Can Allithiamine Help Neuropathy Patients

Today's post from doctorvolpe.com (see link below)is a very interesting piece of new information about a topical cream (or capsules) called Allithiamine, which is a form of Vitamin B1. It is already used as a component of a commonly found version, Bentofiamine but Allithiamine is purely the fat-soluble B1 vitamine and it is commonly used to treat ADHD and Autism, as well as being a cosmetic cream. The point is that it has been shown to provide some dramatic results for people suffering from neuropathy. Now as with all these things, it's wise to err on the side of caution but talking it over with your neuropathy doctor and trying it yourself if you can get hold of it, will prove whether it can help you or not. Tomorrow's video post talks about the same thing and if you're interested, it must be worth while looking at both posts before coming to any conclusions. After that, doing your own research is also advisable.

Allithiamine found to reverse neuropathy 
Dr. Arturo M. Volpe May 20th, 2003

Allithiamine is a fat-soluble form of vitamin B-1. Although vitamin B-1 (thiamin) is most commonly found in its water-soluble form, allithiamine is also a naturally occurring form of this vitamin and is found in many foods, including garlic.

Since it is fat-soluble, allithiamine has the advantage of being excreted at a much slower rate than the common form of thiamin. In addition, while thiamin in any form is associated with health of the nervous system, the fat-soluble form is far more effective in promoting recovery of a damaged nervous system.

The reason for this may be that the nervous system is, in large part, made up of fat. Nerves are encased in a protective fatty cover known as the myelin sheath. Efficient functioning of the nerves is largely dependent on the health of this sheath. Because allithiamine is fat-soluble, it dissolves more easily and is better absorbed in these fatty regions of the nervous system where it can promote recovery.

Vitamin B-1 deficiency is widespread in our society due to the prevalent high-carbohydrate diets. This vitamin is consumed when carbs are digested and used (metabolized) in the body, so the more carbs we eat the more thiamin we need. However refined carbs are a poor source of thiamin and when they become the major component of the diet, people exhaust their thiamin reserves without replenishing them, so they become deficient. In our country some carbohydrate products are enriched with thiamin for this very reason, but the amount added is probably inadequate, at least for a segment of the population (besides, many carbohydrates like French fries are not enriched).

An extreme form of chronic vitamin B-1 deficiency is seen in alcoholics. Alcohol is metabolized like a carbohydrate but provides no nutrients at all and thus robs the body of many vitamins, especially thiamin. This extreme deficiency can lead to a form of dementia known as Wernicke-Korsakoff psychosis that is treated with daily vitamin B-1 injections.

Diabetics are also often deficient in thiamin, although their deficiency is usually not severe enough to cause dementia. A prevalent symptom of deficiency in diabetics is polyneuropathy, a condition characterized by loss of sensation in the extremities. An early sign of this condition is “burning” feet, which explains why many diabetics (and alcoholics) often cannot tolerate sleeping with a blanket covering their feet.

Derrick Lonsdale, MD has found thiamin deficiency to also be prevalent in children with ADHD and autism. Dr. Lonsdale discovered that thiamin deficiency tends to manifest in children as hyperactivity and a sensitivity to touch that he calls “touch-me-not syndrome.”

A recent double-blind controlled study of allithiamine supplementation was performed in Germany on diabetic patients who suffered from polyneuropathy. Patients in the active treatment group were given oral supplements of allithiamine (actually benfotiamine, a form of allithiamine) plus vitamins B-6 and B-12 that have synergistic actions. After the 12-week duration of the study, all patients who received the vitamin combination showed significant improvements. Additional progress was observed nine months later in a group who continued to take the vitamins after the study was completed. Incidentally, no side effects were reported in this study (“A benfotiamine-vitamin B combination in treatment of diabetic polyneuropathy” Exp Clin Endocrinol Diabetes 1996; 104 (4): 311-6).

