Insulin level tracking?
I’m wondering something kind of stupid this morning, which is why we don’t track people’s insulin levels. Or maybe we do and I don’t know about it? In which case, how do I get myself a Quantified Self insulin tracker?
Here’s a bit of background to explain why I’m asking this. Insulin levels in your blood regulate the speed at which sugar in your blood is turned into fat, and similarly they regulate how quickly fat cells release fat into the bloodstream.
If someone without diabetes eats something sweet their insulin levels shoot up to collect all the blood so the blood sugar levels doesn’t get toxic. Because what’s really important, as diabetics know, is that blood sugar levels remain not too high nor too low. Type I diabetics don’t make insulin, and Type II diabetics don’t respond to insulin properly.
OK so here’s the thing. I’m pretty sure my insulin levels are normally a bit high, and that when I eat sugar or bread they spike up dramatically. And although that might sound like the opposite of diabetes, it’s actually the precursor to diabetes, where my body goes nuts making insulin and then my organs become resistant to it.
But first of all, I’d like to know if I’m right – are my insulin levels elevated? – and second of all, I’d like to know how much my body reacts, insulin-wise, to eating and drinking various things. For instance, I drink a lot of coffee, and I’d like to know what that does to my insulin levels. And what about Coke Zero?
I am probably going to be disappointed here. I know that the critical level to keep track of for diabetics, blood sugar, is still pretty hard to do, although recent continuous monitors do exist and are helping. So if anyone knows of a “continuous insulin monitor” please tell me!
One last word about why insulin. I am fairly convinced that the insulin levels – combined with a measure of their insulin resistance – would explain a lot about why certain people retain fat where others don’t with the same diet. And it would be such a relief to stop arguing about willpower and start understanding this stuff scientifically.
One last thing. Please do not comment below telling me how to lose weight or talking about how to have more willpower: I will delete such comments! Please do comment on the scientific issues around the mechanisms of insulin, data collection, and potentially modeling with that data.
mathbabe 
You can have your HbA1C levels checked and it gives you a good estimate of your average blood sugar levels over the past four months.
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But I’m not worried about my blood sugar, which I regulate well since I’m not diabetic. I’m interested in tracking my insulin.
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An interesting discussion of insulin and sugar imbalances can be found on “The Story of the Human Body: Evolution, Health and Disease”, especially on chapter 10. It’s not only about your sugar intake, but how (with or without fiber) you ingest it.
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Ed Aboufadel, one of my colleagues, did some interesting work on his sabbatical trying to use wavelets to help develop better modeling from the continuous blood sugar data. His son has juvenile type I diabetes.
My guess about weight is similar to yours, which would explain the partial genetic link that always shows up in studies. Also there’s this research about the different types of fat, and difficulties among people who don’t store the ‘brown fat’ because of heredity or medication.
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like all preventative care or testing, it has risks (infection for one, false positives for another – if I thought about it I could come with more). The question then becomes, does the risk outweigh the benefits? I would guess no, as I don’t see any thing gained other than satisfying you’re curiosity. If you were really interested you could find a freind that had gestational diabetes and borrow or buy their monitor – then just get test strips. If you drink coffee without sugar it should not matter.
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What? Diabetics measure blood glucose not insulin.
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This is right — glucose is easier to monitor continuously. Why would you want to track insulin — if your body is insulin resistant?
http://en.wikipedia.org/wiki/Insulin_resistance
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But I am not diabetic! I want to track insulin, not blood glucose, in part to avoid becoming diabetic.
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From the article: Some scholars go as far as to claim that neither insulin resistance, nor obesity are really metabolic disorders per se, but simply adaptive responses to sustained caloric surplus, intended to protect bodily organs from lipotoxicity (unsafe levels of lipids in the bloodstream and tissues). …. Sedentary lifestyle increases the likelihood of development of insulin resistance. It’s been estimated that each 500 kcal/week increment in physical activity related energy expenditure reduces the lifetime risk of type 2 diabetes by 6%. A different study found that vigorous exercise at least once a week reduced the risk of type 2 diabetes in women by 33%.
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No, not just curiosity, although I agree there would be risks and costs. I’m interested in seeing how exactly my insulin levels change so I can avoid becoming diabetic. I’d love to do it with someone else who is less “at risk” for diabetes. Or for that matter with an entire population willing to take some risks and to accept some costs for the sake of science.
