Showing posts with label Better. Show all posts
Showing posts with label Better. Show all posts

Friday, 24 February 2017

Will My Neuropathy Get Better


Today's post from neuropathyjournal.org (see link below) asks the simple question that every neuropathy patient asks shortly after hearing the diagnosis for the first time: will it get worse? The answer is that nobody can say with any 100% certainty how the disease will develop and LtCol Richardson makes the point that it's pointless expending too much energy on something that you can't change anyway. He suggests that it's better to find the cause and also a doctor who knows what he/she's doing and concentrate your energies on improving your symptoms and situation, rather than worrying about unknown factors regarding the disease getting worse or not. I'm not sure I agree with him about concentrating on finding the cause. In the end, you have nerve damage; there's no cure for that and you share symptoms with millions of others, irrespective of the cause. It's far better to follow his second suggestion and put all your energies into reducing the impact of the symptoms. Your medical history will point to the cause and various standard tests will indicate the extent of the nerve damage in your system but further than that, all you want as patient, is that the symptoms become bearable enough to live a normal life. Worth a read and worth following the Lt Col's links for more ideas on the subject.


Will My Neuropathy Get Worse?
By LtCol Eugene B Richardson, USA (Retired) BA, MDiv, EdM, MS

One issue neuropathy patient’s face is the fear that their neuropathy will grow progressively worse. Neurologists call this a progressive polyneuropathy. The truth: no one really knows if your neuropathy will worsen, stay the same or disappear. A neurologist shared that this may have more to do with the underlying cause of the neuropathy, genetics, and heaven only knows, issues.

I speak of this very fear in chapter twelve, Focus, in the DVD “Coping with Chronic Neuropathy”, and if you have not viewed this chapter, I suggest that you do so. The viewing will provide a better perspective.

Neuropathy patient fears are often increased by the coming and going (remitting and relapsing) of neuropathy symptoms. These patterns are a medically confirmed fact and also occur in many other chronic illnesses. Better recognized are the same patterns for some forms of MS (Multiple Sclerosis)!

Neurologists confirm that there are acute neuropathies that come on suddenly and then the symptoms disappear. In other neuropathies symptoms occur, disappear and then return at the same level. Other neuropathies occur, disappear and then return at increased levels and in more places of the body. Others come, go and then go away for years only to return with a vengeance!

The chronic neuropathies (affect one set of nerves) and polyneuropathies (affect many nerves), which increase for years are often referred to as progressive polyneuropathies. The mystery is increased as there seems to be no rhyme or reason for these patterns. The only thing I noticed is that when I increased activity, I have increased burning, pain or other symptoms and I neurologist tell me that this is due to making damaged nerves work.

For years between the emotional highs when my symptoms remitted (“Hurrah, they’re gone!”) and the emotional lows when they relapsed (“Oh no, they’re back!”), I was tempted to worry that my symptoms were going to worsen and guess what, they did! But one has to ask the question, did the energy spent on worry change anything? No! What I re-discovered was what I learned in Sunday school. It was better to spend my time and energy finding a doctor who was trained (neuromuscular neurologist) in the clinical approaches to neuropathy then to waste energy on worry. I needed a doctor, not worry, to focus on my symptoms. I needed a doctor working with me as a partner, while treating the symptoms and looking for the TYPE and/or CA– USE. Why finding the type of neuropathy important? Because as Dr. Latov in his book tells us, this can often point in the direction of a cause! I needed a medical Sherlock Holmes, not time worrying about what might happen.

This approach maintained a focus on self empowerment by learning all I could, while prodding the doctors with questions that helped them think and act. The most important question for you is not, will my neuropathy get worse, but what is the type of neuropathy and/or the underlying cause? Spend your energy looking for the type and/or cause, as no one knows if your neuropathy will worsen or not.

