Tag: Heart failure

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Western Diet Ups Heart Attack Risk

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Diets that are rich in fried and salty foods increase heart attack risk, while eating lots of fruit, leafy greens and other vegetables reduces it, a groundbreaking study showed.
Western diet boosts colon cancer risk by 300 per cent .

6/12/2008 – (NaturalNews) People who eat a typical “Western diet” or drink diet soda have a higher risk of developing metabolic syndrome and cardiovascular disease, according to a study published in the journal Circulation. “This is a red-alert wake-up call,”…

Green’s The Way: People who ate a ‘Prudent Diet’ — high in fruits and vegetables — had a 30% lower risk of heart attack…..CLICK & SEE

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The study, called Interheart, looked at 16,000 heart attack patients and controls between 1999 and 2003 in countries on every continent, marking a shift from previous studies which have focussed on the developed world.

The patients and controls filled in a “dietary risk score” questionnaire based on 19 food groups, which contained healthy and unhealthy items and were tweaked to include dietary preferences of each country taking part in the study.

The researchers found that people who eat a diet high in fried foods, salty snacks, eggs and meat — the “Western Diet” — a 35% greater risk of having a heart attack than people who consumed little or no fried foods or meat, regardless of where they live.

People who ate a “Prudent Diet” — high in leafy green vegetables, other raw and cooked vegetables, and fruits — had a 30% lower risk of heart attack than those who ate little or no fruit and veg, the study showed.

The third dietary pattern, called the “Oriental Diet” because it contained foods such as tofu and soy sauce which are typically consumed in Asian societies, was found to have little impact on heart attack risk.

Although some items in the Oriental diet might have protective properties such as vitamins and anti-oxidants, others such as soy sauce have a high salt content which would negate the benefits, the study said. The study was groundbreaking in its scope and because previous research had focused mainly on developed countries, according to Salim Yusuf, a senior author of the study.

“We had focussed research on the West because heart disease was mainly predominant in western countries 25-30 years ago,” Yusuf, who is a professor of medicine at McMaster University in Canada, said.

“But heart disease is now increasingly striking people in developing countries. Eighty percent of heart disease today is in low- to middle-income countries” partly because more people around the world are eating western diets, he said.

“This study indicates that the same relationships that are observed in western countries exist in different regions of the world,” said Yusuf, who is also head of the Population Health Research Institute at Hamilton Health Sciences in Ontario.

The main countries in the study were Argentina, Brazil, Chile and Colombia in South America; Canada and US in North America; Sweden in western Europe; and Egypt, Iran and Kuwait for the Middle East. Nearly all of South Asia — India, Pakistan, Bangladesh, Nepal and Sri Lanka — took part.

Sources: The Times Of India

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Fish Oil is Better Than Drugs for Preventing Heart Failure

A typical fish oil softgel
Image via Wikipedia

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Fish oil supplements appear to work better than a popular cholesterol-reducing drug to help patients with chronic heart failure, according to recently released research.

……………………….CLICK & SEE

Researchers gave nearly 3,500 patients a daily omega-3 pill derived from fish oils. Roughly the same number of patients were given placebo pills. Over a four-year period, fewer patients in the group taking the fish oil pills died of heart failure or were admitted to the hospital with the problem.

In a parallel study, the researchers gave nearly 2,300 patients the cholesterol-lowering drug Crestor and another group of close to 2,300 patients placebo pills. After four years, there was little difference in heart failure rates between the groups, but when the two studies were compared they found that fish oil is slightly more effective than Crestor because the oil performed better against a placebo than the drug did.

Chronic heart failure is a condition that occurs when the heart becomes enlarged and cannot pump blood efficiently around the body. Omega-3 fats have long been proven to offer health benefits such as protecting the heart and brain.

Sources:
Time August 31, 2008
The Lancet August 31, 2008
The Lancet August 31, 2008

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The Unfolding Mystery of Scleroderma

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Scleroderma, an autoimmune disease, tends to afflict middle-age women and can affect many parts of the body, inside and out.

CLICK & SEE

Lung disease, the biggest killer of scleroderma patients, is the main focus of research today..

Doctors have a growing arsenal of proven and potential treatments, some of which are risky and the subjects of current research, including stem cell transplants and powerful but toxic cancer drugs.

