Treatment for Diabetes Nerve Pain

Nerve pain caused by diabetes, called diabetic peripheral neuropathy, can be severe, constant, and difficult to treat. It may start as a tingling sensation, followed by numbness and pain. But there are two key points that everyone with diabetes and peripheral neuropathy should know:

• Controlling your blood sugar levels can help prevent worsening nerve pain and improve your overall health at the same time.
• Medications can help relieve nerve pain, make you more comfortable, and improve your quality of life.

If you have diabetes and peripheral neuropathy, talk to your doctor about ways to better control your blood sugar. You may need to take insulin for better control.

Once you are doing all that you can to keep blood sugar levels under control - including diet, meal planning, exercise, and medication - you should assess with your doctor which pain medication is best to relieve your remaining symptoms.

Fortunately, medications can help relieve nerve pain from peripheral neuropathy so you can function at near-normal levels. You have many pain relief drugs from which to choose. But you may need to try several different types of pain relievers before you find the one that helps you.

Over-the-Counter Pain Relievers for Diabetes Nerve Pain

Some people find relief for mild diabetes nerve pain right on their drug store shelves. Common pain relievers and some topical creams may help, depending on the severity of pain.

As a first line of treatment, these can be very helpful.

Anyone with diabetes should talk to their doctor before taking any medication. Even over-the-counter medications can interact with other drugs or cause severe side effects in people with diabetes.

Here are some over-the-counter pain relief options to consider:

NSAIDs (nonsteroidal anti-inflammatory drugs). These medicines reduce inflammation and relieve pain. NSAIDs available without a prescription include aspirin, ibuprofen (Advil, Motrin), and naproxen (Aleve).

But NSAIDs can cause harmful side effects such as stomach irritation and bleeding in some people if taken for weeks or months. When taken long-term they can also lead to kidney and liver damage, which may be more likely in people with diabetes.

However, In many cases, especially with younger people who are relatively healthy, the risk is quite low.

Acetaminophen. Acetaminophen and other over-the-counter drugs containing acetaminophen relieve diabetes nerve pain without reducing inflammation. These medications do not cause the stomach irritation that NSAIDs do. However, taking more acetaminophen than recommended can lead to liver damage. It is important to read labels and check with your pharmacist.

Capsaicin. Found naturally in chili peppers, capsaicin is found in drug stores under various brand names, including Capzasin-P and Zostrix. "Capsaicin has been shown to relieve pain, but there is some concern. 

Capsaicin is thought to ease pain by reducing a chemical called substance P, which is involved in transmitting pain signals through the nerves. On a short-term basis, it is an effective approach. These same nerves play a big role in wound healing. Drs. are concerned that capsaicin could prevent wound healing, which is already a big problem for diabetes patients.

Lidocaine. Lidocaine is an anesthetic that numbs the area it has been applied to. It is available in gels and creams, both over the counter and by prescription. Some product names include Topicaine and Xylocaine.

Other topical creams. Salicylate is a chemical similar to aspirin, and is found in pain-relieving creams like Aspercreme and Bengay. Cortisone creams contain corticosteroids, which are potent anti-inflammatory drugs that can help relieve pain. Both are available at drug stores, but there is no clear evidence that they help relieve nerve pain from peripheral neuropathy.

Prescription Drugs for Diabetes Nerve Pain

Many people need to turn to prescription medication to find relief for diabetes nerve pain. Your choices include:

NSAIDs. Although some nonsteroidal anti-inflammatory drugs are available over the counter, your doctor may suggest higher doses, or different NSAIDs, that require a prescription. There are many prescription NSAIDs to choose from including, Celebrex, Lodine, and Relafen. People with diabetes are more at risk of kidney damage that can occur with NSAIDs. In addition, people with diabetes are at high risk of heart disease, and prescription NSAIDs may raise the risk of heart problems.

Antidepressants. Although antidepressants were developed for depression, these drugs have also become important in relieving chronic pain - whether the person is depressed or not. Doctors have been prescribing antidepressants for many years for pain control, says Gibbons. Antidepressants used to treat pain include-

Tricyclic antidepressants (TCAs) primarily affect the levels of the brain chemicals norepinephrine and serotonin. These are the most commonly used, the best studied, and the most effective of the antidepressants used for pain.