I know that for so many of you neuropathy has been a progressive illness which worsened over the years. Conversely, my progressive polyneuropathy has not killed me, for my neuropathy symptoms began at age 31 and I am now 76. Thirty-five years into the symptoms with a million denials with a diagnosis from mentally ill to idiopathic neuropathy. I was given one drug which drove me to talk backwards and then another that reduced pain by 80%. Five years later with the miracle of IVIg I am able to keep breathing and the chest muscle spasms stopped while reducing other mind numbing symptoms. This took many doctors, lots of research and knowledge, while asking good questions and giving doctors documents from experts. It may have been fear and anger which drove me forward, but it was these focused actions that brought help, not dwelling on my fears!

It is important to know which issue is important as you set goals for getting help. It is important to focus your energy on learning, getting help with symptoms and finding the cause and solutions for the diagnosed illness. I do not mean idiopathic neuropathy (of unknown cause). It is very difficult to find a solution, other than for symptoms, when the neuropathy is of unknown cause. Help the doctor think and pushing the system to do the testing that is now available. Click here to read about my opinion on Idiopathic Neuropathy.

Tests that are available will allow the doctor to know if the neuropathy is large or small fiber, motor, sensory or autonomic, axonal, immune-mediated, demyelinating or inflammatory and these clues can lead to a possible identification of the type and/or cause that is more helpful than idiopathic.

RESOURCE: Read Dr. Scott Berman’s book, as this book may provide insight on these issues. Click here to view the recommended Books On Neuropathy. Dr. Berman has untreatable CIDP (chronic inflammatory demyelinating polyneuropathy) and his book speaks to all neuropathy patients as one who has been in our shoes with many neuropathies. Dr. Berman empowers us to face creatively the emotional issues we ALL face in chronic illness.

https://www.neuropathyjournal.org/will-my-neuropathy-get-worse/

Thursday, 16 February 2017

Lab Grown Neurons Could Lead Researchers To Better Drugs


Today's post from vectorblog.org (see link below) is somewhat technical but isn't everything you read about stem cell research 'technical'? It's worth reading for neuropathy patients though because it looks at current research across the world which involves 'recreating' nerve cells (neurons) and studying them with a view to creating new drugs designed to target pain signals specifically and that's what we need. Current drugs are prescribed to throw a blanket over the problem and hope that that reduces the strength of the pain signals that so characterise neuropathy symptoms. They often have side-effects as a result, so stem-cell research is clearly the future because then drugs can be developed that target the problem with pinpoint accuracy. It's going to take decades yet but as long as they're going in the right direction, maybe future generations will suffer less than we do.

Modeling pain in a dish: Nociceptors made from skin recreate pain physiology
by Nancy Fliesler on December 12, 2014 

 
Neurons from patients could lead researchers to better drugs for chronic pain. Chronic pain, affecting tens of millions of Americans alone, is debilitating and demoralizing. It has many causes, and in the worst cases, people become “hypersensitized”—their nervous systems fire off pain signals in response to very minor triggers.

There are no good medications to calm these signals, in part because the subjectivity of pain makes it difficult to study, and in part because there haven’t been good research models. Drugs have been tested in animal models and “off the shelf” cell lines, some of them engineered to carry target molecules (such as the ion channels that trigger pain signals). Drug candidates emerging from these studies initially looked promising but haven’t panned out in clinical testing.

“These models don’t tell you what the drug is doing to the whole functioning neuron,” says Elizabeth Buttermore, PhD, a postdoctoral fellow in the F.M. Kirby Neurobiology Center at Boston Children’s Hospital. “They haven’t been holding up.”

Last month in Nature Neuroscience, Buttermore coauthored a report with Brian Wainger, MD, of Boston Children’s and Massachusetts General Hospital, describing a new model that appears to capture pain physiology in a dish, using skin cells as their raw material. Their model, also a technical breakthrough in stem cell research, offers new opportunities to understand how pain is produced and to discover new analgesics.


A nimbler way to make neurons

Labs all over the world are beginning to reprogram skin cells into cells resembling embryonic stem cells, known as induced pluripotent stem (iPS) cells, and transforming those, in turn, to their cell type of choice. But Buttermore, Wainger and colleagues found that they were able to bypass the somewhat cumbersome step of creating iPS cells.

