In 1981, scientists discovered ways to derive embryonic stem cells from early mouse embryos. Since then, they have been the subject of intense scrutiny, controversy, and advocacy.

They are unique cells, which can be derived from human embryos and can be differentiated into virtually any kind of different cells. In humans, there are about 200 different types of cells including bone, muscle, and nerve cells, and within these cells there are about 20 different types of structures or organelles. Essentially, stem cells can be derived from human embryos, and with the right enzymes, can be stimulated. For instance, bone cells can originate from osteocyte cells, or liver tissues can come from hepatocytes.

Stem cell types and research

There are three types of stem cells:

• Embryonic stem cells
• Adult stem cells
• Induced Pluripotent Stem Cells (iPSC)

Embryonic stem cells are derived from human embryos. Adult stem cells are undifferentiated cells (meaning “clean slates” with the potential to change into another cell variant) found throughout the body after development; they multiply via cell division to replenish dying cells and regenerate damaged tissues. Induced Pluripotent Stem Cells (iPSC), which were discovered in 2006, are derived from skin or blood cells that have been reprogrammed back into an embryonic-like pluripotent state that enables the development of an unlimited source of any type of human cell needed for therapeutic purposes. While these types of cells are interesting and certainly worthy of research, this article will focus on embryonic stem cells as they are consistently the most well-known and discussed type by the general public.

Embryonic stem cells are potent and often sought after due to their abilities to proliferate without limit and contribute to any cell type. However, with great power comes great responsibility and stem cells are no exception. Poorly processed cells have been documented to mutate into cancerous tumors that can wreak havoc upon people’s bodies. Bearing this in mind, scientists also do not believe that this should derail stem cell therapies considering that there are DNA tests to check if stem cells will turn out to be problematic or not.

The stem cell project is regularly a subject of ethical debate in both the academic and public sectors. Most embryonic stem cells are derived from embryos that develop from eggs that have been fertilized in vitro—in an in vitro fertilization clinic—and then donated for research purposes with the informed consent of the donors. People willingly donate their eggs for this research, and this process does not constitute child-killing since the eggs are near their zygote phase, not a whole mature embryo. Scientists obtain those types of cells from an embryo which has not yet completed its formation to develop into a human being. Researchers then use these cells for various treatment and research purposes. It is important to stress that they are not derived from eggs fertilized in a woman’s body and that they are produced in a plastic laboratory culture via clinics in vitro.

Some examples of embryonic stem cells being used in research include the following:

1. UCLA stem cell gene therapy cures bubble baby disease

Researchers at UCLA (University of California, Los Angeles) have developed a cure for babies born with Bubble Baby Disease, a rare and life-threatening condition that can be fatal within the first year of life, by using stem cells from multiple patients and gene therapy to correct the genetic mutation of these patients.

2. Asterias biotherapeutics restores some independence to those suffering from paralysis caused by spinal cord injuries

Asterias Biotherapeutics spent much of 2016-2017 developing a stem cell therapy to restore upper body motor function to quadriplegic spinal cord injury victims. Through lengthy and rigorous testing in human clinical trials, the therapy was found to be safe for use in people with all patients treated reporting at least some improvements. Asterias is now expanding its clinical trials to include patients with sub-acute injuries.

3. UC Irvine scientists engineer stem cells to destroy cancer

In a study conducted by University of California, Irvine researchers, a stem cell-based technique was devised to find and destroy breast cancer cells that had already metastasized. The cells “feel” the stiffness of the surrounding tissues and destroy the cancer-causing cells.

Embryonic stem cells can remain undifferentiated when they are grown in a well taken care of culture that is under stable conditions. Problems primarily begin to arise if cells are allowed to clump together to form embryoid bodies in which they begin to differentiate, or change into more specific cell variants, spontaneously. Although spontaneous differentiation is a good indication that shows which cultures of embryonic stem cells are healthy, the process is uncontrolled and, therefore, an inefficient strategy to produce cultures of specific cell types.

The ability of stem cells being able to differentiate into hundreds of other types of cells continues to amaze scientists as this is no small discovery. Researchers believe that the possibilities with stem cells are near endless, especially in regard to “regenerative medicine,” the process of “replacing, engineering, or regenerating human cells, tissues, or organs to restore or establish a new function.” It is even believed that even whole organs could be synthetically grown by using them.” Additionally, stem cells have the potential to rebuild healthy tissues, help people with heart disease, diabetes, ALS, Alzheimer’s disease, liver disease, Parkinson’s disease, cancer, and many more illnesses.

In a stem cell transplant, embryonic stem cells are first specialized into the necessary adult cell type. Then, those mature cells replace tissue that is damaged by a disease or injury. This type of treatment could be used to:

• Replace neurons damaged by spinal cord injury, a stroke, Alzheimer’s disease, Parkinson’s disease, or other neurological problems.
• Produce insulin that could treat people with diabetes and heart muscle cells that could repair damage after a heart attack
• Replace virtually any tissue or organ that is injured or diseased.

Sometimes scientists use stem cells as a drug. For example, it is possible to inject a stem cell into joints to reduce swelling and pain, or in order to promote the healing processes of soft tissues. Stem cell therapy is performed by injecting the patient’s own stem cells to stimulate the body to repair and replace damaged tissue in any joint or soft tissue structures – such as knees, shoulders, hips, wrists, ankles, elbows, tendons, ligaments and non-healing bone fractures. Cellular Dynamics, a large biotechnical company, sells human heart cells called cardiomyocytes that are derived from induced pluripotent stem (IPS) cells. Pharmaceutical companies are adapting to this new and innovative trend on a day-to-day basis. Stem cells can also be used to test the quality and safety of investigational drugs by testing them on stem cells that have been transformed into tissue-specific cells. Researchers are able to monitor the side effects before exposing the drug to a patient and thus have a greater expectancy of how their body may respond to the drug. This allows us to test for cures for potentially fatal diseases in ways that would otherwise be risky or unethical.

With all of the aforementioned advantages, stem cells are a fairly new, but exceptionally promising, research area. For some people, it may seem unethical to use stem cells on the grounds that extracting stem cells damages the blastocyst, which is a structure formed in the early development of mammals, more specifically the sixth or the eighth day of the development of an embryo. In 2006, President Bush vetoed the Stem Cell Research Enhancement Act stating that the federal government should not support “the taking of innocent human life.” Although stem cells are very promising for science and can open new doors to many new treatments in the medical field, it looks like there are still differences of opinion on their ethical use. This is perhaps because there is need for more convincing evidence or people are not informed accurately on the details of this research area.

References

• https://stemcells.nih.gov/info/Regenerative_Medicine/2006Chapter1.htm
• https://www.healthline.com/health/stem-cell-research
• https://www.statnews.com/2017/04/26/stem-cells-cancer-mutations/
• https://plato.stanford.edu/entries/stem-cells/
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5398703/
• https://www.mayoclinic.org/documents/the-amazing-stem-cell/doc-20249792
• https://www.unmc.edu/stemcells/educational-resources/history.html
• https://www.cirm.ca.gov/patients/power-stem-cells
• https://www.nature.com/news/stem-cells-take-root-in-drug-development-1.10713
• https://hsci.harvard.edu/examining-ethics-embryonic-stem-cell-research#:~:text=Opponents%20argue%20that%20the%20research,taking%20of%20innocent%20human%20life.%E2%80%9D

Alzheimer’s disease is “an irreversible, progressive brain disease that slowly destroys memory and thinking skills, eventually even the ability to carry out the simplest tasks” according to the Alzheimer’s Association. Alzheimer’s affects mostly senior citizens, and symptoms first appear in most people between 60 and 70. The first signs of Alzheimer’s, though, can be noticed between the ages of 30 and 65. However, it is very rare for younger people to exhibit symptoms. Most cases of dementia are caused by Alzheimer’s disease [1]. It is known that all Alzheimer’s patients have dementia; however, one cannot say that all dementia patients have Alzheimer’s disease. Alzheimer’s is a deadly disease, finishing predictably in death [2].

Alzheimer’s disease is named after Dr. Alois Alzheimer. In the early twentieth century (1906), Dr. Alzheimer observed alterations in the brain tissue of a woman who had expired of an uncommon mental disease. Her signs involved loss of memory, language difficulties, and erratic conduct. After her death, Dr. Alzheimer inspected her brain and discovered many uncharacteristic clusters (now called amyloid plaques) and scrambled packets of filaments (now called neurofibrillary, or tau, tangles) [1].

Based on his findings, he correctly theorized that these anomalous buildups were accountable for the patient’s loss of memory and other mental complications.

The plaques and tangles in the brain are some of the foremost characteristics of Alzheimer’s disease. Another characteristic is the damage of contacts between nerve cells (neurons) in the brain. Neurons conduct communications between different segments of the brain – for example, they conduct communications from the brain to muscles and organs in the body. Many other multifaceted brain alterations are thought to play a function in Alzheimer’s disease.

In the beginning, this impairment seems to take place in the hippocampus of the brain. The hippocampus is the part of the brain that is indispensable in forming memories. When neurons perish, further parts of the brain are distressed. In the last stage of Alzheimer’s, destruction is extensive, and brain tissue has shortened substantially.

How many Americans have Alzheimer’s disease?

It is estimated   that more than 5 million Americans may have Alzheimer’s disease. If existing population developments continue, the number of people with AD will increase significantly. However, this trend can be stopped if the disease can be effectively treated or prevented.

The reasons people develop Alzheimer’s are still not fully understood. One known reason is aging.   Age is the most significant accepted risk factor for Alzheimer’s disease. In 2010, in the United States, close to 5 million people 65 years and older were living with Alzheimer’s illness. A 2013 report from the Alzheimer’s Association suggests that 1/10^th of all Americans over 65 are suffering from Alzheimer’s. The proportion goes up to about a third of the population for those who are over 85. According to the Alzheimer’s Association, AD incidence is between 60% and 80% of all incidents of dementia [3].