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I really recommend this lecture. It has enough detail to convince that he REALLY knows what he is talking about while remaining mostly accessible to the non-endocrinologist. He explains in great detail at the cellular level how the very complex systems of hormones and enzymes work to metabolize food and regulate hunger and weight.
Robert H. Lustig, MD, UCSF Professor of Pediatrics in the Division of Endocrinology, explores the damage caused by sugary foods. He argues that fructose (too much) and fiber (not enough) appear to be cornerstones of the obesity epidemic through their effects on insulin.
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Yes that’s kind of clear by now but doesn’t really explain what I’m interested in.
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No one makes a continuous insulin tracker. I’m not entirely sure why, but I suspect it could be part due to people with diabetes not wanting to wear yet another device in the skin. Anyone who would wear an insulin monitor is likely already wearing a continuous glucose monitor and an insulin infusion pump. They have to rotate and maintain sites for these, as well as do finger sticks to confirm glucose several times a day. That said, as diabetes technology gets smarter and more algorithm driven (as we head towards an artificial pancreas, in which the pump and CGM talk and an algorithm does glucose control), perhaps the insulin data will become valuable enough that this device will be a reality. When thinking about health and medical devices, keep in mind that technology, standardization, data, use if algorithms, etc., is at least ten years lagging behind other areas : (
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I always thought that glucose levels were a proxy for insulin and how your body produced and utilized insulin, and consequently, metabolized sugar. But, IMHO, no amount of genetic re-engineering can compensate for the piles and piles of refined sugar that we have introduced into the modern diet; nor for the high caloric values of junk food. Evolution never expected us to abuse our bodies the way that we do now.
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Actually, it’s not true. Of course, a big increase in insulin makes sugar go away at a faster rate from the blood stream. But not every person has the same insulin reaction nor the same base rate. That’s why I’m so interested in this.
By the way, I’ve drastically decreased my sugar and carb intake over the past 2 years, so this is particularly interesting to me with respect to non-sugar foods.
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Do you mean artificially sweetened (non-sugar) foods? Same result, apparently! From Wikipedia on “Sugar substitute”:
Animal studies have indicated that a sweet taste induces an insulin response in rats.[6] However, the extension of animal model findings to humans is unclear, as human studies of intragastric infusion of sucralose have shown no insulin response from analogous taste receptors.[7] The release of insulin causes blood sugar to be stored in tissues (including fat). In the case of a response to artificial sweeteners, because blood sugar does not increase there can be increased hypoglycemia or hyperinsulinemia and increased food intake the next time there is a meal.
Rats given sweeteners have steadily increased calorie intake, increased body weight, and increased adiposity (fatness).[6] Furthermore, the natural responses to eating sugary foods (eating less at the next meal and using some of the extra calories to warm the body after the sugary meal) are gradually lost.[8]
A 2005 study by the University of Texas Health Science Center at San Antonio showed that increased weight gain and obesity were associated with increased use of diet soda in a population-based study. The study did not establish whether increased weight gain leads to increased consumption of diet drinks or whether consumption of diet drinks could have an effect on weight gain.[9]
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Thank you, thank you, thank you!
Thank you for requesting information on INSULIN monitoring (not glucose). I too am very interested in monitoring my insulin levels. I really need to lose 40 pounds and I am keenly aware that different people process food differently. My wife eats well and can NOT gain any appreciable weight over 120 lbs. Not so for me. I know how my body reacts to certain foods but with only the coarsest resolution. I need to understand more.
I know caffeine spikes insulin levels. I know certain OTHER foods spike my insulin and others don’t (maybe aspartame, maybe not. Alcohol? Not sure.). Again, I need to understand how MY body reacts to food, sleep, lifestyle, etc. And I too am puzzled and concerned about the lack of information on insulin monitoring. I’ll be following this discussion closely.
Thank you for very actively keeping the discussion on track. It’s not about average insulin levels. It’s not about glucose levels. It’s about insulin monitoring!