Of the TCAs, Elavil has been a very good option for pain, yet it has troublesome side effects. "It tends to have more side effects -- drowsiness, weight gain, dry mouth, dry eyes. For people with peripheral neuropathy, there can be additional side effects. Many patients develop blood pressure and heart rate problems and get dizziness when taking Elavil.

A newer drug in this class, Pamelor, is "quite effective, with fewer side effects, so it is better tolerated. "Norpramin is also good and has the least side effects of all."

Selective serotonin reuptake inhibitors (SSRIs) are a newer form of antidepressant. These drugs work by altering the amount of the brain chemical serotonin. "These are very effective for depression, but less effective for pain. They've been shown effective in some studies, but they're clearly not as effective as TCAs for pain.

Serotonin and norepinephrine reuptake inhibitors (SNRIs) are another newer form of antidepressant medicine. They treat depression by increasing availability of the brain chemicals serotonin and norepinephrine.

Antiseizure drugs. Drugs that prevent epileptic seizures can also relieve certain pain conditions, including neuropathy. The majority of pain patients can be treated with any of these. The drugs work by controlling the abnormal firing of nerve cells - in the brain and in other parts of the body, like legs and arms,the Dr. explains.

Neurontin is the antiseizure drug most commonly used for nerve pain from peripheral neuropathy. It's quite effective in treatment of painful neuropathy. It does tend to cause sedation or dizziness at higher doses. But if the dosage is increased slowly, it is quite well tolerated.

Lyrica is a seizure medication that is FDA-approved for painful neuropathy. "It is designed as the next generation of Neurontin. The most common side effects are dizziness and sleepiness. 

Opioid medicines. When pain is very severe, patients want immediate relief. That's when they may need to see a pain specialist. Sometimes people need strong painkillers called Ultram or Ultracet, possibly in combination with Neurontin.

Both Ultram and Ultracet are FDA-approved painkillers that contain tramadol, a weak opioid (morphine-like) substance. The drug also weakly affects the brain chemicals serotonin and norepinephrine, similar to antidepressants, which reduces the perception of pain.

Often we use tramadol as a back-up for what we call 'breakthrough pain' - pain that suddenly, for no apparent reason, is worse at times. Tramadol is a good replacement for over-the-counter stuff at those times.

Neuropathy specialists shy away from strong narcotic opioid medications. Narcotics can cause severe constipation, and there is the potential for addiction. There's also a stigma about using a narcotic drug. Depending on the type of work a person does, it could be a problem.

More Treatment Options for Diabetes Nerve Pain

For severe, intractable diabetes nerve pain, injections of local anaesthetics such as lidocaine - or patches containing lidocaine - are used to numb the painful area.

Doctors can also:

Surgically destroy nerves or relieve a nerve compression that causes pain.

Implant a device that relieves pain.

Perform electrical nerve stimulation which may relieve pain. In this treatment, small amounts of electricity are used to block pain signals as they pass through the skin. "It's debatable whether this is effective.

Other useful aides to improve quality of life and function include:

Hand or foot braces can compensate for muscle weakness or help relieve nerve compression.

Orthopaedic shoes can improve gait (walking) problems, which will prevent foot injuries. 

WHY FATS ARE IMPORTANT FOR US

Researchers  are studying fats, or lipids, to learn more about normal and abnormal biology in the body.

When you have your cholesterol checked, the doctor typically gives you levels of three fats found in the blood: LDL, HDL and triglycerides.

In human plasma alone, researchers have identified some 600 different types relevant to our health.Many lipids are associated with diseases--diabetes, stroke, cancer, arthritis, Alzheimer's disease, to name a few. But our bodies also need a certain amount of fat to function, and we can't make it from scratch.

Triglycerides, cholesterol and other essential fatty acids--the scientific term for fats the body can't make on its own--store energy, insulate us and protect our vital organs.

They act as messengers, helping proteins do their jobs. They also start chemical reactions involved in growth, immune function, reproduction and other aspects of basic metabolism.

The cycle of making, breaking, storing and mobilizing fats is at the core of how humans and all animals regulate their energy. An imbalance in any step can result in disease, including heart disease and diabetes. For instance, having too many triglycerides in our bloodstream raises our risk of clogged arteries, which can lead to heart attack and stroke.

