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How can I manage my complex regional pain syndrome condition better?

January 25, 2012 by Leave a Comment


Answer:  Try decreasing your intake of Omega 6 fatty acids and trans fatty acids.

It’s a long shot based on the study findings below, but if your current intake of trans fat and Omega 6 fatty acids is high, it’s worth a shot cutting back on your trans fat and Omega 6 fatty acids to see if your symptoms improve.
Pain Med. 2010 Jul;11(7):1115-25. Epub 2010 Jun 8.

Do omega-6 and trans fatty acids play a role in complex regional pain syndrome? A pilot study.

Ramsden C, Gagnon C, Graciosa J, Faurot K, David R, Bralley JA, Harden RN.

Abstract

OBJECTIVES:

The study aims to compare the omega-6 (n-6) and omega-3 (n-3) highly unsaturated fatty acids (HUFA), and trans fatty acid (trans FA) status of Complex Regional Pain Syndrome (CRPS) patients to pain-free controls.

DESIGN:

Case control study. Setting. The setting was at a multidisciplinary rehabilitation center.

PATIENTS:

Twenty patients that met the Budapest research diagnostic criteria for CRPS and 15 pain-free control subjects were included in this study. Outcome Measures. Fasting plasma fatty acids were collected from all participants. In CRPS patients, pain was assessed using the McGill Pain Questionnaire-Short Form. In addition, results from the perceived disability (Pain Disability Index), pain-related anxiety (Pain Anxiety Symptom Scale Short Form), depression (Center for Epidemiologic Studies Depression Scale Short Form), and quality of life (Short Form-36 [SF-36]) were evaluated.

RESULTS:

Compared with controls, CRPS patients demonstrated elevated concentrations of n-6 HUFA and trans FA. No differences in n-3 HUFA concentrations were observed. Plasma concentrations of the n-6 HUFA docosatetraenoic acid were inversely correlated with the “vitality” section of the SF-36. Trans FA concentrations positively correlated with pain-related disability and anxiety.

CONCLUSION:

These pilot data suggest that elevated n-6 HUFA and trans FA may play a role in CRPS pathogenesis. These findings should be replicated, and more research is needed to explore the clinical significance of low n-6 and trans FA diets with or without concurrent n-3 HUFA supplementation, for the management of CRPS.

Filed Under: complex regional pain syndrome, managing less common health problems, physical Tagged With: , , , ,

How can I manage my multiple sclerosis condition better?

January 24, 2012 by Leave a Comment

Answer: Watch this TED video and see if you feel inspired to eat more fruit and vegetables and to cut back on processed foods.

Filed Under: managing less common health problems, multiple sclerosis, physical Tagged With: , , , , ,

How can I manage my multiple sclerosis condition better?

January 24, 2012 by Leave a Comment

Answer: Check out the Overcoming Multiple Sclerosis plan and see if it’s something you’d like to try.


The Overcoming Multiple Sclerosis website gives lots of up-to-date scientific information about MS and management suggestions.


Here’s an excellent video where Professor George Jelinek discusses the results of a scientific evaluation of his MS treatment program:

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Qual Prim Care. 2010;18(6):379-89.

Effect of a residential retreat promoting lifestyle modifications on health-related quality of life in people with multiple sclerosis.

Li MP, Jelinek GA, Weiland TJ, Mackinlay CA, Dye S, Gawler I.

Abstract

AIM:

To evaluate the effect of a residential retreat on promoting lifestyle modification for the health-related quality of life (HRQOL) of people with multiple sclerosis (MS).

METHODS:

A longitudinal cohort study of adults with self-reported MS who voluntarily attended a five-day residential retreat in rural Victoria, Australia. Participants were asked to complete the MSQOL-54 questionnaire just prior to the retreat, and at one year and 2.5 years post-retreat.

