Triglycerides

Triglycerides are a type of fat found in your blood. When you eat, your body converts any calories it doesn't need to use right away into triglycerides. The triglycerides are stored in your fat cells. Later, hormones release triglycerides for energy between meals. If you regularly eat more calories than you burn, you may have high triglycerides (hypertriglyceridemia).

A simple blood test can reveal whether your triglycerides fall into a healthy range.

• Normal — Less than 150 milligrams per deciliter (mg/dL) (less than 1.7 mmol/L)
• Borderline high — 150 to 199 mg/dL (1.8 to 2.2 mmol/L)
• High — 200 to 499 mg/dL (2.3 mmol/L to 5.6 mmol/L)
• Very high — 500 mg/dL or above (5.7 mmol/L or above)

Your doctor will usually check for high triglycerides as part of a test called a lipid panel or lipid profile, which also checks your cholesterol levels. You'll have to fast for nine to 12 hours before blood can be drawn for an accurate triglyceride measurement.

Triglycerides and cholesterol are separate types of fats (lipids) that circulate in your blood. Triglycerides provide your body with energy, and cholesterol is used to build cells and certain hormones. Because triglycerides and cholesterol can't dissolve in blood, they circulate throughout your body with the help of proteins that transport the lipids, called lipoproteins.

Although it's unclear how, high triglycerides may contribute to hardening of the arteries or thickening of the artery walls (atherosclerosis) — which increases the risk of stroke, heart attack and heart disease.

High triglycerides are often a sign of other conditions that increase the risk of heart disease and stroke as well, including obesity and the metabolic syndrome — a cluster of conditions that includes too much fat around the waist, high blood pressure, high triglycerides, high blood sugar and abnormal cholesterol levels.

Sometimes high triglycerides are a sign of poorly controlled type 2 diabetes, low levels of thyroid hormones (hypothyroidism), liver or kidney disease, or rare genetic conditions that affect how your body converts fat to energy. High triglycerides could also be a side effect of taking medications such as beta blockers, birth control pills, diuretics, steroids or the breast cancer drug tamoxifen.

Description and details on Venlafaxine (Effexor) antidepressant drugs

Venlafaxine (Effexor) is an antidepressant of the serotonin-norepinephrine reuptake inhibitor (SNRI) class first introduced by Wyeth in 1993. It is prescribed for the treatment of clinical depression and anxiety disorders, among other uses. Due to the pronounced side effects and suspicions that venlafaxine may significantly increase the risk of suicide, it is not recommended as a first line treatment of depression. However, it is often effective for depression not responding to SSRIs. Venlafaxine was the sixth most widely-used antidepressant based on the number of retail prescriptions in the US (17.1 million) in 2006.

Venlafaxine is used primarily for the treatment of depression, generalized anxiety disorder, social anxiety disorder, and panic disorder in adults.

Effexor is distributed in pentagon-shaped peach-colored tablets of 25 mg, 37.5 mg, 50 mg, 75 mg, and 100 mg. There is also an extended-release version distributed in capsules of 37.5 mg (gray/peach), 75 mg (peach), and 150 mg (brownish red).

Venlafaxine is a bicyclic antidepressant, and is usually categorized as a serotonin-norepinephrine reuptake inhibitor (SNRI), but it has been referred to as a serotonin-norepinephrine-dopamine reuptake inhibitor. It works by blocking the transporter "reuptake" proteins for key neurotransmitters affecting mood, thereby leaving more active neurotransmitters in the synapse. The neurotransmitters affected are serotonin (5-hydroxytryptamine) and norepinephrine (noradrenaline). Additionally, in high doses it weakly inhibits the reuptake of dopamine, with recent evidence showing that the norepinephrine transporter also transports some dopamine as well, implying that SNRIs may also increase dopamine transmission. This is because SNRIs work by inhibiting reuptake, i.e. preventing the serotonin and norepinephrine transporters from taking their respective neurotransmitters back to their storage vesicles for later use. If the norepinephrine transporter normally recycles some dopamine too, then SNRIs will also enhance dopaminergic transmission. Therefore, the antidepressant effects associated with increasing norepinephrine levels may also be partly or largely due to the concurrent increase in dopamine (particularly in the prefrontal cortex).

