP in these target brain regions. With continual stimulation, the reward system becomes more sensitive to the drug, reinforces behaviors of that drug’s use, and motivates the individual to seek out situations in which the drug is available. This combination of factors is what makes addiction especially difficult to combat.

Caffeine functions similarly to nicotine in that it activates the reward system and also binds to a receptor designed for neurotransmitters; in particular, it binds to adeonsine receptors. In the case of caffeine, however, it blocks the adenosine receptors and prevents adenosine from acting on the receptor rather than stimulating the receptor. By blocking the adenosine pathways, caffeine prevents adenosine from calming neural systems and results in arousal. The specifics of these mechanisms have yet to be completely defined, but one place where adenosine has an effect is on dopamine cells. The disinhibition of dopamine cells will prolong their effect and this may be one reason why caffeine makes nicotine more rewarding.

A second mechanism that might play a role in the increased reward experienced by an individual drinking coffee and smoking a cigarette at the same time has to do with the second known mechanism of caffeine. It has a more global effect of altering the metabolic processes of cells throughout the body. Caffeine allows for build up of intracellular energy stores (ATP) by blocking the enzymes that usually breaking them down. This effect is similar to that imparted upon cells by epinephrine, the neurohormone responsible for arousal. Epinephrine is released initially when nicotine is used and the use of caffeine with nicotine may prolong the state of alertness and focus that is experienced in the initial phase of nicotine use.

Ironically, smoking can actually decrease the length of time that caffeine is effective. However, the use of both nicotine and caffeine at the same time initiates an intense feeling of alertness that may help people feel more awake in the mornings. In addition, the use of both drugs together can powerfully activate the brain’s reward system. The reward system will therefore crave continued activation to that degree and other parts of the brain will associate those feelings of well-being with the taste, smell, and situational aspects of nicotine and caffeine consumed with one another, further perpetuating their concomitant use.

1. National Institute of Drug Addiction, National Institutes of Health statistics. Available at: http://www.nida.nih.gov/ResearchReports/Nicotine/nicotine2.html#impact. Accessed: November 29, 2008.

Frequent urination is one of the primary symptoms of diabetes. When people speak of diabetes, they are usually referring to diabetes mellitus. Mellitus means sweet or sugary. The urine of individuals with diabetes mellitus is not only voluminous, but also smells sweet. This is due to their innate issues absorbing sugar, which results from problems with the hormone insulin. Insulin, which increases after the consumption of food in healthy individuals, is important for signaling cells of the body to absorb sugar. If that insulin signal is inefficient or the cells cannot sense it, such as in the case of diabetes mellitus, sugar cannot absorb sugar from the blood stream. One of the things that happen at that point is that sugar is excreted in the urine. Other consequences of consistently high blood sugar (chronic hyperglycemia) include damage to the kidneys, nerves, vasculature, and visual system.

The cause of disrupted insulin is different in Type I and Type II diabetes. In Type I diabetes, there is an underlying auto-inflammatory condition in which the immune system attacks pancreatic beta cells that are responsible for producing insulin. Eventually, these cells die and there is no natural source of insulin. Individuals with Type I diabetes therefore cannot make insulin when they need it and have to take insulin. This form of diabetes is what most children have; it is caused by genetics rather than by lifestyle and accounts for only about 5% of the cases of diabetes in the United States.

Individuals with Type II diabetes are able to make some insulin. The problem in this situation is that they are insensitive to insulin. Down-regulation of insulin receptors means that their cells cannot sense insulin to absorb sugar. Their treatment might include insulin at later stages of the disease, but can also include drugs that increase the body’s production of insulin, decrease the body’s breakdown of insulin, or mediate the body’s resistance to insulin. Doctors treating individuals with Type II diabetes mellitus have to carefully monitor their patients and often change their treatment regimens throughout the course of the disease. Unlike Type I diabetes mellitus, Type II diabetes can be caused by poor lifestyle.

Lifestyle modification is often a component of treatment for people with Type II diabetes. A reduction of adipose tissue, specifically in the gut, can reduce the risk of developing Type II diabetes. This is because the fat itself can release hormones that disrupt the insulin system. These hormones are called adipokines and are known to impair the body’s regulation of glucose. Although there may be a genetic component that predisposes individuals to Type II diabetes, poor lifestyle is a major contributor that is cost our country $174 billion in 2007. Making proper lifestyle choices is therefore important for more reasons than maintaining our body image! If you would like to learn more to help someone with diabetes or to help prevent someone from developing diabetes, a lot more information on this topic can be found at the American Diabetes Association website, www.diabetes.org.

