Why does the common treatment for cancer make body hair fall out? The answer is really pretty simple. It has to do with how different types of Chemotherapy target cancer cells. There are many different Chemotherapy drugs that work in different ways, so I will only speak in general terms regarding their side effects.
Most cells in the human body divide using a process called mitosis. This process has 5 phases {prophase, prometaphase, metaphase. anaphase, and telephase). It is preceded by interphase, and results in the cell dividing, called cytokinesis. When a cell reaches the end of its lifespan, it gets destroyed in a pre-programed process called apoptosis. There are many types of cancer (over 200). All types are a result of the same problem, unregulated cell growth. Cells that divide more rapidly than apoptosis can regulate- effectively, too much mitosis. The result is excessive tissue, known as tumors. These tumors can be localized, or they can spread to surrounding areas through your lymphatic system or your blood stream. Many Chemotherapy drugs work by interrupting mitosis. Most Chemotherapy cannot differentiate between abnormal cancer cells and normal healthy cells. Because of this, cells that have high mitotic rates (multiply rapidly) can also be affected by Chemotherapy-cells like those found in your hair follicles, the lining of your mouth, stomach, and those found in your bone marrow. The result can be hair loss, decrease in production of white blood cells (thus why cancer patients are immune-suppressed), and inflammation of your digestive tract. In the end, chemotherapy will hopefully kill the cancer cells, and in the process unfortunately potentially make your hair fall out. However, the healthy cells of your hair follicles will repair themselves, making your hair loss temporary, as is hopefully your cancer!
Blood pressure is really just that- the pressure at which blood moves around the body in your arteries. The easiest and least invasive way to test what that pressure is at any given moment is to momentarily stop the flow of blood and then slowly allow it to begin again. The pressure at which it begins to flow is the highest pressure the blood exerts on your artery walls.
Medical professionals do this by using a blood pressure meter known as a Sphygmomanometer (say that three times fast while eating peanut butter!) They encircle a limb, usually an arm, with a balloon-like device known as a blood pressure cuff. While pumping the cuff up, they use a stethoscope to listen for your heart beat past where the cuff is cutting of blood flow. When they no longer hear your heart beating, they slowly release the pressure while watching the pressure gauge.
When they start to hear your heart beat again, this is the top number of your blood pressure, known as your systolic pressure. They continue to release the pressure until they once again, no longer hear the heart beating, this is the bottom number of your blood pressure, known as your diastolic pressure. Together these numbers tell them two things: the pressure that is inside your arteries between heartbeats (the bottom number) and the pressure inside your arteries when your heart squeezes (the top number). This information gives doctors the ability to assume several things about what is going on inside the body- things like how well the heart is working, is it working too hard or not hard enough, and is the pressure a factor in the symptoms a patient might be having?
Chickenpox is one form of a Herpes Virus. There are over 25 known viruses that fall into the Herpes' family. Known as Herpesviridae, they are divided into three sub-families, Alphaherpesvirinae, Betaherpesvirinae, and Gammaherpesvirinae. Only 8 are known to infect humans.
Chickenpox is caused by a Herpes virus called Varicella. It can also be called Varicella-Zoster or Human Herpes Virus-3. This is because the Vericella Virus can lay dormant in your nerve roots and then cause the Zoster virus (shingles) later in life. This later infection can also be called the Herpes Zoster Virus. Like all Herpes viruses, it causes itchy papulae (rash or blisters) to appear. Chickenpox mainly shows up on the face, scalp, and trunk, with a small amount presenting on the limbs. This virus can re-appear later in life and is then known as the Varicella-Zoster Virus. Zoster, meaning belt or girdle, is more an explanation of where the rash appears- most commonly around the trunk- it's merely a reactivation of the Vericella Virus.
There are two aspects to this question. The first is temperature. Numerous studies throughout the last century have shown that cold temperatures will not increase your chance of becoming infected by a cold virus. Now that's out of the way, let's attack the second aspect. The fact that there is a "cold and flu season", and it does coincide with cooler temperatures.