Fats help the body stockpile certain nutrients as well. The so-called "fat-soluble" vitamins--A, D, E and K--are stored in the liver and in fatty tissues.

Using a quantitative and systematic approach to study lipids, researchers have classified lipids into eight main categories.

Cholesterol belongs to the "sterol" group, and triglycerides are "glycerolipids." Another category, "phospholipids," includes the hundreds of lipids that constitute the cell membrane and allow cells to send and receive signals.

The main type of fat we consume, triglycerides are especially suited for energy storage because they pack more than twice as much energy as carbohydrates or proteins. Once triglycerides have been broken down during digestion, they are shipped out to cells through the bloodstream. Some of the fat gets used for energy right away. The rest is stored inside cells in blobs called lipid droplets.

When we need extra energy--for instance, when we exercise--our bodies use enzymes called lipases to break down the stored triglycerides. The cell's power plants, mitochondria, can then create more of the body's main energy source: adenosine triphosphate, or ATP.

Recent research also has helped explain the workings of a lipid called an omega-3 fatty acid—the active ingredient in cod liver oil, which has been touted for decades as a treatment for eczema, arthritis and heart disease.

Two types of these lipids blocked the activity of a protein called COX, which assists in converting an omega-6 fatty acid into pain-signalling prostaglandin molecules. These molecules are involved in inflammation, which is a common element of many diseases, so omega-3 fatty acids could have tremendous therapeutic potential.

Low-dose aspirin helps slow breast cancer growth

A new study by scientists including one of an Indian origin has found that aspirin slowed the growth of breast cancer cell lines in the lab and significantly reduced the growth of tumours in mice. 

The age-old headache remedy also exhibits the ability to prevent tumour cells from spreading. 

Results of the study by researchers  suggested that regular use of low-dose aspirin might prevent the progression of breast cancer in humans. 

Anecdotal evidence indicated that breast cancer was less likely to return in women who took aspirin to lower their risk of heart attack or stroke. But the science behind this relationship is not well understood. 

The VA study found that aspirin might interfere with cancer cells` ability to find an aggressive, more primordial state. In the mouse model the researchers used, cancer cells treated with aspirin formed no or only partial stem cells, which are believed to fuel the growth and spread of tumours. 

Senior author said that first-line chemotherapy treatments do not destroy stem cells. 

Eventually, the tumour will grow again. If you don`t target the stemness, it is known you will not get any effect. It will relapse.

In lab tests, aspirin blocked the proliferation of two different breast cancer lines. One of the lines tested is often called triple-negative breast cancer, a less common but more difficult treat form of the disease. We are mainly interested in triple negative breast cancer, because the prognosis is very poor, said a researcher.

Triple-negative breast cancers, which will be addressed in a special thematic program at the ASBMB annual meeting, lack receptors for estrogen, progesterone and Her2. Aspirin also may improve the effectiveness of current treatments for women whose breast cancers are hormone-receptor positive. 

In the team`s study, aspirin enhanced the effect of tamoxifen, the usual drug therapy for hormone-receptor positive breast cancer. 

Aspirin is used in the treatment of a number of different conditions because of its ability to attack multiple metabolic pathways is what makes it potentially useful in the fight against cancer.

Aspirin is a medicine with side effects, including gastrointestinal bleeding. Researchers will continue to explore if the positive effects of regular use of the drug outweigh the risks. 

Bipolar Disorder Drugs May 'Tweak' Genes Affecting Brain

Medications taken by people with bipolar disorder may actually be nudging hundreds of genes that direct the brain to behave more normally, according to new research.

The study suggests that anti-psychotic drugs activate a wide range of genes, changing their function. 

"A gene's activity in any given cell will vary depending on what it's exposed to.

It's not often that scientists stumble upon something in research that they totally weren't expecting to see. "It was a major surprise to us that people treated with an antipsychotic [medication] had changes in the gene expression pattern.

The findings could help point the way to new gene-targeted and stem cell therapies, and provide valuable insight into what causes manic-depressive mood swings.

However, a genetics expert not connected to the study was more cautious about drawing implications from its findings.

