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diabetes FAQ: treatment (part 3 of 5)

Archive-name: diabetes/faq/part3
Posting-Frequency: biweekly
Last-modified: 10 March 2009


Subject: My diabetic father isn't taking care of himself. What can I do? We'll assume your father has type 2 diabetes. See separate section for definition of types. Type 2 diabetics, and those who care for them, are in a difficult situation. Type 2 strikes late in life, so personal habits and patterns are already formed and solidly engrained. Yet in most cases those habits and patterns are exactly what must be changed if a newly-diagnosed diabetic is to care properly for his or her health. This is a difficult psychological problem. The cornerstones for treating type 2 diabetes are exercise, weight control, and diet. A high percentage of type 2 patients who apply these therapies assiduously can control the disease with these therapies alone, without insulin or oral hypoglycemic drugs. Naturally these are also some of the most difficult aspects of life to change. There can be no single or simple answer of how to help or encourage a particular individual find a combination of therapies which not only controls the disease but also is psychologically acceptable and which can be incorporated as a lifetime pattern. Helping depends on knowing the individual's habits, patterns, motivations, desires, likes and dislikes, and working with all the existing conditions and everything brought forward from past life. Doctors and other health care professionals have a choice in treating patients with type 2 diabetes. They can prescribe drugs (oral hypoglycemics) and insulin, or they can try to get their patients to make the difficult lifestyle changes described above. (Many patients need both.) The latter effort is time consuming and often frustrating, as doctors too often see patients failing to make any change at all. Friends and family can help by learning about type 2 diabetes, and doing what you can to encourage your loved one to make diet and lifestyle changes. If this supports the plan a treatment team is urging the patient to follow, you will add your support for difficult changes. If the doctor (or the whole treatment team) falls down on the educational and motivational structure, you can fill in some of the gaps. Your effort is well spent in either case. In particular, if a doctor has left the impression that drugs and insulin are the only treatments, make sure to counter that impression with information about the value of exercise, diet, and weight control. At the same time, it's important to remember that needing oral hypoglycemics and/or insulin injections as additional tools isn't failure. On the contrary, a patient who's been actively involved in self treatment already has an excellent chance of using these additional tools successfully. Those who have learned to use the exercise - weight control - diet triumvirate will also be able to utilize insulin and oral drugs as additional treatments when needed. Choose the appropriate tools and use them effectively. These treatment choices can interact in positive ways as well. Bringing blood glucose under control often increases the body's sensitivity to insulin. So ironically, using insulin may decrease the need for insulin. This is a positive change which can then be reinforced by the other, interacting treatments. You will need far more information than is appropriate for a Usenet FAQ panel. As a start, call the ADA (see ADA section), get a subscription to _Diabetes Forecast_ (see journals), and visit a university library and browse in the diabetes section in the stacks. Beyond the generalizations above, a few specifics are usually of value: Set a good example in your own life. Exercise and eat a good diet. The recommendations for diabetics are healthy choices for anyone. Share your example. Serve a tasty, low-fat diet to family and friends when they are your guests. Suggest joint activities. Suggest a walk instead of watching a ball game. Make sure your diet and activities are visibly enjoyable so your guests will accept your invitiation to join you.
Subject: Managing adolescence, including the adult forms Adolescents have special problems in managing diabetes. These include a variety of physiological problems related to puberty and rapid growth, social problems related to growing up and the general social pressures of adolescent life, and the psychological turmoil caused by the expectations of others. I'm here today to talk about (hey, hold the eggs and tomatoes) expectations. Actually, this all applies to adults as well, though the subtle points may differ. The most important thing to remember, for the adolescent, the parent, and the health care provider, is All Blood Glucose Measurements Are Good. There Are No Bad Blood Glucose Readings. If that doesn't sound right, then please take two steps. First, learn why it is true. Then chant it like a mantra until you internalize it, so that you never give off the slightest vibes to the contrary. Why is it true? There are two kinds of adolescents (to simplify life enormously): those who rebel and those who want to please. Ironically, the rebellious are probably easier to deal with in treating diabetes. "So my blood sugar is 350, so what?" Bad? No, that's good: you know what's going on, and so does your child. The point of blood glucose measurement is to respond -- not to be good or bad -- and only with an accurate report can you and the patient respond. [Compulsory digression: 350 mg/dl = 20.0 mmol/L.] Look what can happen to the eager-to-please child: Child: My blood sugar is 350. Adult: Oh, that's awful! You must try to be better! [next time:] Child: My blood sugar is ... um [to self: I must be good] 140 ... Adult: Oh, that's great! In short order, the log book looks great but the HbA1c doesn't jibe. This all happens with the best of intentions from all parties. The child is trying to please, and is behaving in exactly the ways that elicit approval. The adult is trying to care for the child's health in the most natural ways. And the result is one that neither desires. Thus the positive mantra to replace the half-negative one above: All Blood Glucose Measurements Are Good. Responding To Blood Glucose Readings Is Good. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . An excellent article entitled "Insulin Therapy in the Last Decade: A Pediatric Perspective", by Julio Santiago, MD, of the St. Louis Children's Hospital and the Washington University School of Medicine in St. Louis, Missouri, appears in _Diabetes Care_, volume 16 supplement 3, December 1993, pp. 143-154. The article discusses many aspects of treating pediatric diabetes. Santiago spends several pages discussing how to establish realistic and honest approaches to self-monitoring. I highly recommend the article.
Subject: So-and-so eats sugar! Isn't that poison for diabetics? This is asked from both sides: the non-diabetic who doesn't understand diabetes, and the diabetic who gets tired of hearing "I won't put any sugar on the table" etc etc ad nauseum. Diabetics should eat a high-quality, healthy diet very similar to that recommended for everyone. This will include some sugar, and research indicates that obtaining a moderate amount of carbohydrates in the form of sugar makes little or no difference in controlling blood glucose levels. There isn't room here to describe all the aspects of diabetes treatment that make this so. No one has suggested a really good, uniformly satisfying answer to the public know-alls who insist they know more than you do. Feel free to add to this list: That was true before insulin treatment became available in 1922. Fat is more dangerous than sugar because diabetics have a three-fold higher risk of heart disease. The whole point of injecting insulin is to balance carbohydrate intake. All carbohydrates are converted to sugar in the digestive tract anyway.
Subject: Insulin nomenclature The major types of insulin have both generic designations and brand names used by the manufacturers. Most of the brand names are close enough to the generic ones that the correspondence is obvious. Novo uses totally different names. In those parts of the world where Novo has most of the market, the Novo brand names are used in place of the generic names. To facilitate communication between Novo users and others, here is the correspondence: Generic Novo May also be known as ------- ---- -------------------- Regular Actrapid Soluble NPH Protophane Isophane Lente Monotard Ultralente Ultratard Zn (Zinc suspension) The recently developed lispro (generic name) insulin is sold as Humalog by Eli Lilly. Novo has no comparable insulin as of July 1996, although they undoubtedly have research in progress.