RESULTS:

Of 188 participants 109 (58%) completed the questionnaire. The cohort showed a significant improvement in HRQOL at one year and 2.5 year follow-up. After one year, overall quality of life (QOL) domain had increased from 73.4 to 81.7 (P<0.001), physical health composite from 66.2 to 76.4 (P=0.001) and mental health composite from 73.7 to 83.6 (P<0.001) in the subset of 76 with data at both time points. After 2.5 years, overall QOL had increased from 68.4 to 71.7 (P=0.03), physical health 59.7 to 70.0 (P=0.01), and mental health 66.9 to 76.6 (P<0.01) in the subset of 44 with data at both time points.

CONCLUSIONS:

HRQOL usually deteriorates over time in people with MS. Attendance at a residential retreat promoting lifestyle modification appears to have a significant short-medium term positive effect on QOL for people with MS. General practitioners caring for people with MS should consider the potential benefits of this approach in overall management.


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Qual Prim Care. 2009;17(1):55-61.

Managing multiple sclerosis in primary care: are we forgetting something?

Jelinek GA, Hassed CS.

Abstract

Multiple sclerosis (MS) is the commonest debilitating, progressive neurological disorder in most Western countries. It is important for many reasons, including the personal costs, levels of disability produced, age group affected and the resultant economic burden placed on individuals, families and the community. Although it is thought to be an autoimmune condition, in general little is understood about the causation of MS and the factors that trigger or contribute to exacerbations and deterioration. This overview of the literature will consider some important studies examining the relationship between lifestyle and psychosocial factors and MS progression. These studies suggest that nutrition, sunlight, exercise, stress and social factors can all modulate the rate of progression of MS and the level of disability. Although appearing in respected journals, this information tends to be little known or discussed by clinician and patient alike. If lifestyle approaches do offer potential avenues for therapy, this raises important questions regarding the management of MS in primary care. More widely prescribed conventional medicines have been studied in more detail but are only modestly effective and may have significant side-effects. Are we presently neglecting the most effective approach of combining the non-drug or holistic approach with the best of conventional pharmaceutical therapies, and if so what are the implications of this omission?


Read the complete scientific paper:

Managing multiple sclerosis in primary care: are we forgetting something?

Some good quotes from the paper:

As Ornish was publishing his groundbreaking research
in the holistic management of heart disease (including
a low-fat diet, exercise, stress reduction and stopping
smoking),1 research from Canada was being published
in The Lancet and elsewhere on a dietary intervention
for the management of MS.2,3 The results were possibly
even more startling, but received relatively little notice
in the wider medical community. Swank found that
over a 34-year follow-up only 31% of MS patients
adhering to a low saturated fat diet (less than 20 g/day)
died, compared with approximately 80% of patients
not sticking to the diet.2,3 Furthermore, in the group
who started with a lower level of disability only5%had
died. The rates of disease progression and disability
were also vastly different in the two groups; ‘when those
who died from non-MS diseases were excluded from
the analysis, 95% survived and remained physically
active’.2

The lifestyle approach in primary care, especially for
chronic illness, should be first-line therapy and not an
afterthought. The slowness in adoption of this approach
needs to be examined. In contrast, there is a
tendency to readily embrace heavily promoted drug
treatments with their associated high cost and frequent
side-effects, despite concerns regarding supporting
evidence and patient quality-of-life issues.
Importantly, however, a holistic approach is not an
argument against the judicious and appropriate use
of pharmacological and technological advances. A
balanced approach in primary care uses the best that
every therapeutic modality has to offer.

Filed Under: managing less common health problems, multiple sclerosis, physical Tagged With: , , ,

How can I improve my congestive heart failure condition?

January 21, 2012 by Leave a Comment

Answer: Talk to your doctor about eating more dark chocolate.

Eur Heart J. 2011 Dec 15.

Cardiovascular effects of flavanol-rich chocolate in patients with heart failure.

Flammer AJ, Sudano I, Wolfrum M, Thomas R, Enseleit F, Périat D, Kaiser P, Hirt A, Hermann M, Serafini M, Lévêques A, Lüscher TF, Ruschitzka F, Noll G, Corti R.