Bipolar disorder, also known as manic-depressive illness, affects about 5.7 million American adults, or about 2.6 percent of the U.S. population aged 18 and older, according to the U.S. National Institute of Mental Health (NIMH). The brain disorder causes severe and unusual shifts in mood, energy, activity levels, and the ability to carry out routine daily tasks.

The new research, published in a recent issue of the journal Bipolar Disorders, involved examining 26 brains donated to a nonprofit brain bank. Fourteen of the brains were from people who had bipolar disorder. Of those, seven were from people who had been taking one or more antipsychotic medications -- such as clozapine, risperidone and haloperidol -- when they died. Twelve brains were from those with no mental health condition.

In comparing the brains, the scientists observed that the genes of those that had been exposed to anti-psychotics at the time of death or during their lifetime were similar to those from people who did not have bipolar disorder. This suggests that the drugs may normalize or suppress the kinds of brain pathology one would expect in bipolar disorder, according to the researchers.

The study also supports the idea that the ability of brain cells to effectively communicate with each other may be impaired in people with bipolar disorder. The researchers found that the brains of people who were taking anti-psychotics and those who did not have bipolar disorder showed striking similarities in how their brains relayed signals between cell gaps, or synapses, and on high-speed neuronal "freeways" called the nodes of Ranvier.

While anti-psychotic medications can often be effective in moderating the effects of bipolar disorder, the side effects are often difficult for people to deal with. These include metabolic syndrome -- a combination of symptoms that increase the risk of developing cardiovascular disease and diabetes -- as well as weight gain, increased blood sugar levels, and tremors.

"It's still not known if these changes just happen to occur or play a key role in the therapeutic effect," said a Dr. 

The researchers don't have data on what medications the brains were exposed to during their lifetimes. Patients [with bipolar disorder] are exposed to antidepressants, drugs of abuse, and other medications, and we don't have medication exposure data on the brains [of the people without bipolar disorder].

According to the study, the research represents a step toward a radical evolution in the design of drugs for psychiatric conditions by the pharmaceutical industry.

"A lot of these psychiatric illnesses fluctuate, but now we give medications at a constant rate, almost as if we were giving a diabetic the same amount of insulin no matter what the person's blood sugar is," a  researcher said. "Medications as we know them will change based on our understanding of the biological mechanisms behind disease."

Suppressing protein may stem Alzheimer's disease process

Scientists  have discovered a potential strategy for developing treatments to stem the disease process in Alzheimer's disease. It’s based on unclogging removal of toxic debris that accumulates in patients’ brains, by blocking activity of a little-known regulator protein called CD33.

Too much CD33 appears to promote late-onset Alzheimer's by preventing support cells from clearing out toxic plaques, key risk factors for the disease . Future medications that impede CD33 activity in the brain might help prevent or treat the disorder.

Variation in the CD33 gene turned up as one of four prime suspects in the largest genome-wide dragnet of Alzheimer's affected families. The gene was known to make a protein that regulates the immune system, but its function in the brain remained elusive. To discover how it might contribute to Alzheimer's  the researchers brought to bear human genetics, biochemistry and human brain tissue, mouse and cell-based experiments.

They found over-expression of CD33 in support cells, called microglia, in post-mortem brains from patients who had late-onset Alzheimer's disease, the most common form of the illness. The more CD33 protein on the cell surface of microglia, the more beta-amyloid proteins and plaques — damaging debris — had accumulated in their brains. Moreover, the researchers discovered that brains of people who inherited a version of the CD33 gene that protected them from Alzheimer's conspicuously showed reduced amounts of CD33 on the surface of microglia and less beta-amyloid.

Brain levels of beta-amyloid and plaques were also markedly reduced in mice engineered to under-express or lack CD33. Microglia cells in these animals were more efficient at clearing out the debris, which the researchers traced to levels of CD33 on the cell surface.

Evidence also suggested that CD33 works in league with another Alzheimer's risk gene in microglia to regulate inflammation in the brain.

The study results — and those of a recent rat study that replicated many features of the human illness — add support to the prevailing theory that accumulation of beta-amyloid plaques are hallmarks of Alzheimer's pathology. They come at a time of ferment in the field, spurred by other recent contradictory evidence  suggesting that these presumed culprits might instead play a protective role.

Since increased CD33 activity in microglia impaired beta-amyloid clearance in late onset Alzheimer’s, researchers are now searching for agents that can cross the blood-brain barrier and block it.