Subject: What is Humalog / LysPro / lispro / ultrafast insulin? Except as otherwise noted, this info comes from an article on p396 of the March 1994 _Diabetes_ by researchers at Eli Lilly. Insulin is a protein. Proteins consist of sequences of amino acids. Human insulin has the amino acid lysine at position B28 and proline at position B29. Insulin molecules naturally pair off (like people) and combine into dimers. The dimers interact with small amounts of zinc and combine into hexamers, the form sold as "regular" insulin. From another source, now forgotten: the time required to disassociate the hexamer into the dimer, and then the dimer into the monomer so that it can be absorbed, is the main reason for the delay in the action of regular insulin and the reason for injecting it 30 to 45 minutes before meals. Switching the B28 and B29 positions on the protein has no effect on the normal activity of the insulin but inhibits the formation of the dimer and the hexamer. Thus the insulin is in monomeric form when injected and can be absorbed immediately. The name LysPro comes from the names of the amino acids, lysine and proline, that occupy the swapped positions. According to an article in the August 1996 Diabetes Forecast, the spelling 'lispro' is now preferred. Challenges in the development include the biochemical process for swapping the amino acids, and making the result reasonably stable in the monomeric form. From another source, now forgotten: US FDA approval was not automatic, since the insulin molecule has been modified. In fact, several other amino acid exchanges have been tried and met with unacceptable side effects. Some points from the article in the August 1996 Diabetes Forecast: Patients with gastroparesis, or taking acarbose, should be careful with lispro. Gastroparesis is a condition caused by neuropathy which causes the stomach to empty slowly and erratically. (See the section on gastroparesis later in this section.) Acarbose is a drug which slows the absorption of carbohydrates from the intestine. Either may result in lispro insulin acting too quickly. Response to lispro is variable. Some patients love it, others hate it. On the average, it does not change bg control either for better or for worse, but some patients definitely find it one or the other. Eli Lilly is promoting lispro for convenience, not for better control. Doctors and patients are still experimenting with the best regimens for using lispro insulin. "Best" clearly varies from one patient to another. Typically lispro insulin is injected very close to mealtime. An obvious concern is that hypoglycemic reactions might be more common with a faster acting insulin. A paper presented at the 1996 ADA Scientific Papers conference studied this possibility: Reducing the Incidence of Hypoglycemia with a Novel Insulin Formulation J. Anderson, R. Brunelle, A Pfeutzner et al. Indianapoils, IN and Bad Homberg, Germany In fact, they found the rate of hypoglycemic incidents slightly lower among those using lispro insulin. They found no difference on most other measures, including especially HbA1c. I've only seen the abstract of the paper, so I know nothing about their methodology. (They also state the lispro forms hexamers just like regular insulin but that the hexamers dissociate much more quickly. I don't know who to believe, but from a practical point of view it doesn't matter.)
Subject: Travelling with insulin Insulin does not need to be kept cold. Insulin is stable at body temperature. This is not surprising when you realize that the beta cells often store the insulin they produce for days before releasing it. (Specifically, according to Jens Brange's _Stability of Insulin_, Regular/Actrapid insulin stored at 40C will lose 5% of its potency after 14 weeks.) A general guide to how long it is safe to store insulin at various temperatures: Refrigerated a few years Room temperature several months Body temperature a few weeks Do not allow insulin to freeze. Do not expose insulin to temperatures significantly above body temperature. I don't know how much heat is required to destroy insulin, but leaving it in a closed car in the sun would be a very bad idea. (Two readers have reported that solidly frozen and rethawed regular insulin works just fine. I've been unable to locate any studies documenting the degradation of insulin at extreme temperatures.) Short of such extremes, degradation is gradual. You should always be alert for gradual changes in your blood glucose anyway, since individual sensitivity to insulin changes over time for reasons unknown. Your normal dosage adjustments will handle minor degradation that might occur, say, from keeping insulin in a very hot room for several weeks. So why do drugstores (pharmacies) keep insulin refrigerated, and why are "insulin cold packs" advertised? The drugstores are mosty just following standard procedures. For them, it's a simple precaution not worth violating. As for cold packs, as long as anyone thinks they are needed, someone will sell them. As noted, you do need to protect insulin from extremes of temperature, and the cold packs can help at both extremes. In many situations it may be just as effective to pack the insulin next to a bottle of water, especially during outdoor activities when you are carrying water anyway. Always keep your insulin with you! Keep all your medical supplies with you. Never pack them in checked luggage. Luggage may sit outside in hot sun or freezing rain. If you are delayed, or your luggage is waylaid, you could be without supplies packed in luggage. Meter manufacturers recommend keeping meters and strips from freezing and extreme heat.
Subject: Injectors: Syringe and lancet reuse and disposal Disposable syringes can be safely reused as long as you take reasonable precautions. Recap both ends between uses, and discard the syringe if dropped, dirty, or damaged (especially if the needle is bent). Discard it when it becomes uncomfortable to use. This varies a great deal, being half a dozen uses for some patients and several dozen uses for others. Comfort depends far less on sharpness than on the silicone coating applied to the needle at manufacture. Never wipe the needle with alcohol, as this will remove the silicone coating. Lancets can also be reused safely with the same caveats. Syringe disposal has proven controversial. If you want to be conservative, buy a needle clipper, get a hard plastic bottle designed for medical waste to put the syringes in, and take the full bottle to a facility approved for handling medical waste. Your doctor's office, a local hospital, or a pharmacy may be able to handle it for you. Intermediate positions use one of these techniques. At the least conservative, cap the needle carefully and discard in trash which will not be subject to illicit searching and possible abuse. If you have trouble capping the needle without sticking yourself, definitely get a bottle to drop the uncapped syringes in; a bleach bottle may be adequate. Local or state regulations apply in many places and limit your choices. Know the laws for your area! Where sharps containers are required, the pharmacy where you purchase the container will probably dispose of the full container for you.
Subject: Injectors: Pens A pen injector is a device that holds a small vial of insulin and a disposable needle, and injects an amount measured with a dial. Advantages include being compact, convenient, easy to use circumspectly in public, and accurate and simple in dose measurement. The pen device clicks for each unit (or two depending on the manufacturer) dialed; this can help those with impaired vision. Some pen units only allow setting a multiple of two units of insulin, which many find inadequate. Get a model which measures a multiple of one unit, which should be easy to find among current models. The primary disadvantage is cost, up to twice as much per unit of insulin compared with standard vials. The special vials may be difficult to obtain in remote areas, and widespread shortages have occurred occasionally. Falling back to a standard syringe is always an option. Also, the special vial can be refilled from a standard vial using a syringe, making sure the rubber stopper is not damaged, though the manufacturer will not recommend this. If you do refill, make sure to use the same concentration of insulin. This is not a problem in the US, where only U100 concentration is used. In some parts of the world, U40 concentration is common, but pen refills are always U100. Make sure to match the concentration. Pens are more popular in Europe than in the US, but are being heavily promoted in the US.