By adding just five signals (namely, transcription factors) to skin cells from mice and from patients with an inherited pain disorder, they were able to create nociceptors—specialized pain-sensing neurons. Two of these signals hadn’t been known before and were found by examining mature nociceptors from mice.

In tests, the lab-created mouse nociceptors closely resembled “natural” neurons. They functioned, responded to different pain triggers and became hypersensitized to pain just like their real-world counterparts. The lab-created human nociceptors still have some hoops to jump through, but by early measures, they appear to “beautifully model” patients’ neuropathies and pain hypersensitivities, says Clifford Woolf, MB, BCh, PhD, senior investigator on the project and director of the Kirby Center.

The nociceptor model is already revealing new aspects of pain physiology and could ultimately provide a much more realistic platform for testing new drugs. Woolf, who also co-leads the Harvard Stem Cell Institute’s Nervous System Diseases Program has already found this to be true for amyotrophic lateral sclerosis (ALS).

The nociceptor project’s success was a long time in coming. The team had first tried to make nociceptors from embryonic stem cells. “We spent three years trying to recapitulate the developmental steps involved, and it turned out to be a total bust,” said Woolf.

But he refused to pull the plug, and the approach that finally worked turns out to be the most expedient and the most clinically relevant: Skin cells can be collected directly from patients, making it easier to model their different kinds of chronic pain—neuropathies caused by genetic mutations, diabetes or even chemotherapy, which can sensitize patients to pain.

“We’re trying to get to clinical trials with more success,” says Buttermore. “Hopefully, we’ll avoid drugs that don’t work.”

http://vectorblog.org/2014/12/modeling-pain-in-a-dish-nociceptors-made-from-skin-recreate-pain-physiology/?utm_campaign=Q1%202015%20Innovation%20Social&utm_medium=social&utm_source=twitter&utm_content=Vector%20Pain%20in%20a%20Dish&sf34613949=1



Monday, 13 February 2017

Will Generic Pregablin Lyrica Be Any Better For Neuropathy Patients


Today's post from psnc.org.uk (see link below) is a British view and advice to pharmacists on the changing status of Lyrica, as Pfizer's patent has now run out and generic versions will be coming onto the market. Pfizer in their wisdom, have decided to maintain a Lyrica patent for patients with neuropathy, at least until July 2017. This will effectively prevent other companies from bringing out a generic version until that date. Now in 2013, Pfizer were quite clear that pregabalin (Lyrica) was in their own eyes unsuitable for diabetes and HIV-related neuropathy patients. This was mainly due to adverse study outcomes and many court cases relating to side effect issues. The point is: what's changed? the answer: probably nothing: they still won't approve Lyrica for HIV and diabetes neuropathy patients and the FDA backs that up completely. So is this just a corporate move to prevent rivals from bringing generic Lyrica to the market too quickly? More importantly for neuropathy patients; will generic pregabalin (lyrica) be any more effective and any less dangerous for patients in the future. We'll have to wait and follow the recommendations for the US FDA and similar authorities across the world but until then, if your doctor is still prescribing Pregabalin (Lyrica) (generic or not) for your neuropathic problems, you need to have a serious discussion as to whether this is in fact, the best option.

Pregabalin (Lyrica) – Licensing differences between Lyrica and Generic
January 29, 2015

Pregabalin (Lyrica) patent is changing and generic pregabalin is becoming available. The NPA have issued advice (shown below) regarding the licencing of the products.

The NPA have also informed us that are also in the process of discussing this issue with the MHRA and Pfizer.

Dear Pharmacist

You may find in the coming months that generic pregabalin is available to order. I would like to highlight to you that although the patent for pregabalin expired in July 2014, this patent expiry related to the use of pregabalin in epilepsy and generalised anxiety disorder; Pfizer will retain a patent for the use of pregabalin in the treatment of peripheral and central neuropathic pain in adults until July 2017.
This means that until July 2017, generic manufacturers of pregabalin will only be able to obtain a licence for pregabalin for use in epilepsy and/or generalised anxiety disorder and Lyrica, Pfizer’s branded product, will remain the only product licensed for use in pain as well as epilepsy and generalised anxiety disorder.