Venlafaxine is well absorbed with at least 92% of an oral dose being absorbed into systemic circulation. It is extensively metabolized in the liver via the CYP2D6 isoenzyme to O-desmethylvenlafaxine, which is just as potent a serotonin-norepinephrine reuptake inhibitor as the parent compound, meaning that the differences in metabolism between extensive and poor metabolizers are not clinically important in terms of efficacy. Side effects, however, are reported to be more severe in CYP2D6 poor metabolizers. Steady-state concentrations of venlafaxine and its metabolite are attained in the blood within 3 days. Therapeutic effects are usually achieved within 3 to 4 weeks. No accumulation of venlafaxine has been observed during chronic administration in healthy subjects. The primary route of excretion of venlafaxine and its metabolites is via the kidneys. The half-life of venlafaxine is relatively short, therefore patients are directed to adhere to a strict medication routine, avoiding missing a dose. Even a single missed dose can result in the withdrawal symptoms.

Venlafaxine extended release is chemically the same as normal venlafaxine. The extended release version (sometimes referred to as controlled release) controls the release of the drug into the gastrointestinal tract over a longer period than normal venlafaxine. This results in a lower peak plasma concentration. Studies have shown that the extended release formula has a lower incidence of patients suffering from nausea as a side effect resulting in a lower number of patients stopping their treatment due to nausea.

Generic venlafaxine is available in the United States as of August 2006 and in Canada as of December 2006. A generic form of the extended-release version is available in Canada as of January 2007 and will become available in the United States in 2010. Generic versions of both drug forms are available now in India.

Venlafaxine was shown to be effective for depression in multiple double blind studies. Venlafaxine is similar in efficacy to trazodone and tricyclic antidepressants amitriptiline (Elavil) and imipramine and it was better tolerated than amitriptiline. Venlafaxine appears to have efficacy similar or somewhat better than sertraline (Zoloft) and fluoxetine (Prozac) depending on the criteria and rating scales used. In particular, higher doses of venlafaxine are more effective, and more patients achieved remission or were "very much improved". At the same time the efficacy was similar if the number of patients who achieved "response" or were "improved" was considered. A meta-analysis comparing venlafaxine and combined groups of SSRI or tricyclic antidepressants indicated superiority of venlafaxine.
Based on the same set of criteria, venlafaxine was similar in efficacy to an atypical antidepressant bupropion (Wellbutrin); however, the remission rate was significantly lower for venlafaxine.
Venlafaxine was also marginally inferior in efficacy to a newer SSRI escitalopram (Lexapro) and had twice higher frequency of the side effects, in particular, nausea, ejaculation disorder, somnolence and sweating.

A popular magazine Consumer Reports, which in 2004 had rated venlafaxine as the most effective among six commonly prescribed antidepressants, no longer recommends it. Fluoxetine, citalopram and bupropion have been chosen as Consumer Reports Best Buy drugs in the updated version of their guide, based upon effectiveness, safety, side effects, and cost.

Venlafaxine is not recommended in patients hypersensitive to venlafaxine. It should not be taken by anyone who is allergic to the inactive ingredients, which include gelatin, cellulose, ethylcellulose, iron oxide, titanium dioxide and hypromellose. It should never be used in conjunction with a monoamine oxidase inhibitor (MAOI), due to the potential to develop a potentially deadly condition known as serotonin syndrome. At least 14 days time lag are required between the intake of venlafaxine and MAO inhibitors.

Caution should also be used in those with a seizure disorder. Venlafaxine is not approved for use in children or adolescents. However, Wyeth does provide information on precautions if venlafaxine is prescribed to this age group for the treatment of non-approved conditions. Studies in these age groups have not established its efficacy or safety.

The prescribed dosage of venlafaxine may have to be adjusted for those with liver, thyroid or kidney problems. It is crucial to inform a doctor of any such disorders before taking venlafaxine.

Venlafaxine can increase eye pressure, so those with glaucoma should inform their doctors before taking venlafaxine. More frequent eye checks may be necessary.

The FDA has asked the sponsors of all SNRIs to include the potential risk for persistent pulmonary hypertension (PPHN) in prescribing data as of July 19, 2006. Medications containing Venlafaxine caused a mean heart rate increase of 4 b.p.m in clinical trials, along with a sustained increase in blood pressure in some.

The development of a potentially life-threatening serotonin syndrome may occur with Effexor XR treatment, particularly with concomitant use of serotonergic drugs (including SSRIs, SNRIs, and triptans) and with drugs that impair metabolism of serotonin (including MAOIs). Serotonin syndrome symptoms may include mental status changes (e.g., agitation, hallucinations, coma), autonomic instability (e.g., tachycardia, labile blood pressure, hyperthermia), neuromuscular aberrations (e.g., hyperreflexia, incoordination) and/or gastrointestinal symptoms (e.g., nausea, vomiting, diarrhea).