Subject: Injectors: Jets A jet injector uses no needles, but instead squirts the substance being injected through a narrow orifice under high pressure, producing a fine stream which penetrates the skin as easily as a needle. Jets are popular with anyone who is simply scared of needles, for any reason. The jet disperses the insulin more than a needle does, which probably results in faster absorption. This can be an advantage or a disadvantage, and requires careful monitoring when first used. Technique is just as important as with needles, so jets are no more appropriate than needles for small children. If a jet is used to avoid needles, equipment failure forcing a fallback to needles may be traumatic. High cost is a major factor.
Subject: Insulin pumps An insulin pump provides a Continuous Subcutaneous Insulin Infusion, or CSII, via an indwelling needle or catheter. That is, a small needle (similar to those on insulin syringes) or tube is inserted through the skin and fixed in place for two or three days at a time. An external box pumps insulin through the needle steadily. Pumps don't solve all the problems of treating diabetes for two main reasons: 1) The infusion is still subcutaneous, so the insulin still must be absorbed before it can be used. Insulin from the pancreas goes directly into the bloodstream and takes effect much more quickly. 2) Current pumps are open-loop -- that is, there is no feedback from blood glucose (bG) to the pump. The patient must still self-monitor bG and program the pump. Nonetheless, many patients get much better results with a pump than from intensive therapy without a pump, and those patients tend to be extremely happy with the pump. It isn't clear at present how to decide whether a given patient should use a pump. Different studies have obtained varying results, ranging from 85% success to 85% dropout! Unfortunately, no studies seem to have been done since the mid-1980s, and the manufacturers have little motivation to fund the studies, as advertising is more cost-effective for them. It is likely that the pumps and pump therapy have become much more consistently successful since then. A few important factors seem clear, though: 1) Motivation. A pump takes extra effort and attention. 2) Knowledge. If you aren't already familiar with intensive therapy, think more than twice before jumping for a pump. You should probably try intensive therapy with multiple injections first. 3) Treatment team. Successful users are backed by teams of physicians and educators who are experienced *with pumps*. Don't try a pump on your own (the manufacturers won't let you anyway), and don't try it with inexperienced providers -- these are recipes for unnecessary failure. 4) Funding. Pumps represent a nontrivial capital outlay. If you don't have insurance or other public programs that will pay for the pump, you will need personal financial resources. Most or all pump manufacturers allow a trial period, so you can try a pump without financial risk. You will probably know fairly soon whether you want to continue with the pump. I have removed the oudated insulin pump discussion previously posted here.
Subject: Type 1 cures -- beta cell implants Beta cells can be isolated and implanted, requiring only outpatient surgery for implantation. But foreign beta cells are quickly rejected without immunosuppressant drugs. Even with the recent advances in drugs, especially cyclosporin, using immunosuppressants is much more dangerous than living with diabetes. As a result, beta cell implantation is not currently used to treat diabetes. Current research is investigating two general methods of implanting beta cells without the use of immunosuppressant drugs. The first (immunoisolation) encapsulates the beta cells within a barrier so that nutrients, glucose, and insulin can pass freely through the barrier but the proteins which provoke the immune response, and the cells which respond, cannot pass. The second (immunoalteration) involves altering the proteins on the surface of the cells which provoke the immune response. The first human trial began early in 1993 on immunoisolated beta cells, and human trials were scheduled to begin late in 1993 on immunoaltered beta cells. (As of early 1997, I haven't had the opportunity to try to locate the followup to these trials.) An article in the Journal of Clinical Investigation, September 1996, describes a successful experiment which implanted immunoisolated porcine (pig) islets into monkeys. An accompanying editorial describes the state of islet transplantation. Both are online in full, linked from the issue contents page at http://www.jci.org/content/vol98/issue6/ In early 2000, a lot of hype appeared about the "Edmonton protocol" trials. While an important step, this is still only a small step on a long journey. They made improvements in technique and graft survival, but no progress on the serious problems of beta cell supply (each patient needed beta cells from two cadaver donors) or of immunosuppressant use (they used drugs, albeit carefully). Don't expect these treatments to be available on a standard basis any time soon. I've been reading about this research since the mid-1970s, and the results are always just around the corner. Serious problems remain to be solved: safety of the immunoisolated implants, long-term survival, ability to use beta cells from non-human species or grow usable cells for grafting in the laboratory, perfection of both techniques -- all these must be resolved before beta cell implantation moves beyond the experimental stage. Other problems will likely be encountered along the way, since this is cutting edge medical research. I'll be surprised if it gets out of the lab before the year 2005; 2015 is probably a better guess. And it may fail -- it's always possible that unsolvable problems will yet arise. Finally, it's not yet clear that even completely normal bG profiles will cure all the problems of type 1 diabetes. Some may be related to the autoimmune reaction that is the immediate cause of diabetes. This question cannot be answered until it is possible to normalize bG levels for a period of many years.
Subject: Type 1 cures -- pancreas transplants Whole pancreas transplants have the same rejection problems as beta cell implants, and also require major surgery. For these reasons, whole pancreas transplants are only used 1) in desperate cases in medical schools with exceptional capabilities, and 2) in conjunction with kidney transplants. Kidney transplants are (relatively) common in diabetics with advanced complications. A kidney recipient is taking immunosuppressant drugs anyway, and the same surgery that implants the kidney can stick in a pancreas with little extra effort or trauma. As a result, the double transplant is now recommended, at least for consideration, for any diabetic patient who requires a kidney transplant. The only disadvantage would seem to be that the pancreas donor must be dead; whereas a living kidney donor is feasible. Even this is not strictly true, as a kidney-plus-partial-pancreas transplant from a living donor is possible, and the partial pancreas contains enough beta cells to produce insulin for the recipient. However, this procedure is seldom performed. Combination kidney/pancreas transplants are listed in a different queue than kidney-only. Since the number of people waiting for donor kidneys is quite long (anywhere from a few months to seven or eight years), the kidney/ pancreas list is often a quicker means of receiving a transplant. For example, in January 1998 there were 38,380 people on the UNOS [see below] registrations for a kidney transplant. There were only 355 registrations for a pancreas transplant and 1604 registrations for a kidney-pancreas transplant. [Based on UNOS Scientific Registry data as of January 28, 1998.] Kidney/pancreas transplants, while still considered experimental at some institutions, have been approved by Blue Cross/Blue Shield in the following centers: University of Iowa Hospitals and Clinics, Iowa City; University of Minnesota Hospital and Clinic, Minneapolis; Ohio State University Hospitals, Columbus; and University of Wisconsin Hospital and Clinics, Madison. Though this is for BC/BS only, other insurance companies may follow the BC/BS lead if pushed. [Information from January 2000. Check to see whether additional centers have been approved.] UNOS (United Network of Organ Sharing) has a list of 124 transplant centers that have pancreas transplant programs. For more information, contact UNOS at (800)24-DONOR or see their web page at http://www.unos.org (See the section on sources for additional contact info.) The UNOS handles transplant registrations only in the USA, but can provide contact information for organ-donation agencies around the world. Organ allocation became a political football in the US in the late 1990s, and the details of allocation and waiting lists may change. The transplant mailing list is an excellent resource. See the section on online resources: mailing lists. (Thanks to Alexandra Bost for much of the information in this section.)