Like many autoimmune ailments, scleroderma remains a great unknown. Despite decades of research, the cause of this rare and complicated disease has yet to be discovered. But the good news is that doctors have a pretty clear understanding of how scleroderma progresses — a natural history, they call it — and are better than ever at extending and easing their patients’ lives.

“Lots of patients and lots of doctors used to consider it a ‘black box’ disease, a complete mystery, with little that could be done,” said Dr. Philip J. Clements of the University of California, Los Angeles, who is a scleroderma specialist. “Now there’s a body of evidence that tells us what to watch out for, and when.”

Experts now know, for example, that the gradual hardening of tissues and blood vessels that is a hallmark of scleroderma usually starts on the hands and face, with skin thickening, pitted scars and cool, pale fingertips among the earliest symptoms. Damage can then progress inward to internal organs, though the course varies widely from patient to patient. Of the 10,000 cases diagnosed among Americans each year, mainly women, a small subset will die quickly. But many others are able to manage their condition with a variety of treatments and have normal life expectancies.

Doctors also now know that if a patient’s internal organs are going to be affected as well as the skin, that is likely to happen in the first four or five years of the disease. So early diagnosis and close monitoring of the heart, lungs and kidneys are vitally important.

They have also learned that steroids, once viewed as a cure-all for immune disorders, can worsen the effects of scleroderma, especially in the kidneys, and should be used with caution.

“Learning which drugs to avoid was itself a big step,” said Dr. John Varga, the Gallagher Professor of Medicine at Northwestern University and chairman of the Medical Advisory Board for the Scleroderma Foundation, a nonprofit group that sponsors research and support for patients and families.

Kidney disease used to cause 90 percent of scleroderma-related deaths until the advent of a class of blood pressure drugs called angiotensin-converting enzyme, or ACE, inhibitors in the 1980s. ACE inhibitors prevent kidney damage by slowing down the chemicals that cause the muscles surrounding blood vessels to contract. Complications in the kidneys now account for only 14 percent of scleroderma deaths, Dr. Steen said.

The lungs are still a challenge. About 80 percent of scleroderma patients develop some form of lung problem — either pulmonary hypertension, due to hardening of the veins and arteries in the lung, or pulmonary fibrosis, in which the lung tissue becomes inflamed and then thickened with scarring. Some patients develop both. Either way, breathing becomes more difficult as the lungs become less pliable.

“If you die of a scleroderma-related problem, half of those deaths are from lung disease,” said Dr. Virginia Steen, a professor at Georgetown University and director of the Rheumatology Fellowship Program there. She wrote a seminal 2007 article that documented the shift from kidney disease to pulmonary disease as the biggest cause of death among scleroderma patients.

One successful remedy called Revatio, routinely prescribed since 2005, came from an unexpected source: Viagra. Repackaged from a little blue diamond to a round white tablet and renamed for marketing, dosage and insurance purposes, the drug works by relaxing the blood vessels and improving blood flow, whether for erectile or lung dysfunction.

“No one could understand why all these women were taking it four times a day,” said Frannie Waldron, chief executive of the Scleroderma Foundation.

Doctors also have a growing arsenal of experimental treatments and potential cures, some of which are risky.

Among them is cyclophosphamide, or Cytoxan, a powerful but highly toxic cancer drug that acts on the immune system. The drug decreases the inflammation that causes pulmonary fibrosis and has been used on scleroderma patients for the last 10 years.

But cytoxan has dangerous side effects, including an increased risk of bladder cancer, and usually is not given for more than a year. Moreover, the fibrosis seems to start again once drug treatments stop. Several studies involving the medication are under way, as well as efforts to find alternative treatments, many of them sponsored by drug companies.

Another big push involves stem cell transplant, an extremely risky process in which doctors try to reset the patient’s immune system and bypass the glitch that causes scleroderma. The procedure is the subject of a National Institutes of Health study called the SCOT trial, for Scleroderma: Cyclophosphamides or Transplantation?

Similar to a bone marrow transplant, doctors first draw the patient’s blood and extract the stem cells, the highly malleable building blocks that are thought to be free of the seeds of scleroderma. The patient is then subjected to high doses of radiation or chemotherapy with Cytoxan to kill the bone marrow. The last step is to reinfuse the stem cells, in the hopes that they replicate themselves in a healthy form free of disease.

The study will compare the benefits of the stem cell transplant with giving patients just monthly doses, but high ones, of Cytoxan. Preliminary results have been promising, several experts said.

