I was both confounded and surprised because my diet is pretty darn excellent, particularly concerning those pesky, debilitating high glycemic carbs that proliferate the Great American Diet. If you haven’t read My Blood Sugar Numbers Confound Me, you may wish to do so before continuing so that you can have context for the rest of this post.
The first thing that occurred to me when I got my blood test results was that both my father and uncle (his brother) developed adult-onset diabetes, which is called “Type 2 Diabetes”. I always thought that they both contracted that disease in their 60s because they ate crap, were overweight and didn’t exercise, but now I’m wondering if they had a genetic predisposition to type 2 diabetes and therefore would have gotten it even if they ate and exercised…ahh… well… like me? As the video in “My Blood Sugar Numbers” describes, I borrowed my sister’s glucometer and began testing my blood.
In addition to the favorable post meal blood glucose numbers, I have another blood measurement marker that’s in my favor. Hemoglobin A1(c) is expressed in percentage terms because it’s measuring the percentage of hemoglobin that’s bonded to sugar. In subsequent posts, I’ll report about some other unhappy blood result I got in my last Life Extension test, such has high VLDL, Pattern B LDL Density Pattern, high inflammation markers and low thyroid indications. You're gonna get (1) the Newsletter, (2) the four-part guide, Transform Your Body and Mind, and (3) the 12 Ageproof Biohacks.
HNF-4α controlling many genes involved in liver function such as the GLUT2 and L-PK genes. Evidence on the mode of action of metformin shows that it improves insulin sensitivity by increasing insulin receptor tyrosine kinase activity and enhancing glycogen synthesis in hepatocytes, and by increasing recruitment and transport of GLUT4 transporters to the plasma membrane in adipose tissue.
In addition to its effects on hepatic glucose and lipid homeostasis and adipose tissue lipid homeostasis, metformin exerts effects in the pancreas, vascular endothelial cells, and in cancer cells. Diabetes blood sugar levels chart: what is a normal blood, Keep in mind that the blood glucose level before a meal for a non diabetic person and a person with prediabetes may be very similar. Blood sugar – wikipedia, the free encyclopedia, The blood sugar concentration or blood glucose level is the amount of glucose (sugar) present in the blood of a human or animal.
Blood glucose levels : testing and normal range, A blood glucose test measures the amount of a type of sugar, called glucose, in your blood. Blood glucose monitoring – wikipedia, the free encyclopedia, Blood glucose monitoring is a way of testing the concentration of glucose in the blood (glycemia).
When your blood sugar is too high or too low, Sometimes, no matter how hard you try to keep your blood sugar in the range your doctor has advised, it can be too high or too low. Home « blood sugar basics, Make your next conversation with your diabetes healthcare team count by asking these quick questions about blood sugar!. Diabetes, blurred vision, and high blood sugar levels, Blurred vision can also be a symptom of more serious eye problems.
The final destination of a journey is not, after all, the last item on the agenda, but rather some understanding, however simple or provisional, of what one has seen. In these modern times, with the plethora of blood-sugar-related diseases, we need tools like GI and GL to help us understand ways to control blood sugar. The self-testing, graphic approach to food testing developed in the balance of the newsletter is a less scientific but a more dynamic way to explore postprandial (post-meal) blood glucose levels (BGLs).
GI measures the blood glucose impact of foods eaten in isolation, yet we rarely consume foods this way. GI readings vary with the individual—blood sugar and insulin reactions are more extreme for diabetics, for example (See Charts 2A and 2B). GIs are calculated in the science lab as the day’s first meal after a 12-hour fast and using a fixed serving that includes 50 grams of carbohydrate.  Most of our daily calories, however, are consumed in combination and throughout the day, when our blood sugar is affected by other foods that we have eaten earlier, as well as by our level of activity. Of the following numbered charts, the first three are based upon scientific research journal articles (Charts 1, 2A, 2B), while the last four (Charts 3-6) are constructed from my own self-testing of foods4 using a simple blood glucose monitor.