Subject: Type 2 cures -- barely a dream The treatments described in the preceding sections apply only to type 1 diabetes. Type 2 diabetes is the result of insulin resistance or other forms of improper use of insulin within the body, not in general to an absolute lack of insulin. Type 2 patients usually have normal beta cells at the start, with beta cell insufficiency developing later while the insulin use defects continue. There is nothing on the horizon for type 2 diabetes with promise comparable to that of beta cell transplants for type 1. The sequencing of the human genome, completed in 2000, provides information for research which is likely to help, but that is for the very long term. This is distinct from the *treatment* of type 2 diabetes, which has improved quite significantly even since I first wrote the above paragraph. New drugs are available which improve insulin sensitivity. The UKPDS directly, and the DCCT indirectly, have convinced many more doctors that intensive treatment of type 2 diabetes is worth the trouble and expense. Support and education programs continue to expand. The UKPDS showed clearly that medical nutrition therapy (MNT, diet with proper medical team support) helps type 2 diabetics greatly even without weight loss, and so more doctors are providing the necessary aid. But all this is treatment, not cure.
Subject: What's a glycemic index? How can I get a GI table for foods? The glycemic index, or GI, is a measure of how a given food affects blood glucose (bG). Some complex carbohydrates affect bG much more drastically than others. Some, such as white bread, affect bG even more than sugar (sucrose). This was quite a surprise when the research was first published in 1981. It really should not have been such a surprise. "Sugar", meaning sucrose, decomposes in the gut to equal parts of glucose and fructose. Fructose, as expected, has only a small effect on bG. Even professionals, it turns out, were swayed in their thinking by the evil charm of the word "sugar" and failed to take into account the differences among the many kinds of sugar found in foods. To use the glycemic index in a real-life diet, you must combine the GI of various foods using a weighted average. Rick Mendosa's article (see below) has information on simple calculations for mixed meals, which recent research has shown to be reliable. It remains difficult to predict the GI of high fat meals because of the multiple affects of the fat, especially the way it slows the gut. For example, a baked potato has a very high GI (one of the famous, unexpected examples), but adding butter to it lowers the GI greatly. This is a good reason to reduce dietary fat (if you needed another reason), since doing so makes the effect of carbohydrates more predictable. If you don't want to go to the effort of full GI calculations, the important thing is to understand that foods may affect your bG profile in ways that you wouldn't expect from categorizations such as "simple sugar" and "complex carbohydrate". Build your knowledge about your own response to different foods and meals by monitoring and keeping records, and avoid assumptions. Rick Mendosa <mendosa(AT)mendosa.com> has written an excellent and thorough article about the glycemic index. He also maintains a glycemic index list. I highly recommend that you check out http://www.mendosa.com/gi.htm [Thanks to Rick for information he provided for this section.]
Subject: Should I take a chromium supplement? The short answer is "no". I'll quote the ADA's longer answer, from the May 1994 _Diabetes Forecast_, p.73. The ADA's editorial board says: Some popular books on diabetes have claimed that chromium, which is found in many common foods such as animal meats, grains, and brewer's yeast, is good for people with diabetes. Not so. Though chromium supplements may benefit people who are significantly malnourished and have an actual chromium deficiency, there is no significant evidence that consuming extra chromium helps people with diabetes who are even close to being well nourished. Taken at the dosages listed on the bottle, however, chromium is not likely to be harmful. But your money is better spent on more useful items!
Subject: Does falling blood glucose feel like hypoglycemia? Sometimes. Symptoms of hypoglycemia are divided into the adrenergic and the neuroglycopenic. Adrenergic responses are caused by increased activity of the autonomic nervous system and may be triggered by a rapid fall in blood glucose (bG) or by low absolute bG levels; symptoms include weakness sweating tachycardia palpitations tremor nervousness irritability (sound familiar?) tingling of mouth and fingers hunger nausea or vomiting (unusual) The autonomic nervous system activity also causes the secretion of epinephrine, glucagon, cortisol and growth hormone. The first two are secreted rapidly and eliminated rapidly. The second two are secreted slowly and remain active for 4-6 hours, and may cause reactive hyperglycemia. Neuroglycopenic responses are caused by decreased activity of the central nervous system and are triggered only by low absolute bG levels; symptoms include headache hypothermia visual disturbances mental dullness confusion amnesia seizures coma The above information is from Mayer Davidson's _Diabetes Mellitus: Diagnosis and Treatment_. Remember, as always, that individual responses vary greatly. The exact set of symptoms encountered will vary. It's not impossible that some of the symptoms will fall in the other category for some individuals.
Subject: Alcohol and Diabetes This section provided by Peter Stockwell <peter(AT)sanger.otago.ac.nz>. Having diabetes does not prevent the consumption of alcoholic drinks, but there are some considerations: - Alcohol can metabolised to produce energy and so has dietary consequences. - Alcohol promotes the uptake of blood glucose into liver glycogen causing a drop in bG. - Many alcoholic drinks contain sugar, particularly mixed drinks. - The symptoms of drunkenness and hypoglycaemia are similar - alcohol may mask the effects of a hypo. - Diabetics must remain sober enough to care for themselves (perform injections on schedule, etc). - Excess alcohol consumption can cause increased serum triglycerides. Few difficulties arise if following points are observed. Acceptable in moderation: - Red wines. - Dry or medium-dry white wines. - Dry sherries. - Dry light beers (lagers, light ales fermented with low residual sugar). - Spirits (whiskey, gin, vodka, etc) with "diet" mixers. Use with extreme caution due to high sugar content: - Sweet wines or sherries. - Ports. - Heavy or dark sweetened beers (stout, porters, etc which have high residual sugar). - Wine coolers. - Spirits with normal mixers. - Cocktails. - Liqueurs. Use with extreme caution due to very high alcohol concentration: - Neat (undiluted) spirits. General rules: - Simple drinks (wine, beer) are more reliable than complex mixed drinks, especially in company where you have less control over the contents or concentration. - Drink with or after food to avoid hypo problems. - Approach anything with caution if you are in doubt. - Low alcohol beers are not necessarily preferred - many of them are rather sweet. - Alcohol provides about 7 cal/g of food energy. Some is lost in the urine, but most is converted by the liver into forms which can be used for energy elsewhere in the body or stored as fat. Clearly these succinct rules are simplified and there are exceptions to them (for example, there are dry ports) but they are intended as a general guide. I make no attempt to define the term moderation, this will depend on the individual.