Incidence of Alzheimer’s disease in South Asia

Globally, at least 44 million individuals live with dementia, making the disease a worldwide health catastrophe that must be tackled. In excess of 4 million individuals have some appearance of dementia in India [4].

In the Southern Indian state of Kerala, 1066 qualified members who were cognitively regular at reference, 104 of them acquired dementia (98 of them were found to have AD) over a continuation time of 8.1 years. The occurrence rates per 1000 person-years for AD was 11.67 for persons aged ≥55 years and greater for those aged ≥65 years (15.54). Individuals who were aged ≥65 years, the global age consistent occurrence rate, was 9.19 per 1000 person-years, prevalence rate of AD raised substantially and proportionally with growing age. These are the initial AD occurrence rates to be conveyed from southern India. When compared to reports from rural North India these occurrence rates appear to be much greater. But they are comparable with those reported from China, and slightly lesser than that reported from the western world [5].

Signs of Alzheimer’s disease

Memory difficulties are characteristically one of the first signs of Alzheimer’s; nonetheless, early indications may differ from individual to individual. A decrease in other facets of thinking, for example forgetting words, sight/three-dimensional problems, and diminished thinking or decision making, may additionally indicate the precise initial periods of Alzheimer’s disease. Mild cognitive impairment (MCI) is a disorder that can be an initial mark of Alzheimer’s. However, not everyone with MCI will develop Alzheimer’s.

Patients with Alzheimer’s have difficulty performing routine things like paying bills, driving a car, or cooking food. They repeatedly ask the same questions, go astray without difficulty, misplace things or put them in unusual places, and find even easy things puzzling. As the disease advances, some patients become anxious, wrathful, or furious.

Longevity of a person with Alzheimer’s disease?

At the time of diagnosis, if the person is older than 80, they are only likely to live another three or four years. If the person is younger then 80, they could live for as many as ten years or more.

Currently Alzheimer’s disease is graded as the sixth greatest cause of death in the United States. But fresh evaluations show that the illness may be listed as third, after heart disease and cancer, as a source of death for elderly people.

At the present time, there is no cure for Alzheimer’s. However, treatment can help patients cope with symptoms [1].

In the 21^st century, Alzheimer’s can only be diagnosed with 100 percent precision through a postmortem examination that discloses the occurrence of the distinctive plaques and tangles. However, a complete examination and suitable checkup can afford a dependable diagnosis with better than 90 percent certainty.

Malformed accumulations of particular proteins inside the brain interrupt normal brain performance and produce the reasoning and efficient difficulties characteristically connected with Alzheimer’s Disease. Ultimately, as the sediments expand all over the brain, brain material begins to die. This results in additional intellectual damage. CT scans and MRI scans show the subsequent brain contraction. CT scan shows enlargement of the ventricles in the brain and loss of brain tissue in a patient with Alzheimer’s disease. Recent research is endeavoring to ascertain what produces these accumulations and is watching for techniques to avoid or change them before they cause lasting brain destruction [2].

Alzheimer’s is not curable.
Alzheimer’s is not contagious.
Alzheimer’s is not a natural part of the aging process.
Alzheimer’s is not something you get from using deodorant or cooking in aluminum pans.
Alzheimer’s is not inevitable if you live long enough.

In some families, Alzheimer’s disease is hereditary. But these appearances are very rare, and they account for fewer than five percent of all incidents. If a family member like a mother or a brother has Alzheimer’s disease, it doesn’t inevitably mean that you’re prone to contract it as well.

There is no test that can foretell whether you’ll get Alzheimer’s disease, save tests for the very rare hereditary Alzheimer’s. A blood test can tell whether you have a certain form of cholesterol-carrying protein connected with an elevated occurrence of the disease. This examination can’t convey whether you’ll actually contract the condition; at least 50 percent of people who have an elevated risk factor never get Alzheimer’s.

Taking into consideration medical ethics, healthcare authorities counsel against taking this blood test or undertaking other genetic testing because they want to save their patients from unwarranted fear about something that will perhaps never happen. There are others reasons for which they also advise against testing. If a person has the inherited gene or elevated risk factor, it might negatively affect their ability to acquire health insurance or long-term care.

Causes of AD

All types of dementia are a result of brain cell death. As such, Alzheimer’s Disease is also caused by brain cell death. When there is an ongoing brain cell death occurring over a period of time, then it is called a neurodegenerative disease. When the brain tissue has an increasingly smaller number of nerve cells and connections, then the total brain size shrinks due to Alzheimer’s.

Plaques in the brain are a result of the build-up of a protein called beta-amyloid (also known as “amyloid plaques”). These plaques cannot be seen or tested for in the living brain affected by Alzheimer’s Disease. A postmortem or autopsy will show these plaques and masses. Plaques are found between the dying cells in the brain.

These unusual protein clusters in the brain tissue are always present with Alzheimer’s disease. Scientists are not yet sure if there could be an additional primary activity that is really causing Alzheimer’s Disease. This sort of alteration in brain nerves is also observed in other illnesses. Researchers want to find out how these protein abnormalities progress so that a cure or treatment might be discovered. Researchers have not completely comprehended why the alterations that lead to Alzheimer’s disease befall a patient. It is known that several dissimilar factors are believed to be implicated, aging and a family history of Alzheimer’s, chief among them.

Diagnosis

Alzheimer’s disease is not straightforward to diagnose, as there is no single test for it. The first step physicians take is to rule out other complications before validating whether mental indications and signs are stark enough to be a type of dementia or something else.

Signs and symptoms [6]

Phases of Alzheimer’s Disease:

Aging has effects on memory but not AD.

• Occasionally forgetting things.
• Sometimes items are misplaced.
• Slight temporary memory loss.
• Not recalling precise particulars.

Early phase

• Not recollecting incidences of deprived memory.
• Forgetting names of family or friends.
• Only close friends or relatives may notice the changes.
• Some perplexity in conditions outside the acquainted.

Middle-phase

• Enormous effort recollecting newly acquired knowledge
• Increasing misperception in numerous situations
• Difficulties with slumber or sleep
• Difficulty in recognizing where they are

Late-phase

• Low capability to reason
• Difficulties in talking
• Retelling same dialogues
• Extra rude, nervous, or suspicious

Treatment

For Alzheimer’s there is no recognized treatment. The loss of brain cells cannot be stopped or overturned.

Drug therapy

There are no disease-altering medicines obtainable for Alzheimer’s, but some choices may decrease its symptoms and help recover quality of life. Four drugs are available. They’re called cholinesterase inhibitors. They include Donepezil (brand name Aricept), Rivastigmine (Exelon), and Tacrine (Cognex). Another type of drug, called memantine (Namenda), which is an NMDA receptor antagonist, may also be used. This drug may be used alone or with a cholinesterase inhibitor.

Other therapies

As with other kinds of dementia and neurodegenerative illness, a chief part of therapy for patients with Alzheimer’s comes from the patronage given by healthcare personnel. Quality-of-life care becomes more imperative as needs increase with diminishing freedom [3].

There are other treatments outside the US. In India, Alzheimer’s disease is treated with Ayurveda [7]. Ashwaganda, an ancient Herb used in Ayurveda, is confirmed to be a possible cure for Alzheimer’s [8]. It has also been found that Curcumin (in India it is called Haldi) is more efficient at hindering the formation of the protein fragments than many other potential Alzheimer’s treatments. Optimizing vitamin D and vitamin B12 intake, as well as a nutritious diet rich in folate and coconut oil, have also been tested as to their efficacy at treating Alzheimer’s Disease [9].

Daily mental challenges

Mental stimulation, particularly acquiring something novel, such as learning to play an instrument or a new language, is linked with a reduced risk of Alzheimer’s. Researchers theorize that mental tasks assist in developing the brain, making it less prone to the lesions connected with Alzheimer’s Disease [8].

References

1. What Is Alzheimer’s Disease? National Institute on Aging, U.S. Department of Health and Human Services. https://www.nia.nih.gov/health/what-alzheimers-disease
2. Alzheimer’s for Dummies, Patricia B. Smith, Mary M. Kenan, Mark Edwin Kunik, Leeza Gibbons. October 2003. http://www.dummies.com/health/knowing-what-alzheimers-is-and-is-not/

3. What’s to know about Alzheimer’s disease? Medical News Today. Newsletter. 13 February 2018. https://www.medicalnewstoday.com/articles/159442.php
4. About Alzheimer’s and Dementia. org. India, Alzheimer’s association. https://www.alz.org/in/dementia-alzheimers-en.asp
5. Incidence of Alzheimer’s disease in India: a 10-years follow-up study. Mathuranath PS1, George A, Ranjith N, Justus S, Kumar MS, Menon R, Sarma PS, Verghese J. Neurol India. 2012 Nov-Dec;60(6):625-30 https://www.ncbi.nlm.nih.gov/pubmed/23287326

6. Alzheimer’s disease. From Wikipedia, the free encyclopedia. https://en.wikipedia.org/wiki/Alzheimer%27s_disease
7. Treating Alzheimer’s disease with the help of Ayurveda by Hunila. November 1, 2012 org. http://www.alzheimerindia.org/treating-alzheimers-disease-with-the-help-of-ayurveda/

8. Ashwaganda: Ancient Herb Proven to be a Potential Cure for Alzheimer’s by Dr. Mercola April 07, 2012 https://articles.mercola.com/sites/articles/archive/2012/04/07/ashwaganda-effect-on-alzheimers-disease.aspx

9. Coconut Oil and Alzheimer’s Disease By anh-usa (Alliance for Natural Health) on October 5, 2010. http://www.anh-usa.org/coconut-oil-and-alzheimers-disease/

Embryonic stem cells are cells in the early stages of embryonic development when a fertilized egg cell is divided first into two cells and then into four, eight, and sixteen. Each grows into a brand new cell type and multiplies as per the codes present in its DNA program as tissues form and organization starts. 

