Squaw Vine Information - Side Effects, Uses and Benefits

Taxonomic Class

Rubiaceae

HEPATIC

Common Trade Names

Mitchella repens, Partridge Berry, Squaw Vine
Source

Squaw vine is the dried plant of Mitchella repens Linne, common to the woodlands of the central and eastern United States. The plant blooms in July and is usually harvested late in summer.

Chemical Components

The leaves of the plant contain resin, wax, mucilage, dextrin, and tannin. The leaves are also thought to contain glycosides and saponins.

Actions

Tannic acid has local astringent properties that act on GI mucosa, which is thought to occur through binding and precipitation of proteins, and forms insoluble complexes with select heavy metal ions, alkaloids, and glycosides. It has also been shown to have antisecretory and antiulcerative effects within the GI tract because of an inhibitory action on the gastric enzyme system. Saponins are usually less toxic to humans after oral ingestion, but when administered I.V., they act as potent hemolytics.

Reported Uses

Squaw vine has been used as an astringent, a diuretic, and a tonic. Because its tonic properties are thought to work primarily on the uterus, squaw vine has been used extensively as an aid in labor and childbirth. Native Americans were the first to use the plant to make parturition safer and easier. It has also been used in cases of abdominal pain associated with menstruation, abnormal menstruation, and heavy bleeding . Other claims include its use as a remedy for amenorrhea, diarrhea, dysentery, dysuria, edema, gonorrhea, hysteria, kidney stones, polyuria, and vaginitis. Crushed squaw vine berries have been mixed with myrrh and used for sore nipples. The use of squaw vine is based on traditional and anecdotal reports, not on controlled human clinical trials.

Dosage

Liquid extract: Yo to 1 tsp P.O. t.i.d.

Squaw vine (dried): 30 to 60 grains (2 to 4 g) P.O.

Tincture: 1 to 2 ml P.O. t.i.d.

Adverse Reactions

GI: heartburn, hepatotoxicity (rare).

Other: irritated mucouS membranes.
Interactions

Alkaloid-related drugs (atropine, scopolamine), iron-containing products:Tannic acid may slow metabolic breakdown. Monitor the patient.

Cardiac glycosides: Risk of increased effect of these drugs. Use together cautiously.

Disulfiram: Disulfiram reaction can occur if herbal form contains alcohol Do not use together.
Contraindications and Precautions

Squaw vine is contraindicated during the first and second trimesters of pregnancy. Use cautiously in patients with preexisting hepatic disease or complications.

Special Considerations

* Saponin glycosides have a bitter taste and are irritating to the mucous membranes.

* Monitor liver function test results. Advise the patient to immediately discontinue use of squaw vine if transaminase levels become elevated.

* Urge women to report planned or suspected pregnancy.

* Advise the patient to immediately report symptoms of hepatic dysfunction (fever, jaundice, right upper quadrant pain).

Caution the patient taking disulfiram not to take an herbal form that contains alcohol.

Commentary

Although there appears to be widespread use of squaw vine as a medicinal herb, none of these claims has been studied or proved in animals or humans.

Squaw Vine Information - Side Effects, Uses and Benefits

HEPATIC

Silymarin (Milk Thistle) Extract - Treat Type II Diabetes

Nowadays, people have been finding alternative ways to prevent or treat illnesses. This is because, most synthetic medicines have higher rate of causing undesirable side effects. If you are one of those people who would want a safer yet equally effective way to manage one's health, a daily dose of Silymarin extract is just for you.

Silymarin, or also known as milk thistle, is a flowering plant that belongs to the daisy family. This plant is abundant in certain regions of Europe, North Africa and the Middle East. Like any other plant that belongs to this genus, milk thistles have a tall erect stem. It also has a large alternate leaves which has waxy lobes with thorny spikes.

HEPATIC

Milk Thistle extract comes from the plant's seeds. The extract from the seeds have high medicinal value because it contains around 65 to 80% of silymarin (a flavonolignan complex) and about 20 to 35% fatty acids that includes linoleic acid.

Silymarin, being a complex mixture of polyphenolic molecules, has been clinically proven to treat type II diabetes when taken at high doses. Furthermore, Silymarin is also said to treat patients diagnosed with Hepatitis C at an even higher dose. But taking such high doses would require a doctor's order as it could cause some adverse reactions like brief gastrointestinal disturbances, diarrhea, cramping, mild allergic reactions, and urticaria. However, if you want to take it as a daily supplement, an average of 420 to 480 mg per day is recommended.

This plant benefits the liver because it produces a hepatoprotective effect by stimulating (Ribonucleic Acid) RNA and (Deoxyribonucleic acid) DNA synthesis and scavenges pro-oxidant free radicals and increase intracellular concentration of glutathione (a substance needed to detoxify hepatic cell reactions), thus altering the outer membrane of the hepatic cells. Moreover, it is also said to exert anti-inflammatory effect on the platelets.