As with most antidepressants, lack of sexual desire is a common side effect. In trials, delayed ejaculation and delayed orgasm occurred in 8-16% of men. Delayed orgasm occurred in 2-8% of women. Venlafaxine can raise blood pressure at high doses, so it is contraindicated for persons with hypertension.

It has a higher rate of treatment emergent mania than many modern antidepressants, and many people find it to be a more activating medication (one that increases energy or wakefulness) than other antidepressants.[citation needed] Paradoxically, some users find it highly sedating and find that it must be taken in the evening.

There have been false positive phencyclidine (PCP) results caused by Venlafaxine with certain on-site routine urine-based drug tests. Positive on-site results should always be sent to a qualified drug testing laboratory for confirmation before any action is taken against the employee.

The percentage of occurrences for each side effect listed comes from clinical trial data provided by Wyeth Pharmaceuticals Inc. The percentages indicate the percentage of people that experienced the side effect in clinical trials.

* Nausea (21-35%)
* Headache (34%)
* Apathy
* Constipation
* Ongoing Irritable Bowel Syndrome
* Dizziness (11-20%)
* Fatigue
* Insomnia (15-23%)
* Vertigo
* Dry mouth (12-16%)
* Sexual dysfunction (14-34%)
* Sweating (10-14%)
* Orthostatic hypotension (postural drop in blood pressure)
* Vivid dreams (3-7%)
* Impulsive Actions
* Increased blood pressure
* Decreased Appetite (8-20%)
* Electric shock-like sensations also called "Brain zaps"
* Increased anxiety at the start of treatment
* Akathisia (Agitation) (3-4%)
* Memory Loss

A comparison of adverse event rates in a fixed-dose study comparing venlafaxine 75, 225, and 375 mg/day with placebo revealed a dose dependency for some of the more common adverse events associated with venlafaxine use. The rule for including events was to enumerate those that occurred at an incidence of 5% or more for at least one of the venlafaxine groups and for which the incidence was at least twice the placebo incidence for at least one venlafaxine group. Tests for potential dose relationships for these events (Cochran-Armitage Test, with a criterion of exact 2-sided p-value <= 0.05) suggested a dose-dependency for several adverse events in this list, including chills, hypertension, anorexia, nausea, agitation, dizziness, somnolence, tremor, yawning, sweating, and abnormal ejaculation. Most patients overdosing with venlafaxine develop only mild symptoms. However, severe toxicity is reported with the most common symptoms being CNS depression, serotonin toxicity, seizure, or cardiac conduction abnormalities. Venlafaxine's toxicity appears to be higher than other SSRIs, with a fatal toxic dose closer to that of the tricyclic antidepressants than the SSRIs. Doses of 900 mg or more are likely to cause moderate toxicity. Deaths have been reported following very large doses.

There is no specific antidote for venlafaxine and management is generally supportive, providing treatment for the immediate symptoms. Administration of activated charcoal can prevent absorption of the drug. Monitoring of cardiac rhythm and vital signs is indicated. Seizures are managed with benzodiazepines or other anti-convulsants. Forced diuresis, hemodialysis, exchange transfusion, or hemoperfusion are unlikely to be of benefit in hastening the removal of venlafaxine, due to the drug's high volume of distribution.

Depression After a Heart Attack

The increased risk of death associated with depression after a heart attack persists for at least five years, a study finds.

"We've known for a number of years that depression increases the risk of mortality as well as morbidity [illness] after a heart attack for at least three to six months," said study author Robert M. Carney, a professor of psychiatry at Washington University School of Medicine in St. Louis. "We assumed that we would find a decline in risk, but that was not what we found. The risk remained worse after five years."

Carney and his colleagues followed more than 750 people after their heart attacks, according to their report in the current online issue of the Journal of Affective Disorders. Using diagnostic interviews rather than the self-reporting common in most such studies, the researchers determined that 163 had major depression, and 195 had minor depression. Over the five-year study, the death rate was 87 percent higher for those with major depression and 76 percent higher for those with any form of depression.

In real numbers, 62 people diagnosed with depression died during the study, while 44 non-depressed heart attack patients died.

Why depression should increase the risk of dying is a mystery, Carney said. "We think that because depression is a chronic and recurrent problem, the factors causing that risk recur over time," he said. "But we don't know the mechanism."

The researchers have started a trial to determine whether the omega-3 fatty acids that are found in fish oil can reduce that risk. Heart patients are being given an antidepressant drug and a special formulation of omega-3 fatty acids, comparing them with a similar group that gets only an antidepressant.