After twenty years of research and accompanying debates on the human embryo, we are finally on the threshold of both reshaping our present concepts in biology and moving on to clinical case studies. The first human embryonic stem cells were produced in 1998. Studies researching the question, “Can we treat diabetes by reprogramming the DNA in these cells at the beginning of life?” switched first to how human genes worked and which genes are responsible for the development of particular tissues and then to the embryonic stem cells for these areas and ultimately to replacing or reprogramming a “faulty or deficient” gene.

The most controversial topics in genetics and embryonic studies are related to bioethics. Many scientists are grappling with questions like whether is it ethically correct to intervene with the genetic programming of a fertilized human egg (zygote)? If so, what should be the limits? Are we trespassing a divine domain?

Embryonic stem cells have been an excellent source of information that we lacked throughout history about how living organisms started to develop. Like astronomers who trace their knowledge to the Big Bang in order to obtain fundamental information about the origin of the universe, biologists have been researching how the molecules in a single cell went through sequential and planned changes, how they transformed and acquired new functions that triggered the mind-blowing developments in diverse, miraculous living organisms. Scientists have found out how primordial embryonic cells transformed into more than 200 cell types that constitute various tissues and organs. The number of studies has skyrocketed about which molecule types can be used to regenerate the damaged tissue, say, after a traffic accident. Embryonic studies that focus on the regeneration or reparation of medulla cells (spinal cord) have been a source of hope for some patients with permanent paralysis because of a broken back injury or severed spine in a traffic accident or those who are still stranded in wheelchairs. Similarly, the preliminary findings of research into Parkinson’s and diabetes are extremely promising, and a new study reports of two blind people with macular degeneration (which causes blindness) who have been treated.

Initial studies

In 1981 researchers successfully obtained stem cells from a rat embryo culture. They soon realized that the cells held a secret potential: they could grow into 200 different types of cells. Later Wisconsin-Madison University biologist James Thomson derived stem cells from primates for the first time. Three years afterwards, Thomson derived the first human embryonic stem cells from donated but unused embryos.

The increasing number of research studies into embryonic stem cells sparked off intense debate both in religious circles and among the science community that care passionately about the sanctity of humans. Allegedly, lab studies were conducted on human embryos without restrictions, which were grown until tissues and organs formed but were then killed. In 2001, the US president George W. Bush slashed federal funds, stating that stem cell research was not strictly ethical. Deriving embryonic cells was banned in many countries including Germany and Italy. In other countries, however, studies went full speed ahead. Indeed, reports flooded in about stem cells grown by researchers in Australia, Singapore, Israel, Canada and the USA into nerve cells, immune system cells, and heart cells.

Before long, a new idea emerged about transferring new cells into the egg cell – like nuclei of body cells used in cloning Dolly the sheep – to produce various tailor-made, fully DNA-compatible tissues and organs, as they had the same genome as the donor’s. It became a topic of everyday conversations that spare organs could be cultivated for the human body just like spare parts of cars or other machinery were produced to replace a faulty or damaged part. In fact, if it were not for claims such as “creating a new human” there would be no objections against producing a kidney, lung, or heart from the DNA of a patient and thus overcome the major problem of tissue rejection in transplantation of organs.

If faulty or defective genes could be removed and replaced by healthy genes in the DNA of stem cells, many incurable genetic diseases could easily be fixed and many prospective parents who avoid having a child because of a defective gene they carry would welcome the development enthusiastically.

We are on the threshold of reshaping our present concepts in biology and moving on to clinical case studies. Embryonic studies have been a source of hope for even patients with diseases like paralysis and blindness.

Just in time and in the right amount

Embryonic stem cells are cells in the early stages of embryonic development when a fertilized egg cell is divided first into two cells and then into four, eight, and sixteen. Each grows into a brand new cell type and multiplies as per the codes present in its DNA program as tissues form and organization starts. It is most mysterious and miraculous that the molecules that lead a stem cell to transform into a new type of cell are synthesized at exactly the right moment and in the precise amount.  Scientists are currently trying to figure out which molecule leads a cell to become a nerve, muscle, or bone cell when attached to it. They are likely to decode the molecules by monitoring the tissues that remain undeveloped because of missing genes resulting from DNA mutations observed in certain genetic diseases.

The new field that has developed in the last two decades called regenerative medicine is predicated on tapping into the potential of stem cells by repairing missing or faulty tissues, or completing a link in the chain necessary for the functioning of a dysfunctional metabolic process. In 2006, stem cell biologist Shinya Yamanaka of Kyoto University in Japan successfully transformed adult rat cells into an embryonic state. The following year, human body cells were transformed into embryonic stem cells. The ensuing research has led to the acknowledgement that it was theoretically possible to transform stem cells into any cell type, a promising cure for diseased embryos that have genetically missing parts.

The major problem, however, is keeping these delicate cells alive in a culture medium. In 2007, Yoshiki Sasai discovered a molecule called rock inhibitor that nourished the cell colonies he grew. The success rate in generating new cell colonies rose to 27%. Parmar from Swedish Lund University heralded “a new golden era” by producing new neurons from embryonic stem cells for the treatment of Parkinson’s.

As new techniques were developed for producing cells fast and reliably, these cells turned out to involve a very low risk of developing cancer. “We don’t yet know how this hidden power and balance that can be transformed into any cell type is controlled,” states Hiromitsu Nakauchi, a stem cell biologist at Tokyo University who researches making blood platelets out of stem cells derived from the embryo or somatic cells.

Experiments are underway that aim to treat disorders by activating stem cells stored in the body that have not yet differentiated through the help of proper stimulating molecules. 

Miraculous differentiation

As the techniques for producing and feeding stem cells got easier, researchers aimed at growing and forming tissues and organs. A connective tissue or an outer covering like the skin that lacks a shape but takes the shape of the underlying muscles and bones can be produced even in a Petri dish and then transplanted to a burned or missing area of the skin. The present aim is the production of organs such as the kidney or the heart that has a particular shape and is made up of a number of different tissues. If the correct signal molecules responsible for cell division and differentiation can be identified and readily used where necessary and at the right amount, then organs including any type of tissue can be produced. Researchers like James Wells at Cincinnati Children’s Hospital in Ohio have tested the damage of drugs on intestines by using the partial intestines they developed from stem cells rather than administer them to normal humans, thereby hailing the imminent age of intestine transplants.

In 2004, the doctors who did tube baby experiments for a patient in Chicago known to have a genetic disorder started to produce a series of stem cells from generated embryos. They made models at the cellular level of the emergence of such genetic disorders as thalassemia, Huntington’s disease, Marfan syndrome, and muscle dystrophy. In 2007, they used embryonic stem cells to suppress molecular changes that trigger mental disorders caused by a genetic disorder called fragile X syndrome.

Research shows that multipotent (mesenchymal) cells stimulated at the outset of tissues are even more promising than embryonic cells with respect to diseases because it is easier to repair damaged or missing tissue by guiding them. However, it is essential in a genetic disorder that cells derived at the beginning of the embryonic stage should be used in order to replace faulty genes with healthy ones and address the disorder at its outset.

Experiments are underway that aim to treat disorders by activating stem cells stored in the body that have not yet differentiated through the help of proper stimulating molecules. In this way, as many as ten illnesses are likely to be treated, some of which include diabetes, macular degeneration in the eye, and neurodegenerative diseases such as Parkinson’s.

Douglas Melton from Harvard Stem Cell Institute in Cambridge has worked for fifteen years to transform embryonic stem cells into insulin-producing β-cells. He has produced pancreatic cells that sense glucose and produce insulin and he hopes to transplant them to end the dependence of patients of diabetes type-1 on insulin shots. The last obstacle remains to be the introduction of these cells to the system so that they are not destroyed by the patient’s immune system.

Clinically, it is believed that stimulated multipotent cells have a greater advantage than embryonic cells because the produced cells and tissues have the same DNA as the patient and thus do not cause any immune reaction when they are transplanted. The problem for many genetic disorders including type-1 diabetes is that the patient has the same mutation in his or her genes, and a method should be devised for cleaning and replacing these cells.

Another problem is the cost. It is reported that preparation of a series of multipotent cells will cost about one million dollars. However, the cost is expected to decrease and cells will be developed for the treatment of Parkinson’s disease, which is caused by a loss of neurotransmitter substance, which enable communication between nerves, and dopamine.

Treatment of macular degeneration is a popular target in this field. Patients gained the ability to read, though slowly, one year after the transplantation of part of stimulated multipotent cells to a damaged retina.

Such research studies normally cause some opposition. Playing with genes and embryos involve certain ethical and health risks. Yet, as reported in a Prophetic tradition, with all our God-given abilities like intelligence, curiosity, and willpower, humans can, and hopefully will, find cures for all diseases. Research into stem cells has the potential to provide many breakthroughs in these efforts to find healing for every human. Scientists and ethicists have to work together to determine our direction not to cause any unintended harm to any single soul while moving forward with this research.

Our body is perfectly coordinated to regulate our blood sugar level. But when our insulin levels are artificially altered, serious diseases can occur.