Pfizer has indicated that it will contest any challenges to the patent for pain.

To avoid any possible patent infringement by pharmacists, steps will need to be taken to ensure that where generic pregablin is requested on a prescription the correctly licensed product is supplied. This may mean contacting the prescriber and establishing the indication and requesting that the prescription is amended and ordered by brand as Lyrica if necessary.

Although generic pregabalin is unlikely to differ clinically from the branded Lyrica, supplying the generic version of pregabalin for neuropathic pain may have the following implications for pharmacists:
Generic pregabalin preparations will not include information relating to neuropathic pain in the patient information leaflet and pharmacists will be supplying a product off-licence
Supplying generic pregabalin for neuropathic pain would not be in line with Medicines and Healthcare products Regulatory Agency’s risk hierarchy guidance for the supply of unlicensed medicinal products, which states that a UK-licensed product should always be supplied for the correct licensed indication
Using generic pregabalin for neuropathic pain may be deemed by Pfizer to be a patent infringement by all parties concerned, including the prescriber and the supplying pharmacist

Currently, reimbursement for NHS prescriptions for pregabalin is based on Lyrica. This may change when generic versions become available meaning that pharmacists may not be correctly reimbursed where Lyrica is supplied against a generically written prescription for pregabalin. I advise that where generic prescriptions for pregabalin are received, the prescriber is contacted to ascertain the indication. Where the indication is for neuropathic pain, the prescription should be returned to the prescriber for amendment to Lyrica. Prescriptions for pregabilin for epilepsy or generalised anxiety disorder can be dispensed with either Lyrica or appropriately licensed generic versions.

When supplying pregabalin for the treatment of epilepsy, pharmacists should also consider MHRA guidance issued in 2013 regarding the generic prescribing of antiepileptics. The guidance states that pregabalin does not generally need to be prescribed by brand for the treatment of epilepsy unless there are specific concerns such as patient anxiety and a risk of confusion or dosing errors.

For further information on this or any other query please contact the NPA Pharmacy Services Team on 01727 891 800 / 08447 364 201
or email pharmacyservices@npa.co.uk .

http://psnc.org.uk/sunderland-lpc/our-news/pregabalin-lyrica-licensing-differences-bewteen-lyrica-and-generic/

Monday, 9 January 2017

MORE EXERCISE IS NOT ALWAYS BETTER



There is strong epidemiological evidence of the importance of regular physical activity, such as brisk walking and jogging, in the management and rehabilitation of cardiovascular disease and in lowering the risk of death from other diseases such as hypertension, stroke, and type 2 diabetes. The Physical Activity Guidelines for Americans recommends about 150 minutes per week of moderate-intensity exercise or about 75 minutes of vigorous-intensity exercise. But there is clear evidence of an increase in cardiovascular deaths in heart attack survivors who exercise to excess, according to a new study published in Mayo Clinic Proceedings.

Paul T. Williams, PhD, of the Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA, and Paul D. Thompson, MD, of the Department of Cardiology, Hartford Hospital, Hartford, CT, studied the relationship between exercise and cardiovascular disease-related deaths in about 2,400 physically active heart attack survivors. They conducted a prospective long-term study using the National Walkers' and Runners' Health Studies databases. This study confirmed previous reports indicating that the cardiovascular benefits for walking and running were equivalent, as long as the energy expenditures were the same (although when walking, as compared to running, it will take about twice as long to burn the same number of calories).