“You’d think you’d have trouble recruiting for this,” said Dr. Arthur C. Theodore of Boston University, one of the investigators in the project. “But scleroderma patients are desperate.”

Sources: The New York Times

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Ailmemts & Remedies

Hypoglycemia

Definition:
Hypoglycemia is the clinical syndrome that results from low blood sugar. The symptoms of hypoglycemia can vary from person to person, as can the severity. Classically, hypoglycemia is diagnosed by a low blood sugar with symptoms that resolve when the sugar level returns to the normal range….CLICK & SEE

Risk Factor:
While patients who do not have any metabolic problems can complain of symptoms suggestive of low blood sugar, true hypoglycemia usually occurs in patients being treated for diabetes (type 1 and type 2). Patients with pre-diabetes who have insulin resistance can also have low sugars on occasion if their high circulating insulin levels are further challenged by a prolonged period of fasting. There are other rare causes for hypoglycemia, such as insulin producing tumors (insulinomas) and certain medications. These uncommon causes of hypoglycemia will not be discussed in this article, which will primarily focus on the hypoglycemia occurring with diabetes mellitus and its treatment.

Despite our advances in the treatment of diabetes, hypoglycemic episodes are often the limiting factor in achieving optimal blood sugar control. In large scale studies looking at tight control in both type 1 and type 2 diabetes, low blood sugars occurred more often in the patients who were managed most intensively. This is important for patients and physicians to recognize, especially as the goal for treating patients with diabetes become tighter blood sugar control.

Low Blood sugar is Also Bad:
The body needs fuel to work. One of its major fuel sources is sugars, which the body gets from what is consumed as either simple sugar or complex carbohydrates. For emergency situations (like prolonged fasting), the body stores a stash of sugar in the liver as glycogen. If this store is needed, the body goes through a biochemical process called gluco-neo-genesis (meaning to “make new sugar”) and converts these stores of glycogen to sugar. This backup process emphasizes that the fuel source of sugar is important (important enough for human beings to have developed an evolutionary system of storage to avoid a sugar drought).

Of all the organs in the body, the brain depends on sugar (which we are now going to refer to as glucose) almost exclusively. Rarely, if absolutely necessary, the brain will use ketones as a fuel source, but this is not preferred. The brain cannot make its own glucose and is 100% dependent on the rest of the body for its supply. If for some reason, the glucose level in the blood falls (or if the brain’s requirements increase and demands are not met) there can be effects on the function of the brain.

Our Body’s Natural Protection:
When the circulating level of blood glucose falls, the brain actually senses the drop. The brain then sends out messages that trigger a series of events, including changes in hormone and nervous system responses that are aimed at increasing blood glucose levels. Insulin secretion decreases and hormones that promote higher blood glucose levels, such as glucagon, cortisol, growth hormone and epinephrine, all increase. As mentioned above, there is a store in the liver of glycogen that can be converted to glucose rapidly.

In addition to the biochemical processes that occur, the body starts to consciously alert the affected person that is needs food by causing the signs and symptoms of hypoglycemia discussed below.

Signs and symptoms:
Hypoglycemic symptoms and manifestations can be divided into those produced by the counterregulatory hormones (epinephrine/adrenaline and glucagon) triggered by the falling glucose, and the neuroglycopenic effects produced by the reduced brain sugar.

Adrenergic manifestations

*Shakiness, anxiety, nervousness, tremor

*Palpitations, tachycardia

*Sweating, feeling of warmth

*Pallor, coldness, clamminess

*Dilated pupils (mydriasis)

Feeling of numbness “pins and needles” (parasthaesia) in the fingers

Glucagon manifestations:

*Hunger, borborygmus

*Nausea, vomiting, abdominal discomfort

*Headache

Neuroglycopenic manifestations:

*Abnormal mentation, impaired judgement

*Nonspecific dysphoria, anxiety, moodiness, depression, crying

*Negativism, irritability, belligerence, combativeness, rage

*Personality change, emotional lability

*Fatigue, weakness, apathy, lethargy, daydreaming, sleep

*Confusion, amnesia, dizziness, delirium

*Staring, “glassy” look, blurred vision, double vision

*Automatic behavior, also known as automatism

*Difficulty speaking, slurred speech

*Ataxia, incoordination, sometimes mistaken for “drunkenness”

