10 Best Foods to Cleanse Liver and Gallbladder of Stones

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18 Things You Should Know About Genetics

This is an animated film that presents fundamental background information about genetics, as well as offering some quirky but interesting facts about DNA, genes and genetics. It was created to be an upbeat, fun educational short film to initiate and draw interest to this sometimes daunting and seemingly complex subject matter.

The Origin of Genes

Disorders resulting from mutation in Mitochondrial DNA (mtDNA)



mtDNA Mutation


Cancer:

        Mitochondrial DNA is prone to somatic mutations, which are a type of non-inherited mutation. Somatic mutations occur in the DNA of certain cells during a person's lifetime and typically are not passed to future generations. There is limited evidence linking somatic mutations in mtDNA with certain cancer types, including breast, colon, stomach, liver and kidney tumors. These mutations might also be associated with cancer of blood-forming tissue (leukemia) and cancer of immune system cells (lymphoma).

       It is possible that somatic mutations in mtDNA increase the production of potentially harmful molecules called reactive oxygen species. MtDNA is particularly vulnerable to the effect of these molecules and has a limited ability to repair itself. As a result, reactive oxygen species easily damages mtDNA, causing a buildup of additional somatic mutations. Researchers are investigating how these mutations could be related to uncontrolled cell division and growth of cancerous tumours.

Cyclic Vomiting Syndrome:

Cyclic vomiting syndrome may be related to genetic changes in mitochondrial DNA. Some of these changes alter single DNA building blocks (nucleotides), whereas others rearrange larger segments of mitochondrial DNA. These changes likely impair the ability of mitochondria to produce energy. Defects in energy production may lead to symptoms during periods when the body requires more energy, such as when the immune system is fighting an infection. However, it remains unclear how changes in mitochondrial function are related to recurrent episodes of nausea and vomiting

Kearns-Sayre syndrome:
Most people with Kearns-Sayre syndrome have a single, large deletion of mitochondrial DNA. The deletions range from 1,000 to 10,000 nucleotides, and the most common deletion is 4,997 nucleotides. Kearns-Sayre syndrome primarily affects the eyes, causing weakness of the eye muscles (ophthalmoplegia) and breakdown of the light-sensing tissue at the back of the eye (retinopathy). The mitochondrial DNA deletions result in the loss of genes that produce proteins required for oxidative phosphorylation, causing a decrease in cellular energy production. Researchers have not determined how these deletions lead to the specific signs and symptoms of Kearns-Sayre syndrome, although the features of the condition are probably related to a lack of cellular energy. It has been suggested that eyes are commonly affected by mitochondrial defects because they are especially dependent on mitochondria for energy.

Leigh syndrome Mutations in one of several different mitochondrial genes can cause Leigh syndrome, which is a progressive brain disorder that usually appears in infancy or early childhood. Affected children may experience delayed development, muscle weakness, problems with movement, or difficulty breathing.
Some of the genes associated with Leigh syndrome provide instructions for making proteins that are part of the large enzyme complexes necessary for oxidative phosphorylation. For example, the most commonly mutated mitochondrial gene in Leigh syndrome, MT-ATP6, provides instructions for a protein that makes up one part of complex V, an important enzyme in oxidative phosphorylation that generates the majority of the cell's energy (ATP) in the mitochondria. The other genes provide instructions for making transfer RNA molecules, which are essential for protein production within mitochondria. Many of these proteins play an important role in oxidative phosphorylation. The mitochondrial gene mutations that cause Leigh syndrome impair oxidative phosphorylation. Although the mechanism is unclear, it is thought that impaired oxidative phosphorylation can lead to cell death in sensitive tissues, which may cause the signs and symptoms of Leigh syndrome.

More on mtDNA Mutation Disorders: http://ghr.nlm.nih.gov/chromosome/MT

Vamsi Mootha - Bio-Data Cruncher

While surfing the internet not long ago, a Harvard biologist stumbled upon a pile of research data including unpublished leftovers from an unresolved genetic study. It wasn't unusual: Data like that can be found all over the web.

33 Year-old Indian-American professor Vamsi Mootha using a unique computational method, mined the data and indentified a gene underlying a rare but fatal pediatric disorder called "Leigh Syndrome, French-Canadian" variant or LSFC. Astonishingly, he did it in a single weekend.

For the diabetes study, Mootha applied computational approaches similar to those used on the pediatric study to both found reaserch and data his team generated independently. As a result, he located a set of three genes that revs up the energy-producing ability of muscle cells and might lessen diabetes' harmful effects. Again, the finding was notable not only because of its potential consequence, but also because Mootha has found a way to sort the hay in the genetic haystack to discover the proverbial needle.

Each human cell contains all of the body's approximately 23,000 genes. But not every gene in every cell is active; some are silent. It's the repertoire of active genes that makes a muscle cell different than a liver cell or skin cell. In a diseased cell, the program is altered. The correct genes are activated too much or not enough.

A relatively new technology, called microarrays, enables interrogation of every gene to determine how active it is. Rather than just look at a slice of diseased cell tissue under a microscope, scientists can see how many of the 23,000 genes are switched on or off and to what degree. Multiply all that data by all the patients in research studies such as Mootha encountered, and the result is an intimidating mass of numbers to crunch and assess.

"Vamsi got a hold of the data from the internet, but he said you can't compare gene by gene. You'd be doing so many comparisons, you aren't going to find anything statistically significant," said Alan Attie, a University of Wisconsin biochemistry professor.

"Vamsi re-curated the list of genes, making about 120 categories by functional group," such as genes that make fat or carbohydrates, or control respiration, etc., Attie said. "It turned out that the mitochondrial respiration group showed a big difference. But looking at the individual gene level, there would have been only modest differences."

