What are Traditional and Alternative Medicine Fibroid Treatments?

Do you have pain, irregular and unusually heavy menstrual periods? Talk to your doctor about fibroids. Here’s information on the various fibroid treatments.

Fibrin is a protein that the body creates in response to inflammation or bleeding. Fibroids or fibromuscular tumors occur when excessive amounts of fibrin build up. Hormonal imbalance is a reason this occurs. Specifically, fibroids can be inside the uterus muscle wall, under the uterus lining, on the outside part of the uterus, on long stalks outside the uterus, or on long stalks inside the uterus. Fibroids are typically benign; however they’re very painful and they cause blood clots, urinary urgency, pain during sex, anemia, low back pain, constipation, pelvic pressure, bleeding in between periods, heavier menstrual periods, scarring, infertility, or problems if they occur during pregnancy. In terms of age of occurrence, fibroids typically occur in women anytime from their early 20s to late 40s although occasionally fibroids occur in post-menopausal women or teenagers. There are various treatments for fibroids.

Traditional Treatment and Diet

Treatment options for fibroids are varied. For example, doctors sometimes prescribe birth control pills at low dosage to treat fibroids. Sometimes they may prescribe high dosage ibuprofen to reduce pain and swelling. Or, they prescribe iron supplements to combat the anemia that occurs as a function of heavier menstrual periods.

Other treatments include surgery. For instance, physicians may choose to do uterine artery embolization which stops blood supply to the fibroid. Or, they may do hysteroscopic resectioning or may do a myomectomy to remove the fibroids. Granted, surgery also has risks such as potential regrowth of the fibroids, post-operative infections, or infertility. If the previously mentioned surgeries do not work, then hysterectomy is sometimes an extreme measure that it taken because it removes the uterus as well as removing the fibroids.

Physicians sometimes prescribe hormone therapy for persons with fibroids. Granted, hormone therapy has potential side effects that could include mood swings, depression, excessively heavy menstrual periods, or even ovarian cancer. There are other treatments for fibroids that are reportedly not as harsh on the body. For instance, doctors often prescribe stress reduction, exercise, and a high fiber low fat diet for people who have fibroids. Avoiding foods laden with sugar, flour, or yeast has also been suggested.

Avoiding phytoestrogen foods and avoiding soy has been suggested because some women have reported that consuming soy made their tumors worse. Also, apparently being given soy formula as a baby is a risk factor because a study found that women given soy formula when they were babies were in fact 25% more likely to eventually have uterine fibroids as compared to women who were fed cow’s milk or breastfed. It has also been recommended that some cereals should be avoided due to the presence of sugar and other unhealthy ingredients. Also, it has been suggested that processed foods, pasta, overly acidic foods or carbonated drinks should not be consumed. Additionally, it has been stated that drinking sufficient amounts of water such as eight cups of water each day is very important in the healing effort.

Alternative Medicine Treatments for Fibroids

There are also alternative medicine treatments. Examples of alternative medicine treatments include Cayce castor oil packs, chiropractic spinal adjustments, an insert into the heel of one shoe in cases where there is discrepancy in leg lengths, and colonics. Treatments for leaky gut syndrome are sometimes suggested in cases where the leaky gut syndrome is contributing to the fibroids. Acupuncture is another alternative medicine treatment that is sometimes done for persons with fibroids.

Herbals are another alternative medicine fibroid treatment. One example of an herbal used for fibroids includes the supplement fibrovan. There are anecdotal reports that fibrovan reportedly helps dissolve fibrin deposits and clots. Fibrovan contains ingredients such as epigallocatechin gallate (EGCG) which is an antioxidant typically found in green tea leaves, lycopene which is an antioxidant that is found inside of tomatoes, nattokinase which is an enzyme extract that is found in soy beans, and bacillus natto which is a beneficial bacteria to the human body.

What Is the Pupil and How Does It Change Size? How Your Eyes and Brain Control Light Intensity on Your Retina

Nerve responses and specialized structures control the aperture that regulates the amount of light that enters the eye and falls on the photoreceptors.

The eye is the brain’s window on the world, the first portal to the processes associated with vision. And similar to cameras and taking pictures, either too much or too little light can lead to images that lack for detail, display distorted coloration, and generate lower resolution images than desired. The eye has a specialized structure at its anterior (front) end, the pupil, which plays a critical role in maximizing visual inputs.

The Eye and Refraction of Light

The front part of the eye is most involved in the process of refraction of light. That is, the structures of the anterior segment of the eye are most involved in the process of bending (refracting) light so that the images will focus on the retina, the light-sensitive and sensing structure in the posterior (rear) of the eye. The front part of the eyeball, or globe, contains the cornea, the anterior and posterior chambers, the iris (the visibly colored circle in the front of the eye), the ciliary bodies, the lens, and the pupil.