The human body needs energy. ATP (Adenosine Triphosphate) is to each cell in the body what gasoline is to a car. This energy is stored inside the bonds of the three phosphate molecules attached to an adenosine nucleotide. The light energy that exists in the sun’s rays is converted into chemical energy, stored in the form of carbohydrates, proteins, and fats through the photosynthetic reactions taking place in the chloroplasts of plants. Molecules of chemical energy are broken down in the mitochondria organelle of the cells in order to utilize their energy for ATP synthesis. This chemical energy (ATP) derived from nutrients is used by the eyes to see, the ears to hear, the hands to grab, the feet to walk, the heart to pump blood, the stomach to digest foods, the kidneys to filter blood, red blood cells to carry oxygen, white blood cells to fight germs, and the brain to think, memorize, and remember.

ATP is primarily synthesized from glucose – commonly known as blood sugar (glycolysis) – in approximately 100 trillion cells in our body. Glucose means fast energy. A sensitive metabolic balance is established (homeostasis) to maintain a blood glucose concentration in between 70-100 mg/dl for a nonstop energy flow and to prevent any cellular damage. If this balance is thrown out of order, many medical problems will ensue, primarily cardio-vascular diseases. How is the homeostatic balance of blood sugar maintained in healthy people?

Maintenance of blood sugar balance

The blood sugar balance is provided by the assistance and cooperation of the pancreas, liver, fat tissue, muscle tissue, the brain, the digestive system, and the kidneys. The chiefs of the orchestra here are the insulin and glucagon hormones synthesized in the pancreas, which operate in great harmony and yet have opposite functions. Insulin is in charge of dropping blood sugar; however glucagon increases it.  

The fine balance of blood sugar is conserved before we sense it for various energy situations such as exercise, sleep, or various energy intake cases such as overeating or skipping a meal. The real hunger is the 8-10 hour long “night fasting” period. During this time, since there is no food intake, the glucose that cells require for energy production is obtained from reserves in the liver. Thus, cells get their energy and blood sugar levels are kept at normal levels. If there is no additional food intake and the fasting time becomes longer, the glycogen reserves of the liver get consumed within 10-18 hours and necessary energy is obtained from fats and proteins. However, real fullness corresponds to a period of 4-6 hours “after meal.” During this time, the complex and macro size carbohydrates are converted to glucose in the liver and this glucose is stored as glycogen. Because the glucose storage capacity of the liver, which has numerous tasks, is limited, the excess glucose is stored by conversion into fatty acids. The unspent excess calories from three meals eaten in five hour intervals will be stored in either the liver or as fat tissue during the 12-18 hour long fullness period. The utilization of fats stored in the humps of camels which form by food intake to compensate for their energy and water needs during long desert travel can be given as an example of this.

In fact, when we say “I am hungry,” we acknowledge that the time has come to resupply our ATP reserves of nearly 100 trillion cells. The most important stimulator for the secretion of insulin from the pancreas is glucose. With the first bite, the readied insulin reserves of the pancreas are released into the bloodstream. This event, which takes place approximately within the first 6-10 minutes, is called the first-phase insulin response. With the language of reduced glucagon as a result of increased insulin, the message that it is no longer necessary to release glucose into the blood is transmitted to the liver. The blood sugar levels increase with continuing food intake (hyperglycemia) and this information is relayed to the pancreas through hormones secreted by intestinal cells. As directed by this signal, the proper insulin amount necessary for blood sugar levels is secreted into the bloodstream from the pancreas. This is called the late-phase insulin response.

The tasks of insulin

Cells are in need of insulin to uptake glucose into capillary vessels. Insulin binds itself to its specific receptor on the membrane of a cell, conducting its message, especially to muscle tissue. It’s saying, “The glucose food that you need is brought here by the blood vessels, and you can retrieve it.” After receiving the message inside the cell, GLUT (glucose transporters) molecules, which are in charge of glucose intake and are stored in the cytoplasmic vesicle pool, are carried to the cellular surface. Molecular gates are established once these molecules merge with the cellular membrane for the entrance of glucose through it. Glucose is inserted into the cell via this gate. The retired GLUTs are collected back in the cytoplasmic pools after cellular energy demand is met.

While these events are taking place, commands are given to the liver to prepare for the load of glucose arriving from the intestines and for adipose tissue to store the excess fat. These meticulous processes last for approximately two hours. The blood sugar level recedes back to its normal limits, but the activities of the liver and the adipose tissue continue at a rapid pace. If overeating occurs, the liver cannot take such a load. This can cause a delay in its functions, which will cause the body to feel tired.

The insulin and glucagon hormones have a half life of 3-5 minutes and are rendered ineffective in the liver and kidneys once they conclude their tasks. Thus, the body prevents lower blood sugar levels because of high insulin concentrations (hypoglycemia) or because of higher glucagon levels; it also prevents higher blood sugar levels (hyperglycemia).

The disruption of the blood sugar balance

Diabetes is the chronic observation of blood sugar above normal limits. This happens when the insulin hormone levels secreted from the pancreas are reduced and not able to carry out their function. There might be genetic factors present that contribute to diabetes; however, stress, a lack of exercise, obesity, and the consumption of processed foods containing elevated levels of carbohydrates often lead to the onset of diabetes in adults. The fine balance in between the liver, pancreas, muscles, and fat tissue can be disrupted by the following reasons:

1. If the number of cells in charge of insulin production in the pancreas decreases, sufficient insulin cannot be produced.
2. The message of insulin cannot be retrieved completely because of a disruption occurring at the receptors where insulin binds on cells, or due to lower numbers.
3. There may be a problem with reactions regarding GLUT production in accordance with the internal message retrieved upon bondage of insulin to the receptors.
4. During fullness, if the necessary suppression of glucagon production in pancreatic cells is not adequate, the glucose release from the liver continues.
5. The secretion of late-phase insulin response hormones in charge of pancreatic stimulation from the intestines is reduced.
6. Emptiness of the stomach is delayed, and a longer absorption time of nutrients occurs.
7. The appetite center is over stimulated and the urge to eat increases.

If the reasons above take place, then the blood sugar level is above normal. Normal blood sugar drops below 140 mg/dl two hours after a meal in healthy people, whereas this cannot be maintained in diabetic patients.

An iron pipe with salty sea water running through it for years is similar to a capillary vessel that has blood with high sugar levels inside it in terms of the damage that they undergo. Once hypertension and cholesterol joins diabetes, the heart, eyes, and kidneys will not function properly. These organs are great blessings granted to our body which we often appreciate only once we lose them. Therefore we must follow an intermediate path in eating and drinking, just as in every situation, avoiding excess.

Where am I?

There are 46 chromosomes in your body, carrying 20-25 thousand genes. Chromosomes and the genes they contain shape the genetic memory of a human being. Genes can contain hundreds of features, and these are revealed over time. For instance, you do not have any teeth when you are a newborn, but the time when you will get your teeth is encoded into your genetic memory. Once genes receive the action command, teeth start to emerge.

There are hundreds of genes located on chromosomes, all the way from the chromosome number 1 and 2, to chromosome number 46. For example, there are around three thousand genes found on chromosome number 1. The Y chromosome, in charge of male development, only contains 125 genes. A distinct address (locus) for each gene on the chromosomes is recorded. If you ask about the address of the fibrillin gene that synthesizes me, it is 15q 21.1, i.e., 15th Avenue, Long arm street, 21st pl, Number 1.

In other words my residing address is the 1st subband of the 1st band of the 2nd region located at the long arm of chromosome number 15. We are three siblings, known as fibrillin1, fibrillin2 and fibrillin3.

We stretch and relax like an arch. We can expand and tighten like an inflated balloon and then return to our previous state. If by an error, we happen to fail to restore ourselves after inflation, the tissue’s architecture gets deformed and expanded fibers cannot regain their original shape anymore. When observed in veins, this situation is called an aneurysm. The frequency of this disease is approximately one in ten thousand, which is also called ballooning. That said, my flexing is necessary. Veins flex so that the blood pumping through them doesn’t cause any turbulence, as it would otherwise be during a vacuum occurring inside metal water pipes. Flexible sportsmen who do acrobatic moves do not compare with me. I can bend, curve, flex, relax and constrict, inflate, deflate and transform like elastic, from one shape to another, for your health and overall convenience – all because of the wondrous features granted to my nature.

What kind of a fiber am I?

I provide structural support for the fabrication of elastic fibers in the connective tissue as a protein synthesized according to the code of the fibrillin gene. In case of my failure or absence, weaknesses occur, especially in the connective tissues of organs that are rich in elastic fibers, such as the aorta, lungs, and eye balls. The iris (the colored part of the eye), pupil, and eye lens display changes in accordance with levels of light or distance of objects observed. These changes are controlled perfectly according to my work, and humans often don’t even notice this. We also help the eye lens constrict and relax. It can be understood that we are such a great blessing granted for your service. Of course, if we tried to count all the blessings we’ve been given, and never even consider, it would be impossible!

My weight is 350 kilo daltons. A Dalton is an atomic mass unit approximately equal to one hydrogen atoms’ mass, which is 1.66×10-24. I consist of 2.871 amino acids. I am formed by the sequential arrangement of 20 amino acids that exist in your body as the smallest unit of proteins. We bind each other to become 10-12 nanometers wide microfibers as the result of a process called polymerization that brings loops of a protein chain together. These microfibers are brought together with the elastin protein that provides elasticity in our body. The system that we form with elastic fibrils constantly serves the body’s blood vessels, primarily the vessels located in your eyes, heart, and many of your tissues, such as your skin and nerves.