Mootha and collaborators had found that the master regulator of gene expression for genes in the mitochondria were different between diabetics and non-diabetics. Though Mootha, whose undergraduate degree is in mathematics, calls his approach "relatively simple computation," National Institutes of Health research physiologist Robert Balaban disagrees.

"Vamsi is not attempting to reduce the problem to its simplest elements, but to accept the complexity of biology and develop the tools we will use over the next several decades to unravel the interactions that naturally occur," he said.

One of those tools is a software program that a graduate student is developing, based on Mootha's algorithms, which other scientific researchers can use to profile diseases.

Mootha's diabetes discovery was significant for both the disease and other researchers trying to mine masses of data, but his passion is investigating mitochondrial mutations linked to rarer diseases such as LSFC (.pdf).

That's how he envisions employing his windfall. "$500,000 is really not enough money to fund a large, modern genomics lab, but it might be enough to jump-start a research program focused on developing therapies for rare mitochondrial disorders," Mootha said.

"Big pharma will not develop drugs to combat these disorders anytime soon since the market is so small, so the onus is on private institutions and academic labs to develop new therapeutics."

Source: http://www.wired.com/medtech/health/news/2004/10/65474

Harvard Medical School, Broad Institute team works to better understand Mitochondria

Why do nearly 1 million people taking cholesterol-lowering statins often experience muscle cramps? Why is it that in the rare case when a diabetic takes medication for intestinal worms, his glucose levels improve? Is there any scientific basis for the purported health effects of green tea?

A new chemical tool kit provides the first clinical explanation for these and other physiological mysteries. The answers, it turns out, all boil down to mitochondria, those tiny organelles floating around in cellular cytoplasm, often described as the cell’s battery packs.

A research team led by Harvard Medical School (HMS) assistant professor and Broad Institute associate member Vamsi Mootha has developed a tool kit that isolates five primary aspects of mitochondrial function and analyzes how individual drugs affect each of these areas. These results were published online Feb. 24 in Nature Biotechnology.

Over the past few decades, mitochondria have increasingly been understood as a key determinant of cellular health. On the other hand, mitochondrial dysfunction can lead to many neurodegenerative conditions as well as metabolic diseases such as diabetes. Because mitochondria are responsible for turning the food we eat into the energy that drives our bodies, these and other connections are logical. Nevertheless, there has not yet been a systematic method for thoroughly interrogating all facets of mitochondrial activity.

“Historically, most studies on mitochondria were done by isolating them from their normal environment,” says Mootha, who is also a member of the Center for Human Genetic Research at Massachusetts General Hospital. “We wanted to analyze mitochondria in the context of intact cells, which would then give us a picture of how mitochondria relate to their natural surroundings. To do this we created a screening compendium that could then be mined with computation.”

In order to thoroughly analyze these organelles, Mootha and his team zeroed in on five basic features of mitochondria activity, looking at how a library of 2,500 chemical compounds affected mitochondrial toxic byproducts (like all “chemical factories” mitochondria produce their own toxic waste), energy levels, speed with which substances pass through these organelles, membrane voltage, and expression of key mitochondrial and nuclear genes. (Mitochondria contain their own genome, consisting of approximately 37 genes in humans.)

“It’s just like taking your car in for an engine diagnostic,” explains Mootha. “The mechanic will probe the battery, the exhaust system, the fan belt, etc., and as a result will then produce a read-out for the entire system. That’s analogous to what we’ve done.”

As a result of these investigations, Mootha and his group produced three major findings.

First, the team discovered a pathway by which the mitochondria and the cell’s nuclear genome communicate with each other. They found this by discovering that certain drugs actually break communication between these two genomes. By reverse engineering the drugs’ toxic effects, they may be able to reconstruct normal function.

Second, the team looked at a class of the cholesterol-lowering drugs called statins. Roughly 100 million Americans take statins, and among that group, about 1 million experience muscle cramping and aches. Previous studies suggested that mitochondria were involved, but clinical evidence remained conflicting. Mootha and his colleagues found that three out of the six statins (Fluvastatin, Lovastatin, and Simvastatin) interfered with mitochondria energy levels, as did the blood-pressure drug Propranolol. When combined, the effect was worse.

“It’s likely that a fair number of patients with heart disease are on one of these three statins as well as Propranolol,” says Mootha, “Our cellular studies predict that these patients might be at a higher risk for developing the muscle cramps. Obviously, this is only a hypothesis, but now this is easily testable.”

The third and arguably most clinically relevant finding builds on a paper Mootha co-authored in 2003, a paper that demonstrated how type 2 diabetes was linked to a decrease in the expression of mitochondrial genes. A subsequent and unrelated paper showed a relationship between type 2 diabetes and an increase in mitochondrial toxic byproducts. Mootha’s group decided to query their tool kit to see if there were any drugs that affected both of these functions, drugs that could boost gene expression while reducing mitochondrial waste.

Indeed, they found six compounds that did just that, five of which were known to perturb the cell’s cytoskeleton, that is, the scaffolding that gives a cell its structure.

“Our data shows that when we disrupt the cytoskeleton of the cell, that sends a message to boost the mitochondria, turning on gene expression and dropping the toxic byproducts,” says Mootha. “The connection between the cytoskeleton and mitochondrial gene expression has never been shown before and could be very important to basic cell biology.”

Of the five drugs that did this, one, called Deoxysappanone, is found in green tea and is known to have anti-diabetic effects. Another, called Mebendazole, is used for treating intestinal worm infections. This connection gives a rationale to case reports in which diabetics treated with Mebendazole have described improvements in their glucose levels while on the drug.

The researchers intend to further investigate some of the basic biological questions that this study has raised, foremost being the relationship between the cytoskeleton and mitochondria. They also plan on using this tool kit to develop strategies for restoring normal mitochondrial function in certain metabolic and neurodegenerative conditions where it has broken down.

This research was funded by grants from the American Diabetes Association and the Richard and Susan Smith Family Foundation.

