Autoimmune Thyroid Disease

An Unfortunate and Lengthy Adventure in Misdiagnosis

Aspirin-like compounds increase insulin secretion in otherwise healthy obese people

with 4 comments

And it’s supposed to be a good thing?

Chris sent me this great press release to deconstruct. If you’re in on the joke, it’s downright hysterical.

Aspirin-like compounds (salicylates) can claim another health benefit: increasing the amount of insulin produced by otherwise healthy obese people. Obesity is associated with insulin resistance, the first step toward type 2 diabetes.

Aspirin and other salicylates are known to reduce blood glucose in diabetic patients. New research accepted for publication in the Journal of Clinical Endocrinology & Metabolism reveals a similar beneficial effect among obese individuals by increasing the amount of insulin secreted into the bloodstream.

“The administration of a salicylate led to the lowering of serum glucose concentrations,” said Jose-Manuel Fernandez-Real of the Institut d’Investigacio Biomedica de Girona and CIBEROBN Fisiopatologia de la Obesidad, Spain, and lead author of the study. “These findings highlight the importance of further research on the possible therapeutic benefit of aspirin in the fight against type 2 diabetes.”

For their study, Fernandez-Real and his colleagues evaluated the effects of triflusal (a derivative of salicylate) on 28 subjects (nine men and 29 women). The average age of the participants was 48 years old and their average Body Mass Index (BMI) was 33.9. A BMI of over 30 is considered obese. During three, four-week treatment periods, the study participants received a 600 mg dose, a 900 mg dose, or a placebo once per day.

The researchers found that administration of triflusal led to decreased fasting serum glucose. Contrary to their expectations, insulin sensitivity did not significantly change during the trial. Insulin secretion, however, significantly increased in relation to the dose size.

In conjunction with the human studies, the researchers also conducted laboratory studies on insulin-producing cells (known as islets of Langerhans) from mice and humans. The researchers observed that triflusal significantly increased the insulin secreted by these cells.

Aspirin therapy has been recognized to improve glucose tolerance and to reduce insulin requirements in diabetic subjects,” said Fernandez-Real. “To our knowledge, this is the first study to show that salicylates lowered serum glucose in non-diabetic obese subjects. We believe that this effect was due to a previously unsuspected increase in insulin secretion rather than enhanced insulin sensitivity.”


The paper “Salicylates increase insulin secretion in healthy obese subjects” will appear in the July issue of JCEM, a publication of The Endocrine Society.”

Other researchers involved in the study include Abel Lobez-Mermejo, Ana-Belen Ropero, Sandra Piquer, Angel Nadal, Judit Bassols, Roser Casamitjana, Roman Gomis, Eva Arnaiz, Inaki Perez, and Wifredo Ricart. Aspirin-like compounds increase insulin secretion in otherwise healthy obese people

Were these scientists born yesterday? Aspirin therapy does not “improve glucose tolerance”. It just lowers blood glucose! If anything, it impairs glucose tolerance by inducing the release of too much insulin, which causes hypoglycaemia.

There are two types of diabetics; Type 1 and Type 2. Type 1 diabetics have an autoimmune condition characterised by low to non-existent insulin levels, high blood sugar, and weight loss. Type 2 diabetics have something called ‘insulin resistance’. They have high levels of insulin, high blood sugar, and weight gain. Insulin lowers blood sugar by pushing glucose into cells. T2 diabetics resist the presence of insulin, so they have both high insulin levels and high blood sugar. When doctors talk about improving insulin sensitivity, they are talking about decreasing the resistance to insulin.

Any endocrinologist (in fact, any diabetic) can tell you that insulin is a weight gain hormone. They will also tell you that the more weight you gain, the more resistant to insulin you will be. So why, why would you want to give a T2 diabetic more insulin?

Because you’re using the wrong criteria to assess their health!

Currently diabetes medicine is labouring under a sad misunderstanding. The misunderstanding is that most of the negative symptoms of diabetes are caused by high blood sugar, and that blood sugar must be kept under control at all costs. Unfortunately some of the negative symptoms of diabetes are actually caused by high insulin levels, not high blood sugar. This means that outdated drugs that actually worsen T2 diabetes over time are still being prescribed to T2 diabetics. In fact, Michael Eades MD posted on this subject not so long ago, describing how the large, well-funded ACCORD study has halted its rigorous blood sugar control trials in diabetics because the diabetics who were controlling their blood sugar the best (by raising their insulin levels even higher), were dying faster than the control group.