Abstract

Aims

Flavanol-rich chocolate (FRC) is beneficial for vascular and platelet function by increasing nitric oxide bioavailability and decreasing oxidative stress. Congestive heart failure (CHF) is characterized by impaired endothelial and increased platelet reactivity. As statins are ineffective in CHF, alternative therapies are a clinical need. We therefore investigated whether FRC might improve cardiovascular function in patients with CHF.

Methods and results

Twenty patients with CHF were enrolled in a double-blind, randomized placebo-controlled trial, comparing the effect of commercially available FRC with cocoa-liquor-free control chocolate (CC) on endothelial and platelet function in the short term (2 h after ingestion of a chocolate bar) and long term (4 weeks, two chocolate bars/day). Endothelial function was assessed non-invasively by flow-mediated vasodilatation of the brachial artery. Flow-mediated vasodilatation significantly improved from 4.98 ± 1.95 to 5.98 ± 2.32% (P = 0.045 and 0.02 for between-group changes) 2h after intake of FRC to 6.86 ± 1.76% after 4 weeks of daily intake (P = 0.03 and 0.004 for between groups). No effect on endothelial-independent vasodilatation was observed. Platelet adhesion significantly decreased from 3.9 ± 1.3 to 3.0 ± 1.3% (P = 0.03 and 0.05 for between groups) 2 h after FRC, an effect that was not sustained at 2 and 4 weeks. Cocoa-liquor-free CC had no effect, either on endothelial function or on platelet function. Blood pressure and heart rate did not change in either group.

Conclusion

Flavanol-rich chocolate acutely improves vascular function in patients with CHF. A sustained effect was seen after daily consumption over a 4-week period, even after 12 h abstinence. These beneficial effects were paralleled by an inhibition of platelet function in the presence of FRC only.Trial Registration ClinicalTrials.gov Identifier: NCT00538941.

Filed Under: congestive heart failure, managing less common health problems, physical Tagged With: , ,

How can I improve my chronic fatigue?

January 21, 2012 by Leave a Comment

Answer: Try eating dark chocolate.



Nutr J. 2010 Nov 22;9:55.

High cocoa polyphenol rich chocolate may reduce the burden of the symptoms in chronic fatigue syndrome.

Sathyapalan T, Beckett S, Rigby AS, Mellor DD, Atkin SL.

Abstract

BACKGROUND:

Chocolate is rich in flavonoids that have been shown to be of benefit in disparate conditions including cardiovascular disease and cancer. The effect of polyphenol rich chocolate in subjects with chronic fatigue syndrome (CFS) has not been studied previously.

METHODS:

We conducted a double blinded, randomised, clinical pilot crossover study comparing high cocoa liquor/polyphenol rich chocolate (HCL/PR) in comparison to simulated iso-calorific chocolate (cocoa liquor free/low polyphenols(CLF/LP)) on fatigue and residual function in subjects with chronic fatigue syndrome. Subjects with CFS having severe fatigue of at least 10 out of 11 on the Chalder Fatigue Scale were enrolled. Subjects had either 8 weeks of intervention in the form of HCL/PR or CLF/LP, with a 2 week wash out period followed by 8 weeks of intervention with the other chocolate.

RESULTS:

Ten subjects were enrolled in the study. The Chalder Fatigue Scale score improved significantly after 8 weeks of the HCL/PR chocolate arm [median (range) Exact Sig. (2-tailed)] [33 (25 – 38) vs. 21.5 (6 – 35) 0.01], but that deteriorated significantly when subjects were given simulated iso-calorific chocolate (CLF/CP) [ 28.5 (17 – 20) vs. 34.5 (13-26) 0.03]. The residual function, as assessed by the London Handicap scale, also improved significantly after the HCL/PR arm [0.49 (0.33 – 0.62) vs. 0.64 (0.44 – 0.83) 0.01] and deteriorated after iso-calorific chocolate [00.44 (0.43 – 0.68) vs. 0.36 (0.33 – 0.62)0.03]. Likewise the Hospital Anxiety and Depression score also improved after the HCL/PR arm, but deteriorated after CLF/CP. Mean weight remained unchanged throughout the trial.