Source: http://news.harvard.edu/gazette/story/2008/02/hms-broad-institute-team-works-to-better-understand-mitochondria/

Mitochondrial DNA (mtDNA)

Human Mitochondrial DNA:

What is mtDNA all about?

Mitochondiral DNA (mtDNA) is located in cell organelles called Mitochondira, structures within Eukaryotic cells that convert the chemical energy from food into a form that cells can use, ATP. Most other DNA present in Eukaryotic organisms is found in the cell nucleus. mtDNA can be regarded as the smallest chromosome, and was the first significant part of Human Genome to be sequenced. In most species, including humans, mtDNA is inherited solely from the mother. The DNA sequence of mtDNA has been determined from a large number of organisms and individual (including some organisms that are extinct), and the comparison of those DNA Sequences represents a mainstay in Phylogenetics, in that it allows biologist to elucidate the evolutionary relationships among species. It also permits an examination of the relatedness of populations, and so has become important in Anthropology and Field Biology.

Mitochondrial Inheritance
In most multicellular organisms, mtDNA is inherited from mother (maternally inherited). Mechanisms for this includes simple dilution (an egg contains 100,000 to 1,000,000 mtDNA molecules, whereas a sperm contains only 100 to 1000), degradation of sperm mtDNA in the fertilized egg, and, at least in a few organisms, failure of sperm mtDNA to enter the egg. Whatever the mechanism, this single parent (uniparental) pattern of mtDNA inheritance is found in most animals, most plants and in fungi as well.

Female Inheritance
 In sexual reproduction, mitochondria are normally inherited exclusively from the mother. The mitochondria in mammalian sperm are usually destroyed by the egg cell after fertilization. Also, the most mitochondria are present at the base of the sperm's tail, which is used for propelling the sperm cells. Sometomes the tail is lost during fertilization.

In 1999 it was reported that parental sperm mitochondria (containing mtDNA) are marked with ubiquitin to select them for later destruction inside the embryo. Ubiquitin is a small regulatory protein that has been found in almost all tissues of eukaryotic organisms. Among other functions, it directs protein recycling. Ubiquitin can be attached to protein and label them for destruction. The ubiquitin tag directs protein to proteasome, which is a large protein complex in the cell that degrades and recycles unneeded proteins. This discovery won the Nobel Prize for Chemistry in 2004. Ubiquitin Tags can also direct proteins to other locations in the cell, where they control other protein and cell mechanisms. Ubiquitin is encoded in mammals by 4 different genes. UBA52 and RPS27A genes code for a single copy of ubiquitin fused to the ribosomal proteins L40 and S27a, respectively. The UBB and UBC genes code for polyubiquitin precursor proteins.

Peter Sutovsky Et. el [1], published a Nature Journal "Development: Ubiquitin Tag for Sperm Mitochondria" (25 November 1999). Like other mammals, humans inherit mitochondria from mother only, even though the sperm contributes nearly one hundred mitochondria to the fertilized egg. In support of the idea that this strictly maternal inheritance of mtDNA arises from selective destruction of sperm mtDNA. The journal shows the sperm mtDNA inside fertilized Cow and Monkey eggs are tagged by the recycling marker protein ubiquitin. This imprint is a death sentence that is written during spermatogenesis and executed after the sperm mitochondria encounter the egg's cytoplasmic destruction machinery.

The fact that mtDNA is maternally inherited enables researchers to trace maternal lineage far back in time (Y-Chromosome DNA, paternally inherited, is used in an analogous way to trace the Antage Lineage). This is accomplished in humans by sequencing one or more of the Hypervariable Control Regions (HVR1 or HVR2) of the mtDNA, as with a genealogical DNA Test. HVR1 consists of about 440 base pairs. These 440 base pairs are then compared to the control regions of the other individual to determine maternal lineage.
Because mtDNA is not highly conserved and has a rapid mutation rate, it is useful for studying the evolutionary relationships - phylogeny - of organisms. Biologists can determine and then compare mtDNA sequences among different species and use the comparisons to build an evolutionary tree for the species examined. Since mtDNA is transmitted from mother to child (both male and female), it can be useful tool in geneological research into a person's maternal line.



References:
[1] Peter Sutovsky, Ricardo D. Moreno, João Ramalho-Santos, Tanja Dominko, Calvin Simerly & Gerald Schatten. "Development: Ubiquitin Tag for Sperm Mitochondria". Link: http://www.nature.com/nature/journal/v402/n6760/full/402371a0.html

Significance of Mitochondria

Mitochondria are rod-shaped organelles that can be considered the power generators of the cell, converting oxygen and nutrients into adenosine triphosphate (ATP). ATP is the chemical energy "currency" of the cell that powers the cell's metabolic activities. This process is called aerobic respiration and is the reason animals breathe oxygen. Without mitochondria (singular, mitochondrion), higher animals would likely not exist because their cells would only be able to obtain energy from anaerobic respiration (in the absence of oxygen), a process much less efficient than aerobic respiration. In fact, mitochondria enable cells to produce 15 times more ATP than they could otherwise, and complex animals, like humans, need large amounts of energy in order to survive.

Mitochondria, often referred to as the powerhouse of the cell. These organelles are found in virtually all of our body’s cells and are responsible for generating the bulk of cellular ATP.  In addition, the organelle plays a central role in apoptosis, ion homeostasis, intermediary metabolism, and biosynthesis.  Studies during the past 25 years have demonstrated a clear role of the mitochondrion in rare, inborn errors of metabolism.  More recent studies have implicated mitochondrial dysfunction in a variety of common human diseases, such as diabetes, neurodegeneration, and the aging process itself.

Dr. Vamsi Mootha in Mootha Labs

Contrary to popular belief, the mitochondrion is incredibly dynamic.  Its protein composition and functional properties vary across cell types, remodel during development, and respond to external stimuli.  Mitochondria contain their own genome (referred to as mtDNA) which encode a mere 13 proteins.  All the other estimated 1000+ proteins are encoded in the nuclear genome and imported into this cellular compartment.