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Thanks! Maybe I should ask again in 10 years 🙂
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Delighted that you started this conversation. I can refer you to http://www.diabetes247.com, an excellent resource for the type 1 diabetes community. Its author, Elizabeth Snouffer, has reported at length on her use of a Continuous Glucose Monitor (CGM) and the data she captures about patterns in her blood glucose levels. Medtronic and Dexcom seem to be the primary medical device companies that offer the CGM, data capture/analytics, custom reporting, etc. Their websites likely explain it all clearly, and there are likely many other players in the market. The Medtronic system transmits glucose data to Medtronic insulin pumps, which many type 1 diabetics now use.
Separately, my 11 year old son has used a CGM on and off for a few years. In the next few weeks, he’ll start up again with updated training on use. You are very welcome to join us for this session if you would like to learn more (we’re in the NYC area). We’re flexible and could likely accommodate your schedule.
Best wishes to you.
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Thanks, but I’m not interested (in this post) in blood glucose levels, but rather insulin levels for non-diabetics.
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As a physician (not an endocrinologist), I would say that your understanding of insulin levels sounds fairly accurate–though it is not completely understood by anyone at this point.
It would actually be very useful to know exactly how insulin levels react to ingesting various foods, but we don’t have a test that we can do continuously to follow this in the laboratory setting, much less at home. A site that explains the insulin test ( http://labtestsonline.org/understanding/analytes/insulin/tab/glance/ ) states, “Although glucose levels can be monitored at home, insulin tests require specialized instruments and training.”
You might find the following links interesting, as well–discussing the effect of Splenda on insulin levels, ( http://www.medicalnewstoday.com/articles/261179.php ), and the relationship between insulin levels and obesity, ( http://www.medicalnewstoday.com/articles/253713.php ). I haven’t looked up those particular studies, but the discussion in these articles sounds reasonable. If you wanted to really get into this, you could look up the abstracts on PubMed ( http://www.ncbi.nlm.nih.gov/pubmed ), but they can be difficult for someone without a medical background to interpret.
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Thank you so much! This is exactly the information I am looking for!!
🙂
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Here’s a good resource, a blog called “Diabetes Mine” and Amy is great and debunks a lot of stuff you read that’s not accurate. It’s been around for quite a few years and I interact with her and if have questions, she’s right there to add comments without obtrusive or “telling you what to do”…there’s enough of those out there. As far as devices, they do a good job over there talking about many of them as well.
You can certainly get good information from Amy and others there without being tracked and marketed. Again I like the blog because they put and the bad out there.
http://www.diabetesmine.com/
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Insulin is a signaling hormone; its presence needs to be detected by cell receptors that have evolved to detect insulin. Glucose is a basic fuel required for the body to do much of anything, which includes making insulin. Based on this, one would expect the concentration (in molecules/volume) of glucose in blood to be several orders of magnitude higher than insulin. Wikipedia presents some easily accessible information at http://en.wikipedia.org/wiki/Insulin#Blood_content in particular, see the figure http://en.wikipedia.org/wiki/File:Suckale08_fig3_glucose_insulin_day.png for an “Idealized” graph.
According to Wikipedia, typical blood levels of insulin between meals are 57-79 pmol/L, while glucose levels are 4.4-6.1 mmol/L. pmol:mmol is 10^-9, or parts-per-billion. You want to use molar quantities to think about this instead of mass, because moles are directly proportional to the number of molecules (insulin has a mass of 5.8 kD, glucose only 0.18 kD). I’ll leave the back-of-the-envelope calculation for how much more sensitive an insulin test would have to be to you, but this is one reason that tests for insulin require specialized equipment/training, while tests for glucose are essentially OTC.
As for modeling insulin resistance, there’s probably quite a bit out there. You should look on Pubmed (search for “insulin resistance mathematical models” revealed ~7000 articles). However, my guess is that most of these are epistemological regression models, and if you poke around you’ll (hopefully) find more mechanistic models. Quite a bit of work has gone into the signaling mechanisms (Pubmed for “insulin signaling pathway” returns 20k articles), both in the pancreas and in other cells, and they seem pretty key to understanding type II diabetes.