*Focal or general motor deficit, paralysis, hemiparesis

*Paresthesia, headache

*Stupor, coma, abnormal breathing

*Generalized or focal seizures

Not all of the above manifestations occur in every case of hypoglycemia. There is no consistent order to the appearance of the symptoms, if symptoms even occur. Specific manifestations may vary by age and by severity of the hypoglycemia. In young children, vomiting can sometimes accompany morning hypoglycemia with ketosis. In older children and adults, moderately severe hypoglycemia can resemble mania, mental illness, drug intoxication, or drunkenness. In the elderly, hypoglycemia can produce focal stroke-like effects or a hard-to-define malaise. The symptoms of a single person may be similar from episode to episode, but are not necessarily so and may be influenced by the speed at which glucose levels are dropping, and previous incidence.

In newborns, hypoglycemia can produce irritability, jitters, myoclonic jerks, cyanosis, respiratory distress, apneic episodes, sweating, hypothermia, somnolence, hypotonia, refusal to feed, and seizures or “spells”. Hypoglycemia can resemble asphyxia, hypocalcemia, sepsis, or heart failure.

In both young and old patients, the brain may habituate to low glucose levels, with a reduction of noticeable symptoms despite neuroglycopenic impairment. In insulin-dependent diabetic patients this phenomenon is termed hypoglycemia unawareness and is a significant clinical problem when improved glycemic control is attempted. Another aspect of this phenomenon occurs in type I glycogenosis, when chronic hypoglycemia before diagnosis may be better tolerated than acute hypoglycemia after treatment is underway.

Nearly always, hypoglycemia severe enough to cause seizures or unconsciousness can be reversed without obvious harm to the brain. Cases of death or permanent neurological damage occurring with a single episode have usually involved prolonged, untreated unconsciousness, interference with breathing, severe concurrent disease, or some other type of vulnerability. Nevertheless, brain damage or death has occasionally resulted from severe hypoglycemia.

Causes:-
Hundreds of conditions can cause hypoglycemia. Common causes by age are listed below. While many aspects of the medical history and physical examination may be informative, the two best guides to the cause of unexplained hypoglycemia are usually

1.The circumstances

2.A critical sample of blood obtained at the time of hypoglycemia, before it is reversed.

There are several ways to classify hypoglycemia. The following is a list of the more common causes and factors which may contribute to hypoglycemia grouped by age, followed by some causes that are relatively age-independent. See causes of hypoglycemia for a more complete list grouped by etiology.

Hypoglycemia in newborn infants:-

Hypoglycemia is a common problem in critically ill or extremely low birthweight infants. If not due to maternal hyperglycemia, in most cases it is multifactorial, transient and easily supported. In a minority of cases hypoglycemia turns out to be due to significant hyperinsulinism, hypopituitarism or an inborn error of metabolism and presents more of a management challenge.

*Transient neonatal hypoglycemia

*Prematurity, intrauterine growth retardation, perinatal asphyxia

*Maternal hyperglycemia due to diabetes or iatrogenic glucose administration

*Sepsis

*Prolonged fasting (e.g., due to inadequate breast milk or condition interfering with feeding)

*Congenital hypopituitarism

*Congenital hyperinsulinism, several types, both transient and persistent

*Inborn errors of carbohydrate metabolism such as glycogen storage disease

Hypoglycemia in young children:-

Single episodes of hypoglycemia may occur due to gastroenteritis or fasting, but recurrent episodes nearly always indicate either an inborn error of metabolism, congenital hypopituitarism, or congenital hyperinsulinism. A list of common causes:

*Prolonged fasting

*Diarrheal illness in young children, especially rotavirus gastroenteritis

*Idiopathic ketotic hypoglycemia

*Isolated growth hormone deficiency, hypopituitarism

*Insulin excess

*Hyperinsulinism due to several congenital disorders of insulin secretion

*Insulin injected for type 1 diabetes

*Hyperinsulin Hyperammonia syndrome (HIHA)due toGlutamate dehydrogenase 1gene.Can cause mental retardation and epilepsy in severe cases.