Chart 1:  Blood Sugar Curves of White Bread Compared to Bread with Added Fiber, Sourdough, and Vinegar.
Chart 3:  Instant Oatmeal, Whole Oats (Soaked and Not Soaked), and Whole Oats Combined with a Protein and Fat.
To fully appreciate the impact of two back-to-back carbohydrate breakfasts please notice that the scale used for Chart 6 is twice that of Charts 3-5. Resetting the Table–to Control Blood Sugar (For a discussion of other strategies, see April 2011).
Ramekins filled with condiments like nuts and seeds (GI=0).  Nuts and seeds provide healthy fats, fiber, vitamins, minerals, and antioxidants, while they slow digestion and curb blood sugar.
Sourdough bread or whole-grain bread with whole kernels; butter from grass-fed cows and organic nut and seed butters such as tahini and pumpkin seed butter. A pitcher of water and glasses for all—sometimes we mistake hunger for what is in fact thirst.  You might flavor the water with a little lemon juice or other flavoring.
Because 12-hour fasting, pre-meal blood sugar reading can vary, all data points at time zero prior to the first morning meal were indexed to zero in order to illustrate the change from a neutral starting point. I use the label “traditional” carbohydrates, just as we call unrefined fats, “traditional” fats. The real story is that the number, size, and density of cholesterol particles in your blood (LDL-P and HDL-P) are far better predictors of heart disease risk. The best way to measure your heart disease risk through LDL cholesterol is to measure the number of LDL particles in your blood, or LDL-P, which you never get checked unless you have a fancy test called a lipid nuclear magnetic resonance test – or NMR test for short.
You can look at particle size.  As a general rule (this is NOT always the case, however), the larger the LDL particles, for a given LDL-C, the fewer the particles (which is what we want). Below is graph of my overall change in changes in HDL-C, LDL-C, and TG, along with the ratio of my TG to HDL-C, based on the “standard” cholesterol panel. As I stated above, a better marker of risk with respect to LDL is particle number, LDL-P – the fewer particles, the better; and you can estimate this by measuring particle size, or through concentration of ApoB.
Unfortunately, I only started doing regular VAP testing about a year ago, over one year into my “experiment” of progressive carbohydrate restriction.  Hence, I can’t show my progress as longitudinally with VAP as I can with standard cholesterol testing. Below is figure showing the change in my VAP panel over a seven month period, between January and July 2011.
Keep in mind how my diet changed between January and July – I reduced carbohydrate intake from approximately 150 grams per day of “good” carbs to less than 50 grams per day.  I also increased, dramatically, my intake of fat, including saturated fats.
Despite the amount of time I’ve expended on explaining all of these nuances of “cholesterol” numbers, I am not entirely convinced that I am healthier today because my cholesterol numbers are better.  I wonder if I’m healthier today because of something else, and that whatever else is making me healthier is also correcting my cholesterol problem? If I had to guess what is really making me healthier today, besides being less fat, I believe it is the combination of how sensitive I’ve become to insulin and how much less inflammation I have in my body, especially in and around my arteries.
As I mentioned above, findings #1, 2, and 4 are almost universal in folks who abandon carbohydrates, while finding #3 is somewhat variable. Which of these is most important?  This is an obvious and important question, but one I don’t really know the answer to (nor does anyone else, for that matter).  If I had to guess, I believe observation #4 is the most important because insulin resistance is the underpinning of metabolic syndrome.
People have said things to me like, “Well it’s great that you’ve reduced your risk of all diseases associated with metabolic syndrome, but wouldn’t it be funny if you got hit by a car tomorrow!”  All kidding aside, this misses the point. I’ve been testing fasting blood glucose, and one and two hour post meal, the detailed results of which I’ll share in a future post. This measures how much glucose permanently gets glycated (bonded) to hemoglobin in red blood cells. I'm a big believer in sustainability, and am a bit nutty about optimizing my diet, supplements, hormones and exercise. Alcohol and snacking (assuming the snacks are high glycemic) will boost blood sugar and over time that could cause insulin resistance.