"A number of studies over the years have found an inverse relationship between the amount of fish people eat and depression," Carney said. "The advantage of giving them in heart disease is that they have an effect on the cardiovascular system as well."

The major finding of the study and the use of omega-3 fatty acids are already in the mainstream of research on depression and heart disease, said Dr. Alexander H. Glassman, a professor of psychiatry at Columbia University Medical Center in New York City.

"There is a torrent of information that depression in relation to vascular disease worsens the outcome," Glassman said. "If you look at post-stroke patients, you find the same data. If you look at heart failure, depression has a similar effect on mortality."

The value of the study is that it had the longest follow-up of any trial using diagnostic interviews, which are regarded as more accurate than self-reporting, Glassman said. "It makes the evidence firmer and extends the evidence," he explained.

The use of omega-3 fatty acids is "a hot issue," being tried in cardiac and non-cardiac cases, Glassman said. "It is a logical thing to do," he added.

The study and the omega-3 trial will still leave some major issues about depression and heart disease open, Glassman said.

"The two key questions that remain are: Does treating depression make the outcome better? And what is it about depression that is causing the problem in the first place?" he said.

For hepatitis C sufferers

Adelaide scientists will lead a $2 million five-year project to develop new vaccines and explore better treatment options for hepatitis C sufferers.

University of Adelaide virologists Dr Michael Beard and Dr Karla Helbig will work with colleagues from the University of NSW to develop new strategies to treat and prevent hepatitis C, which infects more than 170 million people around the world.

The scientists, who are also attached to the Institute of Medical and Veterinary Science and Royal Adelaide Hospital, hope to identify antiviral proteins that can be used in the fight against hepatitis C.

Currently there is no effective vaccine and the existing treatment is expensive and often causes severe side effects. The success rate also varies between 50-80% so many sufferers cannot be helped by current approaches.

The funds, awarded by the National Health and Medical Research Council (NHMRC), are part of a larger $17.7 million joint program grant, tackling both HIV/AIDS and hepatitis C and involving nine scientists from across Australia.
This latest grant is an adjunct to three NHMRC project grants awarded to Dr Beard’s team in the past two years specifically for hepatitis C research.

In 2006 the virologist was awarded more than $894,000 to investigate the link between alcohol and hepatitis C, and the basic mechanisms of liver disease.

“In Australia, more than 264,000 people have been infected with the hepatitis C virus and there are approximately 10,000 new infections per year. A proportion of these are intravenous drug users, with alcohol playing a significant role in disease progression,” Dr Beard said.

He said vaccines had been trialled for HIV, but with little success. “There is antiretroviral treatment but this does not eradicate HIV, it only keeps it under control for a period of time. It is also very expensive and therefore not accessible on a global scale”.

Take Action to Prevent Cancer

As part of National Cancer Prevention Month in February, experts at The University of Texas M. D. Anderson Cancer Center encourage participation in cancer prevention studies to help researchers learn more about the causes of cancer and how to avoid the disease.
Cancer prevention studies are designed for people who have not been diagnosed with cancer or for those who have successfully completed cancer treatment. Today’s standard cancer prevention recommendations are the results of research data from past prevention studies.

Hawk predicts prevention studies will begin to focus more on populations with a high risk of developing cancer, such as persons with a family history of cancer (mother, father, brother or sister) as well as those with a personal history of cancer.

High-risk populations are likely to benefit most from taking medications, adopting healthy lifestyle behaviors that may reduce risk or both. Studies involving high-risk populations also can lay the groundwork for follow-up studies addressing those at lower risk of developing cancer.
A large percentage of the nation’s cancer prevention trials are taking place at M. D. Anderson. Hawk’s extensive involvement in cancer prevention studies gives him insight into ways to expand and enhance M. D. Anderson’s role in the field.

People who participate in prevention studies at M. D. Anderson may take medicines, vitamins or other supplements, or obtain screening exams that may lower their risks of developing cancer. Some prevention studies may collect demographic, lifestyle, medical and family history information to learn more about the causes of cancer and how to prevent them.

The Division of Cancer Prevention and Population Sciences is one the largest cancer prevention programs in the nation. It was established to learn more about the causes of cancer, encourage people to adopt health lifestyle habits that may prevent cancer and develop effective medication that lowers cancer risk.

Alzheimer's or depression

Early Alzheimer's and depression share many symptoms, so it can be difficult even for doctors to distinguish between the two disorders. And many people with Alzheimer's up to 40 percent, in fact also are depressed.