*Gastric dumping syndrome (after gastrointestinal surgery)

*Other congenital metabolic diseases; some of the common include

*Maple syrup urine disease and other organic acidurias

*Type 1 glycogen storage disease

*Type III glycogen storage disease. Can cause less severe hypoglycemia than type I

*Disorders of fatty acid oxidation

*Medium chain acylCoA dehydrogenase deficiency (MCAD)

*Familial Leucine sensitive hypoglycemia

*Accidental ingestions

*Sulfonylureas, propranolol and others

*Ethanol (mouthwash, “leftover morning-after-the-party drinks”)

Hypoglycemia in older children and young adults:-

By far, the most common cause of severe hypoglycemia in this age range is insulin injected for type 1 diabetes. Circumstances should provide clues fairly quickly for the new diseases causing severe hypoglycemia. All of the congenital metabolic defects, congenital forms of hyperinsulinism, and congenital hypopituitarism are likely to have already been diagnosed or are unlikely to start causing new hypoglycemia at this age. Body mass is large enough to make starvation hypoglycemia and idiopathic ketotic hypoglycemia quite uncommon. Recurrent mild hypoglycemia may fit a reactive hypoglycemia pattern, but this is also the peak age for idiopathic postprandial syndrome, and recurrent “spells” in this age group can be traced to orthostatic hypotension or hyperventilation as often as demonstrable hypoglycemia.

*Insulin-induced hypoglycemia

*Insulin injected for type 1 diabetes

*Factitious insulin injection (Munchausen syndrome)

*Insulin-secreting pancreatic tumor

*Reactive hypoglycemia and idiopathic postprandial syndrome

*Addison’s disease

*Sepsis

Hypoglycemia in older adults:-

The incidence of hypoglycemia due to complex drug interactions, especially involving oral hypoglycemic agents and insulin for diabetes rises with age. Though much rarer, the incidence of insulin-producing tumors also rises with advancing age. Most tumors causing hypoglycemia by mechanisms other than insulin excess occur in adults.

*Insulin-induced hypoglycemia

*Insulin injected for diabetes

*Factitious insulin injection (Munchausen syndrome)

*Excessive effects of oral diabetes drugs, beta-blockers, or drug interactions

*Insulin-secreting pancreatic tumor

*Alimentary (rapid jejunal emptying with exaggerated insulin response)

*After gastrectomy dumping syndrome or bowel bypass surgery or resection

*Reactive hypoglycemia and idiopathic postprandial syndrome

*Tumor hypoglycemia, Doege-Potter syndrome

*Acquired adrenal insufficiency

*Acquired hypopituitarism

*Immunopathologic hypoglycemia

Treatment:-
Management of hypoglycemia involves immediately raising the blood sugar to normal, determining the cause, and taking measures to hopefully prevent future episodes.

Reversing acute hypoglycemia:-
The blood glucose can be raised to normal within minutes by taking (or receiving) 10-20 grams of carbohydrate. It can be taken as food or drink if the person is conscious and able to swallow. This amount of carbohydrate is contained in about 3-4 ounces (100-120 ml) of orange, apple, or grape juice although fruit juices contain a higher proportion of fructose which is more slowly metabolized than pure dextrose, alternatively, about 4-5 ounces (120-150 ml) of regular (non-diet) soda may also work, as will about one slice of bread, about 4 crackers, or about 1 serving of most starchy foods. Starch is quickly digested to glucose (unless the person is taking acarbose), but adding fat or protein retards digestion. Symptoms should begin to improve within 5 minutes, though full recovery may take 10-20 minutes. Overfeeding does not speed recovery and if the person has diabetes will simply produce hyperglycemia afterwards.

If a person is suffering such severe effects of hypoglycemia that they cannot (due to combativeness) or should not (due to seizures or unconsciousness) be given anything by mouth, medical personnel such as EMTs and Paramedics, or in-hospital personnel can establish an IV and give intravenous Dextrose, concentrations varying depending on age (Infants are given 2cc/kg Dextrose 10%, Children Dextrose 25%, and Adults Dextrose 50%). Care must be taken in giving these solutions because they can be very necrotic if the IV is infiltrated. If an IV cannot be established, the patient can be given 1 to 2 milligrams of Glucagon in an intramuscular injection. More treatment information can be found in the article diabetic hypoglycemia.

One situation where starch may be less effective than glucose or sucrose is when a person is taking acarbose. Since acarbose and other alpha-glucosidase inhibitors prevents starch and other sugars from being broken down into monosaccharides that can be absorbed by the body, patients taking these medications should consume monosaccharide-containing foods such as glucose tablets, honey, or juice to reverse hypoglycemia.

Prevention:
The most effective means of preventing further episodes of hypoglycemia depends on the cause.