Allithiamine is also very effective as a piece of the treatment puzzle in children with ADHD and autism when there is a pre-existing deficiency. Although oral administration is highly effective, this vitamin has a viciously bad taste and it is usually administered as a cream to children who are too small to swallow pills.

http://doctorvolpe.com/neuropathy/allithiamine/

GREATER RATES OF MITOCHONDRIAL MUTATIONS DISCOVERED IN CHILDREN BORN TO OLDER MOTHERS

The discovery of a "maternal age effect" by a team of Penn State scientists that could be used to predict the accumulation of mitochondrial DNA mutations in maternal egg cells -- and the transmission of these mutations to children -- could provide valuable insights for genetic counseling. These mutations cause more than 200 diseases and contribute to others such as diabetes, cancer, Parkinson's disease, and Alzheimer's disease. The study found greater rates of the mitochondrial DNA variants in children born to older mothers, as well as in the mothers themselves. The research will be published in the early online edition of theProceedings of the National Academy of Sciences on October 13, 2014.

 

Mitochondria are structures within cells that produce energy and that contain their own DNA. "Many mitochondrial diseases affect more than one system in the human body," said Kateryna Makova, professor of biology and one of the study's primary investigators. "They affect organs that require a lot of energy, including the heart, skeletal muscle, and brain. They are devastating diseases and there is no cure, so our findings about their transmission are very important."

The multidisciplinary research team set out to learn whether maternal age is important in the accumulation of mitochondrial DNA (mtDNA) mutations, both in the mother and in the child as a result of transmission. Collaborating with Ian Paul, a pediatrician at the Penn State Milton S. Hershey Medical Center, they took samples of blood and of cells inside the cheek from 39 healthy mother-child pairs. Because mtDNA is inherited only maternally, paternal mtDNA was not a factor in the study. Studying healthy individuals gave the researchers a baseline for future studies of disease-causing mutations.

Through DNA sequencing, they found more mutations in blood and cheek cells in the older mothers in the study. Maternal age of study participants ranged from 25 to 59. "This finding is not surprising," Makova said, "because as we age, cells keep dividing, and therefore we will have more mutant genes." But finding greater rates of mutations in children born to the older mothers did come as a surprise. The researchers believe a similar mutation process is occurring both in the cells of the mothers' bodies and in their germ lines.

The study led to another important discovery about egg-cell development. Although it was known that developing egg cells go through a "bottleneck" period that decreases the number of mtDNA molecules, scientists didn't know how small or large this bottleneck is. "If the bottleneck is large, the genetic makeup of the mother's mitochondria will be passed to her children," Makova explained. "However, if it is tiny -- if there is a severe decrease in mitochondrial molecules during the egg-cell development -- then the genetic makeup of the child might differ dramatically from that of the mother. What we discovered is that this bottleneck is indeed very small."

This finding is especially important for mothers who have a mitochondrial disease. For many mitochondrial diseases, 70 to 80 percent of molecules need to have the disease-causing variant for the disease to manifest itself. But for others, only 10 percent of the mtDNA molecules with the variant are needed to cause disease. "If the bottleneck is very small, as we've found in our study, these percentages can change dramatically," Makova said. "Knowing the size of the bottleneck allows us to predict, within a range, the percentage of disease-carrying molecules that will be passed on to the child."

Knowledge about both the maternal age effect and the bottleneck size is useful in family planning. "We have some predictive power now and can assist genetic counselors in advising couples about the chances of mitochondrial diseases being passed to the next generation," Makova said. "Everyone is concerned about Down syndrome because that is a common genetic problem. We have now added another set of genetic disorders that also might be affected by the age of the mother. It is good for couples to have this knowledge as they make family-planning decisions."

Loam

The last leaves of the Cottonwood

Hang on tightly, resisting the wind.

Cruel cold gusts push through the night

Stealing color and leaving mist in its wake

Roots take stock.

Maple leaves explode with beauty -

a plant that knows she works well with deadlines.

Flowers hide invisibly inside capsules of potential

luring animals to eat her flesh, so she may find

Loam to sleep under

for the winter

Until light and warm rain

Crack her heart open again.

Share Sciatica pain treatment by baba ramdev

With this site folks can assist you to have a valuable reference point based on analysis from active content pieces Sciatica pain treatment by baba ramdev probability topic as lots more clients what person frequently prefer him or her. within research Accumulating all of us make use of several search engines like google are graphics who are associated Sciatica pain treatment by baba ramdev .