So, they compromised after many lively debates on the topic and now we all have an 8-minute snooze session. As a scientist, I wanted to determine the neurological basis for keeping a person on the fine line that separates sleep from wakefulness. It turns out, however, that the true basis for the 8 (to 9) minute snooze lies within the clock’s mechanics. Classic alarm clocks are built on a three bit counter that refreshes at the start of the ninth minute. The snooze button taps into this moment to reset itself. Newer digital clocks, however, allow for all different snooze settings. I have reviewed some basic sleep principles for you to consider in the case that you have the luxury of setting your own snooze duration (and actually want to get up).

That magical morning moment when sleep becomes wakefulness requires that many physiological systems line up. When we sleep, our brains cycle through five different stages of sleep that have been defined as stages 1-4 and rapid eye movement (REM) sleep. Stages 1 and 2 are lighter levels of sleep while 3 and 4 are deep sleep (also known as delta sleep). REM is the sleep period during which our brain is the most active, creating dreams. This may also be the most important part of sleep for learning and memory. We move in and out of REM sleep several times during the night and end up spending approximately 20% of our sleep time in REM sleep; when we are awoken during an REM sleep cycle, we often remember our dreams. As we approach morning, our sleep cycles are shorter and the time spent in stage 1, stage 2, and REM sleep increases.

When our alarm goes off in the morning, our body has been preparing for wakefulness by altering its temperature and hormonal milieu. Our brains move out of stage 1 or REM sleep to shut off our alarm. If we turn it off all the way, we may have a bout of sleep-induced amnesia that causes us to forget the brief moment of wakefulness. However, if we have a snooze button that keeps us from moving fully back into stage 1, we can slowly wake up and keep the new day in our consciousness. I am, however, unaware of any scientific publications that define a specific physiological or neurological event that occurs at 8 minutes after waking.

As one final note, it is recommended that adults get seven to nine hours of sleep a night and many factors including insomnia, sleep deprivation, napping patterns, and lifestyle- can alter normal sleep cycles and make it harder to get up in the morning and you may need to adjust your snooze schedule accordingly.

Figure can be accessed at: http://helpguide.org/life/sleeping.htm. September 29, 2008.

The reason is that bacteria thrive in moist environments like those created with sweat and cotton socks. With the right environment, the bacteria feast on the dead skin cells from your feet and produce stinky waste products.

It has recently been discovered that common foot odors are likely caused by Staphylococcus epidermis, a normal resident of the foot (Ara K, et al). One of the byproducts released by Staphylococcus epidermis as it degrades the leucine in sweat is isovaleric acid, or 3-methylbutanoic acid, and this is what causes the stink that is present in your sneakers and in locker rooms. Ironically, isovaleric acid releases volatile esters that are often used in perfumes. It is strange to think that stinky shoes and fine fragrances are so closely related. Although we can discern the difference between stinky isovaleric acid and its ester fumes, we all smell isovaleric acid to different degrees. According one recent set of genetic analyses, one person may be 10,000 times more sensitive to the sweaty stink of isovaleric acid than others (Menashe I, et al)!

More severe bacterial conditions of the foot are caused by Micrococcus sedentarius, or Kytococcus sedentarius, and sufferers of this infection are often left with severe skin damage and the stink from their feet is due to the production of thiols, sulfides, and thioesters, which contain sulfur (English JC, et al).

Preventing these bacteria from taking over your feet is as simple as keeping your feet clean and aired out. So, wash up those dogs and walk around barefoot a bit. Because isovaleric acid is not very water soluble, it is necessary to use some sort of soap to get the stink off your feet when washing them. Once your feet are clean a little bit of citral, citronella, or geraniol can inhibit the production of isovaleric acid (Ara K, et al). As far as remedying the sneakers, try putting them in the freezer for 24 hours (after placing them in a plastic bag, perhaps…). That should kill of some of the bacteria that have taken up residence.

 
English JC. Pitted Keratolyis. WebMD; August 30, 2006. Available at: http://www.emedicine.com/derm/TOPIC332.HTM. Accessed September 12, 2008.

Ara K, Hama M, Akiba S, et al. Foot odor due to microbial metabolism and its control. Can J Microbiol. 2006;52(4):357-364.

Menashe I, Abaffy T, Hasin Y, et al. (2007) Genetic Elucidation of Human Hyperosmia to Isovaleric Acid. PLoS Biology. 2007;5(11):e284.