The risk of further episodes of diabetic hypoglycemia can often (but not always) be reduced by lowering the dose of insulin or other medications, or by more meticulous attention to blood sugar balance during unusual hours, higher levels of exercise, or alcohol intake.

Many of the inborn errors of metabolism require avoidance or shortening of fasting intervals, or extra carbohydrates. For the more severe disorders, such as type 1 glycogen storage disease, this may be supplied in the form of cornstarch every few hours or by continuous gastric infusion.

Several treatments are used for hyperinsulinemic hypoglycemia, depending on the exact form and severity. Some forms of congenital hyperinsulinism respond to diazoxide or octreotide. Surgical removal of the overactive part of the pancreas is curative with minimal risk when hyperinsulinism is focal or due to a benign insulin-producing tumor of the pancreas. When congenital hyperinsulinism is diffuse and refractory to medications, near-total pancreatectomy may be the treatment of last resort, but in this condition is less consistently effective and fraught with more complications.

Hypoglycemia due to hormone deficiencies such as hypopituitarism or adrenal insufficiency usually ceases when the appropriate hormone is replaced.

Hypoglycemia due to dumping syndrome and other post-surgical conditions is best dealt with by altering diet. Including fat and protein with carbohydrates may slow digestion and reduce early insulin secretion. Some forms of this respond to treatment with a glucosidase inhibitor, which slows starch digestion.

Reactive hypoglycemia with demonstrably low blood glucose levels is most often a predictable nuisance which can be avoided by consuming fat and protein with carbohydrates, by adding morning or afternoon snacks, and reducing alcohol intake.

Idiopathic postprandial syndrome without demonstrably low glucose levels at the time of symptoms can be more of a management challenge. Many people find improvement by changing eating patterns (smaller meals, avoiding excessive sugar, mixed meals rather than carbohydrates by themselves), reducing intake of stimulants such as caffeine, or by making lifestyle changes to reduce stress.

Herbal medication for Hypoglycemia:-
THE following HERBS as stated below can help to ease low blood sugar with symptoms that include lightheadedness, headache, irritability, depression, anxiety, cravings for sweets, confusion, night sweats, weakness in the legs and arms, swollen feet, insatiable hunger, eye pain, nervous tics, mental disturbances, insomnia, aggressiveness, hair-trigger temper.

Cinnamon bark extract, coral calcium with trace minerals, L-carnitine, bilberry extract, Mexican wild yam, dandelion root, milk thistle extract.

Quik Tip: Cinnamon bark decreases insulin resistance and improves blood-sugar profiles better than most prescription drugs, USDA studies confirm.

Hypoglycemia as “folk” medicine:-
Hypoglycemia is also a term of contemporary folk medicine which refers to a recurrent state of symptoms of altered mood and subjective cognitive efficiency, sometimes accompanied by adrenergic symptoms, but not necessarily by measured low blood glucose. Symptoms are primarily those of altered mood, behavior, and mental efficiency. This condition is usually treated by dietary changes which range from simple to elaborate. Advising people on management of this condition is a significant “sub-industry” of alternative medicine. More information about this form of “hypoglycemia”, with far more elaborate dietary recommendations, is available on the internet and in health food stores. Most of these websites and books describe a conflation of reactive hypoglycemia and idiopathic postprandial syndrome but do not recognize a distinction. The value of most of their recommendations is – from a scientific perspective – unproved.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://www.medicinenet.com/hypoglycemia/article.htm
http://en.wikipedia.org/wiki/Hypoglycemia
http://www.herbnews.org/hypoglycemiadone.htm

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Co Q10

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Other Names: Coenzyme Q10, Co Q10, Ubiquinone, Vitamin Q

Definition: CoQ10 is a naturally-occuring compound found in every cell in the body. CoQ10’s alternate name, ubiquinone, comes from the word ubiquitous, which means “found everywhere.”Coenzyme Q10 is a benzoquinone, where Q refers to the quinone chemical group, and 10 refers to the isoprenyl chemical subunits.

This oil-soluble vitamin-like substance is present in most eukaryotic cells, primarily in the mitochondria. It is a component of the electron transport chain and participates in aerobic cellular respiration, generating energy in the form of ATP. Ninety-five percent of the human body’s energy is generated this way. Therefore, those organs with the highest energy requirements – such as the heart and the liver – have the highest CoQ10 concentrations

CoQ10 plays a key role in producing energy in the mitochondria, the part of a cell responsible for the production of energy in the form of ATP.