Subject: Necrobiosis lipoidica diabeticorum Necrobiosis lipoidica diabeticorum (NLD) consists of oval plaques, usually on the lower legs. It may start as small red spots or raised areas, which develop a shiny, porcelain-like appearance. The plaques often turn a light color due to extracellular fat (the "lipoidica"). They are often itchy or painful. Typically the spots turn a brownish color, which fades slowly but is permanent. NLD is not related to any other complication of diabetes. In particular, NLD does not presage eye, kidney or vascular problems. NLD is much more common in diabetics, who account for perhaps 2/3 of all cases. Many of the remainder develop diabetes, and NLD should be considered a warning sign of diabetes. Reports vary widely on exactly who is most at risk. About 1% of diabetics have some degree of NLD ... plus or minus 1%, depending on which report you read. Some reports say NLD occurs more often in young women, but some textbooks disagree. The real dangers seem to be ulceration, infection, and the stress from the appearance. Ulceration sometimes occurs spontaneously, and often as a result of trauma. Ulceration is often a result of scratching or trauma, and the ulceration from scratching sometimes heals very slowly. Thus avoiding scratching and trauma decreases the amount of ulceration, though some ulceration will occur anyway. There are some images of NDL lesions at http://tray.dermatology.uiowa.edu/DermImag.htm No particularly good treatment seems to be known. Topical steroids (that is, creams) are the most common first choice. The ulcerations usually heal if cared for properly, and drastic measures are not called for in most cases. William Biggs reports that skin grafts may be necessary in cases of severe ulceration, but do not tend to give results that are cosmetically attractive. Other treatments reported to help sometimes are oral aspirin, pentoxifylline, dipyridamole, locally injected steroids, and systemic steroids. No one claims to be able to predict what will work on any given patient, and often not much of anything is effective. However, the ulcers usually heal if given supportive treatment. Surgery should be avoided. Ineke van der Pol reports finding relief in Chinese herbal treatments. STEROID WARNING: locally injected and systemic steroids raise blood glucose and cause severe problems regulating blood glucose. These should be used only as a last resort. Topical steroids (creams and inhalers) cause no such problems. Note that treatment is not a medical necessity except for ulcerations and infections. Otherwise, the purpose of treatment is to prevent ulcerations and infections, decrease pain and itching, and improve the appearance. NLD is the subject of occasional articles in scientific journals on diabetes and on dermatology. Betsy Butler has researched the medical journals, finding little beyond what I've reported above -- in her words, "no good answers". _Therapy for Diabetes Mellitus and Related Disorders_, published by the ADA, has a section on necrobiosis lipoidica diabeticorum and its treatment. Ineke van der Pol has started a mailing list about NLD at http://groups.yahoo.com/group/necrobiosis. I thank the following people, especially Betsy, who posted the information from which I derived this section: Betsy Butler Polley (who says sorry, she doesn't have any information besides what's here) William Biggs <reddy_biggs(AT)msn.com> Tari M. Birch <tm_birch(AT)pnl.gov> Terence Griffin (who also says he doesn't have any other info) Bill Barner <barner(AT)mail.loc.gov> Ineke van der Pol <fluo(AT)chello.nl> (who has no further information but is happy to correspond about NLD if you wish)
Subject: Has anybody heard of frozen shoulder (adhesive capsulitis)? Short answers: adhesive capsulitis, aka frozen shoulder, is a painful condition that limits motion in one shoulder or both. It's not found exclusively in conjunction with diabetes, but occurs sufficiently more often with diabetes to be considered a diabetic complication. Don't be surprised, though, if your doctor isn't aware of this connection. Avoid surgery (which seldom helps) and cortisone (which plays havoc with blood glucose control); take physical therapy seriously; expect to take about two years to recover. Lee Boylan <lboylan(AT)cisco.com> wrote: There are three treatments usually offered for frozen shoulder: surgery, cortisone shots and exercises. Surgery offers the best transfer of money to a surgeon but the patient ends up needing to do exercises anyway. Cortisone offers quick pain relief but not full shoulder relief, so the patient is told to do exercises. Also, a DMer has drastically changed insulin requirements after taking a cortisone injection. Exercise, with alternating hot and cold packs and optional NSAIDs, offers slow and sometimes painful therapy that gets full or nearly full restoration of movement. Just don't let it discourage you, because improvement comes slowly. Keep at it! Eventually, you will have pain-free motion in your arm. And I'll re-emphasize what Lee says: DON'T TAKE STEROIDS LIGHTLY. Including cortisone. This warning should not be necessary, but unfortunately some doctors are unaware of what steroids do to blood glucose. If your doctor doesn't understand how serious a problem this is, insist on including an endocrinologist in your medical team. Lyle Hodgson <lyle(AT)world.std.com>, who has been through adhesive capsulitis in both shoulders, wrote: I suggest anybody who really wants to know about it who can visit Boston go to see Dr. Gordon Lupien, who used to be an orthopedic surgeon at Joslin and, according to a couple doctors I asked, knows more about adhesive capsulitis in diabetics than anyone else, period. Factoids: o Diabetics get "frozen shoulder" more than non-diabetics. o Women get "frozen shoulder" more than men. o Everybody I talked to who had ever treated "frozen shoulder" said that every patient they'd seen with it got over it in two years, no matter whether they did the exercises or not. o The exercises and ESPECIALLY PHYSICAL THERAPY help tremendously in retaining what range of motion you still have and in keeping the pain (which can be incredible) to a minimum. o The exact cause and pathology is completely unknown, but often adhesive capsulitis follows an untreated injury, or bursitis or tendonitis or even a period of no stretching exercises. o Adhesive capsulitis is often mis-diagnosed as a torn rotator cuff, which may well be involved but which will heal without the surgery most orthopedic surgeons prescribe for it. What's more, an often undiscussed side-effect of the surgery is permanently reduced range of motion, because tendons are snipped and resewn, and thus shortened. o If the exact pathology is unknown, it is certain that it involves scarification of the tissues in the shoulder "capsule", and from what I understand scar tissue is at least partly caused by glycosulation of tissues, so good control is (once again) the best prevention . o Cortisone is often prescribed for non-diabetic patients, and only for diabetic patients by doctors unfamiliar with the dramatic effect cortisone has on bloodsugar levels. Dr. Lupien told me cortisone doesn't even really have any long-term effect except to reduce the pain for awhile, and should be avoided completely since it could also permanently screw up how your body deals with cortisone. o Recommended treatment: daily exercises, biweekly physical therapy, daily (if possible) swimming, and acetaminephen (Tylenol). Extensive use of non-steroidal anti-inflammatories is not recommended. These include aspirin, ibuprofen (Advil/Motrin), and naproxen. Here's a sort-of-a- self test for adhesive capsulitis: 1. Lay on the floor on your back. Can you raise your arm over your head in a 180-degree arc and rest it on the floor without pain or *too* much stretching? 