Your mechanism/hypothesis linking insulin/fat retention is vague, so it’s hard to actually evaluate it. Why isn’t there a simpler answer: some people just burn more calories by existing than others? If there is a link between insulin levels and fat retention, it’s probably not simple. You do need to actually process glucose into fat. This means that glucose has to be taken in by fat cells, presumably through insulin signaling. This suggests that the link, if it exists, may involve downstream pathways, a different uptake mechanism, or a difference in uptake between fat/muscle cells.
There’s a lot already known about this, and an entire NIH institute that funds grants to study it. And there are certainly good opportunities for solid contribution; there may be enough known for models to start being quantitative (if they aren’t already), at least for cultured cell studies. However, it is a situation where I’d be wary of “spending a few months in the lab to save a few hours in the library.”
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Signaling to what, for what? You don’t say.
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Okay. Keep in mind that this is not my field, so this is largely a cartoon of what happens. If you’re actually interested, your local state university library will have these and, if you want to know more, actual access to the research articles.
In multicellular organism, it turns out that different cells need to coordinate with each other, and often use small concentrations of specific molecules for doing so. Cells receive these molecular signals using proteins that sit on the cell membrane; when a signal is received, it is usually amplified internally, and then something happens. The specifics (signaling molecule, receptor, amplification, what happens next) are specific to the process.
Insulin is one of those signaling molecules. Glucose in the blood needs to be tightly regulated. All cells require it to produce the highly-volatile tri-phosphates that let them do anything (ATP and GTP, for example). The process of creating ATP from glucose is the Krebs cycle, and is well-known.
The problem is this: we eat at specific times, but require some amount of glucose at all times, and too much glucose in blood can cause problems (see http://en.wikipedia.org/wiki/Diabetic_ketoacidosis). So the body needs to buffer the amount of glucose in the blood by storing it elsewhere and then releasing it upon demand. The body stores glucose, for the long term, in two basic forms: glycogen (in muscle cells) and fat (in fat cells). The basic problem, then, is how does the body keep a certain range of glucose in the blood, given that we eat large quantities 2-3 times a day. The answer is, partially, through insulin.
Insulin is released by the pancreas in response to elevated blood sugar. It’s detected by specific receptors on muscle and fat cells which, upon its detection, haul out their glucose uptake machinery and prepare to haul in a lot of excess glucose for conversion into a longer-term storage.
Insulin itself plays no direct role in transforming glucose to fat or glycogen, and it plays no direct role in metabolizing glucose. All of these processes are, more or less, well-known. Insulin primarily regulates glucose uptake by specific cells. There’s a whole other side to releasing glucose from longer-term storage when blood sugar levels are depressed, but I don’t believe insulin is involved in those pathways.
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Thanks for clarifying — insulin itself plays no direct role in transforming glucose to fat …. [but] primarily regulates glucose uptake by specific cells.
I also found Dr. Attia’s blog and discussion on this, very deep.
http://eatingacademy.com/weight-loss/how-to-make-a-fat-cell-less-not-thin-the-lessons-of-fat-flux
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there are a couple reason for not tracking insulin levels: (1) it’s tough, compared to sensing glucose levels, due to lower concentrations and more difficult-to-perform bio-assays, and (2) the medicine has all been based to date on controlling the glucose; That is to say it would be quite expensive to develop insulin measuring techniques, and one doesn’t know how much it would pay off (compared to measuring glucose).
Maybe it could be useful for you to use a continuous glucose monitor just to see what happens to your glucose levels under various circumstances (eating, not-eating, resting, exercise, etc.). I use a Dexcom: one injects a subcutaneous sensor with a little radio transmitter module (something like 5 microwatts at 450 MHz), and one carries a receiver with graphical readout. It’s not really continuous — the data points come every 5 mins or so, but compared to finger-sticking, it’s effectively continuous.
I’ve learned from this meter how really some foods will not work their effects until a couple of hours after eating, while others (e.g., orange juice) will work its effects within 15 minutes (YMMV).
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I’m not saying it would be useless, but I’d really like to work with what I suspect is the leading indicator, which in this case is insulin, not blood glucose. Mostly I am just curious about how hard this is and what we know about it.
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The Wikipedia page says it forms up into hexamers and the monomer is the active form. I guess that the UniProtKB sequence length 110 AA means 110 amino acids. So you’d need to detect the specific protein, google says there are monoclonal antibodies available for insulin. So maybe a MEMS device could be used to test for it in blood.