One important difference between Alzheimer's and depression is in the effectiveness of treatment. While Alzheimer's drugs can only slow the progression of cognitive decline, medications to treat depression can improve a person's quality of life dramatically.

People who have both Alzheimer's and depression may find it easier to cope with the changes caused by Alzheimer's when they feel less depressed.

Similar symptoms

Some of the symptoms common to both Alzheimer's and depression include:

• Loss of interest in once-enjoyable activities and hobbies


• Social withdrawal


• Memory problems


• Sleeping too much or too little


• Impaired concentration

With so much overlap in symptoms, it can be hard to distinguish between the two disorders, especially since they so often occur together. A thorough physical exam and psychological evaluation can be helpful in determining a diagnosis. However, many people with moderate to severe Alzheimer's disease lack both the insight and the vocabulary to express how they feel.

Signposts for depression

To detect depression in people who have Alzheimer's disease, doctors must rely more heavily on nonverbal cues and caregiver reports than on self-reported symptoms. If a person with Alzheimer's displays one of the first two symptoms in this list, along with at least two of the others, he or she may be depressed.

• Significantly depressed mood sad, hopeless, discouraged, tearful


• Reduced pleasure in or response to social contacts and usual activities


• Social isolation or withdrawal


• Eating too much or too little


• Sleeping too much or too little


• Agitation or lethargy


• Irritability


• Fatigue or loss of energy


• Feelings of worthlessness, hopelessness or inappropriate guilt


• Recurrent thoughts of death or suicide

Alzheimer's disease with depression is different

Men and women who have Alzheimer's disease become depressed with equal frequency. This differs from the general population, in which women are more likely to experience depression than are men. People with Alzheimer's may also experience depression differently from people without Alzheimer's. For example, individuals diagnosed with Alzheimer's disease:

• May have symptoms of depression that are less severe


• May experience episodes of depression that don't last as long or recur as often


• Talk of suicide and attempt suicide less often

Treatment options

Support groups and professional counseling may help persons with depression in the early stages of Alzheimer's disease, before their communication skills deteriorate. Regular physical exercise, particularly in the morning, also seems to ease the symptoms of depression. But the most common treatment is prescription antidepressants.

Selective serotonin reuptake inhibitors (SSRIs)

SSRIs are the first line antidepressants used for people who have depression and Alzheimer's because of the low risk of side effects and drug interactions. SSRIs include citalopram (Celexa), sertraline (Zoloft), paroxetine (Paxil) and fluoxetine (Prozac).

Serotonin and norepinephrine reuptake inhibitors (SNRIs)

SNRIs are often tried next if the SSRIs don't work. However, SNRIs which include venlafaxine (Effexor), mirtazapine (Remeron) and bupropion (Wellbutrin) have more side effects, such as sedation, dry mouth and constipation.

Tricyclic antidepressants

These older antidepressants, such as nortriptyline (Pamelor) and desipramine (Norpramin), are no longer used as first-choice treatments because they can cause significant side effects, including increased confusion. However, they may be prescribed if other medications aren't effective.

When medications don't help

Some people with depression and dementia may not respond to medication. In many of these cases, electroconvulsive therapy can help relieve symptoms of severe depression. The procedure delivers electricity to the brain for a few seconds, to trigger a seizure. It's performed under general anesthesia in a hospital.

Electroconvulsive therapy is used more frequently for older people than for younger people perhaps because older people may have more side effects from antidepressants or have more severe complications from severe depression.

What's the link?

Scientists aren't sure of the exact relationship between Alzheimer's disease and depression. Some research has found that the biological changes caused by Alzheimer's may intensify genetic predisposition to depression. Other studies suggest that the presence of depression may increase your chances of developing Alzheimer's disease.

It's clear that depression has a strong effect on quality of life for people with Alzheimer's disease. Depression can lead to:

• Weight loss


• Physical fragility


• Earlier placement in nursing homes


• Greater disability involving daily living skills


• Physical aggression toward caregivers

Finding the proper diagnosis and getting appropriate treatment can help make life easier and more enjoyable for both the person with Alzheimer's and his or her caregivers.

Factors of a psychotic disorder

It may be possible to predict who will develop psychotic illnesses, such as schizophrenia and bipolar disorder, very early in the disease process.
The study found five factors that were often present prior to the diagnosis of a psychotic disorder in children who were already at high risk of such disorders.

These included a family history of schizophrenia with recent deterioration in functioning; higher levels of unusual thoughts; higher levels of suspicion or paranoia; greater social impairment; and a history of substance abuse.