2. Stand sideways next to a wall, and walk your fingers up the wall until you can't reach any more. Can you almost press your armpit to the wall? If either of these gives you significant trouble -- you can't quite reach the floor behind your head, you can't touch the wall with your elbow, and either or both gives you pain -- you may (MAY, MAYBE, MIGHT) have adhesive capsulitis. Two doctors and one physical therapist told me that shoulders tend not to get the regular stretching that other joints get: a person can go for long periods of time without moving the shoulder much out of its usual hanging position, and then often the movement doesn't count for much. Hips are stretched at least a little several or many times a day, even with sedentary types who only sit, stand, sit, stand, walk a little, sit, etc.: the tissues are still fairly regularly manipulated so that it is much harder for them to freeze up. Lyle, who is always interested to hear what else anyone has learned about this little-studied, little-mentioned condition
Subject: Gastroparesis J K Drummond (no longer on the net, but well) contributed this section. Gastroparesis (gastroparesis diabeticorum if a diabetes complication) is nerve damage caused delayed gastric emptying. This more common than recognized irregular digestive slowdown interferes with blood glucose regulation and oral medicine absorption. Severity ranges from occasionally recurring bothersome symptoms like nausea, vomiting, constipation and diarrhea to total "stomach paralysis" -- the inability to consume/absorb any food. This worst stage requires tube feedings as the sole source of nutrition, IVs for hydration, and gastric suction for waste elimination. Be aware that "stomach trouble" may be more serious for one with diabetes and report digestive problems to your physician. Do not wait until you have had gastroparesis for several years or end up in the emergency room because you cannot eat. If you are a health professional, please routinely ask diabetics if they have digestive problems. Many with gastroparesis are undiagnosed or misdiagnosed and find little information about it. Often they have been used as guinea pigs in guessing games of hit or miss treatment trials. The scary quest has only just begun to find answers, reason, and solutions to this lesser known and mystifying complication of diabetes. There are people who have found answers in their lonely struggle with gastroparesis. Most folks with gastroparesis are female, with type 1 diabetes for 20-25 years and are age 25-45 at onset of gastroparesis. These incomplete lists of symptoms, treatments, helpful & stressful foods, and social aspects have been compiled mostly from patient reports. There is no all-patient guarantee of experience. CHECK WITH YOUR DOCTOR! S Y M P T O M S Physical Psychological nausea fatigue- muscle weakness vomiting fear constipation frustration diarrhea stress bloating lack of hunger indigestion high stomach acidity reflux weight loss inability to control blood sugars DIAGNOSIS** Symptoms together with gender &/or years of diabetes (clinical intuition) Gastric Mobility Transit Test Manometric Motility Study Diabetics are also subject to all forms of non-diabetic gastropathy so be aware that tests are necessary to eliminate and/or verify other diagnoses. TREATMENTS NUTRITION - MALNUTRITION Dietitians recommend 6 small meals daily Foods more easily digested Foods increasing symptoms fruit juices protein foods - meat, eggs canned fruits & vegetables raw fruits & vegetables soft starches (white bread dairy products & rice, mashed potatoes, cereals) caffeine, chocolate soups nuts & seeds baby foods non-carbonated beverages jello Liquid Nutritional Supplement Drinks Diabetic: Choice dm (Mead-Johnson), Glucerna (Ross Labs) Ensure Glucerna OS (Ross Labs) Non-diabetic: Ensure/Ensure plus, Sustacal (Ross Products Div) Nutrition via: IVs (fluids or TPN) Tube feedings (eq. Osmolite or Supplena) PHYSICAL - Remaining upright at least a half hour after eating, stomach massage, enemas, glycerine suppositories, stool softeners (for example, psyllium husk powder: Metamucil and other brands) DRUGS - May have adverse side effects on other conditions. Ask your MD! Reduce stomach acid: Zantac, Pepcid, Prilosec, Axid, Cytotec Increase motility: Reglan (metoclopramide) erythromycin Propulsid (cisapride) (in U.S. only under compassionate use protocol) bethanechol domperidone (U.S. availability: compassionate use only, and for veterinary use -- it's used to treat fescue toxicosis in horses) Zelnorm (tegaserod maleate), labeled in the US as of 2002 to treat women with irritable bowel syndrome (IBS) dominated by constipation. Zelnorm increases serotonin activity in the bowel by activating some 5HT4 receptors, which increases serotonin in the bowel and increases motility. The percentage of IBS patients who benefit is small but significant. It's not clear why the labeling is limited to women, though it seems likely to be a combination of the fact that 2/3 of IBS patients are women and the clinical studies barely reached statistical significance. If the effects in gastroparesis follow those in IBS, a small percentage of patients will see improvement, and some of those will be helped a lot. Information from the Zelnorm prescribing information on the http://www.zelnorm.com web site. Reduce digestive system spasm: dicyclomine Diarrhea: immodium, clonidine Nausea/vomiting: marinol, thorazine, ativan, inapsine, zephran, phenergan Surgical (physical implants or alterations) portacath or Hickman - IV hydration or Total Peritoneal Nutrition jejunostomy - tube feedings gastrostomy - for stomach suction (PEG tube) gastric resectioning or stomach removal gastric pacing - digestive pacemakers (experimental). Enterra Therapy by Medtronic, gastric electrical stimulation (GES) neurostimulator implants are approved as a humanitarian use device (HUD) since severe gastroparesis (refractory to drugs) has less then 4,000 cases per year. More info at http://www.medtronic.com/neuro/enterra/patient.html insulin pumps SOCIAL & PSYCHOLOGICAL ASPECTS Frustration for patient and physician from the difficulty in balancing insulin dosages and food intake to achieve level blood sugars with unpredictable slowed digestion. Additional psychological impact from delayed treatment due to relative medical unrecognition causing underdiagnosis and even misdiagnosis (ex. as anorexia nervosa if accompanied by vomiting). Lack of ostomy education. If/when eating ability returns following thinking that a normal diet could never again be eaten it may cause physical & emotional anorexia. Often felt burden to friends and family. Most information was collected by the pioneering health professionals of the defunct Gastroparesis Communication Network, updated by J K Drummond. There's an excellent web page on gastroparesis at http://www.uoflhealthcare.org/tabid/473/Default.aspx ** If you have been or are out of work pursue Medicare/Medicaid & Social Security Options IMMEDIATELY!