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Wow that is unbelievably nerdy. Kinda awesome.
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Crikey. I hate to be troll-like, but why was my comment deleted? It was topical, sincere and, I thought, helpful.
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Because it wasn’t related to insulin, and it had a veneer of dieting and exercise advice.
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Sorry. No advice intended, just considering various things that might affect body fat independent of insulin levels. Will try to stay more on topic.
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Thanks!
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Interesting idea. I have read that artificial sweeteners cause insulin to be released, kind of like classical conditioning. You taste something sweet, thus insulin is released but then there is no sugar in your blood to actually get rid of, and thus you have a problem. Those with diabetes are given the ok to ingest artificial sweeteners because it doesn’t mess with their blood sugar, but it does seem to affect insulin levels which is also a problem, but as insulin levels aren’t readily measured, one that isn’t noticeable.
I have a basic biochemistry book, and in the chapter about metabolic profiles it talks about how adipose cells (aka fat cells) interact with glucose and insulin. It seems like triacylglycerols (fatty acid packages) are delivered to adipose cells when insulin is present, and can only be released from the adipose cell, when glucose is scarce. Thus the idea is that with regulated blood sugar and insulin, fatty acids aren’t continuously stored in adipose cells and are instead only transitionally stored until they are needed. At leas that is a simplistic explanation
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You might be interested in seeing that at least one study ( http://www.ncbi.nlm.nih.gov/pubmed/20929998 ) showed that changes in diet alone (Mediterranean vs. low fat diet) can lead to lower incidence of developing DM 2 over 4 years. The next step, as you suggest, is to better understand how various elements of one’s diet trigger this change.
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Clearly a better understanding of insulin’s action should be invaluable to those of us trying to avoid Type 2 Diabetes (that includes me, as my father suffered from this in his later years, and my body type is much like his).
To that end, here’s a very insightful article: http://bit.ly/19gYO3a
Even if you don’t want to read it, because it contains the awful words ‘weight loss’ and ‘exercise’, I think that judging from the comments put forward so far, many of your readers would find it very illuminating.
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Hey, this is awesome!
I’m not allergic to weight loss in the abstract, just people telling me to have more willpower to achieve it. Or saying it’s simply a matter of “not overeating.” I’ve come to believe, like the author of this illuminating link, that overeating is an effect of an underlying metabolic problem. Trying to control the effect is not helping.
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I agree, in fact the whole website is awesome. The author, Dr Peter Attia is completely obsessed by nutritional and lipid science (his series on cholesterol is a complete eye-opener, and will bring you way beyond the average physician in understanding this very important subject).
He is also one of the founders, and the president, of NUSI (Nutritional Science Initiative – see http://nusi.org/), which has been specifically set up to undertake properly controlled (and agenda-free) studies into various aspects of nutrition (so much of what goes for current nutritional science doesn’t really live up to the scientific method).
It’s refreshing to come across someone who is so passionate about his subject, yet apparently completely open-minded about discovering the truth rather than pushing some half baked theory.
By the way, I have absolutely no connection with him, or with NUSI. I just admire his commitment, energy and integrity, and wish there were more like him.
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I was also going to suggest Peter Attia’s excellent work, but Richard King beat me to it :-). As an endurance runner, I’m very interested in fueling and insulin resistance, and have had good results with cornstarch, a low glycemic index / high molecular weight starch.
As the parent of a child with type 1 diabetes, I’m very interested in the dynamic relationships between carbs, insulin, and blood glucose. The JDRF is sponsoring work to develop an insulin sensor, http://jdrf.org/wp-content/uploads/2013/07/EOI__for_Insulin_Sensor_Final.pdf. The technical challenges are huge, including but not limited to the small amounts of insulin to be detected, consumable reagents, battery life, cost, size, and inconsistent diffusion of insulin in different sensing locations.
It is for these reasons I believe it will be a challenge to develop near-real-time monitoring of insulin levels. Alternative approaches include modifying insulin with radioactive or biomarkers and then injecting that insulin to measure its diffusion / absorption / effect on blood glucose. These approaches also have their own set of challenges.
All of these approaches suffer from the same problem: there is no way to measure the production of insulin at its source, the pancreas. Same goes for other important hormones like glucagon and amylin.