CONCLUSION:

This study suggests that HCL/PR chocolate may improve symptoms in subjects with chronic fatigue syndrome.

Read the complete scientific paper:

High cocoa polyphenol rich chocolate may reduce the burden of the symptoms in chronic fatigue syndrome

Filed Under: chronic fatigue, managing less common health problems, physical Tagged With: , , ,

How can I manage my Parkinson’s disease symptoms better?

January 19, 2012 by Leave a Comment

Answer: Check with your neurologist about increasing your caffeine intake.

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J Alzheimers Dis. 2010;20 Suppl 1:S205-20.

Effects of caffeine in Parkinson’s disease: from neuroprotection to the management of motor and non-motor symptoms.

Prediger RD.

Abstract

Parkinson’s disease (PD) is the second most common neurodegenerative disorder affecting approximately 1% of the population older than 60 years. Classically, PD is considered to be a motor system disease and its diagnosis is based on the presence of a set of cardinal motor signs (rigidity, bradykinesia, rest tremor) that are consequence of a pronounced death of dopaminergic neurons in the substantia nigra pars compacta. Nowadays there is considerable evidence showing that non-dopaminergic degeneration also occurs in other brain areas which seems to be responsible for the deficits in olfactory, emotional and memory functions that precede the classical motor symptoms in PD. The present review attempts to examine results reported in epidemiological, clinical and animal studies to provide a comprehensive picture of the antiparkinsonian potential of caffeine.

Convergent epidemiological and pre-clinical data suggest that caffeine may confer neuroprotection against the underlying dopaminergic neuron degeneration, and influence the onset and progression of PD. The available data also suggest that caffeine can improve the motor deficits of PD and that adenosine A2A receptor antagonists such as istradefylline reduces OFF time and dyskinesia associated with standard ‘dopamine replacement’ treatments. Finally, recent experimental findings have indicated the potential of caffeine in the management of non-motor symptoms of PD, which do not improve with the current dopaminergic drugs.

Altogether, the studies reviewed provide strong evidence that caffeine may represent a promising therapeutic tool in PD, thus being the first compound to restore both motor and non-motor early symptoms of PD together with its neuroprotective potential.

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Handb Exp Pharmacol. 2011;(200):267-310.

Impacts of methylxanthines and adenosine receptors on neurodegeneration: human and experimental studies.

Chen JF, Chern Y.

Abstract

Neurodegenerative disorders are some of the most feared illnesses in modern society, with no effective treatments to slow or halt this neurodegeneration. Several decades after the earliest attempt to treat Parkinson’s disease using caffeine, tremendous amounts of information regarding the potential beneficial effect of caffeine as well as adenosine drugs on major neurodegenerative disorders have accumulated.

In the first part of this review, we provide general background on the adenosine receptor signaling systems by which caffeine and methylxanthine modulate brain activity and their role in relationship to the development and treatment of neurodegenerative disorders. The demonstration of close interaction between adenosine receptor and other G protein coupled receptors and accessory proteins might offer distinct pharmacological properties from adenosine receptor monomers.

This is followed by an outline of the major mechanism underlying neuroprotection against neurodegeneration offered by caffeine and adenosine receptor agents. In the second part, we discuss the current understanding of caffeine/methylxantheine and its major target adenosine receptors in development of individual neurodegenerative disorders, including stroke, traumatic brain injury Alzheimer’s disease, Parkinson’s disease, Huntington’s disease and multiple sclerosis.

The exciting findings to date include the specific in vivo functions of adenosine receptors revealed by genetic mouse models, the demonstration of a broad spectrum of neuroprotection by chronic treatment of caffeine and adenosine receptor ligands in animal models of neurodegenerative disorders, the encouraging development of several A(2A) receptor selective antagonists which are now in advanced clinical phase III trials for Parkinson’s disease.