Subject: Extreme insulin resistance Mayer Davidson writes several pages about insulin resistance in his book _Diabetes Mellitus: Diagnosis and Treatment_. Except for what's in [brackets], the following information is from pp 126-132 of the third edition or pp 112-119 in the fourth edition. I'd recommend finding a copy. Most university libraries will have it, even those without medical schools. It's about $65; if necessary you can order from the Rittenhouse Medical Bookstore in Philadelphia at 215-545-6072. In this context, "insulin resistance" refers to patients requiring more than the arbitrary amount of 200 units/day. Davidson uses the term "insulin antagonism" for the phenomenon which is commonly part of type 2 diabetes. Davidson cites ten major causes of insulin resistance. The first eight are obvious major medical problems that you would immediately suspect were related, so I won't bother listing those. Rarely, insulin is destroyed at the subcutaneous injection site; this form can be treated with normal amounts of insulin administered intravenously or intraperitoneally. The most common form of insulin resistance is immune-mediated. Everyone taking injected insulin develops IgG antibodies to insulin. In most, the antibody levels are low. In about 1 in 1000, the levels are much higher, from 5 to over 1000 times higher than usual. In Davidson's words: The reason for this markedly enhanced response and the subsequent decline to normal levels is completely unknown. The antibodies bind to, and neutralize, the insulin. At one time it was thought that the antibodies resulted from impurities in the insulin preparations, and that using highly purified preparations would avoid the problem. This has proven not to be the case; purified insulin helps but usually does not resolve the problem, [though it seems to be worth trying]. Also, switching to a different insulin does not help, as the antibodies bind to beef, pork and human insulin. They may bind to one more than the others, but the titers of antibody are so high as to neutralize virtually all of any of the insulins. Two treatments which are effective are not generally available in the US. First, insulin can be treated with sulfuric acid. The modified molecule retains some biological activity but has reduced affinity for binding to the IgG antibodies to insulin. This treatment was tested by a Canadian laboratory in the late 1960s but is available in the US only by special petition to the FDA. Novo Nordisk Pharmaceutical can provide information at 609-987-5800. Second, fish insulin works in humans but does not bind to the antibodies. Cod insulin, for example, differs from human insulin in 33 amino acid positions compared with 3 differences for beef insulin. But nonmammalian insulins are not available in the US at all. This leaves the two treatments that are actually used on a regular basis, and a promising new treatment. Because this condition is rare, there's been little experience treating it with lispro insulin (Humalog). That experience is promising; it appears that the structural change in lispro may inhibit the antibody binding. If this is borne out by further experience, lispro will be the treatment of choice for extreme insulin resistance. Glucorticoids such as prednisone decrease the extreme insulin resistance, possibly by inhibiting the production of IgG antibodies. As the antibodies have a half life of 3-4 weeks, the response is delayed, during which time bg control is even more difficult due to the effects of the glucocorticoids. After several weeks the dosage can be reduced to maintenance levels or eliminated, but relapse is common. Since glucocorticoids have other nasty effects in addition to the problems listed above, there are significant problems with this course of treatment. Davidson's recommendation is based on The Good News: insulin resistance is self-limited and only lasts a few months to a year. He simply uses as much insulin as is needed in the meantime. U-500 concentration is available for this purpose. The antibodies delay the action, so even though U-500 is regular insulin it acts like a lente or semilente in resistant patients. For unknown reasons, much less U-500 is needed than the equivalent amount of U-100, 50% to 75% less. Since the situation is difficult to manage and is temporary, Davidson advises not trying for good bg control, but just avoiding ketosis and the overt symptoms of hyperglycemia (thirst, excess urination, infections). When insulin sensitivity returns, it can happen quite suddenly. Davidson starts reducing the high insulin doses when fasting bg is under 200 mg/dl (11.0 mmol/L). At these times, large amounts of insulin previously bound to the antibodies may be released, so avoiding hypoglycemia is a major concern. The return to normal sensitivity will take at least several weeks due to the half-life of the antibodies, and insulin requirements may fluctuate a great deal during this time. A fast response to U-500 insulin (2-4 hours from injection to measurably lower bg) may indicate the decline of insulin resistance. [This was the movie. Now go read the book.]
Subject: What is pycnogenol? Where and how is it sold? All sections on pycnogenol are written by Laura Clift <LauraRuss(AT)aol.com>. Numbers in parentheses refer to the section on "Pycnogenol references". Pycnogenol, a.k.a. Revenol, is a substance that has been mentioned in misc.health.diabetes as an aid/cure for several diabetic complications. Pycnogenol is a bioflavanoid, also identified as an oligomeric proanthocyanidin (OPC) and a procyanidin, which is found in the bark of conifers, specifically the maritime pine (_Pinus maritima_) and the Canadian spruce (_Tsuga canadensis_) and in grape seeds. The substance was patented in the US (patent 4,698,360) in 1985 by J. Masquelier of France. Pycnogenol is sold on several web sites in addition to health food stores. The web sites are set up in a pyramid scheme with the claims of quick riches for new distributors. Most of the sales pitches rely on first-person "testimonials". Some pitches include a list of published scientific studies that, according to the pitch, support the claims of the ad. In the following sections I examine the sales claims, investigate the ad's publication list, and establish a bottom line.
Subject: What claims do the sales pitches make for pycnogenol? Written by Laura Clift. Pycnogenol or Revenol (super-enriched pycnogenol) claim to be the world's most powerful anti-oxidant (vitamin C and E are anti-oxidants). The ads state pycnogenol is non-toxic, non-mutagenic, has high bioavailability, crosses the blood-brain barrier, enables vitamin C to remain in the body for 3 days as opposed to 3 hours, increases capillary resistance, decreases capillary fragility and permeability, decreases lower leg volume, strengthens collagen, and remains active in the body for 72 hours. Ads make claims that pycnogenol prevents, aids and/or cures the following conditions: arthritis, cancer, AIDs, stomach pains, aches and pains, aging, abnormal menstrual bleeding, asthma, atherosclerosis, bruises, diabetic retinopathies, dry skin, edemas, excessive blood sugar, fatigue, hay fever, heart attacks due to vascular accidents, hemorrhoids, inflamed tissue, internal bleeding, jet lag, kidney disease, menstrual cramps, phlebitis, poor circulation, skin elasticity, strokes due to cerebral accidents, stress, ulcers, varicose veins, multiple sclerosis, prostate problems, sleep disorders, dog and horse cancers, attention deficit disorders, and increased physical endurance.
Subject: What's the real published scientific knowledge about pycnogenol? Written by Laura Clift. (refs) point to "pycnogenol references" section. In a study examining the anti-oxidant action of several bioflavanoids, (-)-epicatechin 3-O-gallate and (-)-epigallocatechin 3-O-gallate were both more potent than pycnogenol against the free radicals DPPH, superoxide anion, OH, and OOH, although not by much (1). The toxicity of pycnogenol is not established in published reports. Proanthocyanidin mutagenicity is tricky, if it is completely pure it is considered non-mutagenic. However, there is an impurity that is very similar and hard to remove in the purification of proanthocyanidin that is mutagenic (2). No published work could be found on the bioavailability of pycnogenol in particular, but oral ingestion of bioflavanoids in general results in a low bioavailability (3). Pycnogenol does cross the blood-brain barrier in rats when given as an intraperitoneal injection (4). The same study seems to indicate that pycnogenol can increase capillary resistance and decrease capillary permeability in rats. A clinical study on 25 patients indicated an increase in capillary resistance (5). When administered by intraperitoneal injection to rats, chemically induced edema of the paw was decreased (6). There are no published studies on pycnogenol's interaction with vitamin C and most of the preventions, aids and/or cures claimed. However, procyanidol oligomers offered no protection for venous disease from hypoxia (lack of oxygen) (7).