There are two main types of drugs that are given to T2 diabetics: drugs that increase insulin output (or actual insulin), and drugs that increase sensitivity to insulin. The first class of drugs includes the sulfonylurea drugs, which work to lower blood sugar by stimulating insulin release. The second class of drugs includes metformin, which works by increasing the body’s sensitivity to the existing insulin – that is, by reducing insulin resistance. Metformin is the drug of choice for T2 diabetics. Not sulfonylureas, whose side effects include weight gain. Duh!

So here we have this bizarre study of triflusal – which appears to be a drug without real a purpose other than to mimic aspirin – and researchers are looking for some use for it. Some bright spark who read a medical book once comes up with this. What’s the betting triflusal also causes weight gain and hypoglycaemia? Just the same as salicylates cause me weight gain and hypoglycaemia by inducing insulin release. I’m willing to put money on it.


Written by alienrobotgirl

30 April, 2008 at 11:28 am

Posted in Quacktitioners

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4 Responses

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  1. Bizarre, just bizarre. I Pumeded Fernandez-Real. 161 hits and I think he’s a group leader. How come an idiot can get that far? Oh, just thinking of Keys, Joslin, VanItallie… Stupid of me, it actually seems to come with the territory!



    30 April, 2008 at 1:22 pm

  2. That bit about ” another health benefit” made me laugh too.

    I’ve posted abotu it here:


    30 April, 2008 at 2:18 pm

  3. […] How is that a benefit? Useful info but bad analysis. Good deconstruction here. […]

  4. i have feel the same problem every time i have taken aspirins.I think the last time i have taken one aspirin was 1 year ago(i rather preffer headache than insulin elevations and hypoglicemias)

    The next big nutrient that pharmaceuticals are trying to copy as treatment for diabetes,is named resveratrol,and it rises mitochondrial activity and actives the gen sit1.

    But i really bealive that the real problem in diabetes,comes from the low UVb light sun intake,(between 12:00 am and 16:00pm)and the intake of many drugs(like antiepileptics,or corticoids)that have lowered our vitamin d3 production from cholesterol.

    Low vitamin d3 levels,produces a big problem in the calcium/magnesium metabolism,and in my opinion,is the low c amp production,and the loss of magnesium in cells,wich is substituted for the calcium,which takes us to inflamation,low energy and hypoglicemia problem,which blocks the thyroid metabolism(from t4 to t3),and takes us to the diabetes problems.

    Just a theory,of course.
    i let you here a few studyes about this.

    Diabetes Care. 2007 Jun;30(6):1549-55. Epub 2007 Mar 10. Click here to read LinksComment in:

    Diabetes Care. 2007 Dec;30(12):e135; author reply e136.

    Vitamin D, parathyroid hormone levels, and the prevalence of metabolic syndrome in community-dwelling older adults.

    Reis JP, von Mühlen D, Kritz-Silverstein D, Wingard DL, Barrett-Connor E.

    Department of Family and Preventive Medicine, University of California, San Diego, La Jolla, California 92093-0607, USA.

    OBJECTIVE: Accumulating research suggests low-circulating vitamin D concentrations, i.e., 25-hydroxyvitamin-D [25(OH)D], may be associated with an increased prevalence of metabolic syndrome; however, previous studies have not accounted for parathyroid hormone (PTH) levels. We examined the association of 25(OH)D and PTH with the prevalence of metabolic syndrome in a community-based cohort of older adults. RESEARCH DESIGN AND METHODS: Participants included 410 men and 660 women, 44-96 years old, who completed a follow-up clinic visit in 1997-1999 as part of the Rancho Bernardo Study. Sex-specific logistic regression models were fit to estimate the odds of ATP III (Adult Treatment Panel III)-defined metabolic syndrome across quintiles of 25(OH)D and PTH, adjusting for age, season, and major lifestyle factors. RESULTS: In men, there was a significant trend (P = 0.03) of increasing adjusted odds for metabolic syndrome with increasing PTH concentrations, primarily due to an odds ratio of 2.02 (95% CI 0.96-4.24) in men in the top quintile (> or =63 ng/l) of PTH concentration. This association remained unchanged after taking into account 25(OH)D levels and excluding men with diabetes or impaired renal function; it was attenuated after adjustment for the homeostasis model assessment of insulin resistance. Neither PTH in women nor 25(OH)D levels in either sex was related to the metabolic syndrome. CONCLUSIONS: These findings suggest an increased risk of metabolic syndrome with elevated PTH levels in older men and no effect of 25(OH)D concentrations in either sex. The reason for the sex difference in the PTH-metabolic syndrome association is unknown. Prospective studies are necessary to better determine the roles of 25(OH)D and PTH in the etiology of metabolic syndrome.