Importantly, increasing body of the human and experimental studies reveals encouraging evidence that regular human consumption of caffeine in fact may have several beneficial effects on neurodegenerative disorders, from motor stimulation to cognitive enhancement to potential neuroprotection. Thus, with regard to neurodegenerative disorders, these potential benefits of methylxanthines, caffeine in particular, strongly argue against the common practice by clinicians to discourage regular human consumption of caffeine in aging populations.

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J Neurol Sci. 2006 Oct 25;248(1-2):9-15. Epub 2006 Jun 27.

Novel neuroprotection by caffeine and adenosine A(2A) receptor antagonists in animal models of Parkinson’s disease.

Kalda A, Yu L, Oztas E, Chen JF.

Abstract

The adenosine A(2A) receptor has recently emerged as a leading non-dopaminergic therapeutic target for Parkinson’s disease, largely due to the restricted distribution of the receptor in the striatum and the profound interaction between adenosine and dopamine receptors in brain. Two lines of research in particular have demonstrated the promise of the A(2A) receptor antagonists as novel anti-parkinsonian drugs.

First, building on extensive preclinical animal studies, the A(2A) receptor antagonist KW6002 has demonstrated its potential to increase motor activity in PD patients of the advanced stage in a recent clinical phase IIB trial. Second, recently two prospective epidemiological studies of large cohorts have firmly established the inverse relationship between the consumption of caffeine (a non-specific adenosine antagonist) and the risk of developing PD. The potential neuroprotective effect of caffeine and A(2A) receptor antagonists in PD is further substantiated by the demonstration that pharmacological blockade (by caffeine or specific A(2A) antagonists) or genetic depletion of the A(2A) receptor attenuated dopaminergic neurotoxicity and neurodegeneration in animal models of PD.

Moreover, A(2A) receptor antagonism-mediated neuroprotection goes beyond PD models and can be extended to a variety of other brain injuries induced by stroke, excitotoxicity and mitochondrial toxins. Intensive investigations are under way to dissect out common cellular mechanisms (such as A(2A) receptor modulation of neuroinflammation) which may underlie the broad spectrum of neuroprotection by A(2A) receptor inactivation in brain.

Filed Under: managing less common health problems, Parkinson's disease, physical Tagged With: , , ,

How can I manage my gout condition better?

January 18, 2012 by Leave a Comment

Answer: Try changing your diet: cut back on foods associated with an increased risk for gout (e.g. beer and spirits, foods rich in purines, fructose) and consume more of those foods associated with a decreased risk for gout (e.g. coffee).

Surprisingly, the dietary intervention studies haven’t been done yet to test whether dietary changes reduce gout flares, but it makes sense for you to see if changing your diet helps.

Read this scientific article for ideas to try:

Update on the management of hyperuricemia and gout.

Bull NYU Hosp Jt Dis. 2008;66(3):231-9.

Update on the management of hyperuricemia and gout.

Pillinger MH, Keenan RT.

Abstract

Gout is the most common inflammatory arthritis in the United States, with more than three million sufferers. Management of gout has changed relatively little in the past 50 years, despite the fact that many gout patients have contraindications to one or more currently available gout therapies. However, recent insights into gout pathophysiology suggest that time is ripe for a change. This article reviews recent updates in the management of gout, including new insights into dietary management that may permit better control of hyuperuricemia. Also reviewed are the biological and clinical data behind newly-developed drugs for gout that are likely to receive serious consideration for FDA approval, and clinical use, in the foreseeable future.

Here’s the abstract of another scientific review opinion paper that gives some good suggestions to try:

Curr Opin Rheumatol. 2010 Mar;22(2):165-72.

A prescription for lifestyle change in patients with hyperuricemia and gout.

Choi HK.

Abstract

PURPOSE OF REVIEW:

This review summarizes the recent data on lifestyle factors that influence serum uric acid levels and the risk of gout and attempts to provide holistic recommendations, considering both their impact on gout as well as on other health implications.

RECENT FINDINGS:

Large-scale studies have clarified a number of long-suspected relations between lifestyle factors, hyperuricemia, and gout, including purine-rich foods, dairy foods, various beverages, fructose, and vitamin C supplementation. Furthermore, recent studies have identified the substantial burden of comorbidities among patients with hyperuricemia and gout.