Because of such activity in the body, Silymarin extract is used to prevent, treat, or delay the progress of liver dysfunction (including damage caused by acute viral hepatitis or long term phenothiazine or butyrophenone use), dyspepsia, gallbladder disorders, and spleen disorders.

Additional health benefit includes reduction of increased total and high-density lipoprotein levels and as an antidote for Amanita mushroom poisoning. Further claims include: as an oral steroid for body builders, helps in controlling blood cholesterol levels, reducing the resistance of diabetic patients to insulin, slowing the progress of cancer, and to reduce liver damage caused by exposure to chemo drugs. The set of latter claims however does require more evidences to establish its accuracy.

Taking Thistle Milk extract that has been processed to a tablet or as a part of an ingredient of a food supplement is said to be generally safe. However, as soon as you see some allergic reactions when taking Silymarin extract stop it immediately and consult your doctor. Also, extra precautions should be made when giving the said plant extract to women who are pregnant or lactating because the safety of Thistle Milk extract to babies are not yet established.

Silymarin (Milk Thistle) Extract - Treat Type II Diabetes

HEPATIC

Diabetes - Should Our Athletes Be Worried? How to Balance Blood Sugar

Diabetes is a growing problem in the population: according to Diabetes UK there are 3% (1.8 million) diagnosed cases (approximately 250 thousand with type 1 and over 1.5 million with type 2) and another estimated 750 thousand to 1 million undiagnosed cases of type 2 diabetes. No statistics are available for the athletic population.

What is diabetes?

HEPATIC STEATOSIS

Diabetes is a syndrome or group of symptoms arising from failure to regulate the metabolism of glucose by means of the pancreatic hormone, insulin. This occurs due to a lack of insulin because the pancreas does not produce enough, fails to produce any or the body fails to make proper use of the insulin that is available. Diabetes is classified as insulin-dependent (type 1) and non-insulin-dependent (type 2). This paper will focus on the latter and will ignore any genetic predisposition to the disease.

The glycaemic index and diabetes

The Glycaemic Index (GI) can be considered as a measure of carbohydrate quality. It measures the postprandial (after a meal) glycaemia (plasma glucose) raising potential of a single food by expressing the rise in glycaemia in response to a 50g available carbohydrate portion of that food as a percentage of the rise in response to a 50g available carbohydrate portion of a reference food (white bread or glucose).

Foods high on the GI result in a sharp rise of plasma glucose, with a high demand for insulin, followed by a more or less rapid fall of glucose. Foods that are low to moderate on the GI produce a slower rise, with a lower demand for insulin, and a more gradual decline in plasma glucose.

Those in favour of carbohydrate quality, argue that GI is a robust measurement, predicts the relative glycaemic response to mixed meals and is easy to follow and implement. In contrast, opponents who favour giving priority to carbohydrate quantity argue that GI is highly variable, not physiological, cannot reliably predict mixed meal responses and is difficult to learn or follow.

Despite some opposition to low-GI intervention in type 2 diabetes, the interventions are clinically efficacious in diabetes therapy over the mid to long-term. The Canadian Diabetes Association, Diabetes Australia, Diabetes UK and the European Association for the Study of Diabetes all support the application of the GI concept in the management of diabetes.

Insulin resistance

Insulin resistance, a component of the Insulin Resistance Syndrome, also known as Syndrome X and the Metabolic Syndrome, is associated with type 2 diabetes. No statistics for insulin resistance are available in the UK, although, according to Diabetes UK, a national register may be set up in the future.

Obesity is the most significant factor leading to insulin resistance with visceral obesity having a particularly strong negative correlation. It can be reversed with diet modification based on a low-fat intake and limiting refined carbohydrates without the need of caloric restrictions. Physical activity is an important factor in reversing the problem.

Mechanisms leading to insulin resistance are unclear, although the abnormal accumulation of certain fats in the liver (hepatic steatosis) is a contributing factor.

In a study by Pan et al, skeletal muscle triglyceride (mTG) appeared to be another important factor in predicting insulin resistance. Trained athletes and animals show the same or higher levels of muscle triglycerides as sedentary controls but have improved insulin action. The authors postulated that this could be due to the distribution of triglyceride. Endurance exercise increases both the mitochondrial volume and distribution in skeletal muscles. In trained dogs, mitochondria appear virtually in direct contact with triglyceride droplets whereas no such association with mitochondria was found in untrained animals. As a result, trained individuals may have an improved ability to mobilise fats.

Research into sucrose and fructose on animals has consistently shown that high sucrose and fructose diets decrease insulin sensitivity. Studies on humans have been inconsistent.