Mootha's Laboratory uses new tools of genomics in combination with biochemical physiology to systematically explore mitochondrial function in health and in disease.  They focus on rare, monogenic syndromes as well as common diseases.  The long-term goal of the lab is to develop predictive models of mitochondrial physiology that can aid in the diagnosis and treatment of a broad range of human diseases. Hats off to Dr. Vamsi Mootha.

Read more about Mitochondria in "Molecular Expressions - Cell Biology and Mircoscopy Structure and Function of Cells and Viruses"
Follow the link: http://micro.magnet.fsu.edu/cells/mitochondria/mitochondria.html

Probing Mitochondrial Physiology - Forefront of a new Science

Vamsi Mootha is an associate member of the Broad Institute. He is developing experimental and computational strategies to integrate genomic, proteomic, and physiological data to accelerate human disease gene discovery. He has applied these strategies to the successful identification of genes underlying rare, inherited metabolic syndromes, and more recently, has been extending these efforts to more common diseases, such as type 2 diabetes. He utilizes a multidisciplinary approach that includes mathematics, computer science, biochemistry, and genetics.

Vamsi's research program is primarily focused on the mitochondrion, the "powerhouse of the cell," and its role in human diseases. Work previously published by Vamsi and colleagues at the Broad demonstrated that mitochondria are less active in the muscles of diabetics and those at risk for developing diabetes. Recently, Vamsi and colleagues identified three genes that form a regulatory circuit in controlling the activity of mitochondria in a given cell. This gene circuit is a promising drug target for type 2 diabetes.

A 2004 recipient of the Macarthur genius award, Vamsi is associate professor of systems biology at Harvard Medical School and associate professor of medicine in the Center for Human Genetics at Massachusetts General Hospital.

Vamsi received his undergraduate degrees in mathematical and computational science at Stanford University, where he graduated Phi Beta Kappa with highest honors. He received his M.D. in 1998 at Harvard Medical School in the Harvard-MIT Division of Health Sciences and Technology, where his thesis work was focused on mitochondrial physiology. He subsequently completed his internship and residency in internal medicine at Brigham and Women's Hospital in 2001, after which he completed postdoctoral fellowship training at the Whitehead Institute/MIT Center for Genome Research.

ABCC9 Gene - Sleep Control

Scientists have identified the gene responsible for controlling the length of time for which an individual sleeps and why some have their own internal alarm clock.

Karla Allebrandt and her team from the Ludwig Maximilians University of Munich identified a gene called ABCC9 that can reduce the length of time we sleep.

The discovery is expected to explain why light sleepers, such as Margaret Thatcher, are able to get by on just four hours shut-eye a night.

The Europe-wide study of 4,000 people from seven different EU countries saw the volunteers fill out a questionnaire assessing their sleep habits. The researchers then analysed their answers, as well as participants’ genes. They discovered that people who had two copies of one common variant of ABCC9 slept for “significantly shorter” periods than people with two copies of another version.

Having already established that the ABCC9 gene was also present in fruitflies, the team were able to modify it in the animal and shorten the length of time for which it slept.

“Apparently the relationships of sleep duration with other conditions such as heart disease and diabetes can be in part explained by an underlying common molecular mechanism,” the Daily Mail quoted Allebrandt as saying.

“The ABCC9 gene is evolutionarily ancient, as a similar gene is present in fruitflies. Fruitflies also exhibit sleep-like behaviour.

“When we blocked the function of the ABCC9 homolog in the fly nervous system, the duration of nocturnal sleep was shortened,” she added.

How pathogens are killed - Nobel Prize winners in Physiology or Medicine 2011

From left to right: Bruce A. Beutler, Jules A. Hoffmann and Ralph M. Steinman

Inside our body can be found the bloodiest of battlefields, where millions of organisms are massacred daily, without cease. It is a battle waged by our body’s immune system against a wide variety of pathogenic bacteria, virus, fungi and parasites. What makes the defence mechanism powerful is the two-level protection conferred by the immune system. The innate immune system that serves as the first line of defence is not antigen-specific; it readily targets all pathogenic organisms the moment they enter the body. The antigen-specific adaptive immune mechanism acts as the second line of protection to keep us healthy. This year’s Nobel prize in Physiology or Medicine has been awarded to Bruce A. Beutler, Jules A. Hoffmann, and Ralph M. Steinman for revolutionising our understanding of the immune system by discovering the key principles that activate the defence mechanism. Beutler and Hoffmann will share half the prize money for discovering receptor proteins that recognize micro-organisms and activates the innate immunity. In 1996, Hoffmann found that the Toll gene was responsible for sensing pathogenic micro-organisms and that its activation was required for mounting innate immune response. Two-years later, Beutler discovered that components of micro-organisms bind to Toll-like receptors located in many cells. The binding activates the innate immunity, which results in inflammation and destruction of the pathogens.


The other half of the prize money was awarded to Steinmann for discovering, way back in 1970s, that dendritic cells were responsible for adaptive immunity. As they are antigen-specific, dendritic cells take time to react to an invading organism on first exposure; but immunological memory allows them to react more rapidly to the same antigen on subsequent exposures. This is the attribute researchers exploit while designing preventive vaccines.


Adaptive immunity holds great medical promise. The immune system can be directed to attack the tumour. Blocking the excessive production of cytokines when diseases show up can ameliorate autoimmunity. Even preserving autoimmune diseases may become possible when certain cells of the immune system are successfully silenced. Steinmann will go down history as not just a highly worthy Nobel Prize winner. He was (as a Rockefeller University statement explains) “diagnosed with pancreatic cancer four years ago... his life was extended using dendritic-cell based immunotherapy of his own design,” and he died three days before his Nobel was announced. 