An area which I think shows far more promise in terms of developing an understanding of insulin resistance is studying the effect of exogenous insulin delivery in people with type 1 diabetes who have low c-peptide levels (their pancreas no longer works).
Imagine a closed loop system which uses feedback control from a continuous glucose monitor to adjust the level of insulin delivered from an insulin pump in order to maintain blood glucose within a tight range, i.e. 90-160mg/dl. Looking at the trend of insulin delivery over time, one can develop an understanding of insulin resistance as a function of internal and external factors such as circadian rhythms, menses, puberty, illness, stress, exercise, BMI, and genotype.
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Thanks, awesome information!
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And that last sentence is exactly what I hope to achieve.
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What you’re hope to achieve is largely phenomenological, and will likely run into many of the heterogeneity problems inherent in linking medicine to human phenomena without a deeper understand of the mechanisms at work. Which is not to say that the work wouldn’t be valuable, just that there’s a different approach you might consider.
This recent paper presents a systems modeling approach to insulin resistance:
http://www.jbc.org/content/288/14/9867
The authors use existing and new data to construct a model of the insulin resistance signaling pathway within an adipose cell, and propose a molecular mechanism for growing insulin resistance. Models of this sort are basically a system of ODEs, sometimes with diffusion for transport. The system is usually underdetermined, so there’s quite a bit of art in choosing the important factors, weighing the importance of the data, and often choosing the important interactions. However, the results are, in theory, testable in cell culture and would provide more direct targets, both for pharmaceutical approaches and for further research into how fitness and stress affect the adipose cells.
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Is there another chemical or mechanism in the chemical cascade from eating that might be easier to measure and monitor? The new type 2 diabetes medicines, the incretin mimetics such as Byetta and Victoza, insert their pharmaceutical magic earlier in the chemical cascade before insulin is triggered. Maybe there is another way to get at this.
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insulin also has the context of leptin, if you’re looking at variables. also the complex effect of sugar in the context of addiction (endorphins, receptors, etc) reveal more important variables. lustig (sugar the bitter truth) and taubes have a lot of interesting things to say about insulin from a dietary perspective. luck! i’m interested what your analytic powers unveil…
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Despite the availability of various biochemical assays to measure the presence of the insulin molecule in various analytes such as blood, a significant challenge remains. If the insulin is subject to mechanical or thermal stress (shake and bake), then its biological activity can be compromised (it unfolds improperly and can no longer bind to insulin receptors). This is known as denaturing and can be caused by “frying your insulin”, i.e. leaving it out in the sun. It can also be caused by mechanical shear if the syringe is filled too rapidly from the vial. There are even cautions in using pneumatic tubes to transport insulin in pharmacies. Then there is the whole question of dissolved air in insulin pump reservoirs and bubble formation / degassing due to Henry’s Law.
Unfortunately the gold standard for insulin bioavailability rests with our friend the rabbit, http://www.pharmacopeia.cn/v29240/usp29nf24s0_c121.html “The most prominent manifestation of insulin activity, an abrupt decrease in blood glucose, was the basis for biologic assay from the time of its first clinical use. The procedure, although relatively cumbersome, has the great merit of accurately reflecting the effect on the diabetic patient. The advent of practical yet sophisticated physicochemical methods (e.g., liquid chromatography) to measure insulin potency quantitatively has resulted in a more accurate and precise compendial test for insulin and insulin products. However, the bioidentity of insulin and insulin products cannot be assessed by these methods.”.
If you really want to know how much “effective” insulin is in that syringe, you need a rabbit (six rabbits, actually).
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Let me prove that high blood sugar and insulin levels are not caused by being fat. If you take a fat person and do a gastric bypass (bypass top 1/7 of digestive tract) then they will eventually lose weight. But their type2 diabetes (high blood sugar levels) is cured immediately after the operation. QED.
Also note that for given levels of physical activity, the higher the weight the higher the life expectancy. You can reduce weight without exercise, and also reduce blood sugar levels, by going on a low carb diet, but this now seems problematic as a health strategy.
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The best way to check pancreas function is an insulin clamp test. Not cheap but the gold standard. I’ve wondered about the continuous monitor for a few years as I have reactive hypo and not diabetes..
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