In a large cohort study by Janket et al, 38,480 initially healthy postmenopausal women were followed for an average of 6 years. The researchers accrued 918 incident cases of type 2 diabetes but found no definitive influence of sugar intake on the risk of developing type 2 diabetes. It was noted, however, that the median follow-up time of 6 years might not have been long enough to detect a very subtle relationship between sugar intake and incidence of type 2 diabetes.

Assessment on humans is thought to be more complicated because of other factors affecting insulin sensitivity. Some studies found that those consuming a diet consisting of large amounts of sweets and desserts were at increased risk of developing diabetes. However, the diet also included high amounts of saturated fats (red meat, fries and dairy products) which is known to be associated with decreased insulin sensitivity.

No studies have shown a negative effect of sucrose on insulin sensitivity. One explanation for this lack of correlation could be that recruitment of volunteers for nutrition studies is notoriously difficult and many studies have a young or a highly health-orientated population. Both groups are likely to be physically active. Given the strength of the positive influence of physical exertion on insulin sensitivity, such persons are inclined to be resistant to the negative effects of diet. However, this does suggest that the promotion of physical activity may have a greater influence on insulin sensitivity than diet.

Another possible explanation is that the GI concerns only the first 2 hours of the postprandial period. It is postulated that a GI defined by a 4-6 hour postprandial period would alter the ranking of sucrose in a GI table to a higher level. Neither sucrose (a disaccharide: glucose bonded to fructose) nor fructose (a monosaccharide) is high on the GI.

Studies based on high fructose versus high glucose diets have shown that the high fructose diets produce an increase in plasma triacylglycerol, plasma cholesterol, VLDL and LDL cholesterol concentrations, all of which are a risk factor in cardiovascular disease. In addition, some of these effects were seen in men but not women. The reason for this difference is not clear. Although not all studies are consistent with these findings, the positive data cannot and should not be dismissed as it may be of considerable clinical importance. It is also important to note that some individuals are more sensitive to fructose than others.

The risk for athletes

Are athletes at risk of developing type 2 diabetes as a result of their high intake of fructose, sucrose and high glycaemic foods? Although the scientific evidence to-date does not support this notion, athletes may be at risk of developing insulin resistance which is associated not only with diabetes but also with coronary heart disease, hypercholesterolaemia, hypertension, dysglycaemia, osteoarthritis and impaired glucose tolerance.

An over-consumption of refined carbohydrates, over-processed foods, saturated fats and processed vegetable fats are all associated with insulin resistance. The majority of adult athletes we have consulted to-date, over-consume the above with the possible exception of saturated fats. However all our adolescent athletes consumed large amounts of saturated fats.

Although some athletes are becoming more informed on the importance of nutrition for both their long-term health and their performance, there are still a large number who are uninformed or misinformed on nutritional issues. Particularly distressing is the lack of knowledge amongst adolescent athletes which needs to be urgently addressed, not only by nutritionists and dieticians, but also by coaches and parents.

One procedure that can be immediately implemented by everybody is that of chewing our food thoroughly and eating more slowly: it appears that prolonging absorption time by increasing the length of time to complete a meal, consuming smaller and more frequent meals or drinking a beverage over a prolonged period of time all improve glucose tolerance.

In summary, to minimise the risk of insulin resistance, the following points should be adhered to:

Limit sugars and high GI carbohydrates to just before, during and just after exercise.

At other times, consume a large variety of foods avoiding repeating the same food on any one day.

Try to include colourful foods at every meal.

Eat fresh rather than ready-made as often as possible.

Limit all saturated fats found in dairy products and fatty meats.

Avoid fried foods.

Avoid junk foods.

Dilute fruit juices.

2010 Corpotential, All Rights Reserved.

Diabetes - Should Our Athletes Be Worried? How to Balance Blood Sugar

HEPATIC STEATOSIS

Fatty Liver Diet Plan - What You Should Do To Reduce Liver Fat Now Before Catastrophe Strikes

Implementing the right fatty liver diet plan early on can help you enjoy many more years of symptom free living. Although fatty liver disease (FLD) is often an asymptomatic disease in its early stages, it shouldn't be taken lightly.

FLD can be a deadly killer when simple steatosis goes unchecked and worsens to become non alcoholic steatohepatitis (NASH), cirrhosis, liver cancer, or complete liver failure. Diet and exercise will be your best allies against this potentially deadly condition.

STEATOSIS

Fatty liver is closely tied to obesity and if you suffer from FLD, chances are you also struggle to maintain a healthy weight. Perhaps you just need to shed a few pounds or maybe you need to lose hundreds. Regardless, watching your weight and working on a gradual reduction of 1-2lbs per week will go a long way toward reducing fat in your liver.