When two or three of these factors were present, the odds of psychotic illness jumped. Two factors increased the likelihood of psychotic illness to 68 percent, and three factors combined raised the risk to 80 percent.

Not everybody who has early symptoms goes on to develop psychosis. But if we identify the group in which 80 percent will develop psychosis, the efforts of intervention would be best applied to those at highest risk.

Symptoms of psychosis are seen in numerous mental health disorders, such as bipolar disorder, schizophrenia, depression, and with some forms of alcohol or drug abuse.

The two most common psychotic symptoms are delusions and hallucinations, according to AACAP. Delusions are false but firmly held beliefs. Hallucinations are false sensory perceptions, such as hearing voices when no one is talking.

And Major depressive disorder

Major depressive disorder or MDD is the most common major mental illness, afflicting almost one in five individuals. More than 75% of people who recover from an episode of MDD will have at least one recurrence, with the majority having multiple recurrences. Major depressive disorder is the leading cause of disability of all medical illnesses, with substantial functional impairment, morbidity, and mortality. Few studies have assessed the efficacy of antidepressant medications beyond 1 year of maintenance treatment for the prevention of recurrent depression.

The investigators randomly assigned patients with recurrent depression to receive treatment with either venlafaxine extended-release (ER) or fluoxetine, an antidepressant already established as efficacious as a comparative medication. Although the PREVENT study followed patients for over two years, this article reports only on the acute and continuation phases, which were 10 weeks and 6 months long respectively.

The authors found that nearly 80% of the patients achieved at least an adequate therapeutic response to acute phase treatment with venlafaxine ER or fluoxetine, and almost none of the responders who continued on treatment for 6 months relapsed.

In addition to the high response rates by the patients in this study, the rates of adverse events (side effects) were similar among the two treatment groups

Pediatric metabolic syndrome predicts CVD in later life

The cardiovascular risk factors that contribute to the metabolic syndrome are associated with future cardiovascular disease (CVD) in adults; however, it is not known whether the presence of these risk factors in childhood predicts CVD in adult life.
Children aged 5–19 years were evaluated for lipid characteristics, BMI, blood chemistry values, blood pressure and family history of CVD in the initial LRC study period. The PFS established the CVD status of 771 participants from the initial study.
The mean age of participants in the PFS was 38.4 years. Of the 31 patients who had pediatric metabolic syndrome in the LRC study, six (19.4%) experienced CVD during the intervening period compared with an incidence of 1.5% for participants who did not have metabolic syndrome in childhood. Multivariate analysis showed that pediatric metabolic syndrome (odds ratio [OR] 14.7, P <0.0001) and age at follow-up (OR 1.2, P = 0.03) were significant predictors of CVD, whereas sex, race and family history of cardiovascular disease were not.
Pediatric metabolic syndrome predicts CVD during the subsequent 25 years of life. This results highlight the importance of preventative interventions in childhood and early adult life, particularly with regards to weight and BMI control.

Angelman syndrome

Angelman syndrome is a genetic disorder that causes developmental disabilities and neurological problems, such as difficulty speaking, balancing and walking and, in some cases, seizures. Frequent smiles and outbursts of laughter are common for people with Angelman syndrome, and many have happy, excitable personalities.
If your child has Angelman syndrome, you may not see any signs at birth. Angelman syndrome usually isn't detected until parents begin to notice developmental delays when a baby is about 9 to 12 months old. Seizures often begin when a child is between 2 and 3 years old.
There's no cure for Angelman syndrome. Treatment for Angelman syndrome often includes medication and other therapies.

Characteristic Angelman syndrome symptoms include:

* Developmental delays, such as lack of crawling or babbling at 9 to 12 months, and mental retardation
* Lack of or minimal speech
* Inability to walk, move or balance well (ataxia)
* Trembling movement of arms and legs
* Frequent smiling and laughter
* Happy, excitable personality

People who have Angelman syndrome may also have other signs and symptoms, including:

* Seizures, usually beginning between 2 and 3 years of age
* Stiff or jerky movements
* Small head size (microcephaly)
* Crossing of the eyes (strabismus)
* Flatness in the back of the head
* Tongue thrusting
* Walking with arms up in the air
* A lower jaw that juts out
* Light pigmentation in hair, skin and eyes (hypopigmentation)

Angelman syndrome is a genetic disorder. It's most often caused by problems with a gene located on chromosome 15 called the UBE3A gene.

Genes are segments of DNA that provide the blueprints for all of your characteristics. You receive your genes, which occur in pairs, from your parents. One copy comes from your mother (maternal copy) and the other copy comes from your father (paternal copy).