Remarkable dose-dependent reductions in deaths from cardiovascular events of up to 65% were seen among patients who were running less than 30 miles or walking less than 46 miles per week. Beyond this point however much of the benefit of exercise was lost, in what is described as a reverse J-curve pattern.
"These analyses provide what is to our knowledge the first data in humans demonstrating a statistically significant increase in cardiovascular risk with the highest levels of exercise," say Williams and Thompson. "Results suggest that the benefits of running or walking do not accrue indefinitely and that above some level, perhaps 30 miles per week of running, there is a significant increase in risk. Competitive running events also appear to increase the risk of an acute event." However, they point out that "our study population consisted of heart attack survivors and so the findings cannot be readily generalized to the entire population of heavy exercisers."

In the same issue, investigators in Spain report on a meta-analysis of ten cohort studies aimed at providing an accurate overview of mortality in elite athletes. The studies included over 42,000 top athletes (707 women) who had participated in a range of sports including football, baseball, track and field, and cycling, including Olympic level athletes and participants in the Tour de France.
"What we found on the evidence available was that elite athletes (mostly men) live longer than the general population, which suggests that the beneficial health effects of exercise, particularly in decreasing cardiovascular disease and cancer risk, are not necessarily confined to moderate doses," comments senior investigator Alejandro Lucia, MD, PhD, of the European University Madrid, Spain. "More research is needed however, using more homogeneous cohorts and a more proportional representation of both sexes."

"Extrapolation of the data from the current Williams and Thompson study to the general population would suggest that approximately one out of twenty people is overdoing exercise," comments James H. O'Keefe, MD, from the Mid America Heart Institute in Kansas City, MO, and first author of an editorial on "Exercising for Health and Longevity versus Peak Performance: Different Regimens for Different Goals," which appears in the same issue. Along with co-authors Carl "Chip" Lavie, MD, and Barry Franklin, PhD, he explains that "we have suggested the term 'cardiac overuse injury' for this increasingly common consequence of the 'more exercise is better' strategy." Even so, these authors state that about 10 out of every twenty people are not getting the minimum recommended amount of physical activity (>150 minutes/week of moderate exercise).

O'Keefe, Franklin and Lavie point out that a weekly cumulative dose of vigorous exercise of not more than about five hours has been identified in several studies to be the safe upper range for long-term cardiovascular health and life expectancy, and that it may also be beneficial to take one or two days a week off from vigorous exercise, and to refrain from high-intensity exercise on an everyday basis. They propose that individuals from either end of the exercise spectrum (sedentary people and over-exercisers) would probably reap long-term health benefits by changing their physical activity levels to be in the moderate range.

"For patients with heart disease, almost all should be exercising, and generally most should be exercising 30-40 minutes most days, but from a health stand-point, there is no reason to exercise much longer than that and especially not more than 60 minutes on most days," says Lavie, who is a cardiologist at the John Ochsner Heart and Vascular Institute, New Orleans, LA. "As Hippocrates said more than 2,000 years ago, 'if we could give every individual the right amount of nourishment and exercise, not too little and not too much, we would have found the safest way to health.' I and my co-authors believe this assessment continues to provide wise guidance," he concludes.




Thursday, 20 October 2016

Targeting Neuropathy Treatment Better


Today's post from sciencedaily.com (see link below) looks at the studies being made at atomic and molecular level to find ways of treating neuropathic pain more directly and accurately. One of the more extreme and excruciatingly painful, neurological conditions is erythromelagia  ('Man on Fire syndrome'). Scientists have found a mutation at molecular level in the sodium channels of patients and seen that because it responds well to carbamazepine for instance, identifying that mutation may lead to better targeted drug treatment in the future. Talking about sodium channels, genetic analysis and specific amino acids will leave most people cold but the important thing is that scientists are now looking much more closely at specific pain reactions to specific drugs. This can only lead to better treatment for neuropathy sufferers in the future as we know that it's not a 'one size fits all' disease. At the moment, drugs meant for other problems are thrown at neuropathy in the hope that one eventually works. Hopefully in the future. much of the guesswork will be removed.