In her ebook, "Fatty Liver Diet Guide", veteran liver nurse, Dorothy Spencer states, "Since losing weight is the primary concern in treating fatty liver, following a 1200 calorie diet is an excellent way to shed excess body fat." Slow, gradual weight loss is recommended over drastic weight loss measures such as gastric bypass surgery. This prevents the body from going into starvation mode (from the sudden loss of fat) and producing fatty acids that can further congest the liver.

Following Dorothy Spencer's recommendations, a 1200 calorie diet should be comprised of the following:

6 ounces of protein from lean meats and vegetables 5 servings from a starch source such as potatoes or whole-grain bread 4 or more servings of vegetables 3 servings of fresh fruit (citrus fruits are particularly good as they are rich in vitamin C which is gaining popularity as a fatty liver treatment) 3 servings of fat (unsaturated fats are favored over saturated fats, but all fat should be consumed sparingly) 2 servings of low-fat dairy such as cottage cheese or skim milk

If you don't want FLD to worsen, it's important to get started early eating the right foods that help in reducing fatty liver problems. Prevention is the only "cure". Alcohol consumption should be avoided since ethanol blocks the oxidation of fatty acids in the liver and limits the release of low-density lipoproteins (LDL) which are responsible for moving fatty acids out of the liver.

Fatty Liver Diet Plan - What You Should Do To Reduce Liver Fat Now Before Catastrophe Strikes

STEATOSIS

How to Win Your Hepatitis Disability Case

Contrary to what many people suffering from Hepatitis believe, the Social Security Administration (SSA) is very familiar with the disease. In fact, SSA considers Hepatitis to be such a potentially serious medical condition that federal law provides that if their hepatitis is advanced, a person can be found disabled based on laboratory test results alone!

Use this article as the cornerstone to developing and winning your social security disability claim.

HEPATIC

Step 1 Having a Liver Transplant is not a prerequisite to Winning your Disability Claim

While your hepatitis or liver disease must be at a relatively advanced stage, you can win your disability case even if you have not had a liver transplant.

Step 2 Find a compassionate, supportive Gastroenterologist

This may not come as a surprise for you to learn that gastroenterologists are often not overly compassionate with regard to their patients who have hepatitis. In my practice, I talk weekly with doctors of all medical specialties regarding their patients disability claims. Without trying to stereotype, I must confess that I have talked with many gastroenterologists who appeared to lack bedside manner and patient empathy. This is important, because if your gastroenterologist is not compassionate, he or she will likely also be reluctant to support your disability case.

A supportive gastroenterologist is important for two reasons. First, they are the doctors SSA views as the specialists trained to diagnose and treat hepatitis. Second, SSA gives the most weight to the disability opinions are rendered by a claimant's treating physician. Furthermore, SSA gives even more weight to the disability opinions rendered by a specialist such as a gastroenterologist.

Step 3 You must Undergo the Battery of Tests to Confirm the Hepatitis diagnosis and to Determine the Severity of the Disease

One key to winning your Hepatitis case is good laboratory testing. However, laboratory testing alone is not enough to win your case; once the testing is done, the issue will then be how advanced it the disease is.

The information SSA uses to approve a claim based solely on laboratory testing is contained at Listing 5.05 (Specifically 5.05(F)) of the Administration's criteria for Digestive disorders.

F. Confirmation of chronic liver disease by liver biopsy and one of the following:

1. Ascites not attributable to other causes, recurrent or persisting for at least 3 months, demonstrated by abdominal paracentesis or associated with persistent hypoalbuminemia of 3.0 gm per deciliter (100 ml.) or less; or

2. Serum bilirubin of 2.5 mg. per deciliter (100 mg.) or greater on repeated examinations for at least 3 months; or

3. Hepatic cell necrosis or inflammation, persisting for at least 3 months, documented by repeated abnormalities of prothrombin time and enzymes indicative of hepatic dysfunction.

In my experience, many people win their disability case based on meeting the criteria in #3. The reason is that necrosis or inflammation can be confirmed by liver biopsy, and prothrombin time and liver enzyme abnormalities can be measured by a simple blood panel.

In my opinion, in order to have any chance of winning your hepatitis disability case, you should have a relatively recent liver biopsy performed and have blood work dating back for at least 6 months prior to the date you allege you became disabled.

One benefit many hepatitis claimants have is they usually have undergone all the required medical testing prior to or during the time their disability claim with SSA is pending. Thus, if your Hepatitis is at an advanced and serious stage, winning your claim may be as simple as obtaining (or having SSA obtain) your relevant medical records and submitting them to SSA for review to see if it meets the criteria.

Step 4 If your Hepatitis is not advanced enough to meet the SSA Criteria, you can still win your Disability Claim (i.e. Don't Quit!)

It is important to understand that if your Hepatitis does not meet the criteria set forth above, you can still win your disability case. How? By proving that you are unable to work full-time in an unskilled sedentary (sit down) job.