Activity of a regulator protein called CD33 (green) clogs removal of brain-damaging debris, beta-amyloid protein (red), by support cells, microglia. Left: Microglia of normal control mice (A”) show more CD33 and less beta-amyloid than mice in which CD33 expression is experimentally knocked-out (B”). Right: Little beta-amyloid can be seen in microglia of a mouse line in which CD33 is over-expressed (C”), compared to microglia of mice in which CD33 is experimentally inactivated (D”). Evidence from post-mortem human brains indicates that CD33 is similarly overactive in Alzheimer’s disease, suggesting that a treatment that impedes it might help treat or prevent the disease. Source:Rudolph Tanzi, Ph.D. , of Massachusetts General Hospital and Harvard University

Foods which help to QUIT SMOKING

Great Detoxifier- beetroot, carrot, apple, lime juice !

BEWARE OF SPIDERS IN TOILET SEAT, THEY CAN BE VERY TOXIC

Three women in North Florida turned up at hospitals over a 5-day period, all with the same symptoms. Fever, chills, and vomiting, followed by muscular collapse, paralysis and finally, death. There were no outward signs of trauma. Autopsy results showed toxicity in the blood. Thesewomen did not know each other and seemed to have nothing in common. It was discovered, however, that they had all visited the same Restaurant (Olive Garden) within days of their deaths. The Health Department descended on the restaurant , shutting it down. The food, water, and air conditioning were all inspected and tested, to no avail.. The big break came when a waitress at the restaurant was rushed to the hospital with similar symptoms. She told doctors that she had been on vacation, and had only went to therestaurant to pick up her check. She did not eat or drink while she was there, buthad used the restroom. That is when one toxicologist, remembering an article he had read, drove out to the restaurant, went into the restroom and lifted the toilet seat .  Under the seat, out of normal view , was a small spider. The spider was captured and brought back to the lab, where it was determined to be the Two-Striped Telamonia (Telamonia dimidiata), so named because of its reddened flesh color. This spider's venom is extremely toxic, but can take several days to take effect. They live in cold, dark, damp climates, and toilet rims provide just the right atmosphere. Several days later a lawyer from Jacksonville showed up at a hospital emergency room.Before his death, he told the doctor, that he had been away on business, had taken a flight from Indonesia , changing planes in Singapore , before returning home.He did NOT visit (Olive Garden), while there. He did (as did all of the other victims) have what was determined to be apuncture wound, on his right buttock.Investigators discovered that the flight he was on had originated in India . The Civilian Aeronautics Board (CAB) ordered an immediate inspection of the toilets of all flights from India and discovered the Two-Striped Telamonia (Telamonia dimidiata)spider's nests on 4 different planes! It is now believed that these spiders can be anywhere in the world . So please, before you use a public toilet, lift the seat to check for spiders. It can save your life!

Metals that are wrecking you

Two laboratories come up with shocking results. Experts 

blame pollution, construction activity and ayurvedic 

medicines for toxicity.

It's been 10 years since lead-free petrol was introduced. Lead 

in pencils is gradually being replaced by graphite and clay, 

and most paint and cosmetic companies are now going out 

of their way to convince consumers that their product is 

'metal-free'. And yet, lead poisoning continues to top the 

chart of heavy metal toxicity in humans. Medical experts 

claim extreme level of pollution, construction activity and 

haphazard use of ayurvedic medicines are the culprits.

Figures from the city-based laboratories reveal the 

worrisome trend. Of the 600 odd samples received every 

month by a diagnostics centre for Atomic Absorption 

Spectroscopy, which detects metal content in body fluids, 

about 350 contain lead. It is followed by copper (125), zinc 

(50) and other metals such as arsenic, mercury, aluminium 

and chromium.

Even a small amount of exposure to lead can lead to long-

term health hazards, especially in children. It is known to 

cause anaemia, hypertension, impaired fertility and so on. 

Doctors say foetuses can be affected by lead exposure, as it 

reaches them through the placenta.

In addition, lead does not allow other metals such as zinc 

and copper to be flushed out of the body, leading to their 

build-up as well. The dangerous metal can remain inside the 

body for more than 45 years.

Apart from being carcinogenic or toxic, most metals 

adversely affect the central nervous system, kidneys, liver , 

skin, bones and teeth.