    PMID: 17351276 [PubMed – indexed

    A study from Bulgaria shows that giving vitamin D supplements to diabetics during the winter markedly improved control of their blood sugar levels.
    The majority of North Americans require sunlight to meet their needs for vitamin D because they do not meet their needs from the foods that they eat. Many people in temperate climates therefore are deficient in vitamin D by the end of winter. Lack of vitamin D impairs a person’s immunity and ability to produce insulin and respond to insulin. This study shows that giving vitamin D pills to Type 2 diabetics during the winter improved control of blood sugar levels by increasing the first response of insulin from the pancreas to a rise in blood sugar, and by improving cell response to insulin. If this study can be confirmed, all diabetics should take vitamin D-rich foods or pills whenever they cannot get adequate exposure to sunshine. See report #D222.

    The effect of vitamin D-3 on insulin secretion and peripheral insulin sensitivity in type 2 diabetic patients. International Journal of Clinical Practice, 2003, Vol 57, Iss 4, pp 258-261. AM Borissova, T Tankova, G Kirilov, L Dakovska, R Kovacheva. Borissova AM, Univ Hosp, Dept Endocrinol, 6 Damjan Gruev Str, Sofia 1303, BULGARIA

    : Diabetologia. 2005 Jul;48(7):1247-57. Epub 2005 Jun 22. Click here to read LinksComment in:

    Diabetologia. 2006 Jan;49(1):217-8.

    Vitamin D and diabetes.

    Mathieu C, Gysemans C, Giulietti A, Bouillon R.

    Laboratory of Experimental Medicine and Endocrinology (LEGENDO), Catholic University of Leuven, Herestraat 49, 3000, Leuven, Belgium.

    Vitamin D deficiency predisposes individuals to type 1 and type 2 diabetes, and receptors for its activated form-1alpha,25-dihydroxyvitamin D3-have been identified in both beta cells and immune cells. Vitamin D deficiency has been shown to impair insulin synthesis and secretion in humans and in animal models of diabetes, suggesting a role in the development of type 2 diabetes. Furthermore, epidemiological studies suggest a link between vitamin D deficiency in early life and the later onset of type 1 diabetes. In some populations, type 1 diabetes is associated with certain polymorphisms within the vitamin D receptor gene. In studies in nonobese diabetic mice, pharmacological doses of 1alpha,25-dihydroxyvitamin D3, or its structural analogues, have been shown to delay the onset of diabetes, mainly through immune modulation. Vitamin D deficiency may, therefore, be involved in the pathogenesis of both forms of diabetes, and a better understanding of the mechanisms involved could lead to the development of preventive strategies.

    PMID: 15971062 [PubMed

    Diabetes Obes Metab. 2008 Mar;10(3):185-97. Click here to read Links

    Role of vitamin D in the pathogenesis of type 2 diabetes mellitus.

    Palomer X, González-Clemente JM, Blanco-Vaca F, Mauricio D.

    Institut de Recerca, Hospital de Santa Creu i Sant Pau, Barcelona, Spain.

    Vitamin D deficiency has been shown to alter insulin synthesis and secretion in both humans and animal models. It has been reported that vitamin D deficiency may predispose to glucose intolerance, altered insulin secretion and type 2 diabetes mellitus. Vitamin D replenishment improves glycaemia and insulin secretion in patients with type 2 diabetes with established hypovitaminosis D, thereby suggesting a role for vitamin D in the pathogenesis of type 2 diabetes mellitus. The presence of vitamin D receptors (VDR) and vitamin D-binding proteins (DBP) in pancreatic tissue and the relationship between certain allelic variations in the VDR and DBP genes with glucose tolerance and insulin secretion have further supported this hypothesis. The mechanism of action of vitamin D in type 2 diabetes is thought to be mediated not only through regulation of plasma calcium levels, which regulate insulin synthesis and secretion, but also through a direct action on pancreatic beta-cell function. Therefore, owing to its increasing relevance, this review focuses on the role of vitamin D in the pathogenesis of type 2 diabetes mellitus.

