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High Glucose and Insulin Resistance
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05/03/05 02:40
Andrew 
05/03/05 02:40
Andrew 
Arthritis and Dupuytren~sq~s (continued)

Although it is obviously possible for people to have both Dupuytren's and arthritis (as contributors to this forum have witnessed), and frozen shoulder is also commonly associated with Dupuytren's, yet it is a curious fact that, according to the Reykjavik study (Google 'Iceland Dupuytren arthritis'; and for another article on this topic Google 'Arafa Dupuytren arthritis') Dupuytren's sufferers in general are LESS prone to getting other joint complaints, specifically rheumatoid arthritis. Why this should be (unless it's genetic) is a puzzle. One pertinent fact may be that 80% of rheumatoid arthritis sufferers are women, whereas (according to the Reykjavik study) 80% of Dupuytren's sufferers are men.

05/06/05 02:19
Theresa M. Lynch

not registered

05/06/05 02:19
Theresa M. Lynch

not registered

Diabetes and Dupuytren~sq~s

I have Diabetes for 19 years. I am using an insulin pump for about two years. Now, I have developed Dupuytren Contraction. It is a year now that I contracted this problem. Is this a big problem for me. Is there anything that can be done. I have this contraction in my left hand, the fourth finger with a lump. Having a sharp pain and having a bit of a lump. I am having a difficult time using my hand and closing my fingers. Pain and stiffness presisted.
Please let me know what I can do for this situation.

Sincerely, Theresa M. Lynch San Diego Residences

05/07/05 02:13
Andrew 
05/07/05 02:13
Andrew 
Diabetes and Dupuytren~sq~s

Dear Theresa,

I am sorry to hear that your Dupuytren's is painful. If it is any consolation, Dupuytren's is supposed to be usually less aggressive in diabetics. A study by Fossati and others says: "The contracture is usually not severe in diabetes, is nodular in form, and usually crushes the palmar surface of the long and ring fingers. It is usually well tolerated by the patients and surgery is rarely indicated, particularly in view of the advanced age of many patients."

However, if you think surgery is needed in your case, Dr Eaton's excellent "Dupuytren's Faqs and Facts" webpage has everything you need to know about the disease and its treatment, as well as links to all the studies that back up his points. (To find the page, just type "Dupuytren Faqs" into Google.)

Speaking for myself, I have the impression that my nodule becomes more active when I occasionally indulge (e.g. drink alcohol), and quietens down when I am strict about my diet. I would guess that if somehow you could change your diet in order to lower your blood sugar and reduce your dependence on insulin (some type 2 diabetics have been able to do this, though I don't know if it would be possible in your case), your Dupuytren's might quieten down too.

agdg@supanet.com

05/15/05 02:25
Andrew 
05/15/05 02:25
Andrew 
Blood test

In my posting of a few days ago I mentioned evidence that Dupuytren's disease might be evidence not only of abnormally high blood sugar but also of abnormal levels of lipids (fats) in the blood. At that time I went for a blood test to check out my own levels. Sure enough, when the results came back the level of LDL (the 'bad') cholesterol was higher than it should be, which I had never realised before, so it was worth having the test for that reason alone. My glucose was normal, although at 5.4 (97 mg/dl) a little on the high side, and unexpectedly (unless there was an error) my triglyceride level at 0.73 (65 mg/dl) was unusually low. If anyone has had similar results it would be interesting to hear. I am hoping that whatever diet proves successful in stabilising the levels of sugar and lipids will also prove successful in stabilising the Dupuytren's. I don't think I've found the right diet quite yet but I'm working on it.

Incidentally, in case anyone thinks that my high cholesterol is due to the South Beach-type diet which I mentioned earlier, I have moved away a little from that diet, since I didn't think it quite suited me, and in the past few weeks I have eating much less protein but more fruit and vegetables. For a while my weight remained stable, but when I added a couple of spoonfuls of cider vinegar with a little honey in warm water every morning it began to fall again. I have now lost about 20 lbs in three months.