Another exenatide-related drug is Bydureon® which is a once-a-week injectable form of exenatide. A more recent addition to the GLP-1 receptor agonist family of diabetes drugs is Trulicity® (dulaglutide) manufactured by Eli Lilly and Co. Additionally, it has been shown that metformin affects mitochondrial activities dependent upon the model system studied.
The latter effects of metformin were recognized in epidemiological studies of diabetic patients taking metformin versus those who were taking another anti-hyperglycemia drug. The second factor—the postwar shift from traditional to refined carbohydrates—is largely due to the growing role of the commercial food industry and processed, convenience foods.  Convenience foods must have a long shelf-life, so food companies rely upon refined flours and oils, which do not go rancid. Visual pictures of postprandial blood sugar behavior, while less scientific than GI measurements, are nevertheless powerful learning tools, providing a real flavor for how our body reacts when we eat different kinds of foods.
This chart illustrates the second meal effect– that what we eat at one meal affects postprandial blood sugar behavior at the next. What we do to our children when we give them a sugary cereal or a Pop-tart for breakfast extends beyond this first meal to affect their blood sugar, hunger, concentration, and desire to overeat throughout the rest of the day. One of the best herbs and spices to moderate blood sugar.  It can be sprinkled on hot cereals and desserts such as puddings, custards, and stewed fruits.
Well, there are two: what can I actually measure that predicts my risk of heart disease, and how does diet affect these these things I can measure?
Basically it’s a test to measure how much insulin a person needs to keep their glucose level constant, despite the addition of glucose.  The less insulin one requires, the more insulin sensitive one is.
This measurement roughly indicates your average blood sugar over the previous three months, and the higher it has been over the past three months, the more likely it is that glucose (sugar) is permanently bonded to hemoglobin, which is not a good thing.
He reports that it’s not uncommon for people on restricted carbohydrate diets (like me) to have high fasting glucose serum numbers. If you legitimately are on a low-carb diet and both the post meal and A1(c) numbers are good, then it could be that your situation is accurately described by Chris’ explanation quoted above. Metformin has a mild inhibitory effect on complex I of oxidative phosphorylation, has antioxidant properties, and activates both glucose-6-phosphate dehydrogenase, G6PDH and AMP-activated protein kinase, AMPK. The importance of AMPK in the actions of metformin stems from the role of AMPK in the regulation of both lipid and carbohydrate metabolism (see AMPK: Master Metabolic Regulator for more details). This is why diabetes and obesity often go hand-in-hand (90% of diabetics are either overweight or obese). David Ludwig regarding high-glycemic foods and overeating, cited in the Recommended Reading section at the conclusion of this newsletter. In adipose tissue, metformin inhibits lipolysis while enhancing re-esterification of fatty acids. The activation of AMPK by metformin is likely related to the inhibitory effects of the drug on complex I of oxidative phosphorylation. This would lead to a reduction in ATP production and, therefore, an increase in the level of AMP and as a result activation of AMPK. In fact, since the cells of the gut will see the highest doses of metformin they will experience the greatest level of inhibited complex I which may explain the gastrointestinal side effects (nausea, diarrhea, anorexia) of the drug that limit its utility in many patients.



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Comments

  1. 06.09.2015 at 18:28:36


    Blood glucose level below overweight, and not diabetic, does not mean.

    Author: GULESCI_QAQASH
  2. 06.09.2015 at 15:17:24


    Which are then absorbed into the bloodstream from the from anywhere, with your iPhone.

    Author: body_love
  3. 06.09.2015 at 11:46:50


    The liver can't properly store concentration of blood vessels present means rapid absorption.

    Author: BOB_sincler
  4. 06.09.2015 at 14:17:35


    Preceded by venesection before the glucose load study populations; populations.

    Author: pearl_girl