What do I do? We fulfill commands that are requested from us in many tissues and organs, without any flaws. Scientists call us the wonderful building blocks of the body’s architecture. We can extend twice as much of our length. We are always on task: while you are breathing, when your heart is pumping blood and your stomach is digesting food, or the moment you are gazing at nature with your eyes. We are given the duty to prevent many organs from tearing, including the heart, lungs, stomach, and blood vessels. One of the places I work most frequently is the aorta, the body’s major artery. Your heart beats approximately a hundred thousand times a day. A high level of pressure develops in the arteries during the pumping process. You would suffer greatly without the help of our elastic fibers. Blood vessels would rupture, ending your life. This high pressure is tolerated only through the expansion of the vessel’s diameter without any decrease in length of the artery. This diameter regulation is designed so wondrously that blood flow remains the same; no shaking or waves are observed. This diameter control happens via the fibrillin protein located inside the vessel.

I also play a role in the vitality and tension of your skin. Skin is essentially a dense fibrous connective tissue composed of a protein called collagen. I am also one of the main elements of this connective tissue. As you age, this layer starts to dry and has lesser fibrous proteins; therefore, as fibers decrease, so does my tension, and I start to wrinkle. Elderly people do not like getting wrinkly, but this is your fate. Whatever you do, I will also age and die.

I cannot go without pressing this important issue: Staying under the sun for a long time degrades me. If done properly, sun light is useful for skin. But solar radiation damages the live tissues and organs. This radiation is an effective factor both in degradation of protein structures, and the formation of varicose veins and skin damage. It is reported in various sources that exposure to sun rays leads to alterations in the genetic material of skin. Ultraviolet rays speed up the degradation of skin. In medical language, this is called oxidation via free radicals. Please do not burn us and yourself while sunbathing. Even if you do not care for yourselves, you should still be considerate of us. If you say that sunbathing both helps, with vitamin D synthesis and reducing the risk of osteoporosis, I would like to remind you that for the vitamin D synthesis of skin, it is sufficient to expose your hands, feet and face to the sun.

How is life without me?

Though we were wisely designed, sometimes, you are tested by certain diseases in which we are not present. Absence, as they say, makes the heart grow fonder!

Life without me is unbearable. I could give a couple of examples, should you like. If I was not created, your skin would not be flexible. You wouldn’t be able to control your eye lenses. Your aorta would not be flexible and your heart, which beats thousands of times a day, would be torn under the high pressure in a short amount of time. Major problems would occur with the development of your stomach, lungs, and other organs.

I also have a significant job keeping TGF-Beta (which helps cells grow) function under control. To give you an idea of how important this is, imagine your communication system turned upside down. Now imagine how complicated are the communication systems connecting billions of people around the world, how a mess it would be when they are out of service. These are nothing when compared to the human body. There are 100 trillion cells in the human body, communicating with each other instantaneously. A cellular community that is fifteen thousand times more crowded than the earth’s population communicates via small molecules, like us. Cellular proliferation and tissue differentiation would fail if cells failed to communicate. The full spoon of food in your hand would not end in your mouth but maybe in your ear or your eyes.

If a mutation happens with the Fibrillin-1 gene, Marfan syndrome can occur. This disease, which was defined in the 1800s, is named after its discoverer. The frequency of this disease is one in five thousand. One of the major lethal consequences of Marfan syndrome is an aorta tear. This is in addition to many problems with the eyes, skeleton, and cardio-vascular systems. Many of the patients die in their 30s or 40s because of the flaws in the cardio-vascular system. Of course, death may occur at any age because of an aorta rupture. 14% of the patients with Marfan syndrome display chronic obstructive pulmonary disease (COPD), which is associated with breathing problems, because the integrity of lung tissue is compromised. Another disease I help prevent is called Ektopia lentis, in which the eye lens is displaced from its original position. Normally, I help eye functioning. When my fibers relax or constrict, depending on light, I help the eye to relax, enabling both near and far sightedness. With Ektopia lentis, anomalies on the front vestibule of the eye, a high degree of myopia, and retina damage occur.

If overproduced, I can cause another problem with the eye, called exfoliation syndrome. This is when fibrous connective tissue, like me, accumulates in the eye – it’s commonly called glaucoma, or ocular hypertension. In some people, as they age, a fibrous material like hair dandruff collects on the eye lens. This material, dislocated by movements of the iris, blocks the drainage channels that discharge the intraocular fluid. Eye pressure increases as the result of failed drainage. As you see, I am not a problem when I am synthesized normally, but can be trouble if over produced! My final request from you!

You have seen our amazing works and complicated functions. Therefore, please remember me and my friends. Please do not ignore our efforts and activities. Be grateful for the blessings provided through us, even if you can’t see them. And take care of us, please – don’t get carried away with too much tanning!

A sugar is a monosaccharide if it is made up of a single sugar molecule; it is disaccharide if it is built by two sugar molecules; and a polysaccharide if it is composed with multiple sugar molecules.

Sugars that we ingest are broken, in the digestive system, into monosaccharides of glucose, fructose, and galactose. Almost all of the absorbed monosaccharides are first converted into glucose in the liver. This conversion is a very important task of the liver: 80% of the sugars passing into the blood are glucose. As a result, very limited amounts of fructose and galactose are present in the blood. Therefore, when blood sugar is mentioned, normally glucose is taken into consideration and the fructose and galactose levels in the blood are ignored. Glucose, which is also called grape sugar, is most abundantly found in grapes, while fructose is called fruit sugar, as it is plentiful in fruits, and galactose is named milk sugar after its dense presence in milk. The most important characteristic of fructose is that it is sweeter compared to other simple sugars.

Insulin is secreted from the pancreas in order to lower elevated blood glucose levels after digestion. Insulin functions in the transport of glucose from the blood into cells to provide necessary energy, therefore reducing blood sugar levels; furthermore, it also plays a role in the storage of excess glucose as glycogen, which is found primarily in the liver. Once glycogen storage limits are reached in the liver and muscles, glucose is then stored as fat. Fat tissue acts as sustenance during long fasting periods.

Differences between fructose, glucose, and galactose

Glucose and galactose are absorbed actively, depending on salt. They cannot be absorbed without salt while passing through the intestines. Salt is necessary for the absorption of glucose which is present in the starches of potatoes and other foods. Thus, when potato is consumed with salt, the transport of glucose into the blood is facilitated.

However, salt is not necessary in the case of fructose absorption. The intestinal absorption of fructose contained in fruit is delayed by fruit fibers, since these fibers prevent or balance the transport of fructose into the bloodstream. However, when fructose is ingested as a fruit juice, it is absorbed and joins the bloodstream much faster because of the lower fiber content.

A person feels full after a meal when neurons in the satiety center of the hypothalamus are stimulated by elevated blood glucose. Then, hunger center neurons are repressed, eliminating the feeling of hunger. Therefore, a person reduces their food intake during a meal as their blood glucose levels increase. Increased levels of amino acids and fatty acids in the blood also suppress hunger and stimulate fullness after meal. However, one important point is that fructose does not stimulate fullness in the brain. Therefore, if the blood fructose levels are elevated instead of glucose, a person cannot generate a sensation of fullness sensation. As a result, a person desires to intake more food during consumption of fructose. It is only possible for fructose to generate fullness after it has been converted into glucose by liver.

How to consume fruits?

We should prefer direct consumption of fruits instead of drinking natural or industrial fruit juices because of the high fructose content of fruits. The Prophet Muhammad, peace be upon him, consumed fruits before meals, the wisdom of which we learn only today. Fruits should be consumed at least an hour before or two hours after a meal, for sufficient time should be given for the fructose of an ingested fruit to be absorbed by the intestines and converted to glucose by the liver. Such practices will result in a reduced appetite and food intake. If fruit is consumed after a meal, a delay occurs in the conversion of fructose into glucose since the liver will be occupied by other biochemical processes, along with a full storage of nutrients; this will increase blood fructose levels and fail to reduce appetite. Fatty liver occurs as a consequence of high fat content of the blood. Arteriosclerosis and cirrhosis of the liver may be seen in people with a habit of excessive post-meal fruit consumption.

In a research carried out on laboratory animals, it was found that glucose induces fullness in the hypothalamus and suppresses food intake, whereas fructose was found to repress this effect of glucose, stimulating food intake.¹ Insulin reduces the harms of accumulating sugar in the blood by increasing lipid synthesis. Insulin also takes place in leptin secretion from adipose (fatty) tissue. Leptin is important in the prevention of obesity; therefore, insulin helps in weight loss, too. The leptin hormone causes reduced food intake by stimulating nerve cells in certain parts of the hypothalamus.² Fructose does not cause any leptin secretion because it does not stimulate an insulin release; therefore, it is not effective in generating a sense of fullness.

Ghrelin is a hormone secreted into blood by stomach cells during hunger. This hormone, which produces stomach acids, is enacted through the hypothalamus. It induces hunger, and therefore increases appetite. Insulin secretion increases along with the blood glucose levels during satiety. This eventually causes the increase of the leptin hormone, which also leads to a decrease in ghrelin secretion. As a result, fructose gets absorbed more than glucose in the intestines. Elevated fructose in the blood leads to insufficient or reduced insulin secretion. In this case, a person continues eating.

Fructose and diseases

Free circulation of lipids in the blood damages arteries and veins. For this reason, lipids are transported in “molecular vehicles” that are called as high, low, and very low density lipoproteins (HDL, LDL and VLDL). Neutral lipids (triglycerides) that are present on VLDL (very low density) vehicles are broken down with an enzyme. These lipids are then unloaded from the vehicles by cellular uptake and stored as fats. This transfer of lipids into adipose (fatty) tissue is enhanced via the insulin hormone. In the case of fructose intake, without its insulin secretion effect, lipids accumulate in the blood and liver and eventually prepare ground for liver damage and arteriosclerosis.As the result of a fructose based diet in laboratory animals, it was discovered that lipid production shifted from adipose tissue into the liver, therefore elevating the risk of high blood and liver fat levels.

There are two reasons for this shift. The first one is that fructose acts on the fat producing enzymes of the liver whereas it does not act likewise in adipose tissue.