Interesting Link: http://www.dendriticcellresearch.com/denvax (Institute of Cellular Therapy)

Nobel Prize winner list @ http://society.ezinemark.com/2011-nobel-prize-winners-in-pictures-737146e00cb.html

Crabs - Protiens and Minerals

Crab Nutrition :
Rich in Protein
Crabs protein content of less than about 22 gr/100 gr. Amino acid content is also complete. Amino acids are the highest amount per 100 gram is 3474 mg of glutamate, aspartate 2464 mg, 1946 mg of arginine, lysine and leucine 1939 mg 1768 mg.
Rich in omega-3 fatty acids
As with the results of other marine animal, crabs is also rich in omega-3 fatty acid that is equal to 407 mg / 100 gr.
High levels of vitamin B12
Crabs also contain high vitamin B12 which is about 10.4 mcg/100mg. The content is already able to meet the daily requirement of vitamin B12 by 174%. In addition, crabs also contains niacin and riboflavin in sufficient quantities good for health.
Rich in minerals zinc, copper and selenium
For seafood, crabs is also rich in mineral content. The highest mineral content to 100 g crabs is selenium 48 mcg (68% daily requirement), copper 0.7 mg  (37% daily requirement) and zinc 5.5mg (36% daily requirement)
Crab Nutrition Benefits :
* a high content of protein-forming function as enzymes, organ and muscle cell formation, forming hormone, repair damaged cells, regulating metabolism, and forming the immune system.
* The content of vitamin B12 is good for energy and growth, improve the metabolism of amino acids and fatty acids, red bloodcell production, and to improve the health of nerves and skin.
* omega-3 fatty acids in crabs functioning lower bad cholesterol in the blood there by preventing cardiovascular disease (heart), boost immunity, enhance nervous system function and eye health, and improve the intelligence of the brain when administered early.
* Mineral selenium act as antioxidants to prevent cell damage from free radicals cause cancer and heart disease. Selenium is believed to play a role in preventing cancer and chromosomedamage, as well as increase body resistance to viral infection sand bacteria and prevent inflammation.
* Mineral copper serves as a component of redox enzymes, the formation of red blood Selda, muscles, nerves, bones and brain,and prevent bone disease and nerve.
* Mineral zinc functions to the fundamental building blocks the body’s enzymes, red blood cells, the immune system, prevent prostate enlargement, prevent hair loss.
* Shellfish is very suitable for a high protein diet because it contains saturated fat which is very low at 0.2 grams / 100gram.

Healthy Tips Crab Consumption :
* We recommend that you do not process the crabs with fried
* Though containing a variety of healthful nutrients, crabs also contain a moderately high cholesterol 76 mg / 100gr. Consumption of cholesterol per day the recommended maximum of about 300mg. Medium-sized crabs dish every day was enough to get all the benefits.
* Crab contain purine base that can raise levels of uric acid in the blood. People with gout disease or gout better avoid or severely limit the consumption of crabs.
* For soft shell crabs / soft-shelled, skin does not need to be set aside, also of high nutritional value, especially the content of chitosan and carotenoids are usually widely available in the shell.

Oily Fish for Better Health

What types of oily fish are there?

There are many types of oily fish to choose from. You might find some, like kippers, quite strong tasting if you aren’t used to them, there are plenty of others to try!

• Anchovy (நெத்திலி மீன் )
• Carp (கெண்டை மீன்)
• Eel (விலாங்கு மீன்)
• Herring (Bloater)
• Hilsa
• Jack (also known as Scad, Horse mackerel and Trevally)
• Mackerel
• Orange roughy
• Pilchards
• Salmon
• Sardines (சூடை மீன்கள்)
• Sprats
• Swordfish
• Trout
• Tuna (fresh)
• Whitebait

Why should I eat oily fish?

As fish contains essential vitamins such as niacin, and minerals such as selenium and iodine, it makes a great addition to your meal. Oily fish in particular is said to be rich in omega 3 and vitamins A and D. White fish does contain some omega 3 fatty acids, but at much lower levels than oily fish. Oily fishes are power house of Omega-3 Fatty Acids which can lift your mood. Most fish are rich in Vitamin B12 and Vitamin B6, which are responsible for the Serotonin production. To get the best out of your fish, experts recommend opting for steamed, baked or grilled fish rather than fried; fried food often contains a much higher fat content, especially if they are cooked in butter. 

Healthy fat:
Oily fish such as sardines, herring and mackerel are very rich sources of certain polyunsaturated fats known as omega-6 and omega-3 essential fatty acids. These fatty acids cannot be manufactured by the body and have to be obtained from food. We have only recently become more aware of how important these types of fats are and what a positive effect they have on our health. There are small amounts of these fats in white fish, but oily fish have significantly higher levels. 100g of cod (white fish), mackerel, sardines and fresh tuna contain 0.3g, 3.3g, 1.7g and 1.6g of omega-3 fatty acids respectively.


Benefits of Omega-3:
Researchers have now discovered and identified the many benefits of omega-3 essential fatty acids and we have listed them below:

• They reduce the levels of "bad" LDL cholesterol in the blood.
• They can alleviate inflammatory diseases such as arthritis and help to reduce the amount of medication taken for them.
• They lower blood pressure.
• They prevent the blood from forming clots, which therefore reduces the risk of heart attack and stroke.
• Omega-3 protects against heart and circulatory problems.
• It is good for the healthy development of the brain and eyes.
• It reduces the risk of thrombosis.
• It is good for sufferers of gout.
• Omega-3 clears cholesterol from the arteries, widening the artery walls and increasing elasticity.
• Omega-3 increases the levels of "good" HDL cholesterol in the blood, which protects the heart.
• People who regularly consume oily fish are less likely to suffer dementia or Alzheimer's.
• Oily fish consumption reduces the risk of depression and helps people who are depressed to overcome it.
• Omega-3 is good for the development of a healthy baby, although pregnant women should limit themselves to no more than two portions of oily fish a week.