A missing or defective gene
Both genes in a pair usually are active. This means that information from both the maternal copy and the paternal copy of each gene pair are used by your cells. But in a small number of genes, only one copy of a gene pair is active. The activity of each gene copy depends on whether it was passed from your mother or from your father. This parent-specific gene activity is called imprinting. In these genes, when the copy that is usually active is missing or defective, it causes problems in the functions and characteristics controlled by that gene.
Normally, only the maternal copy of the UBE3A gene is active in the brain. Most cases of Angelman syndrome occur when part of the maternal chromosome 15, which contains this gene, is missing or damaged. In a small number of cases, Angelman syndrome is caused when two paternal copies of the gene are inherited, instead of one paternal and one maternal copy (paternal uniparental disomy).

Angelman syndrome is rare. In most cases, researchers don't know what causes the genetic changes that result in Angelman syndrome. Most people with Angelman syndrome don't have a family history of the disease. In a small percentage of cases, however, Angelman syndrome may be inherited from a parent, so a family history of the disease may increase a baby's risk of developing Angelman syndrome.
Most babies with Angelman syndrome don't show signs or symptoms of the disorder when they are born. The first signs of Angelman syndrome are usually developmental delays, such as lack of crawling or babbling, between 9 and 12 months.

If your child seems to have developmental delays, or if your child has other signs or symptoms of Angelman syndrome, make an appointment to talk with your child's doctor.
Your child's doctor may suspect Angelman syndrome if your child has developmental delays and other signs and symptoms of the disorder, such as problems with movement and balance, small head size and flatness in the back of the head, along with frequent laughter.

Confirming a diagnosis of Angelman syndrome requires taking a blood sample from your child for genetic studies. A combination of genetic tests can reveal the chromosome defects related to Angelman syndrome. These tests may include:

• Chromosome analysis (karyotyping). In this test, the size, shape and number of chromosomes in a cell sample are examined.
• Fluorescent in situ hybridization (FISH). This test can show if any chromosomes are missing.
• 
  DNA methylation test. This test reveals a gene's imprinting pattern. Normal results show both a paternal and maternal DNA pattern. A person with Angelman syndrome shows only a paternal pattern in the affected gene.

Because there isn't a way to repair chromosome defects, there's no cure for Angelman syndrome. Treatment focuses on managing the medical and developmental problems that the chromosome defects cause.
A team of health care professionals will likely work with you to manage your child's condition. Depending on your child's signs and symptoms, treatment for Angelman syndrome may involve the following:
Anti-seizure medication. Medication may be necessary to control seizures caused by Angelman syndrome.
Physical therapy. Children with Angelman syndrome may learn to walk better and overcome other movement problems with the help of physical therapy.
Communication therapy. Although people with Angelman syndrome usually don't develop verbal language beyond simple sentences, communication therapy can be helpful. Nonverbal language skills may be developed through sign language and picture communication.
Behavioral therapy. Behavioral therapy can help children with Angelman syndrome overcome hyperactivity and a short attention span, which can aid in developmental progress. Although the level of development people with Angelman syndrome can achieve varies widely, many are outgoing and are able to build relationships with friends and family.

In rare cases, Angelman syndrome may be passed from affected parent to child through defective genes. If you're concerned about a family history of Angelman syndrome, or if you already have a child with Angelman syndrome, you may wish to talk to your doctor or a genetic counselor for help planning future pregnancies.

Smokers Who Quit Have Less Money Stress

A team of Australian researchers found that smoking could lead to living with financial stress, such as difficulty paying household bills and going without meals because of a shortage of money.
Was asked 5,699 “ever smokers” (quitters, ex-smokers or current smokers) about their smoking habits and whether in the past six months they had a problem paying a bill because of shortage of money.

Of the ever smokers, 55.1 percent were quitters. The researchers found that a smoker who quits could expect to have about a 25 percent lower chance of financial stress. While 71 percent of current smokers said they had experienced financial stress, only 49.6 percent of quitters did.
The study does not report the cost of cigarettes or how many packs per year the smokers consumed, previous research has shown that heavier smokers have more financial stress than those who smoke less, which might also be due to the cost of health conditions linked to smoking.