What Is the Pupil?

Most simply, the pupil is an aperture, an opening. In this case, it is the opening through the iris that lets light pass to and through the ocular lens and onward towards the retina. The pupil is the dark spot in the center of the iris. It appears dark because light that enters the eye is absorbed by the internal structures of the eye and doesn’t reflect back through the pupil.

What Controls the Pupil?

The size of the opening through the iris, known as the pupil, is controlled in response to contraction and relaxation of the different muscles that are part of the iris. The dilation (widening) or constriction (narrowing) depends on numerous signals in a circuit that involves the pupillary muscles, the retinal ganglion cells, the optic nerve (the second cranial nerve, CN II), regions of the brain and brainstem and the oculomotor nerve (the third cranial nerve, CN III).

How Does Pupil Size Change?

When light shines into the eye, the signals from the retina travel to the higher centers of the brain for the processing of visual input. But when it comes to constricting the pupil, neural signals exit the retina and then pass through a different circuit that goes to deeper, older structures of the brain and a signal goes back out through a different nerve back to specific muscles of the iris, the sphincter pupillae, causing them to constrict, narrowing the pupil. This is known as the pupillary reflex. It can not be consciously controlled and serves as a useful indicator of neural function through specific parts of the brainstem. More importantly, this reflex is “consensual”; that is if light is shone specifically into one eye, the pupil of the other eye will constrict right along with the pupil that is being illuminated.

There are another set of muscles in the iris that are known as the dilator pupillae. When these muscles are activated, via a different neural pathway than the sphincter pupillae muscles, the pupil will dilate. Both the constricting and dilating pathways are themselves countered by other neural signals that can inhibit their action. Ultimately, the size of the pupil is determined by the intensity of contraction of the different muscles, regulated by both their positive and negative signals.

Drugs That Change Pupil Size

When someone has a dilated exam at the eye doctor, specific drugs are used that block the action of the muscles controlling pupillary constriction. This aids in the examination of the eye and its internal structures. So drugs like tropicamide, phenylephrine and atropine can cause dilation of the pupil, but so can cocaine, amphetamines and other illicit drugs. Constriction of the pupil can be caused by drugs such as pilocarpine or neostigmine, but can also be caused by drugs of abuse such as heroin or morphine.

In everyday use, the pupil changes size in response to ambient illumination. A lot of light and the pupil constricts to help with visual acuity and keep the light sensing cells of the retina from getting “overexposed”. When it is dark out or a person is in a dimly lit room, the pupil dilates to allow as much light as possible to enter the eye. A remarkably involved system for something that seems so simple.

To learn more about the eye, visit the interactive eye diagram at the US National Eye Institute

G Protein Coupled Receptors: The Most Frequent Target of Pharmaceutical Agents

The G-protein-coupled receptor (GPCR), or 7-transmembrane (7-TM) receptor, superfamily is one of the largest groups of related genes in the entire genome with more than 300 members. Owing to the large number of physiological processes controlled by signaling through these receptors, the superfamily members make up the largest group of “druggable” targets in the body.

GPCR Family Groups

Sequence analysis of the genes contained within the human genome has identified large numbers of GPCR genes (>300) and remarkably enough the function of a sizable portion remain unknown. But based on sequence similarities, the GPCRs have been divided into 6 different classes. All of the members of this group of proteins have seven transmembrane spanning segments. The biochemical and pharmacologic characterization of the original members of the superfamily identified them as utilizing small GTP binding proteins to transduce their intracellular signal once activated.

Examples of GPCR Proteins and Their Functions

GPCRs are involved in many different cellular processes. One of the best characterized members is the light-transducing protein known as rhodopsin. This protein and several close relatives are responsible for the specialized pigment present in the rods and cones of the retina that allow for sensing of light, and the sense of vision. The receptors in cells that respond to the hormone adrenaline, the adrenoreceptors, are GPCRs. Many important neurotransmitter receptors are members of the GPCR superfamily including receptors for serotonin and for glutamate. One of the most widely known by the public at large, and seasonally appreciated members of the GPCR superfamily are the histamine receptors. The sense of smell is possible because of GPCRs that detect odor molecules.

Common Drugs That Target GPCRs

Because of the widespread distribution of GPCRs throughout the body, their presence on the surface of cells and the vast array of cellular processes that they can modulate, GPCRs are the target of more drugs than any other targeted protein in the body. Name a body response and a need to control it and there is likely a GPCR involved and a drug available to modulate it.