Secondly, fructose plays an inhibitory role in the conversion of glucose into lipids in adipose tissue. Also, fructose consumption in humans has been linked to elevated blood fat levels.

Overconsumption of fructose causes increased liver fat synthesis. Phosphofructokinase is the limiting enzyme regarding the breakdown of glucose in the liver. This enzyme is regulated by citrates and ATP produced by glucose catabolism and the Krebs cycle, limiting glucose breakdown. However, there is no such limitation in fructose breakdown. Through fructose catabolism, glucose, glycogen, pyruvate, lactate, glycerol and the acyl part of acylglycerol are synthesized. This synthesis can not be limited. As a result of this excessive output and high amounts of triglycerides, VLDL is produced.³ It has been found that persons who consume two or more boxes of fructose sweetened beverages every day carry a 35% higher risk of heart disease.⁴

This isn’t the only disease associated with fructose. In some studies on laboratory animals, it has been reported that a high fructose diet is associated with hypertension.⁵ A lot of research exists suggesting that excessive fructose consumption leads to insulin resistance in both the liver and peripheral tissues, which can often cause diabetes.⁶ In a recent study, it was claimed that excessive fructose intake poses risks for renal diseases leading to glomerular hypertension, renal damage, and inflammation and damage to renal tubules and tissues.⁷

In a study conducted on 21,483 Americans who were older than two years, daily consumption of 37 gr. of fructose (8% of total calorie need) was found to be elevated to 54.7 grams (10.2% of total calorie need) gradually between the years of 1988-1994, mostly consumed by younger people. Increased use of fructose syrup was linked to obesity during the last 35 years.⁸ Furthermore, in a study carried on 1,749 male and female children and teenagers, a positive relation was found between body mass index (BMI) and excessive consumption of carbonated beverages containing high fructose concentrations.⁹ There many studies that support this report.¹⁰ Excessive fructose consumption is known to cause “metabolic syndrome” in which many diseases like obesity, arteriosclerosis, and diabetes emerge together.

Are fruit juices harmful?

Fructose syrup is being used at increasing rates in the food industry. According to the annual report of US Food and Drug Administration (FDA) for the year 2000, fructose syrups are sugar solutions containing approximately more than 50 % fructose. It is often synthesized by a conversion of corn starch into glucose by glucose isomerase.¹¹ There is also a third syrup type containing 90% fructose, however this has limited uses.

The sweetness of fructose syrup is similar to that of table sugar. It prevents the dehydration of food with its hydrophilic character. It is mostly used in aromatic foods, especially carbonated beverages and fruit juices. It prevents the proliferation of microbes with its high osmotic pressure property and makes food more resistant against them. Syrups containing 42 to 55% of fructose are used in baked goods, cereal products, dairy products, processed foods, both carbonated and regular beverages, ice creams, and frozen desserts. High fructose syrups are used in foods to decrease water activity and prevent spoilage.

Fructose syrups have a very low ash level due to application of intense purification processes during production and product color is water-white. Therefore colors of fructose used industrial foods are white as well. Fructose syrups have a lower viscosity and density compared to glucose syrups and therefore it is runny like water and not as sticky.

How to consume sugars after a meal?

Especially after a fatty meal, our body seeks sugar. The reason behind this is the requirement of sugar for the storage of lipids into fat tissue. However, this sugar should absolutely be glucose instead of fructose. Therefore, some amount of sugar can be consumed to facilitate the removal of lipids from blood after meals. This is recommended to lower blood lipid levels. However, this should not be done with fruits but with natural sugars like grape molasses. A baklava or a dessert made with industrial sugars (fructose) will not be beneficial but harmful.

In conclusion, the consumption of corn-derived fructose syrup is gradually increasing in recent years. Fructose syrup is used both in various carbonated or regular soft beverages, and in desserts. The reason for our fructose syrup preference is that it helps preserve foods longer and it leads to food addiction because it enhances appetite due to its strong sweetness. Fructose syrup is synthesized by the conversion of natural glucose in corn into fructose by isomerase enzymes. In this sense, today’s increased consumption of fructose is altering the existing sugar balance of natural food items. Overconsumption of fructose can pave the way to obesity, metabolic syndrome, arteriosclerosis, diabetes, hypertension, and arteriosclerotic heart and kidney diseases.

Arifagaoglu is a professor of medicine in Ankara, Turkey.

References

1. Wolfgang MJ, Cha SH, Sidhaye A. et al. Regulation of hypothalamic malonyl-CoA by central glucose and leptin. Proc Natl Acad Sci USA. 2007; 104: 19285-19290.
2. Guyton AC, Hall JE. “Dietary Balances; Regulation of Feeding; Obesity and Starvation; Vitemans and Minerals.” Textbook of Medical Physiology, Saunders, 2010, 843.
3. Rutledge A, Adeli K. Fructose and the metabolic syndrome: pathophysiology and molecular mechanisms. Nutr Rev. 2007; 65: 13–23.
4. Fung TT, Malik V, Rexrode KM, Manson JE, Willett WC, Hu FB. Sweetened beverage consumption and risk of coronary heart disease in women. Am J Clin Nutr. 2009;89:1037–42.
5. Barone BB, Wang NY, Bacher AC, Stewart KJ. Decreased exercise blood pressure in older adults after exercise training: contributions of increased fitness and decreased fatness. Br J Sports Med. 2009;43:52–6.
6. Blakely SR, Hallfrisch J, Reiser S, Prather ES. Long-term effects of moderate fructose feeding on glucose tolerance parameters in rats. J Nutr. 1981;111:307–314.
7. Johnson RJ, Sanchez-Lozada LG, Nakagawa T. The effect of fructose on renal biology and disease. J Am Soc Nephrol. 2010; 21(12): 2036-9.
8. Bray G. Fructose: should we worry? Int J Obes 2008;32: S127-131.
9. Forshee RA, Storey ML. Total beverage consumption and beverage choices among children and adolescents. Int J Food Sci Nutr. 2003; 54: 297–307.
10. Forshee RA, Anderson PA, Storey ML. The role of beverage consumption, physical activity, sedentary behavior, and demographics on body mass index of adolescents. Int J Food Sci Nutr. 2004; 55: 463-478.
11. Melanson KJ, Angelopoulos TJ, Nguyen V, Zukley L, Lowndes J, Rippe JM. High-fructose corn syrup, energy intake, and appetite regulation. Am J Clin Nutr. 2008; 88(6):1738S-1744S.

Skin is composed of two main interwoven layers of dermis, on the inside, and epidermis, on the outside. The epidermis, which is composed of five sub units, possesses the most important sign of our identity. Each thin layer is arranged in a way to carry out different tasks. A significant amount of elasticity and flexibility is provided to skin via these five layers. These layers can glide on each other slightly and can also be compressed under pressure. They are compressed when we sit on a hard surface. This situation can be similar to the compression of the spring in a click pen, or the suspension of a vehicle under a load. They regain their previous state upon termination of the pressure, like standing up. This elasticity is crucial for skin’s integrity.

The thin construct of our skin contains sweat glands that are embedded in the fibrous connective tissue. There are sensory receptors, hair roots, and hair muscles connected to them, and also loose nerve endings, and a network of capillary vessels. Free nerve endings are created to specialize in various functions so as to sense hot, cold, pressure, and pain. Likewise, the continuation of blood flow relies on very intricate calculations that are hard to explain. When blood vessels arrive at the skin, they are dispersed like a net in the form of capillaries.

The blood pressure of the arteries located at lower section of the skin is higher than the pressure of pulmonary veins. If pressure is applied to skin for a long duration from outside, the pressure in the pulmonary veins builds up and regional blood flow is disrupted. Therefore oxygen, glucose, and other nutritional substances cannot be delivered to these areas; along with inhibition of waste product removal, it leads to a nutritional abnormality in the tissue.

Sensory cells within our skin detect and report nutritional abnormalities of tissue to our brain via various chemical substances (like acetylcholine, bradykinin, and histamine). Thus we change our position consciously or subconsciously with the intervention of our brain to avoid the danger of a nutritional abnormality, and therefore the area regains normal circulation. In this stage, the process is still reversible; however, should the pressure continue, skin cells will start to die from, from the outside in. These systems do work well in healthy persons but in cases of stroke or coma, the intervention system does not work.

This critical picture can be understood better with an example. Just like roads need to be used in order to carry goods and remove trash, the transportation of minerals, vitamins, and many other life saving substances to the distant parts of the body and removal of waste products requires blood vessels to remain open. This must continue in a perfect balance without any interruption throughout our lives.

If a pressure ulcer occurs, it is like being exposed to external dangers in a house if a door or window breaks. It is like a free entrance visa is granted to germs that were blocked. Our back and pointy areas, like, thighs knees, heels, and shoulders are under more pressure, and therefore at more risk when we lie down. Two to six hours of pressure to one of these areas is enough time to disrupt skin integrity. Our daily sleep requirement is around 6-8 hours, therefore we need to switch positions a couple of times during our sleep. Therefore we face this risk everyday in our sleep; however, thanks to the perfectly functioning protective systems, without noticing during our sleep, our position is changed and this dangerous situation is avoided. Intensive care doctors and staff know better what a great blessing that is are since intensive care patients are mostly unable to move. Despite the use of many preventive efforts, like turning the patients in certain periods or the use of air beds, pressure ulcers still occur and a significant portion of patients die of the microbial infections caused by these wounds.