'Man On Fire Syndrome': In a World of Chronic Pain, Individual Treatment Possible, Research Shows
ScienceDaily (Nov. 13, 2012)

 
An investigation into the molecular causes of a debilitating condition known as "Man on Fire Syndrome" has led Yale researchers to develop a strategy that may lead to personalized pain therapy and predict which chronic pain patients will respond to treatment.

More than a quarter of Americans suffer from chronic pain and nearly 40 percent do not get effective relief from existing drugs. In many common conditions such as diabetic neuropathy, no clear source of pain is found.

The new study published in the Nov. 13 issue of Nature Communications used sophisticated atomic modeling techniques to search for mutations found in a rare, agonizing, and previously untreatable form of chronic pain called erythromelagia, commonly referred to as "Man on Fire Syndrome." Researchers discovered that one of those mutations seem to predicted whether a patient would respond positively to drug treatment.

"Hopefully we can use this knowledge to help chronic pain patients in more systematic ways, and not depend upon trial and error," said Yang Yang, postdoctoral research associate in the Department of Neurology and lead author of the paper.

Under the leadership of Stephen Waxman, the Bridget Marie Flaherty Professor of Neurology, professor of neurobiology and of pharmacology, and senior author of the new paper, Yale has been a leader in identifying the sodium channel Nav1.7 at the base nerve cells as the regulator of several forms of chronic pain. The members of the Waxman lab were intrigued when it was reported the anti-seizure medicine carbamazepine relieved pain in members of a family suffering from erythromelagia, apparently by working on the Nav 1.7 sodium channel.

Yale researchers conducted an exhaustive genetic analysis and discovered that a specific variant -- a difference of a single amino acid among 1,800 -- in the sodium channel explained why this family responded to the drug. In this new paper, the Yale team developed a three-dimensional structural model of human Nav1.7 channel and systemically looked at different erythromelagia mutations at the atomic level. The Yale team found an additional, second mutation that was sensitive to carbamazepine treatment. In theory, chronic pain patients with this mutation should respond to treatment with carbamazepine.

"This work shows us that the goal of personalized, genomically-guided drug treatment for pain is not unrealistic," Waxman said.

The U.S. Department of Veterans Affairs funded the work.

Other Yale authors include Sulayman D. Dib-Hajj, Lynda Tyrrell, and Mark Estacion.


http://www.sciencedaily.com/releases/2012/11/121113122040.htm

Sunday, 28 August 2016

Why Isnt Neuropathy Better Known


Today's post from ihavepn.com (see link below) asks the question why so many Americans suffer in silence with neuropathy but the same question can be applied across the world. You can safely bet that 9 out of 10 people on the street will never have heard of it, let alone pronounce it, yet it is so widespread - how's this possible? You get the feeling that we need a sort of advertising organisation on the scale of Saatchi and Saatchi, to promote awareness of neuropathy and the fact that it's one of those diseases that's actually growing instead of decreasing. Modern lifestyles, diets and choices are contributing to this growth and yet there's nothing about neuropathy that makes it sexy for the media. Maybe we need highly visible role models! What do you think?
Why 42 Million Americans Suffer in Silence with Peripheral Neuropathy
July 2015 (no author mentioned)

Imagine that your feet feel like they are asleep while simultaneously on fire, all the while 10,000 pins and needles are poking at them. Your toes and balls of your feet are numb to your touch, and over time this feeling is progressing in your legs and hands too. What if this feeling were chronic and never went away, causing misery both day and night? This is what 42 million Americans are dealing with everyday, it is a condition called “Peripheral Neuropathy” or PN.

President Clinton famously once said “I feel your pain”, and well, unfortunately I do too. you see, I have Peripheral Neuropathy, the condition listed above, and fortunately at this point I just have these awkward feelings in my feet but my fear is that over time it will spread into my legs and my hands and eventually become debilitating.