Pictured earlier you'll be able to acquire along with preserve the software throughout the laptop computer hard disc drive in order that if you want it is usually specifically looked at simply. Sciatica pain treatment by baba ramdev could be the important to suit your needs what person likes to corresponding ideas. For this reason people procured any step to take root the comprehensive data to get the main advantage of all of our targeted traffic. Lesemarke some of our web-site the fact that will allow you to search for a great deal more articles or reviews relevant to this key terms

Sciatica pain treatment by baba ramdev - that will build up the eye of the customers are usually pleased in making these pages. strengthening the products this great article definitely will we tend to test a later date so you can in fact appreciate once discovering this place. In conclusion, this isn't a small number of sayings that must be made to convince you. although a result of the disadvantages connected with dialect, we could simply current the particular Sciatica pain treatment by baba ramdev conversation way up below

Is Nerve Decompression Surgery The Answer For Neuropathy

Today's post from dlife.com (see link below) suggests that there is a new surgical treatment for neuropathy but doesn't expand enough to tell the reader that this is a limited option that only applies to people living with trapped nerves with still some element of function. It discusses decompression surgery which relieves the entrapment of a nerve (either by releasing the nerve, or removing the impediment but the vast majority of people with neuropathy have nerves that are so severely damaged that a surgical procedure doesn't have any point any more. This decompression surgery has been around a long time and has led to wild claims from unscrupulous operators that neuropathy can be 'cured'. It can if, as in this case, the nerve is only trapped but not destroyed (through recent injury for instance) but it can't if the nerve has been 'broken' or been stripped of its protective myelin sheath and lost all function (being effectively 'dead'). So yes, if your neuropathy problem falls under the general title of entrapment (herniated discs, carpal tunnel and cubital tunnel syndromes amongst others for instance) decompression surgery is an expensive and risky option and worth exploring with the experts but if your pain, tingling, numbness etc comes from damaged nerves, then surgery can't do the necessary repairs.

Hope for Neuropathy
Nerve decompression surgery offers treatment for symptomatic neuropathy. 
By Theresa Garnero, APRN, BC-ADM, MSN, CDE Last Modified Date: January 27, 2014

Many people react with skepticism when hearing that surgery can relieve the pain of neuropathy. Why haven't we heard about this before? Even though it is a relatively novel surgical procedure, it has been performed for over 15 years and is based upon principles learned from more commonly performed operations which surgeons have been performing for decades. Moreover, the results can be life-changing and important for dLife community members to consider.

Have you ever had a pinched nerve or had your arm fall asleep after laying on it? If that's all you've had, consider yourself lucky. How long would it take for your arm to wake up if you had fallen asleep on the nerves for a few years? What if the pressure on your arm nerves continued—would the arm ever wake up? For many people with diabetes, this is the manner in which their nerves become injured and is the reason the symptoms of neuropathy appear. Neuropathy caused by uncontrolled diabetes can be very painful and in severe cases, debilitating. Treatment options typically focus on medications that reduce the painful symptoms while the root cause of the problem, pressure on the nerve, continues (see related article about neuropathy by clicking here).

That was until Dr. Ziv Peled enlightened us with the latest surgical treatment options. Dr. Peled is Director of The Dellon Institute for Peripheral Nerve Surgery and Plastic Surgery in San Francisco, California. He gave a recent educational program on surgical nerve decompression for the Center for Diabetes Services staff at California Pacific Medical Center in San Francisco, California. Dr. Peled explained that the body has many known nerve compression sites where nerves pass through tight tunnels (fascial bands). If the nerves swell within the fixed space of these tunnels (as is the case of people with diabetes), the nerves effectively become compressed or entrapped and the symptoms of neuropathy rear their ugly heads. Common sites include, but are not limited to:

Arms

The median nerve (wrist), which may get caught in the carpal tunnel (i.e. carpal tunnel syndrome).
The ulnar nerve (elbow), which may get caught in the cubital tunnel.
The radial sensory nerve (arm), which may get caught in the dorso-radial forearm.
The radial nerve (just past the elbow), which may get caught in the radial tunnel.

Legs
The common peroneal (knee), which may get caught near the fibular head.
The superficial peroneal nerve, which may get caught approximately 12 cm above the outside ankle bone.
The deep peroneal nerve, which may get caught in the dorsum (top) of the foot.
The distal tibial nerve, which branches to give the medial/lateral plantar nerves (providing sensation to the bottom of the foot), and the calcaneal nerves (providing sensation to the heel region), which may get caught in the tarsal tunnel (behind the inside ankle bone).