The story of sleepers

“The Seven Sleepers” story in the Christian tradition is retold in the Qur’an as “the People of the Cave.” The story is about a group of young believers who took refuge in a cave fleeing the oppression of the pagan Roman emperor. Both traditions narrate that they fell asleep in the cave, where they stayed asleep for hundreds of years. The Qur’anic account, however, mentions that they were made to change position during their centuries-long sleep: “You would have thought them awake though they were asleep. We caused them to turn over to the right and the left…” (18:18). It is an interesting nuance that they were made to change position, for it sounds rather irrelevant to the rest of the story. However, with the medical conditions of our skin that were explained above, this nuance makes perfect sense as advice to us on how we should treat patients who are unable to move.

What possible similarities could there exist between a human and a tree? Interestingly, the open wounds of human beings and trees are subject to the same laws and are healed in similar ways.

Have you ever wondered what kinds of similarities exist between human skin and the bark of a tree?

Trees are subject to major and minor injuries just like humans are. These injuries could be the result of a broken branch, insect infestation, animal damage, fire and human related damages. These kinds of injuries can lead to the infection of a plant which can cause rotting and damage to the transport tissues like phloem (nutrients) and xylem (water) by microorganisms and insects (bacteria, fungi, parasites).

Fluid excretion in wounds and development of scar tissue

Blood serum is secreted in human wounds, whereas gum and resin type fluids are secreted in various trees (Figure 2 and 3). Serum plays an important role in sterilization of the wound, along with blood coagulation. Defense mechanisms in trees involve excretion of different fluids (resin in needle-leaf trees, gum in broadleaf trees) that are synthesized via composition of various chemicals. The most important feature of these fluids is that with their special chemical make up, they can protect the wound from organisms like bacteria, fungi, and insects that are potentially harmful to the tree. These fluids also feature coagulation like the human serum; they congeal and solidify after excretion and trigger a biological healing process while physically covering the wounded area.

Wounds are repaired with new connective tissue cells (fibroblasts) in humans and by callus in trees. Healing of the wound following the coagulation takes place with proliferation of cells in this region (epithelialization). First, epithelial cells wrap the wound via proliferation. New transport tissue is developed during this process. Next, fibroblasts that are in charge of wound repair are transferred into coagulate via this transport tissue. Fibroblasts synthesize collagen protein of the required fiber structure needed for the wound repair. Injured area is woven with these, and recovers its former shape in time depending on the size of the wound.

Healing is granted through timely reproduction, transformation and maturation of paranchimatic cells that make up the callus, when only a portion of tree bark is damaged. Paranchimatic cells are fused side by side and they form a thick elevation of callus tissue around the wound (Figure 4). At the end, these are activated for the development of a new, healthy cambium and bark. Cambium tissue is responsible for vertical and lateral growth of a tree therefore it is vitally important that it does not suffer any damage. This tissue in growth season proceeds from the perimeter of the wound towards the center for a complete healing. The productive efficiency of the tree medium can speed up or slow down the curing process similar to humans.

The reality is that all living things are created with a dress suited for their environments so that their bodies can be protected from negative elements from the outside world. Organisms are armored from many harmful physical (mechanical, extreme temperatures, light etc.) and chemical effects with this perfectly bestowed dress as a manifestation of the divine compassion in the universe just as in the case of the wounds of humans, animals and plants which are subject to the similar laws found in nature.

Heart regeneration in mammals

Such heart regeneration holds the promise for the treatment of heart failure following heart attacks. But so far, the adult human heart is known not to show adequate regeneration or replacement of dead tissue with functional tissue such as beating cardiomyocytes (cardiac muscles) and arteries. When a patient has successive heart attacks and myocardial infarctions (death of cardiac muscle resulting from interruption of the blood supply), the number of dead cells increases due to the decreased level of oxygen reaching the heart tissue. That’s one of the reasons heart disease is so deadly.

The rates of cardiac regeneration, from fish to amphibians to mammals, demonstrates a decreasing trend — high in fish, moderate in amphibians, and limited in mammals. The regeneration mechanism is thought to occur via incorporating stem cells, using differentiation into cardiac muscle and other cell types, or via dedifferentiation of cardiomyocytes. It is known that the heart of an adult zebra fish can regenerate without scar formation, whereas adult rodents and humans respond with a fibrous scar, without obvious cardiomyocyte regeneration. This remarkable phenomenon had been demonstrated in other fish and amphibians, but never before in a mammal. Recently, researchers at UT Southwestern Medical Center showed that a newborn mouse’s heart can fully heal itself.

Sadek’s group at UT Southwestern Medical Center at Dallas showed that the mammalian heart demonstrates a temporary regeneration capacity in newborn mice. After slowing down the body functions by cooling the body of a mouse, they performed a very delicate heart surgery, removing about 15 percent of the apex of a 1-day-old newborn mouse heart. Within a short period (three weeks), they showed that heart had healed and the function of heart had returned to normal. But when mice are a week old, this remarkable ability of regeneration disappears, and damage to the heart results in the thinning of the heart wall at the site of injury, and the loss of the pumping capacity of heart, also known as heart failure. There seems to be a barrier to regeneration after 7 days. This 7-day window in mice could correspond to a few months after birth in humans. Several reports suggest that human heart may also have some ability to regenerate in infancy.

If newborn animals and infants are able to regenerate their hearts, there could be ways to remind the heart how do this or restart this ability in adulthood to allow regeneration in a broader window. Could there be means to induce regeneration by gene therapy, using small molecules, drugs or hormones? This new discovery brings new approaches to study heart disease and hopes that one day, heart disease — the number one killer in the world — could be treated. More studies are needed and a number of labs have already started to invest in this new model of heart regeneration.

Human heart cell turnover and regeneration

The heart is the least regenerative organ in our body. Once cardiomyocytes are damaged through heart attacks, the heart heals by scar formation instead of regeneration. This results in a loss of contractile function and often ends in heart failure. Lack of regeneration in an adult heart is associated with the complexity and inability of cardiomyocytes to divide, along with the absence of adequate muscle-producing cardiac stem cells in the heart.

Cardiomyocytes proliferate extensively during embryonic development but slow dramatically around birth. The growth of heart continues after birth through the increase in cardiomyocyte size, known as hypertropy. This allows DNA synthesis and nuclear division and results in binucleated cardiomyocytes.

Increasing evidence strongly suggests that the human heart shows a degree of cardiomyocyte repopulation (introduction of new cardiomyoctes). It is always challenging to study human heart cellular homeostasis, as it is limited in the availability of human samples and the means to work on it. Who knew nuclear testing during the Cold War would help to uncover dynamics of human cardiomyocyte turnover? Using a technique based on radiocarbon dating of DNA with carbon-14, released from nuclear tests, Bergmann and his colleagues from the Karolinska Institute in Sweden showed that the cardiomyocyte turnover rate is about 1 percent per year at age 20, with a decline to 0.4 percent per year at age 75. This is based on the idea that people born during nuclear tests following World War II until the Limited Nuclear Test Ban Treaty (1963), any cardiomyocyte repopulation should result in lower carbon-14 concentrations. These findings imply that around age 50, about half of the cardiomyocytes in the human heart are generated after birth. However, another study puts emphasis on the importance of cell deaths (apoptosis) for heart cell turnover, asserting that these rates could be much higher (7-40 percent per year). Those findings bring new hopes to heart disease. If the repopulation potential of heart could be therapeutically targeted, the rate of turnover could be extended to overcome the inability to recover cardiomyocyte loss and cardiac contractility after heart attacks.

The better regenerative capacity of fish and amphibians, compared to that of mammals, seems to stem from the presence of species-specific differences. It has been suggested that the limited regeneration potential of mammalian hearts following injury increases survival by prioritizing homeostasis and fibrosis (scar formation by excess connective tissue). Bleeding from the heart in a high-pressure circulation probably favors the more rapid fibrous healing, instead of regeneration, whereas small animals have a low-pressure circulatory system and oxygenation isn’t needed all the time. This phenomenon probably applies to the regeneration of the newborn mouse heart, which also made the removal of the apex of the newborn mouse heart possible.

Cardiac stem cells for regeneration

The heart is a mosaic of various cell types including valvular, arterial, smooth muscle, pacemaker, endothelial, autonomic ganglia, fibroblasts and cardiomyocytes. Those cells have essentially the same genetic makeup but they show a great diversity. Could there be a common cardiac stem cell that gives rise to all those cell types in the heart? There are a number of studies suggesting the presence of such stem cells, though why they fail to regenerate the heart following heart attacks remains unknown.

There have been a number of attempts to discover cardiac stem cells. Some stem cells have been studied in animals and even considered as possible therapies in human trials. Sources of those stem cells could be classifies as resident and non-resident (exogenous) cells of heart. Exogenous stem cell types include skeletal myoblasts, hematopoietic stem cells, mesenchymal stem cells from bone marrow and circulating endothelial cells. Many approaches to identify resident cardiac stem cells are based on knowledge from hematopoietic stem cells. Using surface proteins on the cells known to enrich bone marrow stem cells, several types of resident stem cells are shown to exist in the heart. There are limited improvements in cardiac function using those cells, but the benefits of those cells are thought to be through other mechanisms instead of replacement of dead tissue in the damaged heart.

A study demonstrating the renewal of a newborn mice heart does not completely rule out resident cardiac stem cells as a source of new beating heart cells, but points out the likelihood of their originating from cardiomyocytes by dedifferentiation. Along with a number of attempts to treat heart failure by using stem cells, recent findings offer hope that researchers and doctors will one day able to cure heart disease. Knowing that “there is no disease that God has created, except that He also has created its treatment,” our duty is to study hard and to develop new technologies to find the prospective treatments for heart failure to serve humanity.