First, there is a need to break through some societal tendencies before this second aspect can be evaluated. When people get sick, they tend to describe mild symptoms as "colds" and severe ones as "the flu". Unfortunately, you can't diagnose an illness simply by the perceived severity of symptoms. If any given group of people were exposed to the same cold virus, many would have mild to no symptoms, and some would have more severe reactions. The same can be said for flu viruses. The distinction between the two also gets blurred by some people's tendency to over-exaggerate their symptoms. In truth, a person's reaction to them aside, these are two very different types of viruses. There are over 200 different strains of "cold" viruses, mainly made up of rhinoviruses (up to 50%). The average adult in the US will get 2-4 colds per year and the average child about 6-8. These types of viruses usually are associated with mild symptoms. Up to 25% of infected people won't show any symptoms at all. Most won't get a fever, and if you do, it will be low-grade- around 100 degrees Fahrenheit. Your Runny nose (thus rhinovirus) and cough will tend to be mild. These viruses primarily don't transmit through the air. Instead, people become infected by coming into direct contact with someone who has an infection, or touch something that an infected person touches.
Influenza, however, is a much more sinister beast, affecting approximately 10% of the US population every year. This virus tends to start with sudden onset of a higher fever between 100-104 degrees Fahrenheit. It then progresses into chills, headache, muscle aches and a loss of appetite.
So why the increase in these illnesses in the winter? It seems this knowledge has been around for many centuries. The word influenza comes from an older Italian phrase "influenza di freddo" or "influence of the cold". The flu-season usually ranges from November to March in the northern hemisphere (the coldest months) and May to September in the lower. In fact, in tropical climates, there tends to be extremely low incidences of flu and certainly no true "flu season". There are several contributing factors to why cold temperatures increase influenza infection rates, all of which seem to be well known and promoted by health officials in numerous publications. The most common is that people tend to stay indoors when the temperatures get colder. This allows people to be in closer contact with each other and therefore makes it easier to pass the virus from person to person. Another contributing factor could be that in large parts of the country children are going back to school and interacting more with their fellow infected. In fact, most epidemics can be traced back to children.
Another factor lies in how the influenza virus reacts to temperature and humidity. The virus is extremely stable in colder temperatures, 41 degrees Fahrenheit optimally. The warmer you go, the less stable it becomes. Around 86 degrees, the virus isn't transmitted at all. Humidity also plays a very important role. Influenza is primarily transmitted on the droplets from your respiratory tract (cover your mouth when you cough kids!) The more humid the environment, the more water is available for those droplets to "pick up". The heavier the droplets become, the faster they will fall to the ground and out of the way of our mucus membranes. In drier environments, those death droplets hang around in the air longer for others to breathe in. In fact, one study showed that the virus was best transmitted at a humidity of 20% and not transmitted at all once the humidity reached 80%. So what does all this mean? You are no more likely to get a cold in the winter then you are in the summer. The flu, however, is a different animal altogether. You are more likely to get this virus in the winter.
There is no single mechanism that will definitively determine which hand you will prefer. Technology and further studies will continue to help shed light on the subject. What is known is that it essentially comes down to genes and biological asymmetry in the human brain. What tends to be true in so many other aspects of human preference, handedness also seems to be more of a spectrum. You have some people who strongly prefer right or left handedness, and some that can use both with the same level of comfort. Then there are countless people who have different degrees of ability using their non-dominant hand.
The biological side of the question has been known for quite a while and there are countless published articles on the topic. Most people control speech and language (including writing) with the left hemisphere of their brain, no doubt resulting from millennia of evolutionary mediated natural selection. This asymmetry is an extremely important factor in our brains. Since the left side of the brain tends to control the right side of the body, it leaves a majority of the population with the preference for being right handed. Depending on which study you read, approximately 80-90% of the population is right handed. This idea is further backed up with the ancillary evidence residing in our closest animal relatives, apes. Their brains are much more symmetrical than ours and apes don't typically show any tendencies towards a type of handedness.