How does venlafaxine differ from other antidepressants

Venlafaxine seems to have the relative freedom from side-effects associated with the SSRIs [fluoxetine (Prozac), sertraline (Zoloft), paroxetine (Paxil), and fluvoxamine (Luvox)] and the impact on both serotonin and norepinephrine associated with the tricyclic antidepressants [amitriptyline (Elavil), imipramine (Tofranil), etc.]. It is hypothesized that the action of the venlafaxine molecule upon both serotonin and norepinephrine will cause venlafaxine to be a successful antidepressant for some people who have not responded to treatment with SSRIs.

Pharmacokinetics:

Suction and distribution after the single method Of efektina of depot Cmax of venlafaxine and its active metabolite are achieved during 5.5 and 9 h respectively. The method of preparation with the food does not have an effect on absorption and biotransformation of venlafaxine. Binding with the proteins of the plasma of venlafaxine and its metabolite composes 27% and 30% respectively. Metabolism and removal Of venlafaxine under action P450 CYP2D6 to a considerable degree biotransform in the liver with the formation of active metabolite O -desmetilvenlafaxine . Venlafaxine and its metabolites are derived predominantly by kidneys. Approximately 87% of dose for 48 h are derived with the urine, 5% - in the unchanged form, 29% - in the form unconjugated O -desmetilvenlafaxine , 26% - in the form conjugated O -desmetilvenlafaxine and 27% - in the form of other metabolites. Pharmacokinetics in the special clinical cases age and sex of patients do not have an effect on the pharmacokinetic parameters of preparation. In patients with the disturbances of the function of the liver (c by cirrhosis in the stage of compensation) was noted reduction in the metabolism of venlafaxine and removal of its active metabolite, which led to an increase in their concentration in the plasma of the blood. In patients with the moderately expressed or heavy disturbances of the function of kidneys was noted reduction in the clearance and increase T1/2 in venlafaxine and O -desmetilvenlafaxine. Reduction in the general clearance was more expressed in patients with the clearance of endogenous creatinine below 30 ml/min.

Side-line actions. side effects

Side-line actions: Tablets with the immediate liberation the side effects, connected with the curtailment of treatment by 19% of patients (537/2897) with the depression, obtained Venlafaxine, with conducting of studies of phase 2 and phase 3 ended treatment in connection with the appearance of side effects. Most general effects (?1%), which were been the reason for the curtailment of therapy and those considering as the caused by method medicines (i.e. observed approximately 2 or more times more frequent with the method of Venlafaxine in the comparison with the placebo), they were following (in the brackets it was indicated percentage in the group of placebo): sleepiness 3% (1%), insomnia 3% (1%), vertigo 3% (1%), headache 3% (1%), anxiety 2% (1%), nervousness 2% (1%), asthenia 2% (1%); dryness in mouth 2% (1%), nausea 6% (1%), the disturbance of ejaculation 3% (1%), sweating 2% (1%). The side effects, which were being observed in the controlled tests by the most frequent side effects, connected with the method of venlafaksina of the hydrochloride (frequency of occurrence 5% and more), not equivalent in the frequency of occurrence in the group of placebo, i.e., with the method venlafaksina of hydrochloride were observed at least 2 times more frequently than in the group of the placebo (see Table 1), there were asthenia, sweating, nausea, bolt, anorexia, vomiting, sleepiness, dryness in the mouth, vertigo, nervousness, anxiety, tremor, carelessness of sight, disturbance of eyakulyatsii/orgazma and impotence in men. The side effects, which were being observed with a frequency of?1% in patients, treated of Venlafaxine by hydrochloride (tabl.y). Table 1 presents the side effects, noted in patients, who obtained Venlafaxine hydrochloride in the form of tablets at the doses of 75-375 mg/day with conducting of short term tests (4 and 8- weekly). These effects were observed with a frequency of?1% and exceeded in the frequency of placebo. Table shows the percentage of the patients in each group, in whom was noted at least one case of separate side effect within the period of treatment.

Description, contra-evidence, the application

Latin name: Venlafaxine The pharmacological groups: Acting Substance (MNN) Of venlafaksin * (Venlafaxine *)
According to the data Physicians Desk Reference (2004), venlafaksina hydrochloride in the form of tablets with the immediate liberation is shown for treating the depression. Venlafaxina hydrochloride in the form of capsules with the modified liberation is shown for treating of depression, generalizovannogo alarming disorder and social phobias. Contra-evidence: Hypersensitivity, the simultaneous method of the inhibitors OF MAO (see the "precautionary measures"). Limitations to the application: Recently transferred myocardial infarction and unstable , change AD, the increased intraocular pressure and glaucoma, maniacal states in anamnesis, the initially lowered mass of body, insufficiency, age of up to 18 years (safety and the effectiveness of application they are not established).