SUMMARY:

Lifestyle and dietary recommendations for gout patients should consider overall health benefits and risk, since gout is often associated with the metabolic syndrome and an increased future risk of cardiovascular disease (CVD) and mortality. Weight reduction with daily exercise and limiting intake of red meat and sugary beverages would help reduce uric acid levels, the risk of gout, insulin resistance, and comorbidities. Heavy drinking should be avoided, whereas moderate drinking, sweet fruits, and seafood intake, particularly oily fish, should be tailored to the individual, considering their anticipated health benefits against CVD. Dairy products, vegetables, nuts, legumes, fruits (less sugary ones), and whole grains are healthy choices for the comorbidities of gout and may also help prevent gout by reducing insulin resistance. Coffee and vitamin C supplementation could be considered as preventive measures as these can lower urate levels, as well as the risk of gout and some of its comorbidities.

Filed Under: blog, gout, managing less common health problems, physical Tagged With: , , , , ,

How can I improve my sensitivity to insulin?

January 13, 2012 by Leave a Comment

Answer:  If you are overweight, lose weight through diet.

Hepatology. 2009 Jan;49(1):80-6.

Orlistat for overweight subjects with nonalcoholic steatohepatitis: A randomized, prospective trial.

Harrison SA, Fecht W, Brunt EM, Neuschwander-Tetri BA.

Abstract

The aim of this study was to determine if orlistat, an inhibitor of fat absorption, combined with caloric restriction in overweight subjects with nonalcoholic steatohepatitis results in weight loss and improved liver histology. Fifty overweight subjects (body mass index = >or=27) with biopsy proven nonalcoholic steatohepatitis were randomized to receive a 1,400 Kcal/day diet plus vitamin E (800 IU) daily with or without orlistat (120 mg three times a day) for 36 weeks. Liver biopsies were repeated at week 36. Twenty-three subjects in the orlistat/diet/vitamin E group and 18 in the diet/vitamin E group completed the study. The mean age was 47 +/- 9.0 (standard deviation) years and mean body mass index was 36.4 +/- 6.3 kg/m(2). Four subjects were diabetic. The orlistat group lost a mean of 8.3% body weight compared to 6.0% in the diet plus vitamin E group (not significant). Both groups also had similarly improved serum aminotransferases, hepatic steatosis, necroinflammation, ballooning, and nonalcoholic fatty liver disease activity scores. Stratified according to weight loss instead of treatment group, a loss of >or=5% body weight (n = 24) compared to <5% body weight (n = 17) correlated with improvement in insulin sensitivity (P = 0.001) and steatosis (P = 0.015). Comparing subjects who lost >or=9% of body weight (n = 16), to those that did not (n = 25), improved insulin sensitivity (P < 0.001), adiponectin (P = 0.03), steatosis (P = 0.005), ballooning (P = 0.04), inflammation (P = 0.045), and nonalcoholic fatty liver disease activity score (P = 0.009) were seen. Increases in adiponectin strongly correlated with improved ballooning and nonalcoholic fatty liver disease activity score (P = 0.03). Orlistat did not enhance weight loss or improve liver enzymes, measures of insulin resistance, and histopathology. However, subjects who lost >or=5% of body weight over 9 months improved insulin resistance and steatosis, and those subjects who lost >or=9% also achieved improved hepatic histologic changes.

Filed Under: insulin resistance, managing less common health problems, physical Tagged With: , ,

How can I improve my fatty liver condition?

January 13, 2012 by Leave a Comment

Answer:  If you are overweight, lose weight through diet.

Hepatology. 2009 Jan;49(1):80-6.

Orlistat for overweight subjects with nonalcoholic steatohepatitis: A randomized, prospective trial.

Harrison SA, Fecht W, Brunt EM, Neuschwander-Tetri BA.