Activation of the sympathetic nervous system and the resultant release of epinephrine is responsible for physiological reactions in addition to increased heart rate. These other responses also help the body prepare to react and include dilation of the pupils to increase visual acuity, the breakdown of liver glycogen so that glucose is readily available to fuel muscles, enhanced lung function, hypervigilance, and the redirection of blood flow from central organs to the muscles. During this time, the parasympathetic nervous system, the part of the central nervous system that is responsible for digestion, reproduction, and energy storage, is shut down. The body is focused on survival and the activities of the sympathetic nervous system.

From day to day, our brains primarily utilize glucose as fuel. Glucose is a simple sugar that is the most convenient form of fuel for cells. Although the brain is only two percent of the body’s total weight, it consumes an average of 70 percent of the body’s glucose, which comes as no surprise because we have up to 100 billion energy-hungry neurons in our brains. Glucose, a simple sugar, is absorbed by brain cells directly from the blood stream. Glycogen, a larger carbohydrate, can be broken down by the liver and kidney to release more glucose into the bloodstream if necessary. The body continually adapts its metabolism to ensure that plenty of glucose is available for the brain. During times of extreme stress, blood flow is decreased to muscles and other organs that also consume glucose to ensure that the brain has a continuous supply of glucose.

The second way to address this question is from a longterm perspective. As we age, our brains must protect themselves from free radicals that are generated during normal cellular metabolic processes. During stressful times, our bodies are exposed to greater loads of free radicals. Throughout our lives, brain cells can be damaged by free radicals. It is thus important to consume foods with antioxidants because antioxidants protect brain cells from free radicals. One food that is especially high in antioxidants is blueberries. It has been demonstrated that diets high in blueberries may assist in rapid recovery from severe oxidative brain injury (Stromberg I, et al.), may reverse age-related cognitive decline (Lau FC, et al.), and help with memory (Andres-Lacueva C, et al.). Other fruits high in polypheonls, the specific antioxidant component in blueberries, are kiwis, plums, cherries, blackberries, currants and apples.

Stromberg I, et al. Neurol. 2005 Dec;196(2):298-307.

Lau FC, et al. Neurobiol Aging. 2005 Dec;26 Suppl 1:128-32.

Andres-Lacueva C, et al. Natr Neurosci. 2005 Apr;8(2):111-120.

Pullman, Washington

When there is a topic of great interest, several groups will often design experiments to learn more about that topic. These decisions are made simultaneously and it can take several years for the results from these studies to be reported. When designing experiments, researchers must take several factors into account. Among these might be: the group of people who will be tested, the duration of the experiment, the outcome that is to be measured, and how that outcome will be measured. As one might imagine, the choices made in each of these categories have the potential to affect the final conclusions of the study. For example, one experiment might test how a high fat diet affects the waistline of middle-aged women over five years while another study might test a high fat diet on sleep quality in adolescent boys over one week. These two studies could be interpreted quite differently and different conclusions regarding high fat diets might be reported.

One real life scenario in which confusing results have been reported is in the consumption of coffee. Coffee has been blamed for transient increases blood pressure (Childs E and de Wit H) and increased cholesterol (Higdon JV and Frei B). Other experiments, however, have shown that female lifelong coffee drinkers perform better on cognitive tests late in life (Johnson-Kozlow M, et al.). Finally, recent studies have shown that coffee may be a valuable source of antioxidants (Halvorsen BL, et al.) and folic acid (Child Health Alert) and might even prevent certain diseases (Higdon JV and Frei B). This plethora of results is clearly confusing, but if the different experimental questions and designs are taken into account, it is understandable how these different results came to be. Coffee has many different aspects (caffeine, antioxidants, processing chemicals) that could be used as the basis of experimental questions. The populations of individuals tested in these examples range from general populations of caffeine and non-caffeine users to aged women and pregnant women. The experimental time frame ranged anywhere from one day to a lifetime. The outcomes were measured by surveys, blood tests, laboratory tests and clinical tests of cognition. Each study provides unique information, but the results might seem contradictory when synopsized into a headlines. If you are curious, read more about the details of the study to understand the context of the results. And, with coffee, the real take-home message is what we have heard many times before: anything is okay within moderation.

Child Health Alert. 2007 Mar;25:5-6.

Childs E and de Wit H. Psychopharmacology (Berl). 2006 May;185(4):514-523.

Halvorsen BL, et al. Am J Clin Nutr. 2006 Jul;84(1):95-15.

Higdon JV and Frei B. Crit Rev Food Sci Nutr. 2006;46(2):101-123.

Johnson-Kozlow M, et al. Am J Epidemiol. 2002 Nov 1;156(9):842-850.