I had never heard of Peripheral Neuropathy until I started researching the nature of my symptoms. Consider that 42 Million Americans suffer from some form of peripheral neuropathy whether very light beginning stage symptoms or late stage debilitating symptoms. That is 14% of the American population. But hold on, that seems like a very high number for a condition that most people don’t even know how to pronounce let alone have heard of. Well the fact is that about half of the 14% or 7% (21 million Americans) just have a very mild form of PN that may manifest itself in just a few numb, tingly toes. Because of this the PN subject does not pay much attention to the symptoms to the degree that they don’t even mention it to their doctor during the official start of their symptoms. Given that, it means there are 21 Million Americans that suffer from much more sever symptoms of PN some of them debilitating to the degree that it affects mobility. Still, I am at a loss to understand why more people do not know about this condition. Several people I have talked to recently have never heard of it let alone pronounce it. With a world population of 7 billion people, more than 500 million people may have this condition today around the world. This is one of those conditions that can really make your life miserable. I know it sounds morose and negative but we suffer in silence, not really sharing our pain and frustration with anyone other than our doctor and close family most of the time. But I think it is time to elevate awareness.

Over time as Peripheral Neuropathy progresses it can become crippling and debilitating. Sure there are drugs that will relieve the pain and discomfort to some degree, often not much more than by a factor of 20%. That is partially due to the fact that many of these drugs were designed to control epileptic seizures that in essence slow down the rate at which the mind perceives pain so that sensation is also slowed and thus abated. The side effects inhibit the thought process of the brain and make people feel like they are zombies. Because of these irritating side effects we have no choice but to look for other alternative treatments.

Let’s first go on the hunt for the primary root cause of this condition. Although there are many contributing factors that cause Peripheral Neuropathy to develop, the leading cause is high glucose or blood sugar levels. You don’t have to be diabetic to be considered having high glucose levels anymore, pre-diabetics are also on the list. Higher than normal glucose levels damage the micro veins and arteries starting with those which are furthest from the heart and have the least amount of circulation, that means your feet and hands. Pre-diabetics and diabetics alike are predisposed to impairing the micro veins and arteries in their extremities.

Once the micro veins and arteries are damaged they no longer can supply oxygen to the nerves in the extremities which ultimately means that the nerve cells begin to die. As these nerve cells die they essentially create intermittent signals of sensation to the brain which are felt as pins and needles, burning, numbness and the occasional shooting of lightening pain in the feet and hands.

Diabetes is growing by leaps and bounds in the United States and many of the western cultures around the world. Fine, but how did we get here? Well it boils down to the fact that in order to provide foods that are fast and economical, our society has opted to consume processed foods over whole foods. Processed foods are foods that contain highly refined ingredients like white rice, bleached flour, white sugar or any unnatural form of food and more important they are extremely high in carbohydrates and low in fibre. Carbohydrates are what you have to keep at reasonable levels in your body because carbohydrates are converted to glucose by your body. Too much glucose in your body ultimately leads to glucose intolerance by your cells which is diabetes. Whole foods are those that are whole and cooked in the home like roast chicken with broccoli or green beans. And no, green beans are not whole if they are from a can because they often add salt and preservatives to the broth. Fresh green beans and other fresh produce from the grocer are what we need to be consuming.

The American fast food diet has been killing us and it is taking its toll, causing us to develop various miserable conditions ultimately related to our diet like Peripheral Neuropathy.

Our first lady, Michelle Obama, has been spreading the word to help our young generation have an appreciation for whole fresh foods and I think she is doing a great job by growing veggies in the White House back yard. What we are really facing here is a very influential processed food industry and lobby that does not want to behave in a way that will promote a healthy lifestyle.

If you really want to make a change with yourself and those companies that are supplying us currently with unhealthy processed foods, then you really need to consider making a change by reducing your carbohydrate intake by preparing your own whole foods. I know that we can’t always do that every single day and there are food deserts in America where it is very challenging. Let’s learn how to read food labels properly so that we really understand what we are about to put in our families bodies. Yes, there are actually good healthy foods that come in paper or plastic packages but you have to read the nutrition information to make sure that you are getting what you want and is right for you.