Anatomical jargon aside, you can see we have a lot of places along a nerve's path in which these nerves can become entrapped. A nerve that is wrapped up and bound may result in pain and/or decreased sensation, which lead to a higher risk for ulcers, wounds and potentially the need for amputations. The further out the nerve is from the spinal cord, the higher the rate of nerve problems (e.g. the feet are more often involved than the thighs).

Dr. Peled shared his research and multiple cases of surgically released nerves with a resulting dramatic improvement in pain and sensation. If tight compressive band is cut, the nerve can go on doing its job.

Who qualifies?
Not everyone is a surgical candidate. The first step is to be examined so that your doctor can check if the nerve is still able to function (the Tinel sign). In addition, a sophisticated type of neurosensory testing is used to corroborate the severity of nerve dysfunction. This testing with the Pressure Specified Sensory Device (PSSD), detects exactly how much pressure is required to elicit a sensation of being touched. The PSSD has been demonstrated to be more sensitive than a needle conduction study (i.e. EMG) and best of all, is completely painless (needle conduction studies are painful—trust me).

How long is the surgery?
Surgery is usually about a 2-hour outpatient procedure. One extremity (arm or leg) is done at a time; as soon as six weeks later, the other lower extremity can be done. Patients can use their extremity immediately after surgery (walk, use their arm). Many insurance plans cover the procedure.

What kinds of surgeons perform this procedure?
Specialized plastic surgeons who have completed at least a six-month fellowship in peripheral nerve surgery are the most qualified to perform surgical nerve decompression for diabetic neuropathy, a procedure pioneered by Dr. Lee Dellon. For example, after completing his plastic surgery training at Harvard University, Dr. Peled spent an entire year studying these procedures at the Dellon Institute in Tucson, Arizona. Dr. Dellon is an accomplished plastic surgeon as well as a professor of Plastic Surgery and Neurosurgery at the Johns Hopkins University School of Medicine in Baltimore, Maryland. The Dellon Institutes for Peripheral Nerve Surgery owe their name to him.

Where can I have this done?
To date, this surgery is only available in San Francisco, Tucson, St. Louis, Boston, New York, Tennessee, and Baltimore. For more information, check out www.dellon.com and click on the "contact us" link on the left side of the home page. The clinical results are promising so perhaps this vital procedure will be more widely available in the near future.

http://www.dlife.com/diabetes/complications/neuropathy/garnero_0108

HOMOEOPATHIC REMEDIES FOR MARASMUS

Marasmus is a form of severe malnutrition characterized by energy deficiency. A child with marasmus looks emaciated . Body weight is reduced to less than 60% of the normal (expected) body weight for the age. Marasmus occurrence increases prior to age 1, whereas kwashiorkor   occurrence increases after 18 months. It can be distinguished from kwashiorkor in that kwashiorkor is protein deficiency with adequate energy intake whereas marasmus is inadequate energy intake in all forms, including protein. Protein wasting in kwashiorkor may lead to edema  

Marasmus is caused by a severe deficiency of nearly all nutrients, especially protein, carbohydrates, and lipids.

 Marasmus is commonly represented by a shrunken, wasted appearance, loss of muscle mass and subcutaneous fat mass.Buttocks and upper limb muscle groups are usually more affected than others. Marasmus is not always linked to severe edema. Other symptoms of marasmus include unusual body temperature (hypothermia, pyrexia), anemia, edema, dehydration (as characterized with consistent thirst and shrunken eyes), hypovolemic shock (weak radial pulse, cold extremities, decreased consciousness), tachypnea (pneumonia, heart failure), abdominal manifestations (distension, decreased or metallic bowel sounds, large or small liver, blood or mucus in the stools), ocular manifestations (corneal lesions associated with vitamin A deficiency), dermal manifestations (evidence of infection, purpura, and ear, nose, and throat symptoms (otitis, rhinitis).