The second and more recently known aspect of handedness is genetic. Technology has allowed us to explore with more accuracy the countless genes associated with all types of human tendencies and behaviors. In 2007, researchers found that a gene (LRRTM1) was involved in the development of handedness. There are two manifestations (alleles) of that gene- one known as the D gene and the other C gene. The D is more frequent in all populations and promotes right handed preference. The C gene does not promote left handedness but instead is a gene of chance. It appears that 50% of people with this allele are left handed and 50% are right handed. The discovery also helps explain some of the well known phenomenon regarding handedness. More specifically, that you can "teach" someone to use their non-dominant hand, and become ambidextrous. This was a well known practice when it was once believed that left handedness was the result of the Devil and it promoted evil behaviors. How the manifestation of this gene affects people's handedness isn't fully understood. The leading theory is that it affects the asymmetry of the brain.
Dandruff is simply dead skin cells that shed from our heads, some can be dry, some oily. Depending on the medical professional, some will only describe simple dry skin as dandruff. Others will describe dandruff as the result of other conditions and thus refuse to call it dandruff proper- conditions such as Psoriasis and Eczema are examples. These skin conditions can cause an over production of skin cells that slough off and result in dandruff. Some doctors, however, are reluctant to call this sloughage true dandruff, instead, choosing to say it's a complication of the skin disorder. However you choose to classify your dry skin, the result is the same- flaky stuff that others around us find a little gross. Let's touch on several of the most common types of dry skin causing afflictions.
The most common cause of dandruff is simply dry skin. You can commonly get this in the winter when the air is cold and the rooms we're in overheated. You might have other signs of dry skin on your legs and arms. If you don't get a chance to shower regularly, this will cause a buildup of those flakes.
The second most common cause of dandruff is known as seborrheic dermatitis. You've probably heard it described as "cradle cap" when infants have it. It's thought to be caused by either an over production of oil on our skin, irritation from a fungal yeast Malassezia, or a combination of both. The result is flaky white-yellowish scales that form around the oily areas of your body, like the scalp, ears, chest, back and sometimes your armpits. It will often times be associated with some redness and irritation.
Psoriasis is another common cause of skin flakes and is a chronic disease of the immune system. The exact cause isn't yet known, but it's thought to be an immune system problem where skin cell production is mistakenly sped up. This increase in the growth cycle, causes itchy thick patches of flaky lesions to form. The flaky bits can fall off in the form of dandruff.
Testosterone is a steroid hormone from a group called androgen. Androgen affects many characteristics in our bodies, like the development of the male sex organs, the deepening of the voice during puberty, muscle and bone strength, and hair growth. Interestingly, the same circulating androgen, like testosterone, con increase hair growth in one area of our bodies and inhibit it in others. Thought to be gene dependent, these differences affect our appearance in several ways.
Once testosterone is made, it begins to circulate around the body looking for receptor sites to attach too. Known as "androgen receptors" (in the case of hair), they reside in an area of your hair follicle called your dermal papilla. Once there, the testosterone (androgen) binds to androgen receptors and initiates any altered gene expression. This will either help the follicle or hurt it, depending on the gene expressed.
Testosterone regulates hair growth by affecting the follicle and how it can produce the different types of hair, like facial, pubic and scalp hair. These follicle changes affect the growth phases of hair, producing different reactions. The result is changes in hair growth, or lack thereof, occurring over time, as the growth cycle of hair can take as long as 7 years to complete. What has baffled researchers for decades is how can a hormone like androgen cause some hair's growth to be inhibited in one area of the body, while helping it in others? This paradox appears to be gene related.
There are two types of hair follicles within our bodies, Vellus and Terminal. Vellus hair follicles are the ones that create fine, virtually colorless hair, like the ones found on infants. They are usually tiny and don't reside very deep wifhin the skin. Terminal hair follicles are created from Vellus hair follicles by androgen. They are deeper and longer follicles that form thicker, longer and more pigmented hair. To change from Vellus to Terminal, or from Terminal to Vellus, the follicle must go through the hair growth cycle to regenerate as one type or another.