"The number of samples with metal content has gone up 

over the years. We started in 2010 with about 250 samples 

monthly and today we screen around 600," said  a Dr. 

Another laboratory, tests about 250 samples in a month, of 

which 150 contain lead. "Most samples are from people 

working in industrial set-ups, which expose them to such 

metals on a daily basis. Samples with arsenic generally 

come from people who use ayurvedic drugs containing 

heavy metals," said a Dr. 

While advanced technology is available to test the metal 

content, many metals generally go undetected. That is 

because the process to detect each metal is different and 

doctors check only for that metal which is producing 

adverse symptoms. Ayurvedic medicines have been blamed 

for high amount of metals in them. The practitioners, 

however, claim that their medicines were always made with 

various metals but qualified practitioners know how much 

to prescribe.

According to a consultant physician , these metals are 

present in food, water, even the very air we breathe in. 

"They first enter the blood stream. Liver tries to process 

these metals out of our body, which puts pressure on it. It 

can cause jaundice and liver cell disease. These metals can 

cause renal failure and neurological problems too," said 

a Dr.

According to the Dr., if detected in the initial stages, patient 

can be provided with metal chelationtherapy, which helps 

remove these toxins in two-three months.

Heavy metal poisoning 

Heavy metals may enter the body by ingestion, inhalation or 

absorption through the skin or mucous membranes. They 

are then stored in the body's soft tissues. Once absorbed, they 

compete with other ions and bind to proteins, impairing 

enzymatic activity and damaging many organs.

researchers identify pathway that may protect against cocaine addiction

A study by researchers  gives insight into changes in the reward circuitry of the brain that may provide resistance against cocaine addiction. Scientists found that strengthening signalling along a neural pathway that runs through the nucleus accumbens — a region of the brain involved in motivation, pleasure, and addiction — can reduce cocaine-seeking behaviour in mice.

Research suggests that about 1 in 5 people who use cocaine will become addicted, but it remains unclear why certain people are more vulnerable to drug addiction than others.

A key step in understanding addiction and advancing treatment is to identify the differences in brain connectivity between subjects that compulsively take cocaine and those who do not. 

Until now, most efforts have focused on finding traits associated with vulnerability to develop compulsive cocaine use. However, identifying mechanisms that promote resilience may prove to have more therapeutic value.

In the study, mice were conditioned to receive an intravenous dose of cocaine each time they poked their nose into a hole in their enclosure. Cocaine was then made unavailable for periods of time during the day. Some of the mice would stop seeking the drug once it was removed while others would obsessively continue to poke the hole in an effort to obtain the drug.

Mice that quickly stopped seeking the drug were found to have stronger connections along the indirect pathway — a neural tract that forms indirect projections into the mid-brain and contains cells called medium spiny neurons expressing dopamine D2 receptors (D2-MSNs). A parallel pathway — known as the direct pathway -- forms direct projections into the mid-brain neurons and contains medium spiny neurons expressing D1 receptors (D1-MSNs). These two pathways are thought to work together in complementary but sometimes opposing ways to affect behaviour.

Researchers were very surprised by the results of the study because we were originally looking for vulnerability factors for developing compulsive drug use. Instead,they found changes that only happened in subjects that show a resilience to becoming compulsive drug users. Resilient mice had a strong inhibitory circuit that allowed them to exert better control over their drug intake.

To test this observation, researchers used lasers to activate individual neurons, and found that stimulating D2-MSNs in the nucleus accumbens decreased cocaine seeking in the mice. Blocking D2-MSN signalling with a chemical process increased motivation to obtain cocaine.

This research advances the understanding of how the recruitment, activation and the interaction among brain circuits can either restrain or increase motivation to take drugs.

Previous studies have shown that people with lower levels of dopamine D2 receptors in the striatum, a brain region associated with reward and working memory, are more likely to develop compulsive behaviours toward stimulant drugs.

Dopamine is a key neurotransmitter involved in reward-based learning and addiction. Cocaine disrupts communication between neurons at the synapse, the small junction between nerve cells, by blocking the re-absorption of dopamine into the transmitting neuron. As a result, dopamine continues to stimulate the receiving neuron, causing feelings of alertness and euphoria.