  • Stomach Acid Relief: Histamine H2 Receptor blockers like Zantac and Tagamet
  • Allergy or Hayfever Relief: Histamine H1 Receptor blockers like Benadryl and Claritin
  • Blood Pressure or Heart Rate Control: beta-Adrenoceptor blockers like sotalol, timolol, atenolol, propranolol, and many, many others
  • Motion Sickness: Muscarinic Acetylcholine Receptor blocker scopolamine
  • Dilated Eye Examination: Muscarinic Acetylcholine Receptor blocker tropicamide
  • Severe Psychiatric Disorder: Dopamine Receptor blocker haloperidol

The list of potential GPCR targets and the drugs that have been developed to affect their function is extremely long. And as the functions of the 100 or so other GPCRs with as yet unknown physiological effects are identified, the list of drugs that target GPCRs will grow ever longer.

Wild Atlantic Salmon Stocks Declining: Fish Farms are Causing Depletion of Wild Fish Stocks

Crowded condition of farmed fish encourages parasitic sea lice.

Parasites attack young wild salmon as they return to the sea and are threatening the sustainability of wild stocks.

Wild Atlantic Salmon Stocks

Atlantic Salmon (Salmo salar) come into fresh water to spawn. The young travel down to the sea, and then spend a couple of years feeding in the ocean. The adult fish are genetically programmed to return to the river system of their birth, and the cycle continues. Since the 1970’s the number of adults returning to spawn has reduced by over 50%, and there are now thought to be less that four million wild salmon in the ocean.

Fish Farming Atlantic Salmon

The farming of Atlantic Salmon began in the 1970’s, initially in Norway and Scotland. Eggs are ‘stripped’ from adult salmon, hatched and raised in fresh water. When they are big enough they are put in cages, usually in estuaries, where they are fattened up for market. It is estimated that there are currently around 270 million farmed salmon (compared to 4 million wild!).

Effects of Fish Farming on Atlantic Salmon Stocks

  • The crowded conditions of the farmed salmon in their cages are ideal for encouraging parasites (see ‘Sea Lice Affect Wild Salmon’ and ‘Sea Lice and Salmon’). Unfortunately wild salmon often need to swim past these fish farms to get to the open sea, and in doing so they can pick up heavy infestations of these parasites – enough to threaten their survival.
  • Sometimes cages get damaged allowing farmed salmon to escape into the wild, and although this might initially appear to be a ‘good thing’, these escapees are genetically different from the truly wild fish, and their effect on the wild stock is detrimental.

(Watch the very impressive ‘National Geographic Multimedia Presentation’).

History of Salmon as Food

  • As far back as 20,000 BC salmon were an important food. (A carving of a salmon has been found in a cave in the Vezere region of the Dordogne – France – of this date.) There is also evidence of salmon traps in the same river system dating to around 10,000 BC.
  • More recently the site of Westminster Abbey in London is said to have been determined by the presence of salmon fishermen over a thousand years ago. (The fishermen believed they had ferried St.Peter across the Thames, and this superstition led to the building of first a chapel, and later an Abbey, where he was supposed to have been landed.)
  • Even more recently salmon was so cheap and plentiful in London that mediaeval apprentices had it written into their agreements that they would not be fed salmon more than once a week.

Like oysters, salmon were once thought of as ‘food for the poor’, but have now become a luxury food.

Genealogical Surname Studies and the Home DNA Test

While DNA tests are certainly useful for paternity testing, there are many other applications, including some that can be quite helpful from the point of view of genealogy and family heritage research. Surname studies, in which people who carry the same last name can determine how closely they are related to one another, is one such use of DNA testing.

Home DNA Tests

To participate in a surname study, one must have Y-chromosome DNA tested. DNA companies will provide a kit that allows for the collection of a saliva sample at home. A personal DNA test kit consists of a mouth swab or scraper, a collection tube, and a mailing envelope. Home DNA testing kits can be ordered online, and range in price from less than $100 to several hundred dollars, depending on how many markers and how many tests are wanted. Most websites offering tests provide explanations of the various tests, with recommendations for their use. Only men carry the Y chromosome, so male DNA must be collected. Women may participate in a surname study, but only by providing a test from a close male relative with the same surname.

Surname Studies in Genealogy

Surname studies involve compiling the Y-chromosome profiles of men who carry a particular family name. While compiling these profiles will not produce a family tree, it will allow people to determine the probability of relationship. Y chromosome testing can show if two men share a common ancestor. In a surname study, once a Y-DNA test has been completed, the results can be compared with those of other men who carry the same surname.

Joining a Surname Study

The first step in joining a surname study is to find an existing one. Be sure to check variations of the last name, since names like Edmond, Edmonds, Edmund, Edmonde, etc., might easily all be part of the same family. People in the past were not always as concerned about spelling as people tend to be today.