Alternatively, if you have other medical and/or psychological disorders in addition to Hepatitis, SSA will consider the combined effects of your symptoms and limitations from all your medical diagnoses. It is common for many Hepatitis patients to also have a depressive or anxiety disorder. It is possible for the combination of the Hepatitis and psychological problems to equal in severity the criteria listed above. If SSA deems this to be the case, your claim would likely be approved.

It is also possible for you to be unable to work due to severe side effects from taking medications to treat the Hepatitis. Many people are unable to work during the time and for a significant time thereafter they have received interferon treatment. The side effect of overwhelming fatigue from medication can also help you to equal in severity the criteria listed above.

Step 5 Be Free from any Alcohol or Illegal Substance Abuse

As of 1996, a person cannot be approved for disability benefits based on alcoholism and/or substance abuse. In fact, your claim will be denied by SSA if alcoholism or substance abuse is a material factor in your inability to work. You can be sure SSA will likely scrutinize your disability claim because Hepatitis can be contracted through alcoholism or substance abuse. If either of these conditions is a part of your past, to have your best shot at winning, you should be prepared to show that it is not a material factor in your inability to work.

Remember, one key to winning your disability case is to never quit and keep fighting for the benefits you deserve!

How to Win Your Hepatitis Disability Case

HEPATIC

What Is A Fatty Liver?

Steatosis, or fatty liver, is a condition where triglycerides and other fats collect in liver cells. It is caused from altered fat metabolism from mobilization of fatty acids. Sometimes, as much as 40% of the liver's weight is accounted from these fat cells. A normal liver has only 5% fat. A normal liver weighs about 3 lbs., but a severe case of fatty liver may increase its weight as much as 11! That's nearly 4 times its normal weight!

Mild Steatosis is temporary and asymptomatic. Mild fatty liver is usually reversible by simply changing your diet and alcohol intake. But don't neglect it. Severe or persistent fatty liver may cause liver dysfunction. It may result in recurrent infection, and in the worst case, sudden death from fat emboli in the lungs.

STEATOSIS

The most common cause of fatty liver is chronic alcoholism, but there are other non-alcohol-related causes, such as pregnancy or malnutrition or prolonged total parenteral nutrition (TPN). Prescription and non prescriptioned drug use can result in steatosis.

What can you do if you suspect Steatosis, or Fatty Liver? Go to your doctor and describe your symptoms and tell him about your diet and lifestyle, including drug and alcohol uses. Talk to him about possible immunodeficiency syndrome (HIV). In cases of malnutrition caused steatosis, protein deficiency is usually at the root cause.

If you are diagnosed with any kind of liver damage or dysfunction, show your doctor this scientific, clinical double-blind study of sixty people with alcohol-related diseases (damaged livers), 70% had normalized their liver enzymes after only 30 days' using Bio-Directed Liver Formula, composed of artichoke buds and sarsaparilla extract. The case study was done by administering a therapeutic dose of 3 capsules twice a day and ask if it would be safe for you to do.

Two other double blind studies were published and copywrited in the Townsend Letter for Doctors and Patients, Date: 12/1/2002, by author: Dr. Charles Cochran showing the effectivness of this same product..

What Is A Fatty Liver?

STEATOSIS

Fatty Liver - Symptoms and Treatment

Fatty liver is the infiltration of fat inside your liver cells. That fat takes up space and gradually the liver loses its efficiency, filling your body with fat and toxic waste. Thirty three percent of all Americans suffer from this condition and don't even know about it. Identifying steatosis, its medical name, is important and in this article I will explore how to identify and treat this condition.

What are the symptoms of liver disease?

STEATOSIS

Most symptoms of mild fatty liver are, well, mild. They are not the kind of symptoms that rush you to the doctor's office, but they can signal more dangerous complications.

Mild steatosis causes bad breath, coated tongue, circles under the eyes, headaches or dizziness, and a permanent feeling of being bloated. If you are overweight, fatty liver is more likely if you don't seem to be able to lose weight even when you follow a diet. However, being overweight is not a hallmark of this disease and many people who suffer from this condition are not.

Steatosis is also linked to metabolic syndrome, diabetes type 2, hypertension, and increased cholesterol levels. Note however that having a negative liver test does not guarantee that you don't have mild fatty liver disease.

How to treat fatty liver disease?

Treating this diseases is based on changing your diet and exercising more. As for the diet, eating more vegetables and fruit is essential. You should also reduce animal products and processed food, especially sugar-rich food. Although this may seem standard diet recommendation, studies show that only people who follow these guidelines have success reversing liver disease.

Herbs can also help. Milk thistle, artichoke, dandelion, turmeric, and ginger, among others, all have proved to help reversing liver disease. You can take tons of individual supplements or chose a combined one instead.