Abstract

The aim of this study was to determine if orlistat, an inhibitor of fat absorption, combined with caloric restriction in overweight subjects with nonalcoholic steatohepatitis results in weight loss and improved liver histology. Fifty overweight subjects (body mass index = >or=27) with biopsy proven nonalcoholic steatohepatitis were randomized to receive a 1,400 Kcal/day diet plus vitamin E (800 IU) daily with or without orlistat (120 mg three times a day) for 36 weeks. Liver biopsies were repeated at week 36. Twenty-three subjects in the orlistat/diet/vitamin E group and 18 in the diet/vitamin E group completed the study. The mean age was 47 +/- 9.0 (standard deviation) years and mean body mass index was 36.4 +/- 6.3 kg/m(2). Four subjects were diabetic. The orlistat group lost a mean of 8.3% body weight compared to 6.0% in the diet plus vitamin E group (not significant). Both groups also had similarly improved serum aminotransferases, hepatic steatosis, necroinflammation, ballooning, and nonalcoholic fatty liver disease activity scores. Stratified according to weight loss instead of treatment group, a loss of >or=5% body weight (n = 24) compared to <5% body weight (n = 17) correlated with improvement in insulin sensitivity (P = 0.001) and steatosis (P = 0.015). Comparing subjects who lost >or=9% of body weight (n = 16), to those that did not (n = 25), improved insulin sensitivity (P < 0.001), adiponectin (P = 0.03), steatosis (P = 0.005), ballooning (P = 0.04), inflammation (P = 0.045), and nonalcoholic fatty liver disease activity score (P = 0.009) were seen. Increases in adiponectin strongly correlated with improved ballooning and nonalcoholic fatty liver disease activity score (P = 0.03). Orlistat did not enhance weight loss or improve liver enzymes, measures of insulin resistance, and histopathology. However, subjects who lost >or=5% of body weight over 9 months improved insulin resistance and steatosis, and those subjects who lost >or=9% also achieved improved hepatic histologic changes.

Filed Under: managing less common health problems, nonalcoholic fatty liver, physical Tagged With: , ,

I have Type 2 diabetes. How can I gain better control over my blood sugar?

December 20, 2011 by Leave a Comment

Answer: Exercise!

“This review found that exercise improves blood sugar control and that this effect is evident even without weight loss. . .Exercise improved the body’s reaction to insulin and decreased blood lipids. . .No adverse effects with exercise were reported.”

Cochrane Database Syst Rev. 2006 Jul 19;3:CD002968.

Exercise for type 2 diabetes mellitus.

Plain language summary


Exercise, dietary changes and medications are frequently used in the management of type 2 diabetes. However, it is difficult to determine the independent effect of exercise from some trials because exercise has been combined with dietary modifications or medications, or compared with a control which includes another form of intervention. The review authors aimed to determine the effect of exercise on blood sugar control in type 2 diabetes.

This review found that exercise improves blood sugar control and that this effect is evident even without weight loss. Furthermore, exercise decreases body fat content, thus the failure to lose weight with exercise programmes is probably explained by the conversion of fat to muscle. Exercise improved the body’s reaction to insulin and decreased blood lipids. Quality of life was only assessed in one study, which found no difference between the two groups. No significant difference was found between groups in blood levels of cholesterol or blood pressure. A total of 14 randomised controlled trials were assessed. These included 377 participants and compared groups that differed only with respect to an exercise programme intervention. The duration of the interventions in the studies ranged from eight weeks to one year. Two studies reported follow-up information, one at six months after the end of the six month exercise intervention and one at twelve months post-intervention. Generally, the studies were well-conducted, but blinding of outcome assessors was not reported and although all studies reported that randomisation was performed, few gave details of the method.

No adverse effects with exercise were reported. The effect of exercise on diabetic complications was not assessed in any of the studies.

The relatively short duration of trials prevented the reporting of any significant long term complications or mortality. Another limitation was the small number of participants included in the analyses for adiposity, blood pressure, cholesterol, body’s muscle and quality of life.

Filed Under: managing less common health problems, physical, Type 2 diabetes Tagged With: , , ,
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