One place to check for studies is Family Tree DNA, where a simple search engine will tell you if a study exists, and how many people are currently part of the study. People who have had their DNA tested at other labs, including the National Genographic Project, may also join a surname project using the results of that earlier test.

Other ways to check for surname studies are by searching Google for a particular name and the words “surname study,” and on the DNA page on Cyndi’s List. If no existing study can be found, a new one can be started. Family Tree DNA provides a link to start a new project.

Non-Paternal Events

There is one aspect of participating in a surname study that may come as a surprise. A significant number (somewhere between 1 and 10%, according to various studies) of people discover that there is a break in the line. For example, a man named Martindale, while participating in a Martindale surname study, may have a genetic profile that does not correspond to anyone else in the group – in fact, he might match a group of people name Edwards.

This is what is referred to as a “non-paternal” event, denoting that somewhere in the line the surname and the DNA don’t correspond. This can be the result of adoption, a name change, or illegitimacy, often many generations in the past. Many name changes were informal, as when a recent immigrant simplified or Americanized his name, or when an orphan was adopted by a relative, step-parent, or neighbor. Until recently, no legal papers were required for these changes.

Genealogy and DNA Tests

Traditional genealogy relies on paper documents to prove relationships between family members, but sometimes those documents are hard to find or non-existent. That’s when DNA and surname studies can help fill in the blanks, by providing clues, opening up new avenues for research, or even disproving kinship theories.

Human Leukocyte Antigens and Autoimmunity: The Role of HLA markers in the Immune Response

Various protein antigenic molecules found on white blood cells determine what substances our immune system cells will react with and to what degree.

Various HLA markers highly influence the immune response. These markers are comprised of the class I and class II Human Leukocyte antigens (HLA). To date, 3,3731 different antigen alleles have been identified. The HLA type represents one’s HLA antigen profile just as the blood type represents the antigen markers on one’s red blood cells.

HLA antigens were first studied as a means of tissue typing compatible donors for transplant matching. Tissue donors with the same HLA profile as the recipient are likely to donate organs that aren’t rejected. Today, tests for HLA antigens are also used to understand patterns of autoimmunity, vaccine efficacy, and one’s response to therapeutic agents.

HLA Testing

Today, tests for HLA typing are also more sophisticated than the early tests, and they rely on DNA-based sequencing technologies rather than antigen-antibody reactions. With these technological advances, HLA testing is more specific and sensitive.

Class I and II HLA Antigens

Class I HLA molecules identify the internal contents of cells and display these contents on the cell surface. Class I molecules act as the cell’s internal alarm system, sounding an alert when changes suggest cancer or viral infections.

Class II HLA molecules act as an external alarm system, initiating an immune response when the body encounters extracellular microorganisms. These HLA antigens prompt the recruitment of antibodies and other immune system components that can fight and eliminate cancerous changes and infected cells. Everyone has their own unique HLA alarm system depending on their HLA type. Different HLA molecules typically send alarms in dissimilar ways.

For instance, the class I HLA antigen B5701 is thought to efficiently alert immune cells to the presence of the HIV virus. This antigen helps to control HIV infection. This is an example of how HLA typing can help identify host resistance or susceptibility to particular organisms as well as drug therapies.

When the HLA-directed immune response is working properly, it protects the body. However, if this immune response is too weak or too strong, it can lead to rheumatoid arthritis, transplant rejection, cancer and infection.


HLA typing has become increasingly important in the study of autoimmune diseases. It’s long been known that certain HLA antigens confer susceptibility to specific autoimmune diseases, and certain HLA antigens offer protection. For instance, a majority of (but not all) Caucasion patients with Graves’ disease have been found to have HLA B8 and HLA Dr3 but not HLA B7. HLA B8 and DR3 are associated with susceptibility to Graves’ disease and HLA B7 is thought to protect against the development of Graves’ disease. Genetic susceptibility can vary among different ethnic groups.

Because there are adequate diagnostic tests and procedures available for the diagnosis of most autoimmune diseases, HLA testing is not routinely performed. An exception is testing for HLA B27. This antigen is often seen in patients with ankylosing spondylitis, uveitis, seronegative spondyloarthropathies, and Reiter’s syndrome. Tests for HLA B27 are often used to help diagnose these conditions.

Adverse Drug Reactions

HLA typing is also useful in identifying the immune system’s response to various drugs. For instance, patients with HLA B1502 treated for seizure disorders with carbamazepine (Tegretol) have a high risk of developing Steven Johnson Disease. Patients infected with HIV who have HLA B5701 and a slower risk of disease progression are likely to react with hypersensitivity reactions to the antiviral drug Abacavir