NOTICE: Posting schedule is irregular. I hope to get back to a regular schedule as the day-job allows.

Friday, March 23, 2012

The GUIDE: Diabetic Neuropathy [Full link to blog for email clients.]

In the previous Guide blog, I discussed to diabetes in the brain. One of the follow-up comments requested a discussion diabetic neuropathy. So before moving onto the next topic - by special request: today's Guide blog is on Diabetic Neuropathy.

Copyright O2Creationz, 2012
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As previously mentioned, neurons in the brain are not dependent on insulin for their uptake of glucose from the blood. This is not to say that neurons are insensitive to insulin or that insulin has no effect on neurons. In fact, we are still discovering the many effects of insulin in the brain, and it may very well be the case that insulin has a beneficial effect in glucose uptake, it's just that insulin is not necessary at low levels of activity. Thus, in the brain the effects of high blood glucose are largely due to the osmotic properties of the glucose molecule dissolved in the liquid component of blood. In this manner, glucose acts very much like high salt concentrations.  It is fairly well known that one means of preserving food is to dehydrate it, quite frequently with salt. High salt concentrations draw water out of the cells, and prevent contamination or spoilage because bacteria, being cells, cannot live without water. Likewise the cells of the body, and the brain, do not function well without the normal concentrations of water surrounding them and in them.  As you look at the neuron diagrammed to the upper right, it is important to understand that the size of the neuron is determined by how much water is inside. The large round "Soma" at the top is primarily water, simply enclosed by a membrane. In fact, most of any cell in the body is water, filled with proteins, fats, and  salts. While there is a protein "skeleton", removing even part of the water will cause the cell to shrink. This in turn changes the concentration of the salts and proteins inside the cell. Since the concentration of ions is so important to the function of a neuron – due to the electrochemical gradient that is produced by charged ions – any change in concentration affects the function of the neuron.

Thus even the osmotic effects of blood glucose can alter the function of neurons. High blood glucose has additional effects that are less well understood. It appears that high concentrations of glucose can actually be toxic to neurons. This may occur because the high concentrations "saturate" the glucose transporter which allows glucose to pass from the blood to the inside of the cells, or may be due to interference by glucose at neurotransmitter receptors. While the reasons are not well understood, the effects are quite well known. Prolonged exposure to high blood glucose causes damage to neurons – particularly peripheral neurons. In this case the peripheral neurons that are most affected are the sensory neurons that convey that sense of touch to the brain. One of the first indications of diabetic peripheral neuropathy is tingling or numbness of the toes or fingers. For the reasons cited above, the sensory neurons appear to be most sensitive to high blood glucose. The onset of the symptoms varies from person to person. However, it's fairly well-established that the neuropathy develops over months to many years of high blood sugar.

At the same time, high blood glucose also affects the cells which line the inside of small blood vessels, weakening them, and predisposing them to damage. The small blood vessels of the retina in the eye are particularly sensitive, but the damage can appear to blood vessels anywhere in the body, and maybe another causative factor in peripheral neuropathy. The combination of numbness, or loss of fine touch sensation, with the potential for damage to small blood vessels, leads to frequent complications in the feet in which damage can occur but the patient not be aware of it. In this manner, diabetes can have many similar effects to leprosy, Hansen's disease, in that damage to the skin can occur without the patient detecting it, and infections and gangrene can result in considerable skin and limb damage.

Damage to small blood vessels and sensory neurons, therefore count for many of the cases of diabetic peripheral neuropathy, as well as diabetic "retinopathy"in which small blood vessels in the retina burst, scar over, and result in gradual loss of vision. In addition to the peripheral neuropathy, advanced cases can be accompanied by uncontrolled pain from damaged nerve endings, damage to the nerves around muscles and joints, and eventually the nerves which serve the internal organs. Long-term consequences of diabetic neuropathy can include damage to the nerves and muscles which serve the bladder, resulting in bladder control problems and incontinence. Damage to the nerves serving the gastrointestinal tract, in particular the esophagus, and result in gagging and swallowing problems. Very advanced cases can even involve the nerves and muscles which control the diaphragm, leading to difficulty breathing.

This cascade of problems is one reason for regular medical checkups in persons with a family history or suspicion of diabetes. Much damage can result from very small processes that accumulate over many years. Moreover, these effects occur with prolonged uncontrolled high blood glucose, and are much less likely to occur in individuals with good control of their blood sugar. Yet there is another, much less well understood, consequence of diabetes – particularly type I, insulin insufficiency diabetes. The role of insulin in the health of neurons besides control of glucose uptake is not very well known. It may very well be the case that insulin is required for the structural strength of proteins in the cells. We are certainly discovering that the effects of insulin in the brain can be quite remarkable in terms of protecting neurons from damage due to injury or chemical insult.  It may very well be that without sufficient insulin circulating through the blood, cell membranes may be weakened, and show structural damage over the long-term. It's sad to say, that as much as doctors and researchers know about the disease diabetes, we still have much to learn about insulin itself.

Thus, diabetic neuropathy arises from the indirect effects of glucose on the water content of neurons, from direct effects of glucose on proteins in the cell membrane, and possibly from the lack of insulin to strengthen the cells. For diabetic, the best protection against diabetic neuropathy is control og blood glucose.  In addition, diabetics should pay particular attention to tingling, numbness, joint pain, bruises, or any change in normal sensation. With proper treatment and restoration of blood glucose control further damage can be slowed or even stopped, but some permanent long-term damage may still occur. This is certainly a case where the best defense is a good offense.


I wish to thank my readers for their patience, I'm still dealing with a form of neuropathy myself, due to carpal tunnel syndrome. While it is getting better, it's still a bit difficult to type long blogs, and dictating them with Dragon NaturallySpeaking is taking a little bit of getting used to.

In addition, the day job has taken a few "interesting" turns, one of which will require me to travel next week, also interfering with my progress in posting these blocks. Please bear with me, there is much more content still to come.

Until next time, take care of your brain, your neurons, and your blood sugar!


  1. Nice Blog! Thanks for sharing with us.

    Type 2 Diabetes

  2. Very informative and in depth post on diabetic neuropathy. Thanks for sharing


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