References

• Porrello et al. 2011. “Transient Regenerative Potential of the Neonatal Mouse Heart.” Science 25 February: 1078–1080.
• Bergmann et al. 2009. “Evidence for Cardiomyocyte Renewal in Humans.” Science, 3 April: 98–102.
• Charles E. Murry and Richard T. Lee. 2009. “Turnover after the fallout.” Science, V324.
• O.Bergmann et al. 2009. Science 324, 98.
• Simonetta Ausoni and Saverio Sartore. 2009. “From fish to amphibians to mammals: in search of novel strategies to optimize cardiac regeneration.” JBC. 184 (3).
• Martin-Puig et al. 2008. “Lives of a hear cell: Tracing the origins of cardiac progenitors.” Cell Stem Cell 2. April.
• Nevada Nuclear Testing Site: http://mason.gmu.edu/~kcherrix/atomichome.html
• Sahih al-Bukhari, Vol. 7, Book 71.

Dear Peter! I, your muscular system, would like to talk to you today; I allow you to walk and do all kinds of movements very easily. In the most recent essay of this department, the skeletal system, which works together with me, discussed how it protected your body and enabled you to stand straight and firm. Sure, this is true. However, as you know, huge rocks and trees can stand straight, too; but they do not have what you do-the ability to move. They are rigid and inflexible because they do not have a system that allows them to move.

You on the other hand, as the most splendid creation in the entire universe, have mobility. All animals have mobility at different levels, thanks to the muscular tissues, which work dynamically behind all the moving organs. However, you, human beings are like neither the animals nor the plants. You have not been created to live like a tree that is pegged down in earth or like an animal that unconsciously tries to meet only its biological needs. Our Designer, God, has made you and your descendants the most important of all creation. He has given you qualities that help you to discover the world, learn, invent and establish new civilizations. To realize such potential and to carry out such duties, you need to first have the freedom to make changes in your small immediate world, which can only be done through motion. In order to enable you with this ability to move, my Creator has put me at your service. I am a system that comprises hundreds of muscles and millions of packed cells.

My most important feature is the cells that move by burning sugar, like a motor consuming fuel in order to work. My cells can shorten and lengthen thanks to the intracellular fibrils (myofilaments) that contract and expand. As a result of each contraction, I pull the bone or the organ that I am attached to and cause it to move or change shape. With the exception of your heart, your bones and organs cannot move on their own. Their ability to move depends on the nature of the muscle they are attached to.

Indeed, I can be called both an organ and a form of tissue. I can use my contraction ability not only as muscle tissue, but also as an organ and a system which runs throughout your body. That is the reason why I appear in so many different types and shapes of muscle bundles. Let me give you an example to help you better understand what a muscle consists of: Let us imagine that a thin thread is like a basic muscular cell. Let us now bring together a great number of threads and make string out of them. Then, let us bring together those strings and make a clothes line. Next, let us bring together a great number of clothes lines and make a very thick rope. Now, imagine this thick rope as a muscle and an organ. Yet, this example is too basic compared to the sophisticated muscle.

Very thin cotton fibrils make up the thin threads. In the muscle fiber, like those cotton fibrils, there are two filaments formed by the two types of protein molecules called actin and myosin, which help in the contraction function. Those little filaments are placed facing one another and they slide past each other during the contraction, which causes the muscle fibers to shorten. That is how the contraction and relaxation of a muscle occurs.

Peter, do you think that coincidence plays a role in this complex and wonderful mechanism and the incredible structure which I have attempted to simplify with an example? Not even a simple thread can be produced without a thread-maker or a machine. Each of your muscles comprises billions of fibers, wrapped all around your bones and giving shape to your body. Can such a complex and delicately intricate structure exist on its own and be positioned in the best place it could possibly be?

My muscles consist of bundles that are made of thousands of muscle fibrils; the size and shape of each muscle depends on which bone it is attached to and what function it does. For example, the muscles that move the bones in your arms and legs are long and spindle-shaped; whereas the ones that are attached to your body can be circular, or triangular, or spread over a broad area. Whatever shape they have, the red skeletal muscles, which are attached to your bones, are very strong and they are voluntary muscles, which mean you can control their movement. When you walk, run, do something with your hands, lie down or stand up, you always use my red striated muscles. The strias (stripes) can only be seen under a microscope because of the histological structure of these skeletal muscles that make up a great part of your body.

My smooth muscles are involuntary muscles that work without your control. Their movements are slow and their contractions last longer, which is the reason why they do not tire easily. The smooth muscles lie in the walls of digestive system, blood vessels, and urinary tract, but I will not talk much about them since each system has referred to the smooth muscles within itself and in detail in previous talks. Because they are not attached to your skeleton to work, the smooth muscles do not play a role in your movements, such as walking around; they only work for the movements of your inner organs.

The third type of muscle belongs to your heart (cardiac muscle) and although the heart has a little striated muscle tissue, it, too works involuntarily. Therefore, you should be aware of the fact that it is the striated muscles which work for the movement of the skeleton and do the major job, and that it is this that we refer to when we say “muscle.”

A great number of bones have been created in order to support your body, and joints have been placed between those bones for them to take the proper shape according to every movement. However, none of those joints have the ability to move by itself. A door or a window, no matter how good it is, cannot be opened or closed without an outside force to pull or push it. In the same way, a joint needs a force to move it and that force is produced by your muscular system. There are around 340 muscles included in your muscular system. It has been estimated that all the muscles in your body perform 510 different functions! While some of those functions are bone movements in your joints, other muscles can perform movements without moving a bone at all. Muscles that are placed in your forehead, face, eye lids and abdomen are those kinds of muscles. They can help you look worried by wrinkling your forehead or grimacing when you are disgusted by something.

Keeping with tradition, the muscles that are included in my system have been named based on the function they perform. For example, the muscle which moves an organ part towards another part is called an abductor, while the muscle that straightens a joint is an extensor, and the muscle that bends a joint is a flexor; the muscle that raises a part of the skeleton is a levator, that which the muscle makes a part of an organ prone is a pronator, the muscle that rotates a part of an organ is a rotator and that which brings an organ into a supine position is called a supinator.

In order for you to make all the movements that your body needs, my muscle components have to be both very strong and flexible. The most important feature of my muscle components is that they can be trained and strengthened with a systematic workout. The main goal of all sportsmen who compete is to increase the strength and the endurance of their muscles. As a result of intense exercises with weight and speed, the number, the diameter and the length of my muscle fibers will increase. Thus, I can gain more power to be able to do more work and also gain the ability to contract faster.

However, in addition to all this training and exercise, genetic factors also play a role in my health. For this reason, not everybody who works out can become a good sportsman; but if the person has innate muscular and skeletal capacity, with good exercise this capacity can certainly be enhanced and developed. However, if a person does not have the proper muscular structure for a particular sport, it would be unfair to expect them to be a champion! Although my muscles always seem to be of the same type at first sight, I might show different behavior depending on the distribution of the special fibers inside them. Some of my fibers twitch fast and tire easily, some of them twitch slowly and tire later. Depending on the distribution of these different fibers, the movements and sport that every person can do differ from person to person. In this case, an athlete who can run only 100m and an athlete who can run 10,000m do not have the same development of muscles; they have different amounts and distributions of special muscle fibers.

The contraction of any of my muscles can occur in two different ways: If the pressure put on my muscle is stronger than the resistance of the tissue, the tension remains constant and the muscle shortens. This is called an isotonic contraction. If the pressure put on my muscle is equal to the resistance, the tension of my muscle increases and its length does not change. That is called an isometric contraction. The amount of force that occurs during the contraction of my muscle depends on its length and the amount of the stimulus.

In order to produce muscle contraction, an electrical signal is sent through a motor neuron to the synaptic gap, which is positioned between the muscle cell membrane and the nerve cell. As a result, a chemical reaction occurs, which, in a very short time, causes the actin and myosin proteins in the muscle fibril to slide past each other and thus shorten the fibril, contracting the muscular cells. During this reaction, the temperature also rises a little and the total heat generated by all the muscles determines your body temperature. For this reason, in cold weather, my muscles vibrate, increasing your body temperature and trying to maintain it. You may now understand why moving the parts of the body in cold weather helps people avoid from getting sick or freezing. As you can see, every act of my Creator is quite purposeful. He can create two or even more functions within one task: Through your muscles, He not only provides you with the ability to move freely, but heat is also produced and you are protected from getting cold.

When a muscle fiber contracts frequently as a result of successive electrical impulses from a nerve fiber, it becomes tired after a while and needs rest. In this case, other muscle fibers which have not contracted for a while will take over and continue the job. However, if the electrical impulses from the nerve come too frequently and my muscle fibers do not have an opportunity to rest, a condition of constant contraction, which is known as physiologic tetanus, occurs.

The tension receptors that are placed on my muscles help maintain the harmony and coordination of all your movements including walking and running, bouncing and sitting down. They do this by constantly signaling the nerve system and providing feedback about the condition of my muscles, and about the speed and the intensity of contraction. Thus, through these receptors which control and coordinate my muscle activities, the well-being of my system is ensured. It is this that prevents you from wobbling when you walk, or helps you to take a spoonful of soup to your mouth without spilling it.

Like any other tissue or system, I, too, have some special disorders. The most common disorders are: weakness, malformation, muscles that develop and move involuntarily and habitually, especially in your face (tic), infected muscles (myosite), muscle dystrophy, muscle rigidity (the Stiffman Syndrome), benign or malignant muscle tumors (leiomyom, rhabdomyoma, or Rhabdomyosarcoma). These disorders differ in their degree of severity and risk.

Dear Peter! You have now seen that each muscle helps your organs to move, holding your bones and giving shape and function to your body, making you a beautiful model and an inspiration for sculptors. You may have understood that this is a work of knowledge and might; there is no way that the myofibril in my one cell could form by itself as a result of a coincidence.

Irfan Yilmaz is a professor of biology at Dokuz Eylul University, Izmir, Turkey.