What else do Oily fish contains?

Oily fish are also rich in many vitamins and minerals that are vital for the correct functioning of the body.

Fat-soluble vitamins are plentiful in oily fish, due to the fact that they are absorbed by the fats contained within the fish. The fat-soluble vitamins are A, D, E and K and all are found in significant amounts in oily fish.

Vitamin D can be manufactured by the body when exposed to sunlight every day, but in the UK, you are not necessarily guaranteed sunshine every week let alone every day and therefore it may be necessary to acquire vitamin D from foods.

Oily fish is also a very good source of important minerals such as iodine, selenium, calcium, zinc, phosphorous and magnesium.

Calcium is obtained when the bones of small fish are eaten such as in sardines, whitebait or anchovies and iodine is important for the thyroid to work properly. A deficiency in iodine will cause the thyroid gland in the neck to swell and it will leave you feeling extremely tired and lethargic. It can often cause people to put on weight and make it very difficult for them to subsequently lose it.

How much is too much?

As mentioned above, we should be including one portion of oily fish in our diet, but there are maximum levels recommended for health reasons and concerns about numbers of fish; after all, we want to protect the environment for generations to come.

For those who still wish to have an intake of omega 3 fatty acids can choose to take supplements with a combination of omega 3 6 9 or just the single omega 3. These supplements can be found in most good health stores.

Omega-3 Supplements: Cod-Liver Oil Tabs

Reference:

Food Standards Agency. (2010). Fish and shellfish. http://www.eatwell.gov.uk/healthydiet/nutritionessentials/fishandshellfish/


HelpwithCooking.com
http://www.helpwithcooking.com/fish-guide/oily-fish.html

Foods that can make you Happy - Yahoo! Lifestyle

We all go through periods of feeling anxious, irritable or depressed. However, there are many things you can do to help boost your mood. The foods you eat can directly influence the way you feel, so check out these top five foods to beat the blues.

Vitamins B12

If you’re feeling anxious, stressed or depressed, a dose of B vitamins could help to lift your mood. B vitamins are important for normal brain function and producing mood-boosting serotonin, with vitamins B12 and B6 being particularly beneficial for regulating your mood.

To up your intake of B vitamins, try snacking on Marmite on wholegrain toast. As Marmite is fortified with vitamin B12, this is a particularly good choice of food for vegans and vegetarians who may struggle to get their recommended intake.

Oily fish

Omega-3 fatty acids found in oily fish are well known for being good for the heart. However, they are equally beneficial for our brain health and mood. A study by researchers from the University of Pittsburgh School of Medicine found that participants who had lower levels of omega-3 fatty acids in their blood were more likely to be moderately depressed and have a negative outlook.

Furthermore, a study has found surprisingly low rates of seasonal affective disorder in Icelanders, where the diet is high in omega-3 rich fish. To follow in their footsteps and help ward off the blues, try eating two portions of oily fish a week, or up to four for men.

Chocolate

Many people find themselves reaching for chocolate to ease a bad mood, and this could in fact be no bad thing. Research has shown that chocolate contains many chemicals which can help beat the blues, including relaxing magnesium, calming anandamide and pleasure-inducing phenylethylamine.

To up the mood-boosting benefits further, try snacking on chocolate-dipped strawberries for a healthy treat. Strawberries are not only a good source of vitamin C, which helps in the production of endorphins, but they are high in mood-enhancing flavonoids too.

Bananas

Bananas are high in natural sugars, making them a great remedy for low energy levels which can leave you feeling down. On top of this they are packed with mood-lifting nutrients to help put a smile on your face.

Bananas are a great source of tryptophan, an essential amino acid which boosts serotonin levels, helping to regulate your mood. Furthermore, they are rich in magnesium, which can help you to relax and vitamin B6, which can help to relieve depression.

Nuts

Walnuts are the perfect good-mood food, offering the combined mood-boosting properties of omega-3 fatty acids, vitamin B6 and tryptophan. The nuts are also a good source of folate (vitamin B9); the deficiency of which has been linked to depression.

As well as snacking on walnuts, another good nut to add into your diet is the Brazil. Brazil nuts are an extremely rich source of the mineral selenium, with research suggesting that just one Brazil nut a day can provide you with your recommended daily intake. As low levels of selenium can lead to depression, irritability and anxiety, snacking on Brazils could be the perfect healthy way to boost your mood.