    Inadequate vitamin D status: does it contribute to the disorders comprising syndrome ‘X’?

    Boucher BJ.

    Academic Medical Unit, St. Bartholomew’s and the Royal London Hospital Medical & Dental School, UK.

    Environmental factors are important in the aetiology of glucose intolerance, type II diabetes and IHD. The lack of vitamin D, which is necessary for adequate insulin secretion, relates demographically to increased risk of myocardial infarction. These disorders are connected, degenerative vascular disease increasing with glucose intolerance and diabetes and, with its risk factors, comprising syndrome ‘X’. Evidence is presented suggesting that vitamin D deficiency may be an avoidable risk factor for syndrome ‘X’, adding another preventative measure to current recommendations which are aimed at reducing the worldwide epidemic of these disorders. Experimentally, vitamin D deficiency progressively reduces insulin secretion; glucose intolerance follows and becomes irreversible. Relationships between vitamin D status, glucose tolerance and 30 min insulin secretion during oral glucose tolerance tests are reported in British Asians; insulin secretion, but not glycaemia, improving with short-term supplementation. Studies showing reduction in blood pressure and in risk of heart attack and diabetes with exercise (usually outdoor), rarely consider the role of vitamin D status. Glycaemia and insulin secretion in elderly European men, however, relate to vitamin D status, independent of season or physical activity. Prolonged supplementation can improve glycaemia. Hypertension improves with vitamin D treatment with or without initial deficiency. Vitamin D status and climate are reviewed as risk factors for myocardial infarction; the risk reducing with altitude despite increasing cold. Glycaemia and fibrinogenaemia improve with insulin secretion increases in summer. Variation in vitamin D requirements could arise from genetic differences in vitamin D processing since bone density can vary with vitamin D-receptor genotype. Vitamin D receptors are present in islet beta cells and we report insulin secretion in healthy Asians differing profoundly with the Apa I genotype, being independent of vitamin D status. Those at risk of vitamin D deficiency include the elderly, those living indoors or having a covered-up style of dress, especially dark-skinned immigrants, and pregnant women, and these are groups recognized as being at increased risk of diabetes.

    Baseline serum 25-hydroxy vitamin d is predictive of future glycemic status and insulin resistance: the Medical Research Council Ely Prospective Study 1990-2000.

    Forouhi NG, Luan J, Cooper A, Boucher BJ, Wareham NJ.

    Medical Research Council Epidemiology Unit, Institute of Metabolic Science, Cambridge, UK.

    OBJECTIVE: Accumulating epidemiological evidence suggests that hypovitaminosis D may be associated with type 2 diabetes and related metabolic risks. However, prospective data using the biomarker serum 25-hydroxyvitamin D [25(OH)D] are limited and therefore examined in the present study. RESEARCH DESIGN AND METHODS: A total of 524 randomly selected nondiabetic men and women, aged 40-69 years at baseline, with measurements for serum 25(OH)D and IGF-1 in the population-based Ely Study, had glycemic status (oral glucose tolerance), lipids, insulin, anthropometry, and blood pressure measured and metabolic syndrome risk (metabolic syndrome z score) derived at baseline and at 10 years of follow-up. RESULTS: Age-adjusted baseline mean serum 25(OH)D was greater in men (64.5 nmol/l [95% CI 61.2-67.9]) than women (57.2 nmol/l [54.4,60.0]) and varied with season (highest late summer). Baseline 25(OH)D was associated inversely with 10-year risk of hyperglycemia (fasting glucose: beta = -0.0023, P = 0.019; 2-h glucose: beta = -0.0097, P = 0.006), insulin resistance (fasting insulin beta = -0.1467, P = 0.010; homeostasis model assessment of insulin resistance [HOMA-IR]: beta = -0.0059, P = 0.005), and metabolic syndrome z score (beta = -0.0016, P = 0.048) after adjustment for age, sex, smoking, BMI, season, and baseline value of each metabolic outcome variable. Associations with 2-h glucose, insulin, and HOMA-IR remained significant after further adjustment for IGF-1, parathyroid hormone, calcium, physical activity, and social class. CONCLUSIONS: This prospective study reports inverse associations between baseline serum 25(OH)D and future glycemia and insulin resistance. These associations are potentially important in understanding the etiology of abnormal glucose metabolism and warrant investigation in larger, specifically designed prospective studies and randomized controlled trials of supplementation.


    16 December, 2008 at 7:26 pm

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