agdg@supanet.com

05/19/05 02:07
Andrew 
05/19/05 02:07
Andrew 
More on cholesterol

Concerning the MRFIT heart disease study which I mentioned in my last posting, there is more information which is instructive. From the 316099 white American men screened, the researchers went on to select 12866 who, because of their smoking, high cholesterol, and high blood pressure, seemed particularly at risk of heart disease. This group was divided into two: half were encouraged to give up smoking, change their diet, and take a drug to reduce their blood pressure, while the other half were left to their own devices as a control. The results were surprising: after 7 years, deaths from heart disease in the intervention group were slightly lower than in the control group, but deaths from other diseases were slightly higher, so that overall there was no difference at all in mortality between the two groups. After 16 years, however, there was a slight difference: in the intervention group about 6% fewer people had died than in the control group. Curiously, in the intervention group (more of whom had given up smoking) there were significantly more deaths from lung cancer than in the control group (135 deaths compared with 117), a fact which the researchers found it difficult to explain. (For details of the studies, Google 'PubMed MRFIT'.) I believe that other studies, such as the Oslo study and the LRCCPPT study, had similar results.

One point here surely is that taking a drug to reduce cholesterol may possibly slightly reduce your chances of dying of a heart attack, but on the other hand it may increase your chances of dying of cancer. Maybe that cholesterol is there for a reason! But general measures to improve health - stopping smoking, sleeping 8 hours a night, walking half an hour a day, avoiding fried food, sugar, and caffeine etc. - surely cannot do anything but good.

agdg@supanet.com

05/20/05 02:08
Andrew 
05/20/05 02:08
Andrew 
Cholesterol lowering studies (continued)

A correction to my posting of yesterday: not all the men in the MRFIT trial were white: they were mostly white but 7% were black.

In my comment that the LRS-CPPT study and the Oslo study produced similar results to the MRFIT trial (which I took from a book by Dr James Le Fanu) I think I overstated the case. In fact these studies seem to have produced more encuraging results than the MRFIT trial. In the Oslo study (Google 'PubMed Oslo Diet Smoking'), half of 1232 at-risk men were encouraged to improve their health by giving up smoking and eating a healthier diet. At the end of 9 years, 19 of the intervention group had died (of all causes) compared with 31 of the control group (i.e. 39% fewer); so this trial was quite successful.

The LRC-CPPT trial (in which half a group of 3806 men were given a drug called cholestyramine to reduce their cholesterol), did not pay attention to smoking, but only to reducing cholesterol. After 7 years of this trial, deaths due to heart-disease were 19% fewer in the drug-treated group than in the control group (although total deaths were only 7% fewer, due to a greater number of violent and accidental deaths in the cholestyramine group). A follow-up after 13 years found that the group who had taken the drug during the 7-year trial had had about 9% fewer deaths overall, mostly because of fewer heart-disease deaths. Deaths from other causes did not seem to have increased, although the group who had taken the drug did have a greater number of non-fatal cancers. (Google 'Lipid Research Clinics 1992'.)

More up-to-date studies using statins have reported similar results. For example, the MRC/BHF Heart Protection Study, which followed 20536 British people for 5 years, treating half of them with simvastatin, found at the end of the period that overall mortality was 1328 in the treated group compared with 1507 in the control group (about 12% less). (Interestingly, for those of you who like vitamins, the researchers in this study also gave half their subjects a daily antioxidant vitamin A/C/E tablet, but found that there was no effect at all, adverse or beneficial, on mortality between the two groups. For details, Google 'PubMed MRC/BHF heart vitamin'.)

The Scandinavian Simvastatin Survival Study (known as the '4S' study) likewise found, after ten years, that the number of overall deaths in the group treated with simvastatin was about 11% lower than in the control group.

In all of these trials using drugs there seems to have been a large fall (about 19%) in the number of deaths from heart attacks and stroke, but deaths from other causes are more or less the same in the treated and untreated groups. Whether this would continue to be so if the trials were extended over 20 or 30 years is unclear. Speaking for myself, although my total cholesterol at 5.23 mmol/l (202 mg/dl) is slightly high, I intend to try to lower it by natural means first before I take a drug the long-term effects of which are still unknown.

05/22/05 02:23
Michael

not registered

05/22/05 02:23
Michael

not registered

Dup~sq~s and diet


The following is a good synopsis of current scientific thinking on the causes of Dup's. To paraphrase it, the triggering events for Dup's are tiny local ischemias (hemorrhages of the blood vessels) in the palmar tissue. This explains the association of Dup's with diabetes, smoking, and alcoholism, for those conditions are also characterized by ischemias. The ischemias expose the fascia tissue to free radicals and certain growth factors in the blood. It is believed that the fibroblast cells in Dup's sufferers are genetically hypersensitive to the growth factors. They respond by growing inappropriately, which eventually results in hypovascularity (tissue with lack of blood vessels), which causes more ischemias, which causes more fibroblast production, and so on.