Drinking water in Empty Stomach

It is popular in Japan today to drink water immediately after waking up every morning. Furthermore, scientific tests have proven its value. We publish below a description of use of water for our readers. For old and serious diseases as well as modern illnesses the water treatment had been found successful by a Japanese medical society as a 100% cure for the following diseases:
Headache, body ache, heart system, arthritis, fast heart beat, epilepsy, excess fatness, bronchitis asthma, TB, meningitis, kidney and urine diseases, vomiting, gastritis, diarrhea, piles, diabetes, constipation, all eye diseases, womb, cancer and menstrual disorders, ear nose and throat diseases.
METHOD OF TREATMENT
1. As you wake up in the morning before brushing teeth, drink 4 x 160ml glasses of water
2. Brush and clean the mouth but do not eat or drink anything for 45 minute
3.. After 45 minutes you may eat and drink as normal.
4. After 15 minutes of breakfast, lunch and dinner do not eat or drink anything for 2 hours
5. Those who are old or sick and are unable to drink 4 glasses of water at the beginning may commence by taking little water and gradually increase it to 4 glasses per day.
6. The above method of treatment will cure diseases of the sick and others can enjoy a healthy life.
The following list gives the number of days of treatment required to cure/control/reduce main diseases:
1. High Blood Pressure (30 days)
2. Gastric (10 days)
3. Diabetes (30 days)
4. Constipation (10 days)
5. Cancer (180 days)
6. TB (90 days)
7. Arthritis patients should follow the above treatment only for 3 days in the 1st week, and from 2nd week onwards – daily..
This treatment method has no side effects, however at the commencement of treatment you may have to urinate a few times.
It is better if we continue this and make this procedure as a routine work in our life. Drink Water and Stay healthy and Active.
This makes sense .. The Chinese and Japanese drink hot tea with their meals ..not cold water. Maybe it is time we adopt their drinking habit while eating!!! Nothing to lose, everything to gain...
For those who like to drink cold water, this article is applicable to you.
It is nice to have a cup of cold drink after a meal. However, the cold water will solidify the oily stuff that you have just consumed. It will slow down the digestion.
Once this 'sludge' reacts with the acid, it will break down and be absorbed by the intestine faster than the solid food. It will line the intestine.
Very soon, this will turn into fats and lead to cancer. It is best to drink hot soup or warm water after a meal.
A serious note about heart attacks:
· Women should know that not every heart attack symptom is going to be the left arm hurting,
· Be aware of intense pain in the jaw line.
· You may never have the first chest pain during the course of a heart attack.
· Nausea and intense sweating are also common symptoms.
· 60% of people who have a heart attack while they are asleep do not wake up.
· Pain in the jaw can wake you from a sound sleep. Let's be careful and be aware. The more we know, the better chance we could survive...
A cardiologist says if everyone who gets this mail sends it to everyone they know, you can be sure that we'll save at least one life.

Please be a true friend and send this article to all your friends you care about.

-----DRINK SPRING WATER, PROTECT UR LIFE-----

Eat, Drink, and Be Healthy: The Harvard Medical School Guide to Healthy Eating - Book Review

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There is an interesting dilemma for those who would influence nutrition. In many places in the world, there are governmental agencies concerned with food security, food safety, agriculture, health, and trade that may, from time to time, implement policies that are at least intended to reduce the risk of chronic diseases. Most often, when the goals of agriculture and human health clash, it is the will of the agriculture sector that prevails (remember the European Union's ``butter mountain'' and ``wine lake''?). In the United States, perhaps more than anywhere else, this has left an opening for self-help nutrition books. In a land where individuality and self-reliance are valued above many other virtues and where disease is sometimes seen to be a mark of personal failure, gaining access to the best data on health-related food consumption may be central to maintaining control over one's health. The quality of such books varies enormously, from the bizarre to the mundane. The feature they share is the promise of better health and control over one's destiny. Only occasionally do bona fide researchers step into the maelstrom. Enter Walter Willett of Harvard University and Eat, Drink, and Be Healthy.

Willett's book is based on evidence derived almost exclusively from large cohort studies of diet and disease. He has been the architect of several such studies and is a major contributor to what we know about methods of collecting and analyzing data; he formerly served the Journal well in this capacity. His position in this regard is preeminent but not unchallenged. He encapsulates his position on the evidence in a new ``Healthy Eating Pyramid,'' a gauntlet thrown at the feet of the U.S. Department of Agriculture (USDA). He notes that the USDA Food Guide Pyramid, like Rudyard Kipling's elephant's child, got pulled into shape by competing interests, few of which cared about human health. He goes on, ``You deserve more accurate, less biased, and more helpful information than that found in the USDA Pyramid.'' Thus, the book brings us the promise of science in the service of nutrition, and as with any good scientific claims, Willett makes sure we know, up front, that all findings are provisional and all recommendations subject to change.

The central chapters of the book are derived from and explicate the layers of the new pyramid. Central to Willett's recommendations is the control of body weight, in which exercise, rather than caloric restriction, has the primary role. However, there is also helpful and practical advice on defensive eating strategies; for example, Willett states, ``Recognize that we are victims of our culture, one that glorifies excess.''

Indeed, much of what is presented in the book is sensible and practical and demystified. For example, the data and associated recommendations on fluid intake include the following: we should drink water; tap water is OK; soft drinks are full of empty calories; and fruit juice contains more beneficial substances and less sugar than soft drinks but cannot simply be substituted for water, because, of course, it does contain calories. There is also useful information on more arcane subjects: for instance, we should be careful of grapefruit juice because it modifies the absorption and metabolism of a variety of drugs in ways that may be detrimental. And there is a proper assessment of coffee drinking that I like to summarize as follows: If drinking moderate amounts of coffee is your worst nutritional vice, you are in excellent shape. Even in the area of alcohol, Willett, who has been and remains a champion of the beneficial effects of moderate consumption (which he has the courage to define), notes that if you do not drink alcohol you should not ``feel compelled'' to start. Possibly, this is a nice antidote to the widely held notion that if some is good, more is better, but his choice of words is just a little disturbing. Finally, although many self-help books with much poorer pedigrees than this one offer recipes, it is not often that they include useful rules of thumb about shopping and places to shop and even practical tips on how to make substitutions in recipes.

Are there areas where Willett's Healthy Eating Pyramid and the associated information may not be warmly embraced by others in the nutrition-and-disease research community? Certainly the switch from vilifying total fat (a position Willett abandoned early) to asserting that carbohydrate is the bad guy (a position that Willett has made his own) and that there are ``good fats'' and ``bad fats'' does not meet everybody's sniff test. The field of nutrition and chronic disease is populated by those who will agree with Willett on none, one, two, or all three of these positions. It is probably fair to say that reality is not as clear as this book suggests. It is quite clear that diets high in potatoes, olive oil, or even sugar are not harmful to all (or beneficial to all). It seems probable that in the future there will be increasingly clearer advice that is based on metabolic variations -- variations in body shape and fat distribution and subtle genetic differences in the capacity to handle major nutrients -- and that echoes what we already know about micronutrients. It may well be that the ability to handle specific foods and nutrients differs substantially from person to person and that the only universal may prove to be Willett's central tenet: match the energy ingested to the energy expended by controlling both eating and exercise.