Fatty Liver - Symptoms and Treatment

STEATOSIS

Buff Mice Show 'Weight Training' Muscles Reduce Fat And Improve Metabolism

It may not be time to start pumping iron just yet, but, as strange as it sounds, there is evidence in recent mice studies published in the February 6th issue of Cell Metabolism that indicates that the type of muscles that are developed by weight lifting may play a bigger role in regulating body weight than we think.

You're saying, someone has a lab full of bench-pressing mice in some medical school somewhere? Although a great image, you would only be right about the medical school part. It turns out that a team of researchers at the Whitaker Cardiovascular Institute of Boston University Medical Center (BUMC) has been bulking up their test mice using a technique that genetically turns on the type of fast skeletal muscles (type II) that are used for tasks like managing heavy objects.

HEPATIC STEATOSIS

No, really- somewhere in a lab in Boston, there was a team of muscular mice who were bulked up like weight trainers by genetic manipulation. Interestingly, the researchers didn't see what they expected.

The research group had expected their gene tweaking to result in fat but strong mice, more like sumo wrestlers than body builders, since the mice were being fed a fast-food-like, high-fat and high-sucrose, diet causing them to be fat to begin with all the expected problems. What they got instead was a test group that showed positive metabolic improvements when the type II fast muscle genetic switch was turned on and the muscles developed. "Remarkably, type II muscle growth was associated with an overall reduction in body mass, due to a large decrease in fat mass. In addition, blood tests showed that these mice became metabolically normal and their fatty liver disease rapidly resolved," said senior author Kenneth Walsh, PhD, a professor of medicine and head of Molecular Cardiology at the Whitaker Cardiovascular Institute at BUSM. The beneficial changes occurred despite the fact that the mice continued to eat the same high-calorie diet and did not display any increase in physical activity. "This work shows that type II muscle just doesn't allow you to pick up heavy objects, it is also important in controlling whole body metabolism," added Walsh.

Further analysis found that the mice burned fat because of changes in the physiology and gene expression of their fat and liver cells. "Thus, it appears that the increase in type II muscle fiber orchestrates changes in the body through its ability to communicate with these other tissues," he said.

So, here is what all of this may mean to us. We've always known that activities like weight lifting that form fast, type II muscles were good for burning calories that might otherwise convert to fat. What we didn't know was that the existence of this muscle type could have such far-reaching effect in other metabolic areas as well, such as reducing hepatic steatosis (fatty liver). Walsh believes there might well be an extended connection to humans suggesting that "strength training, in addition to the widely prescribed therapy of endurance training, may be of particular benefit to overweight individuals."

The researchers are still busy revealing the interplay between diet, muscle type, and the body's metabolic systems. Their initial research is clearly the beginning of a longer process, and hopefully the further insight can lead to improvements in the treatment of those in need of weight loss and further reduce conditions like diabetes, heart disease, stroke, and hypertension.

Who would have thought that paying attention to a bunch of buff mice would have such far-reaching results.

Remember, too, that this article is for information purposes only. If you have or think you have a health issue, including weight or diet issues, consult your primary care physician for proper diagnoses and treatment.

Personal Fit Weight Loss Guide dx.doi.org/10.2121/Weight-Loss-Guide-020808

Buff Mice Show 'Weight Training' Muscles Reduce Fat And Improve Metabolism

HEPATIC STEATOSIS

Hepatic Encephalopathy

Hepatic encephalopathy is manifested by waxing and waning alterations in mental standing that happen as a consequence of superior decompensated liver disease or portal-to-systemic shunting. Abnormalities range from subtle alterations in psychological status to profound obtundation.

Changes within the rest pattern beginning with hypersomnia and progressing to reversal of the sleep-wake cycle are frequently an early sign. Cognitive changes consist of a full spectrum of psychological abnormalities, ranging from mild confusion, apathy, agitation, euphoria, and restlessness, to marked confusion as well as coma.

HEPATIC

Motor changes range from fine tremor, slowed coordination, and asterixis to decerebrate posturing and flaccidity. Asterixis is really a phenomenon of intermittent myoelectrical silence manifested by many muscle groups and improved by exhaustion. It is greatest demonstrated by asking the individual to flex the wrists with fingers extended ("stop traffic") after which observing a flapping motion from the fingers.

It is thought to become because of reduced sensory input to the brainstem reticular formation, leading to transient lapses in posture. Cerebral edema, which is an important accompanying feature in patients with encephalopathy in acute liver illness, is not seen in cirrhotic patients with encephalopathy.

Common precipitants of encephalopathy are onset of GI bleeding, elevated dietary protein intake, and an increased catabolic rate producing from infection (including spontaneous bacterial peritonitis). Similarly, because of compromised first-pass clearance of ingested medicines, affected individuals are exquisitely delicate to sedatives along with other medicines normally metabolized within the liver.