Subject: How reliable is the literature cited by the pycnogenol ads? Written by Laura Clift. Masquelier J, Michaud J, Laparra J, Dumon MC. Flavanoids et pycnogenols. Int J Vit Nutr Res 1979;49(3):307-11. Article in French. Abstract states that the article describes pycnogenol chemically designating the compound as "pycnogenol" to distinguish it from the hundreds of other bioflavanoinds. Uchida S, Edamastu R, Hiramatsu M, et al. Condensed tannins scavenge active oxygen free radicals. Med Sci Res 1987;15:831-2. Pycnogenol is a free radical scavenger (anti-oxidant) in vitro (outside of a living animal, or, in a petri plate). Lagrue G, Oliver-Martin F, Grillot A. Etude des effects des oliomeres du procyanidol sur la resistance capillaire dans l'hypertension arterielle et certains nephropathies. La semaine des Hopitaux de Paris 1981; 57:1399-1401. French article. Abstract states capillary resistance increased in 25 patients. No dose amount or route of administration in the abstract. Cahn J, Borzeix MG. Etude de l'administration des oligomeres du procyanidoliques chez le rat: Effets observes sur les alterations de la permeabilite de la barrier hematoencephalique. La semaine des Hopitaux de Paris 1983;59:2031-4. French article. Abstract states that pycnogenol crosses the blood-brain barrier in the rat and affects capillary permeability. Route and dose not presented in abstract. Tixier JM, Godeau G, Rober AM, Hornebeck W. Evidence by in vivo and in vitro studies that binding of pycnogenols to elastin affects its rate of degradation by elastases. Biochem Pharmacol 1984;33(24):3933-9. Study with (+) catechin and pycnogenol (states they are related substances, but act differently, including the results of this study). Pycnogenol prevents the break down of elastin in vitro and in rabbits. Kuttan R, Donnelly PV, DiFerrainte N. Collagen treated with (+)-catechin becomes resistant to the action of mammalian aollagenase. Experentia 1981;37:221-3. (+) catechin is not pycnogenol (see above). Study does not investigate pycnogenol. Reimann HJ, Lorenz W, Fischer M, et al. Histamine and acute hemorrhagic lesions in rat gastric mucosa: prevention of stress ulcer formation by (+)-catechin, an inhibitor of specific histidine decarboxylase in vitro. Agents and Actions 1977;71:69-72. (+) catechin is not pycnogenol (see above). Study does not investigate pycnogenol. Markle RA, Hollis TM. Rabbit aortic endothelial and medical histamine synthesis following short-term cholesterol feeding. Exp Mol Pathol 1975;23:117-23. Markle RA, Hollis TM. Variations in rabbit aortic endothelial and medical histamine synthesis in pre- and early experimental atherosclerosis. Proc Soc Exp Biol Med 1977;155:365-8. Hollis TM, Furniss JV. Relationship between aortic histamine formation and aortic albumin permeability in atherogenesis. Proc Soc Exp Biol Med 1980;165:271-4. Does not study pycnogenol or any bioflavanoid. Logic may go like this: pycnogenol is similar to (+) catechin which can effect histamines. Here are some cardiac/circulatory problems that are affected by histamine. Therefore, pycnogenol will prevent these diseases. Logic may be OK for a hypothesis but is flawed as a conclusion, especially since (+) catechin and pycnogenol act differently in most studies (see above). Feine-Haake G. A new therapy for venous diseases with 3,3,4,4,5,7-hexa-dihydro-flauan. Z Allgemeinmed 1975;51(18):839. German article, no abstract translation; chemical name implies (+)-catechin was studied. Blazso G, Gabor M. Oedema-inhibiting effect of procyanidin. Acta Physiol Acad Sci Hung 1980;56(2):235-40. Chemically induced edema of a rat's paw was decreased with intraperitoneal injections of pycnogenol.
Subject: What's the bottom line on pycnogenol? Written by Laura Clift. (refs) point to "pycnogenol references" section. All bioflavanoids are anti-oxidants (1,8,9) and may effect capillary hyperpermeability (8,9), inflammations (3,8), and edemas (8). However, there is no bioflavanoid deficiency condition, and they have "no accepted preventive or therapeutic role in vascular purpura, hypertension, degenerative vascular disease, rheumatic fever, arthritis, cancer, or any other condition" (9). This was as of 1988; no mention of bioflavanoids is made in the 1994 edition of this reference. Most pycnogenol studies and/or claims come from the early 70's to mid 80's. Promising starts are never followed up on. Most later studies seem negative (both pycnogenol and bioflavanoids), especially about the oral route. With all but one study performed in rodents, there is a very definite lack of information on how this substance acts in humans and what possible side-effects it produces. The sales pitch seems to be taken from the 1985 patent. Filing a medical patent doesn't mean the substance is thoroughly studied and its applications are determined. A patent is filed when preliminary studies look promising and you try to come up with every possibly use for the compound, no matter how far out in left field it may be. If you do not hold the patent for the application, someone else could conceivably use your compound for that application and owe you nothing or a very reduced royalty. In short, patent claims have no medical significance.
Subject: Pycnogenol references Written by Laura Clift. This is the section to which the (refs) point. 1. Uchida S, Edamastu R, Hiramatsu M, et al. Condensed tannins scavenge active oxygen free radicals. Med Sci Res 1987;15:831-2. 2.Yu CL, Swaminathan B. Mutagenicity of proanthocyanidins. Food Chem Toxicol 1987;25(2):135-9. 3. Namgoong SY, Son KH, Chang HW, Kang SS, Kim HP. Effects of naturally ocurring flavanoids on mitogen-induced lymphocyte proliferation and mixed lymphocyte culture. Life Sci 1994;54(5):313-20. 4. Cahn J, Borzeix MG. Etude de l'administration des oligomeres du procyanidoliques chez le rat: Effets observes sur les alterations de la permeabilite de la barrier hematoencephalique. La semaine des Hopitaux de Paris 1983;59:2031-4. 5. Lagrue G, Oliver-Martin F, Grillot A. Etude des effects des oliomeres du procyanidol sur la resistance capillaire dans l'hypertension arterielle et certains nephropathies. Las semaine des Hopitaux de Paris 1981; 57:1399-1401. 6. Blazso G, Gabor M. Oedema-inhibiting effect of procyanidin. Acta Physiol Acad Sci Hung 1980;56(2):235-40. 7. Michiels C, Arnould T, Houbion A, Remacle J. A comparative study of the protective effect of different phlebotonic agents on endothelial cells in hypoxia. Phlebologie 1991;44(3):779-86. 8. Lonchampt M, Guardiola B, Sicot N et al. Protective effect of a purified flavanoid fraction against reactive oxygen radicals. in vivo and in vitro study. Arzneimittelforschung 1989;39(8):882-5. 9. Shils ME. Modern nutrition in health and disease. Philadelphia: Lea and Febiger, 1988. p472.
Subject: Who did this? -- Edward Reid <edward@paleo.org> Tallahassee FL -- Art works by Melynda Reid: http://paleo.org eid: http://paleo.org Melynda Reid: http://paleo.org

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