Fun Stuff About Diabetes

No, diabetes is NOT fun; I'm not suggesting it is. I had two family members with the disease, and now I have one. No, the other was not cured. However (how's THAT for a depressing blog intro!?) I am a geek, and I find facts that connect dots to be fun. So when I recently went googling about for academic articles on the science of diabetes, and came up with some results I hadn't expected, I was so excited I had to share. Perhaps you will be surprised too, and perhaps that will trigger some rabbit-hole reserach of your own. If so, let me know what you find! I'm always good for an "oooh! Cool!" when another tidbit falls into place and a picture grows more complete - or a whole new panel opens up.

These are all abstracts from PubMed. I no longer have access to an academic database, so I haven't been able to read more than these freely-available summaries of research. I typed in things like diabetes+CHO and diabetes+hear* and here is an overview of what I got.

First of all, for some stuff, maybe all diabetes is the same:
“Subjects with type 1 diabetes mellitus (T1DM) eventually develop insulin resistance and other features of T2DM such as cardiovascular disorders. The exact mechanism has been not been completely understood. In this study, we … found that continuous exposure of mice with non-obese diabetes to insulin … induced severe insulin resistance, whereas untreated hyperglycemia for the same amount of time (2 weeks) did not cause obvious insulin resistance. Insulin resistance was accompanied by decreased mitochondrial production … increased … triglyceride content, and elevated oxidative stress.” [J Biol Chem. 2009 Oct 2;284(40):27090-100

Which runs smack up against crap stuff like this:
“Type 1 diabetes is primarily an autoimmune disease and type 2 diabetes is primarily a metabolic condition. However, medical nutrition therapy is an integral part of management for both types of diabetes to improve glycaemic control and reduce the risk of complications… Specific strategies include a kilojoule controlled diet with reduced saturated fat, trans fat and sodium; moderate protein; and high in dietary fibre and low glycaemic index carbohydrates. Carbohydrates should be spread evenly throughout the day and matched to medication.” [Aust Fam Physician. 2010 Aug;39(8):579-83

Which in turn directly contradicts what we already know about the effects of CHO on blood sugar and thus health:
"Replacing dietary saturated fat (SAFA) with carbohydrates (CHO), notably those with a high glycaemic index, is associated with an INCREASE in cardiovascular disease risk in observational cohorts" [Neth J Med. 2011] Emphasis original

Fortunately some researchers are willing to consider the preferences of the effected people, rather than just the official guidelines. This is probably my favourite find in this list, for that reason:
“This systematic review focuses on randomized controlled trials of low-carbohydrate diets compared with low-fat/low-calorie diets... There was a higher attrition rate in the low-fat compared with the low-carbohydrate groups suggesting a patient preference for a low-carbohydrate/high-protein approach as opposed to the Public Health preference of a low-fat/high-carbohydrate diet. Evidence from this systematic review demonstrates that low-carbohydrate/high-protein diets are more effective at 6 months and are as effective, if not more, as low-fat diets in reducing weight and cardiovascular disease risk up to 1 year.” [Obes Rev. 2009 Jan;10(1):36-50

So, what’s for supper? Steak and salad, baby:
“This systematic review focused on the effects of diets high in monounsaturated fat (MUFA) versus diets low in MUFA on important risk factors of T2D (i.e. plasma glucose, insulin, homeostasis model assessment of insulin resistance and glycosylated haemoglobin, HbA1c)… Conclusions: In summary, this systematic review found that high MUFA diets appear to be effective in reducing HbA1c, and therefore, should be recommended in the dietary regimes of T2D.” [Ann Nutr Metab. 2011;58(4):290-6 Okay, so where do we get MUFAs? From Wikipedia: “Monounsaturated fats are found in natural foods such as red meat, whole milk products, nuts and high fat fruits such as olives and avocados. Olive oil is about 75% monounsaturated fat. Canola oil and Cashews are both about 58% monounsaturated fat. Tallow (beef fat) is about 50% monounsaturated fat and lard is about 40% monounsaturated fat.”