History
Coenzyme Q was first discovered by professor Fred L. Crane and colleagues at the University of Wisconsin-Madison Enzyme Institute in 1957. In 1958, its chemical structure was reported by Professor Karl Folkers and coworkers at Merck.

Chemical properties:
The oxidized structure of CoQ, or Q, is given here. The various kinds of Coenzyme Q can be distinguished by the number of isoprenoid side-chains they have. The most common CoQ in human mitochondria is Q10. The image to the right has three isoprenoid units and would be called Q3.

If Coenzyme Q is reduced by one equivalent, the following structure results, a ubisemiquinone, and is denoted QH. Note the free-radical on one of the ring oxygens (either oxygen may become a free-radical, in this case the top oxygen is shown as such).

If Coenzyme Q is reduced by two equivalents, the compound becomes a ubiquinol, denoted

Biochemical role
CoQ is found in the membranes of many organelles. Since its primary function in cells is in generating energy, the highest concentration is found on the inner membrane of the mitochondrion. Some other organelles that contain CoQ10 include endoplasmic reticulum, peroxisomes, lysosomes, and vesicles.

Supplementation
Because of its ability to transfer electrons and therefore act as an antioxidant, Coenzyme Q is also used as a dietary supplement. When one is younger the body can synthesize Q10 from the lower-numbered ubiquinones such as Q6 or Q8. The elderly and sick may not be able to make enough, thus Q10 becomes a vitamin later in life and in illness.

Why People Use CoQ10:

*Heart failure

*Cardiomyopathy

*Heart Attack Prevention and Recovery

*High Blood Pressure

*Diabetes

*Gum Disease

*Kidney Failure

*Migraine

*Counteract Prescription Drug Effects

*Parkinson’s disease

*Weight loss

The Evidences For CoQ10:
*Heart failure
People with heart failure have been found to have lower levels of CoQ10 in heart muscle cells. Double-blind research suggests that CoQ10 may reduce symptoms related to heart failure, such as shortness of breath, difficulty sleeping, and swelling. CoQ10 is thought to increase energy production in the heart muscle, increasing the strength of the pumping action. Recent human studies, however, haven’t supported this.

In one study, 641 people with congestive heart failure were randomized to receive either CoQ10 (2 mg per kg body weight) or a placebo plus standard treatment. People who took the CoQ10 had a significant reduction in symptom severity and fewer hospitalizations.

In another study, 32 patients with end-stage heart failure awaiting heart transplantation received either 60 mg of CoQ10 or a placebo for 3 months. Patients who took the CoQ10 experienced a significant improvement in functional status, clinical symptoms, and quality of life, however there were no changes in echocardiogram (heart ultrasound) or in objective markers.

A study randomized 55 patients with congestive heart failure to receive either 200 mg per day of CoQ10 or a placebo in addition to standard treatment. Although serum levels of CoQ10 increased in patients receiving CoQ10, CoQ10 didn’t affect ejection fraction, peak oxygen consumption, or exercise duration.

A longer-term study investigated the use of 100 mg of CoQ10 or a placebo in addition to standard treatment in 79 patients with stable chronic congestive heart failure. The results indicated that CoQ10 only slightly improved maximal exercise capacity and quality of life compared with the placebo.

*Cardiomyopathy
Several small trials have found CoQ10 may be helpful for certain types of cardiomyopathy.

*Parkinson’s disease
Lower levels of CoQ10 have also been observed in people with Parkinson’s disease. Preliminary research has found that increasing CoQ10 may increase levels of the neurotransmitter dopamine, which is thought to be lowered in people with Parkinson’s disease. It has also been suggested that CoQ10 might protect brain cells from damage by free radicals.

A small, randomized controlled trial examined the use of 360 mg CoQ10 or a placebo in 28 treated and stable Parkinson’s disease patients. After 4 weeks, CoQ10 provided a mild but significant significant mild improvement in early Parkinson’s symptoms and significantly improved performance in visual function.

A larger 16 month trial funded by the National Institutes of Health explored the use of CoQ10 (300, 600 or 1200 mg/day) or a placebo in 80 patients with early stage Parkinson’s disease. The results suggested that CoQ10, especially at the 1200 mg per day dose, had a significant reduction in disability compared to those who took a placebo.