Normally, during puberty, our bodies begin to produce more androgen. This circulating androgen then turns our young Vellus follicles into more Terminal ones. The boy becomes a man! As time goes on, certain Terminal hair follicles (like the ones found on our scalp) can begin to regress back into Vellus follicles. This too is mediated by testosterone. The result is slowly dying hair follicles that don't grow back. (See What Causes Baldness below.)
Hair loss is simply termed "alopecia". This refers to any type of hair loss no matter the cause. There are numerous things that can cause hair loss, from medical treatments like like chemotherapy, to scalp infections and stress. Countless other disease processes can also result in hair loss. The type we think of as "male/female pattern balding" is known as androgenetic alopecia (AGA). This is by far the most common type of balding and accounts for approximately 90% of all male cases. It's also the leading cause of female balding.
Hair, like cells in our bodies, have a growth cycle. There are three phases: Anagen- the active growth stage (80-85% of hair is in this phase); Catagen- this phase is also known as the transitional phase, when hair begins to stop growing; and telogen- this phase is when hair growth is completely shut down and the fibers fall out (10-15% of our hair is in this phase at any given time). Affer your hair goes through the Telogen phase, Anagen begins again and voila! More hair! This cycle repeats itself throughout our lifetimes.
In the case of AGA, as we age, our hair follicles begin to shrink. The result is hair that begins to develop abnormally causing lighter, finer, and shorter hairs. In the end, the hair falls out, never to return. They also tend to have shorter Anagen phases. There are currently two known pathways that seem to work together to mediate this process. The first is hormonal and has been known about for decades. The second was discovered in 2011 and made public in 2012. It involves the genes associated with baldness. At the base of our hair follicles is a structure known as the papilla. It is in direct contact with blood capillaries that feed it the essential nutrients for proper hair follicle growth. These papilla have a large number of receptors that allow certain hormones to attach to them. They are called androgen receptors.
There is a type of androgen hormone in our bodies known as Dihydrotestosterone (DHT). Our bodies make this from the testosterone that appears in normal blood levels. When testosterone is aided by an enzyme (type 2 5-alpha reductase) which lies in hair follicle oil glands, it turns into DHT and begins to bind to the androgen receptors. Once there, it shrinks the follicle, over time, causing androgenetic alopecia (male/female pattern balding).
Named after Dr. George N. Papanicolaou, who, in 1928, found that cancer cells in vaginal smears could help Doctors find early stages of cervical cancer. The procedure, also known as cervical cytology, involves a women lying on the exam table in stirrups. The doctor places a tool, known as a speculum, into the vagina. The speculum then expands and allows the doctor a better view of your cervix. They then scrape away cells, put them on a glass slide and send them off to the lab for analysis. The pathologist looks at what are known as squamous cells to see if they're normal, or possibly pre-cancerous.
What doctors are looking for are abnormal squamous cells. Unlike other cells in the body that are square (cuboidal) or rectangular (columnar), these cells are flat. Coming from the Latin word "squamosus", meaning scales, they resemble the scales on reptiles. These types of cells are found in numerous areas of the body, like the mouth/lips, in the outer layer of your skin (epidermis), and on the cervix. Any squamous cell can become cancerous. In fact, Squamous cell carcinoma accounts for 20% of all skin cancers.
The test, at first, was not taken seriously by many in the medical profession, most likely because Dr. Papanicolaous' first study on the topic was full of typos and inaccuracies. In 1941, he did a much better job on a paper published in the "American Journal of Obstetrics and Gynecology". The theory was then embraced by OB-GYN's and the American Cancer Society, who started promoting the test. It has become so popular, as of 2005, 86% of women age 18-64 had at least one Pap test in the previous 3 years. Forty years ago cervical cancer was the leading cause of cancer deaths among women. Thanks to this screening technique, those death rates have decreased dramatically, though in 2008, it was still the third leading cause of cancer in women, accounting for 8.8% of cancers.