And, as a diabetic, how should you handle your steak and salad? Well these guys can’t tell you, but if you’re having a cheat night they have some tips:
“Our study examines the hypothesis that in addition to sugar starch-type diet, a fat-protein meal elevates postprandial glycemia as well, and it should be included in calculated prandial insulin dose accordingly... pizza dinner, consisting of 45 g/180 kcal of carbohydrates and 400 kcal from fat-protein … There were no statistically significant differences involving patients' metabolic control, C-peptide, glucagon secretion, or duration of diabetes… the significant glucose increment occurred at 120-360 min, with its maximum at 240 min: 60.2 versus -3.0 mg/dL (P=0.04), respectively... Conclusions: A mixed meal effectively elevates postprandial glycemia after 4-6 h. Dual-wave insulin bolus, in which insulin is calculated for both the carbohydrates and fat proteins, is effective in controlling postprandial glycemia.” [Diabetes Technol Ther. 2011 Oct 20

These folks are likely pretty adamant that intermittent fasting is a bad idea for diabetics:
“Basal insulin dose requirements in patients with type 1 diabetes may be derived from the course of glucose concentrations in the fasting state; i. e. by skipping meals. The present study examined whether fasting tests could be replaced by carbohydrate-free meals… Plasma glucose concentrations significantly increase in patients with type 1 diabetes following the intake of carbohydrate-free meals. Carbohydrate-free meal-tests cannot replace skipping meal tests to determine the basal insulin requirement in patients with type 1 diabetes.” [Exp Clin Endocrinol Diabetes. 2010 May;118(5):325-7

There are some other effects of increased blood sugar among diabetics that might interest you, specifically hearing loss (who knew?):
“Induction of diabetes in … mice promotes amplification of age-related peripheral hearing loss ... On the other hand, initial results of effects from very high blood glucose level (T1DM) on the auditory midbrain showed disruption of central inhibition, increased response synchrony or enhanced excitation in the inferior colliculus.” (I don’t know if you want an excited colliculus or not, but there you have it) [Hear Res. 2009 Mar;249(1-2):44-53

“Wolfram syndrome, also named "DIDMOAD" (diabetes insipidus, diabetes mellitus, optic atrophy, and deafness), is an inherited association of juvenile-onset diabetes mellitus and optic atrophy as key diagnostic criteria. Renal tract abnormalities and neurodegenerative disorder may occur in the third and fourth decade. The wolframin gene, WFS1, associated with this syndrome, is located on chromosome 4p16.1. Many mutations have been described since the identification of WFS1 as the cause of Wolfram syndrome. We identified a new homozygous WFS1 mutation (c.1532T>C; p.Leu511Pro) causing Wolfram syndrome in a large inbred Turkish family. The patients showed early onset of IDDM, diabetes insipidus, optic atrophy, sensorineural hearing impairment and very rapid progression to renal failure before age 12 in three females.” (I’ve never encountered the word “inbred” in an academic journal article title before.) [Eur J Med Genet. 2011 Sep 23

“The study subjects were workers in one automobile manufacturing company. …The hearing thresholds at 4,000 Hz frequencies for both ears were significantly higher in 2009 than those in 2005. The changes in the hearing thresholds of the subjects with an impaired fasting glucose (100-125 mg/dl) and diabetes (≥126 mg/dl) were greater than those of the normal (<100 mg/dl) group. After adjusting for variables such as age, smoking and alcohol history, environmental noise, hypertension and serum creatinine, fasting glucose was found to be a significant variable. Impaired fasting glucose (100-125 mg/dl) was significant (β=1.339, p=0.002) for the right ear, whereas it was not significant (β=0.639, p=0.121) for the left ear.” [J Occup Health. 2011 Aug 4;53(4):274-9

A whole whack of diabetes experts got together and did a meta-analysis of trials and articles on insulin injection, and put together a definitive guide. You can access the full text for free here. It looks quite long to print, or you could buy the PDF, but the text seems to be there for your perusal.

Lastly, here’s an interesting one on the impact of parenting style on self-care behaviours of T1D adolescents.

What interested you? What surprised you? What geeky googleholes have you fallen down lately?

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