*CoQ10 and Statin Drugs
Some research suggests that statin drugs, or HMG-CoA reductase inhibitors, a class of drugs used to lower cholesterol, may interfere with the body’s production of CoQ10. However, research on the use of CoQ10 supplements in people taking statins is still inconclusive, and it is not routinely recommended in combination with statin therapy.

You may click to see:->Statin Drugs May Lower CoQ10 Levels

Diabetes
In a 12-week randomized controlled trial, 74 people with type 2 diabetes were randomized to receive either 100 mg CoQ10 twice daily, 200 mg per day of fenofibrate (a lipid regulating drug), both or neither for 12 weeks. CoQ10 supplementation significantly improved blood pressure and glycemic control. However, two studies found that CoQ10 supplementation failed to find any effect on glycemic control.

Gum disease
A small study looked at the topical application of CoQ10 to the periodontal pocket. Ten male periodontitis patients with 30 periodontal pockets were selected. During the first 3 weeks, the patients applied topical CoQ10. There was significant improvement in symptoms.

Dosage
A typical CoQ10 dosage is 30 to 90 mg per day, taken in divided doses, but the recommended amount can be as high as 200 mg per day.

CoQ10 is fat-soluble, so it is better absorbed when taken with a meal that contains oil or fat.

The clinical effect is not immediate and may take up to eight weeks.

Mitochondrial disorders
Supplementation of Coenzyme Q10 is a treatment for some of the very rare and serious mitochondrial disorders and other metabolic disorders, where patients are not capable of producing enough coenzyme Q10 because of their disorder. Coenzyme Q10 is then prescribed by a physician.

Migraine headaches
Supplementation of Coenzyme Q10 has been found to have a beneficial effect on the condition of some sufferers of migraine headaches. So far, three studies have been done, of which two were small, did not have a placebo group, were not randomized, and were open-label, and one was a double-blind, randomized, placebo-controlled trial, which found statistically significant results despite its small sample size of 42 patients. Dosages were 150 to 300 mg/day.

Cancer
It is also being investigated as a treatment for cancer, and as relief from cancer treatment side-effects.

Brain health and neurodegenerative diseases
Recent studies have shown that the antioxidant properties of coenzyme Q10 benefit the body and the brain in animal models. Some of these studies indicate that coenzyme Q10 protects the brain from neurodegenerative disease such as Parkinson’s, although it does not relieve the symptoms. Dosage was 300 mg per day.

Cardiac arrest
Another recent study shows a survival benefit after cardiac arrest if coenzyme Q10 is administered in addition to commencing active cooling (to 32–34 degrees Celsius).

Blood pressure
There are several reports concerning the effect of CoQ10 on blood pressure in human studies.[19] In a recent meta-analysis of the clinical trials of CoQ10 for hypertension, a research group led by Professor Frank Rosenfeldt (Director, Cardiac Surgical Research Unit, Alfred Hospital, Melbourne, Australia) reviewed all published trials of Coenzyme Q10 for hypertension, and assessed overall efficacy, consistency of therapeutic action, and side-effect incidence. Meta-analysis was performed in 12 clinical trials (362 patients) comprising three randomized controlled trials, one crossover study, and eight open-label studies. The research group concluded that coenzyme Q10 has the potential in hypertensive patients to lower systolic blood pressure by up to 17 mm Hg and diastolic blood pressure by up to 10 mm Hg without significant side-effects.


Lifespan
Studies have shown that low dosages of coenzyme Q10 reduce oxidation and DNA double-strand breaks, and a combination of a diet rich in polyunsaturated fatty acids and coenzyme Q10 supplementation leads to a longer lifespan in rats

Safety
*Consult your doctor before trying CoQ10, especially if you have heart disease, kidney failure, or cancer.

*Side effects of CoQ10 may include diarrhea and rash.

*CoQ10 is used in combination with standard treatment, not to replace it.

*CoQ10 may lower blood sugar levels, so people with diabetes should not use CoQ10 unless under a doctor’s supervision. CoQ10 may also lower blood pressure.

The safety of Co q10 in pregnant or nursing women or children has not been established.

Possible Drug Interactions:-

You may click to see:-> CoQ10 drug interactions.

Resources:
http://altmedicine.about.com/cs/supplements/a/CoenzymeQ10.htm
http://en.wikipedia.org/wiki/Coenzyme_Q10

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