So now you understand that our love of excessive carbohydrates is what has lead most of us to develop the condition of Peripheral Neuropathy. Now that we know what to do to prevent it, what are we going to do about the millions of people that already have it or are in the process of developing it? Drug companies have medications available that will relieve the discomfort to some degree but you would have to weigh the benefits with the side effects, particularly the ongoing drowsiness and “the zombie lifestyle” you will experience. That is not to say that drugs will not work for some as it likely will be just right for some but a complete flop for others.

Those with PN (Peripheral Neuropathy) need to be on an exploratory quest to 1) stop the symptoms from spreading and 2) relieve the pain and discomfort.

There are many products and services available to those with PN. First and foremost, get as much information from various sources as possible. This will help guide the PN sufferer to make better decisions about treatment options.

Also PN sufferers need to open the lines of communication. The more interest around this topic the more likely that big money will be looking for a real cure. PN sufferers need to start local interest groups that meet regularly on the topic. There are great organization like the Foundation for Peripheral Neuropathy and the Peripheral Neuropathy Association that a PN sufferer or loved one can take part in.

http://ihavepn.com/million-american-suffer-silence-peripheral-neuropathy/

Friday, 24 June 2016

Words To Help You Understand Neuropathy Better


Today's short post from pain.com (see link below) is a useful one for both newcomers to neuropathy and those who have been living with it for some time. There are very few diseases with as much associated vocabulary as neuropathy! You can guarantee that whatever words your doctor uses at your diagnosis, there are 10 or more alternatives. more or less describing the same thing, that you will hear of or read about during the following months and years. It's a disease that prefers to use 10 scientific terms when actually one or two will do. This makes it a minefield for patients, who think they've finally got a handle on their condition, only to find that they've still got a whole new lexicon of descriptive words to learn. That comes from the fact that there are over 100 sorts and over 100 causes of neuropathy and each comes with its own descriptive vocabulary. This article at least tries to narrow it down to a few key words but even then, I find myself thinking, 'Why haven't they included this one or that one?' I also had to admit...'dermatomes' is a new one for me too. It's like being back at school again but at least articles like this try to help navigate the obstacle course.

Neuropathy: 10 Terms to Know
Pain.com May 2016
 
Neuropathy, simply put, is pain from nerve damage. Here are ten terms you should know about the condition.

Peripheral nervous system: the system of nerves outside the central nervous system (which is made up of the brain and spinal cord). The peripheral nervous system sends signals from the central nervous system to the rest of your body.

Peripheral neuropathy:
damage to these nerves, which leads to pain, numbness, weakness, and burning or tingling sensations in the limbs, hands, and feet. It can be caused by genetics, toxin exposure, traumatic injury, infection, or metabolic conditions.

Diabetic neuropathy: nerve damage that occurs specifically as a result of complications from undiagnosed or untreated diabetes.

Sensory nerves: nerves that perceive sensations on the skin, such as heat, cold, pain, vibrations, or physical contact.

Motor nerves: control the movement of muscles

Autonomic nerves: control automatic bodily functions like digestion, bladder function, heartbeat, and blood pressure.

Dermatomes: connect peripheral nerves to the spinal cord; because the dermatomes coordinate with certain areas of the body, the symptoms can be used to trace which nerves are damaged.

Mononeuropathy: damage to a single nerve.

Multiple mononeuropathy: damage to two or more nerves that affect different areas of the body.

Polyneuropathy: damage that affects many nerves.

If you are experiencing symptoms such as muscle weakness, tingling or numbness, burning or shooting pains in the limbs, loss of control over muscles or bowel and bladder function, consult your doctor for tests.


References:
http://www.mayoclinic.org/diseases-conditions/peripheral-neuropathy/basics/definition/con-20019948
http://www.medicinenet.com/peripheral_neuropathy/article.htm
http://www.webmd.com/brain/understanding-peripheral-neuropathy-basics
http://www.diabetes.org/living-with-diabetes/complications/neuropathy/


http://pain.com/archives/2016/05/04-neuropathy-10-terms/