So the claims put forth in this board topic about insulin resistance and diet and so forth are largely nonsense. It seems the original triggering ischemias can in some cases be hastened or delayed by lifestyle factors, but our genes dictate the sensitivity of our fibroblasts to growth factors. So once the Dup's starts, changing diet can have little or no effect. The solution must be medical.

'Lappi et al. (1992) have proposed a model of the pathophysiology of Dupuytren's contracture based on the potential contribution of growth factors. They suggest that the palmar fascia will be exposed to repeated microhemorrhages due to ischemic vascular disease, liver pathology, trauma or other causes. Because of their genetic predisposition, these normal palmar fascia fibroblasts will respond abnormally to the enduing release of platelets and inflammatory cells. Cells in the fascia are now exposed to PDGF and TGF-beta, both known to be released in high quantities from platelets. PDGF stimulates fibroblasts proliferation and exposure to TGF-beta initiates the production of collagen. In patients who develop Dupuytren's contracture, the genetically altered fibroblasts ate more sensitive to these growth factors. The fibroblasts proliferate and produce abundant collagen. As this proliferation continues unchecked, the thickened fascia eventually becomes hypovascular and more prone to hypoxia and microhemorrhages. The production of oxygen-free radicals stimulates further proliferation of abnormal fibroblasts. A vicious cycle ensues.'

05/24/05 02:18
Andrew 
05/24/05 02:18
Andrew 
Dupuytren~sq~s and diet

Now the debate is getting interesting! What you say about fibroblasts is highly relevant, Michael. However, to go on from there to claim that all the speculation on this thread about insulin resistance and diet is largely nonsense is going too far. Your second paragraph is a nonsequitur. You are like the blind man who had hold of the elephant's tail and declared the elephant was like a rope; he refused to listen to the other blind man who had hold of its leg and insisted it was like a tree.

You might as well argue about hayfever, that, since the cause is known (namely pollen in the air), it can have nothing to do with what we eat or drink. On the contrary: if you eat a lot of yoghurt on a polleny day, you will sneeze more; and if you fast for 24 hours, your sneezing will stop. So diet, even though not the primary cause, does have something to do with it, in that it creates the conditions for disease to take effect. It may well be that Dupuytren's is the same.

I was interested to read on www.frozenshoulder.com that frozen shoulder is five times more common in diabetics. We have already learnt that both diabetes and frozen shoulder frequently go together with Dupuytren's. So here again is a complex of diseases (frozen shoulder, Dupuytren's, and diabetes) that are all associated with each other. Dupuytren's and diabetes are also linked by associations with hypothyroidism and dylipidemia.

In view of this association, it is fair to ask: what kind of disease is Dupuytren's? Is it a disease like Huntingdon's, which, as far as we know, is purely hereditary and cannot be helped or prevented by diet? Or is it more like diabetes and cardiovascular disease, which can often be alleviated and sometimes even completely cured by diet and exercise?

You may be right that once the process of nodule formation has started it can't be stopped. However, some people have reported that their nodules have ceased growing or even reversed when they stopped taking glucosamine chondroitin; and Peyronie's disease plaques have also been reported to come and go. It seems not impossible, therefore, that if we can find and remove the cause of Dupuytren's (whether it is glucosamine or some other cause in our individual case), we might be able to halt the disease, or at the very least prevent it from starting up in another place or in the other hand.

Moreover, as I said earlier, since Dupuytren's is associated more often than not with high fasting glucose, high cholesterol, sooner than average death, etc., it is not merely a disease in its own right but also a sign of a generally unhealthy body. Even if it is impossible to stop the Dupuytren's itself once the process has begun, it would still be worth investigating and correcting these factors simply in order to improve our general health and life expectancy.

agdg@supanet.com

06/05/05 02:20
Andrew 
06/05/05 02:20
Andrew 
Dupuytren~sq~s and retinopathy

The theory quoted by Michael a couple of postings ago which suggests that Dupuytren's disease arises from microhemorrhages and ischemic vascular disease in the hand is interesting but does not address the question, why is Dupuytren's disease more common in diabetics than in non-diabetics? And what causes this vascular disease in the first place?