Other causes consist of electrolyte imbalance as a result of diuretics, vomiting, alcohol ingestion or withdrawal, or procedures such as Ideas. The pathogenesis of hepatic encephalopathy is badly understood. One proposed mechanism postulates that the encephalopathy is caused by poisons in the gut such as ammonia, extracted from metabolic degradation of urea or protein; glutamine, extracted from degradation of ammonia; or mercaptans, derived from degradation of sulfur-containing compounds.

Because of anatomic or functional portal-systemic shunts, these toxins bypass the liver's detoxification processes and produce alterations in psychological status. Elevated amounts of ammonia, glutamine, and mercaptans could be found in the blood vessels and cerebrospinal fluid. However, blood ammonia and spinal fluid glutamine levels correlate badly using the presence and severity of encephalopathy.

Alternatively, there may be impairment from the regular blood-brain barrier, rendering the CNS susceptible to various noxious agents. Elevated levels of other substances, including metabolic products for example short-chain fatty acids and endogenous benzodiazepine-like metabolites, have also been found in the blood vessels. Importantly, some patients show enhancement in encephalopathy when treated with flumazenil, a benzodiazepine receptor antagonist.

A third proposed system postulates a part for GABA, the principal inhibitory neurotransmitter from the brain. GABA is created within the gut, and increased levels are found in the blood vessels of patients with liver failure. A fourth proposal postulates that there's an elevated entry of aromatic amino acids to the CNS, resulting in elevated synthesis of "false" neurotransmitters for example octopamine and decreased synthesis of regular neurotransmitters for example norepinephrine.

Hepatic Encephalopathy

HEPATIC

Hepatic Failure is Cats

Hepatic failure is cats can cause your pet to rapidly develop jaundice where their skin and mucus membranes will turn yellow in color, and it can causes seizures, stupors and if severe, comas. This medical condition is almost impossible to prevent unless as an owner you understand the various drugs as well as the toxins that trigger this very dangerous condition in your cat.

This condition can be fatal to your cat, with two of the largest causes being heat stroke and fungi infections, especially from poisonous mushrooms.

HEPATIC

Hepatic failure in cats is a condition where your pets liver has lost over 75 percent of its functioning capabilities, and as a result, can very easily lead to a complete and massive liver failure called necrosis. Necrosis is the death of your cats liver, and when this occurs, it takes your cats life as well.

This massive amount of lost liver function can be the result of an extremely poor blood flow which in turn causes a decreased delivery of oxygen to your pet, or it can also be the result of a reaction to hepatotoxic drugs or chemicals, as well as infectious agents such as fungi. However, in several cases, it is the result of a heat stroke that has so badly affected your cat that it has interfered with and started to destroy their liver.

However, Hepatic failure can affect a lot more than just the liver; it can also affect your cats gall bladder, nervous system, gastrointestinal tract, and their blood system. But it is the affects on destroying the liver in your cat that are most the most devastating.

Your cats liver performs as many as 1,000 different tasks that can not be done anywhere else in their body and most of them are essential to the life. The liver helps in the production of the essential protein albumin, it stores all of the fat soluble vitamins, and it manufactures a vast majority of your cats digestive enzymes.

However, perhaps it most important functions are in the detoxification of wastes and poisons, the production of blooding clotting agents, and the storage of energy. It is by far and away the most complicated organ in your cats body and can immediately react and fight off several attacks against it simultaneously.

But once it has been attacked by a toxic agent or drug that overpowers all of its protective mechanisms, it can be damaged. Once damaged, especially by Hepatic failure, it deteriorates very rapidly.

Causes:

There are several potential causes of Hepatic failure in cats, but the leading causes are from a reaction to a drug, a biologic toxin, or from heat stroke. There are two forms of heat strokes; one produced obviously from a dangerous overexposure to heat, but the other form is from what is referred to as a post-whole body hyperthermia.

Hepatotoxins are drugs that are extremely harmful to your cats liver. One of the livers major functions is to remove chemicals that are toxic to your cat, but some of them are so over powering that the liver can not clear them out of itself, let alone the rest of the body. The list is very extensive of harmful drugs, but they include any type of an exposure to heavy metals, certain antibiotics, as well as anticonvulsants.

However, the most common cause of hepatotoxins is found in chemical dips and sprays. These are extremely dangerous to cats and you should only use those that are bought through and recommended by your veterinarian. Chemotherapy agents used for cancer treatment are also among the leading causes of Hepatic failure.

These agents act by killing cells that divide rapidly which is one of the main properties of cancer. However, like any type of major treatment, they do have side affects. One of these side affects is that they can also suppress the production of blood cells. Once these cells have been affected, it can slow down the supply of blood as well as oxygen which damages the liver.