It is an interesting paradox that doctors, scientists, and engineers are highly regarded in Western societies but that only a minority of people in those societies like reading about science or are even interested in the topic. Couple that with data from Robin Dunbar of the University of Liverpool in Britain, who found that perhaps two thirds of all human speech is gossip, and it will not be surprising if Willett's book (perhaps like those by Stephen Hawking) sells well but has no impact at all on human behavior or even understanding.

John D. Potter, M.D., Ph.D.

Copyright © 2002 Massachusetts Medical Society. All rights reserved. The New England Journal of Medicine is a registered trademark of the MMS. --This text refers to an out of print or unavailable edition of this title.

Pigments in Retina - Vitamin-A

Chemistry of Vitamin-A

Vitamin-A is a fat soluble vitamin. Its active form is present only in animal tissues. The pro-vitamin, beta-carotene is present in plant tissues. Beta-Carotene has two beta ionone rings connected by a polyprenoid chain. One molecule of beta-carotene can theoretically give rise to two molecules of Vitamin-A; but it may produce only one in biological systems. All compounds with Vitamin-A activity are referred to as retinoids. They are poly-isoprenoid compounds having a beta-ionone ring system. Three different compounds with Vitamin-A activity are:

1. Retinol (Vitamin-A Alcohol)
2. Retinal (Vitamin-A Aldehyde) &
3. Retinoic Acid (Vitamin-A Acid)

Retinal may be reduced to Retinol by Retinal Reductase. This reaction is readily irreversible. Retinal is oxidized into Retinoic Acid, which cannot be converted to other forms. The side chain contains alternate double bounds, and hence many isomers are possible. The all-trans variety of Retinal, also called as Vitamin-A1 is the most common. Vitamin-A2 is found in Fish oils and has an extra double bond in the ring. Biologically important compound is 11-cis-retinal.                          

Absorption of Vitamin-A

Beta-Carotene is cleaved by a di-oxygenase to form Retinal. The Retinal is reduced to Retinol by an NADH or NADPH dependent retinal reductase present in the intestinal mucosa. Intestine is the major site of absorption. The absorption is along with other bile salts. In biliary tract obstruction and steatorrhoea, Vitamin-A absorption is reduced. Within the mucosal cell, the retinol is re-esterified with fatty acids, incorporated into chylomicrons and transported to liver. In the liver stellate cells, vitamin is stored as Retinol Palmitate.

Transport from Liver to Tissues                                 

The Vitamin Theory

Frederick Gowland Hopkins (1861-1947)

Vitamins may be defined as Organic Compounds occurring in small quantities in different natural foods and necessary for growth and maintenance of good health in human beings and in experimental animals. Vitamins are essential food factors, which are required for the proper utilization of the proximate principles of food like carbohydrates, lipids and proteins.

Discovery of vitamins started from observation of deficiency manifestation, e.g. Scurvy, Rickets, Beriberi, etc. "The Vitamin Theory" was suggested by Hopkins in 1912 (Nobel Prize, 1929). The term "vitamine" was coined from the words 'vital' + 'amine', since the earlier identified ones had amino groups. Later work showed that most of them did not contain amino groups, so the last letter 'e' was dropped in modern term 'Vitamin'.

Although vitamins are important nutritionally, their role has been over-emphasized in clinical practices. They are useful to correct deficiencies. But taking higher doses of vitamins will not boost up the health.  

Fredrick G. Hopkins (NP: 1929) [1861-1947]
Suggested "The Vitamin Theory". n 1912 Hopkins published the work for which he is best known, demonstrating in a series of animal feeding experiments that diets consisting of pure proteins, carbohydrates, fats, minerals, and water fail to support animal growth. This led him to suggest the existence in normal diets of tiny quantities of as yet unidentified substances that are essential for animal growth and survival. These hypothetical substances he called “accessory food factors”, later renamed vitamins.[3] It was this work that led his being awarded (together with Christiaan Eijkman) the 1929 Nobel Prize in Physiology or Medicine.                                

Richard Kuhn (NP: 1938) [1900-1967]
Isolated Vitamin-A in 1913, identified carotenes.
Kuhn's areas of study included: investigations of theoretical problems of organic chemistry (stereochemistry of aliphatic and aromatic compounds; syntheses of polyenes and cumulenes; constitution and colour; the acidity of hydrocarbons), as well as extensive fields in biochemistry (carotenoids; flavins; vitamins and enzymes). Specifically, he carried out important work on vitamin B2 and the antidermatitis vitamin B6.



Paul Karrer (NP: 1937) [1889-1971]
Karrer's early research concerned complex metal compounds but his most important work has concerned plant pigments, particularly the yellow carotenoids. He elucidated their chemical structure and showed that some of these substances are transformed in the body into vitamin A. His work led to the establishment of the correct constitutional formula for beta-carotene, the chief precursor of vitamin A; the first time that the structure of a vitamin or provitamin had been established.




Otto P. Diels(NP:1950) [1876-1954]
A German chemist who won a Nobel Prize in chemistry with Alder in 1950. He was awarded the prize for diene synthesis work which led to improved methods of analyzing and synthesizing organic compounds. His research resulted in the discovery of carbon suboxide, methods of dehydrating cyclical hydrocarbons using selenium, and determination of the structure of steroids. A student of Fischer's, Diels graduated from the University of Berlin.






Kurt Alder (NP: 1950) [1902-1958]
Alder received several honorary degrees and other awards, most famously the 1950 Nobel Prize in Chemistry which he shared with his teacher Diels for their work on what is now known as the Diels-Alder reaction. The lunar crater Alder is named in his honour. The insecticide aldrin, created through a Diels-Alder reaction, is also named after the scientist.