HOMOEOPATHIC REMEDIES

TUBERCULINUM 1000- Treatment should be started with this remedy and no other remedy should be given  for the next 24 hours

ABROTANUM 30-An excellent remedy for marasmus , especially of lower extremities with good appetite

BARYTA CARB 30- Child is weak and sluggish with tonsillitis. Abdomen is large

CALCAREA PHOS 6X- An excellent remedy for marasmus . Skin dry and wrinkled

IODUM 200-This remedy in lower potencies reduces weight and in higher potencies increases weight. There is extreme hunger , the child eats well and yet emaciates rapidly. The skin appears yellow and there is a problem with the thyroid gland

MAGNESIA CARB 30- Children who have a tendency to sinking in of the occipital bone or the back of the head and jutting out over it of the parietal bone creating a depression

NATRUM MUR 30-Marasmus of neck in children. Utterly dehydrated . Sad and wistful. Child looks like a tiny hairless monkey

PEPSINUM 30-Marasmus of children fed on artificial food

PICRIC ACID 30- Wasting with great appetite

PLUMBUM MET 30- Emaciation due to anemia

SANICULA 30-Child looks old, dirty and greasy . Progressive emaciation. Skin wrinkled about neck and hands in folds. Mentally obstinate and head strong, constantly changing . Sweating of head at night which wets the pillow. Offensive foot sweat

SYPHILINUM 1000- It should be given after Tuberculinum .Follows it advantageously but it should be given only if there is history of syphilis in the fa

GENES DETERMINE TRACES THAT STRESS LEAVES BEHIND ON BRAINS

Our individual genetic make-up determines the effect that stress has on our emotional centres. These are the findings of a group of researchers from the MedUni Vienna. Not every individual reacts in the same way to life events that produce the same degree of stress. Some grow as a result of the crisis, whereas others break down and fall ill, for example with depression. The outcome is determined by a complex interaction between depression gene versions and environmental factors.

The Vienna research group, together with international cooperation partners, have demonstrated that there are interactions between stressful life events and certain risk gene variants that subsequently change the volume of the hippocampus forever.

The hippocampus is a switching station in the processing of emotions and acts like a central interface when dealing with stress. It is known to react very sensitively to stress. In situations of stress that are interpreted as a physical danger ('distress'), it shrinks in size, which is a phenomenon observed commonly in patients with depression and one which is responsible for some of their clinical symptoms. By contrast, positive stress ('eustress'), of the kind that can occur in emotionally exciting social situations can actually cause the hippocampus to increase in size.

According to the results of the study, just how stressful life events impact on the size of the hippocampus depends on more than just environmental factors. There are genes that determine whether the same life event causes an increase or decrease in the volume of the hippocampus, and which therefore defines whether the stress is good or bad for our brain. The more risk genes an individual has, the more negative an impact the "life events" have on the size of the hippocampus. Where there are no or only a few risk genes, this life event can actually have a positive effect.

Examining life crises

As part of the study, carried out at the University Department of Psychiatry and Psychotherapy (led by Siegfried Kasper), the study team obtained quantitative information from healthy test subjects about stressful life events, such as deaths in the family, divorce, unemployment, financial losses, relocations, serious illnesses or accidents.

A high-resolution anatomical magnetic resonance scan was also carried out (at the High-Field MR Centre of Excellence, Department of MR Physics, led by Ewald Moser). The University Department of Laboratory Medicine (Harald Esterbauer and colleagues) carried out the gene analyses (COMT Val158Met, BDNF Val66Met, 5-HTTLPR). At the University Department of Psychiatry and Psychotherapy, primary author Ulrich Rabl measured the volume of the test subjects' hippocampi using computer-assisted techniques and analysed the results in the context of the genetic and environmental data.

"People with the three gene versions believed to encourage depression had a smaller hippocampus than those with fewer or none of these gene versions, even though they had the same number of stressful life events," says study leader Lukas Pezawas, describing the results. People with only one or even none of the risk genes, on the other hand, had an enlarged hippocampus with similar life events.

The study highlights the importance of gene and environment interaction as a determining factor for the volume of the hippocampus. "These results are important for understanding neurobiological processes in stress-associated illnesses such as depression or post-traumatic stress disorder. It is ultimately our genes that determine whether stress makes us psychologically unwell or whether it encourages our mental health," explains Pezawas.

The study, published in the Journal of Neuroscience, was funded by a special research project of the FWF (Austrian Science Fund) (SFB-35, led by Harald Sitte) and presented as a highlight at the international conference on "Organization for Human Brain Mapping."