Moreover, the description given in the theory, even if not exactly the same, sounds not at all dissimilar to the similar microhemorrhages and ischemic vascular disease that occur in diabetic retinopathy (see for example http://www.stlukeseye.com/Conditions/DiabeticRetinopathy.asp for a good account). Is there a connection? If so, then diet is indeed very relevant to slowing the progress of Dupuytren's. I quote from the above-mentioned website on diabetic retinopathy: "Researchers have found that diabetic patients who are able to maintain appropriate blood sugar levels have fewer eye problems than those with poor control. Diet and exercise play important roles in the overall health of those with diabetes." I would guess that exactly the same is true of Dupuytren's.

Genetics doubtless also plays a role, but there is no reason to throw in the towel and say nothing can be done! Genetics also plays a role in fatness - some people are inclined to be skinny and others to be chubby - but is that any excuse for obesity?

So my money is still on diet. Could it be that your penchant for coffee-drinking, Michael, and my fondness for wine are contributing to the disease?

agdg@supanet.com

06/16/05 02:00
Andrew 
06/16/05 02:00
Andrew 
More statistics from the Reykjavik study

I have managed to get hold of the full article published in 2000 reporting on the Reykjavik Study (of which the abstract is available on the Internet - Google 'Dupuytren Reykjavik' to find it) and thought it might be interesting to pass on a few of the further details which are not mentioned in the abstract.

The researchers examined 1297 Icelandic men and 868 Icelandic women aged between 45 and 74. 249 (19.2%) of the men and 38 (4.4%) of the women had signs of Dupuytren's. Of the men 184 had stage 1 of the disease (i.e. without contractures) and 65 had stage 2 (i.e. with contractures). Of the women 34 had stage 1 but only 4 had stage 2. Stage 2 was found in all age-groups of the men, but in the women only in those above 65. The disease was equally common in left and right hand in both sexes.

Because the number of women with the disease was too small to draw significant statistical conclusions, all the remaining statistics reported below (concerning blood sugar, cholesterol, age, weight, occupation and smoking) refer to the men only.

Comparing the two groups (Dupuytren's and non-Dupuytren's) the researchers surprisingly (in view of what has been published in other studies) found no significant difference in the incidence of diabetes or in levels of cholesterol or triglycerides. If anything the mean cholesterol level of the Dupuytren's men (231.0 mg/dl) was lower than that of the non-Dupuytren's men (234.4), but the difference was not significant. Blood pressure and incidence of arcus senilis (a white ring round the eye) were also similar in both groups.

Where the researchers did find significant differences were in age, weight, fasting blood glucose, occupation, and smoking.

(a) Age. The mean age of the Dupuytren's men was 60.8, of the non-Dupuytren's 56.0. This is to be expected since the disease grows commoner with age.

(b) Weight. The mean weight of the Dupuytren's men was 76.5 kg, of the non-Dupuytren's 81.9 kg. The mean heights were 1.756 m vs. 1.770 m. The body mass index (BMI = kg/mXm) of the two groups was 25.0 and 26.1 respectively. This was judged to be highly significant, with a probability of it happening by chance of less than 1/1000. So although neither group was exactly skinny (a BMI of 25 is on the cusp between 'normal' and 'overweight') the Dupuytren's men were skinnier.

(c) Fasting blood glucose. The mean fasting glucose of the Dupuytren's men was 84.7 mg/dl and non-Dupuytren's 81.1. [Converting, that would be 4.7 vs. 4.5 mmol/l.] The researchers calculated a 1/25 probability of this happening by chance.

(d) Occupation. Dupuytren's was more common among manual workers (labourers, seamen, farmers, masons, carpenters, blacksmiths, etc.) (29.7% of the Dupuytren's men were manual workers compared with 17.2% of the non-Dupuytren's group). Conversely Dupuytren's was less common among university-educated men (5.6% of the Dupuytren's men were in occupations requiring a university degree compared with 11.7% of the non-Dupuytren's men).

(e) Smoking. Dupuytren's was slightly commoner among smokers. 82% of the Dupuytren's men were smokers or former smokers, compared with 77% of the non-Dupuytren's. The probability of this happening by chance was 1/20.

The researchers noted that smoking and elevated blood glucose are both known to affect peripheral circulation. They also speculated that cold weather might be a factor in causing the disease.

agdg@supanet.com

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