The next major cause of this potentially deadly condition is from a mushroom referred to as Amanita phylloides. It is absolutely beautiful in appearance and equally attractive in smell, especially to cats. However, it does have another name that fits it very sinister affect on cats, the Death Cap mushroom. It is found extensively throughout Europe and several parts of the United States.

Once your cat has ingested this mushroom, it is only a matter of time before it starts to destroy their liver.
Heat stokes are the final major cause of Hepatic failure in cats. The normal range of temperature in your cat should be between 100 and 102 degrees. Once your cats temperature reaches 106 from over exposure to heat, it can cause brain damage as well as shutting down liver functions.

Cats that are the most at risk of a heatstroke are usually very old or very young, overweight, or primarily indoor cats. If your cat spends most of their time indoors and than suddenly are exposed to a strenuous amount of exercise on a very hot day, they are prime candidates for a heat stroke.

There is another form of heatstroke that most owners have never heard about, and it is an alternative form of cancer treatment called post-whole body hyperthermia. This is a situation where portions of your cats full body or the portion affected by cancer is heated to 106 degrees. It is done in a clinical setting and monitored very closely and has produced some results with cancer, but it has only very serious side affect; it can cause Hepatic failure.

Summary:

Hepatic failure in cats can be extremely difficult to prevent, but it is not impossible. The symptoms that you can watch for that your cat is developing this deadly liver failure will first be jaundice that is usually followed by a deep depression in your pet.

If your cat shows any signs at all of seizures or a stupor, you will need to seek medical attention as quickly as possible. If they show these symptoms, a coma could be the next symptom as their liver is shutting down and affecting other organs.

Hepatic Failure is Cats

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Hepatic Cancer Causes, Symptoms And Treatment

Hepatic is a term used by medical professionals for issues related to the liver. Therefore, hepatic cancer is another name for liver cancer. Hepatic cancer is one of the most common forms of cancer.

The causes of most cases of hepatic cancer are unknown, but some cases appear to be connected other liver problems such as hepatitis. Interestingly, hepatic cancer often doesn't start in the liver. It spreads to the liver from other diseased organs through a process known as metastasis. But there are four different kinds of primary hepatic cancer, or cancer that starts in the liver itself.

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Hepatocellular carcinoma, which begins with the hepatocytes, the main type of liver cells. This form of hepatic cancer is often referred to by its initials: HCC.

Cholangiocarcinoma is another type. Cholangiocarcinoma originates in tiny bile ducts inside the liver. This type is also known as bile duct cancer.

Hepatoblastoma is a rare form that strikes children less than 4 years of age. Although the diagnosis is often frightening to parents, hepatoblastoma can usually be treated successfully.

The fourth type of primary hepatic cancer is angiosarcoma or hemangiosarcoma, a rare type that starts in the liver's blood vessels.

There are usually no symptoms of hepatic cancer in the early stages of the disease. But in the later stages, the following symptoms are likely to appear.

pain in the upper abdomen, possibly accompanied by swelling in the area tiring easily and a general feeling of weakness lack of desire to eat along with a noticeable weight loss nausea and vomiting

Jaundice may also appear. Jaundice is a condition in which the skin and the whites of the eyes begin to look yellow. This disorder is sometimes called yellow jaundice. The liver is also likely to become enlarged.

To treat hepatic cancer, the doctor must determine the stage the disease has reached. Age and general state of health are also important. Eliminating the cancer completely will be a priority. If this is impractical, the goal then becomes limiting its growth and keeping it from spreading. The doctor will also look for ways to relieve pain and discomfort caused by symptoms.

Treatment options include surgery, with the goal of removing the diseased section of the liver. This is usually done when liver function is still good, the tumor is small, and cancerous cells haven't spread to nearby tissues or organs. This type of operation is known as a partial hepatectomy.

A liver transplant is also an option. In this procedure, the diseased liver is removed and replaced with a healthy liver from a donor.

Another treatment option involves killing cancer cells with extreme cold or heat. This is a relatively recent technological advance.

Alcohol injection is another recent development in the treatment of cancer. This procedure is done by injecting pure alcohol directly into a tumor. This may dry out the cancer cells and eventually kill them.

Targeted drug therapy can be used to limit the tumor's ability to generate blood vessels. This is another promising recent advance and more research is necessary.

Of course, there's also radiation therapy and chemotherapy. Most people are familiar with these forms of treatment. Both of these treatment options, unfortunately, can have serious side effects.

Hepatic cancer strikes nearly 25,000 individuals each year in the United States alone. The disease results in approximately 18,000 deaths. Hepatic cancer is the fifth leading cause of cancer death among men, and ninth among women. As with all other forms of cancer, early detection offers the most hope for long term survival.

Hepatic Cancer Causes, Symptoms And Treatment

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