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My Son's Type I Diabetes - A Year After Mind Blowing Nutritional Realizations

Good to see another type 1 in here! Did you train before dx? I assume so, but just curious. I have long wondered how much more difficult this journey would be if I didn’t have experience being physical and understanding macros and their roles already at dx. God knows the docs couldn’t tell me anything I didn’t know, and some advice would have hurt if followed. I remember the docs mind being blown when I told them how much protein I ate. “That’s not what the fda says I should eat!” Nutrition as taught by them is a joke IMO. That is why mertdawg’s son is so blessed! He has an advocate who can filter dumb docs advice and give him a real chance! I have known a few t1’s who struggle with weight and control too much because of docs.
Anyway, I am glad to have come across t1s who train and care about nutrition!

The 1:10 is for the most active individuals. There are T1D teenagers who need 75 units a day, and girls who will vary between 40-100 over the course of a month. The typical range for Lantus in non insulin resistant individuals is between 1 and 2 units per 10 pounds being low the more muscular you are.

Generally total insulin needs vary between .6 and 1 unit per kilogram per day. If you are using less than .5 per kilo and have an A1C in the low 6’s or better you are considered to still be in the honeymoon phase. So for you that would be about 38-39 total units per day. It sounds like you are taking well under that, and also staying under 6.0.

Most of the pediatric docs are focused on research in genetics or developing new types of insulin and have no idea about day to day management. They insist on my son getting 15 grams of juice if his blood sugar hits 69, but that would spike him to 180. The truth is that if you AVERAGED under 200 10 years ago it was considered to be tight control for a kid under 12 (8.5 A1C). My son was diagnosed at 8.7 and had felt terrible for a couple of weeks. Then again there is a difference between being 8.5 but having the insulin to let your muscles USE glucose and being 8.5 and peeing it all out during the night.

I will post some amazing articles I have come across. For one, I found that insulin actually raises your muscles level of glycolytic enzymes, and also other non-insulin requiring pathways. When someone has a high blood sugar, say 300 ,their muscle cells actually have the sugar inside, but don’t have the insulin to signal the muscle cell to burn glucose. Also most hyper glycemia is the result of the liver releasing too much glucose after a meal, not the inability of the body to move glucose into cells.

When a non diabetic person has low insulin they will turn ON fat burning, turning protein into glucose, and ketones because low insulin is the signal that there is low blood sugar, but when a T1D has low insulin they have high blood sugar, and get all of the other things turned on too, basically creating a gluco, lipo, protein toxic, ketone toxic cesspool in the blood causing body tissues to be exposed to toxic levels of these energy containing compounds.

If you take the mmol/Dl level and multiply it by 18 you get the American version. So a 4 would be 72, and a 6 would be 108.

When non-diabetics eat a reduced carb diet their fasting blood sugar rises such that at around 30% carbs normal fasting level is about 95. At under 20% carbs then fasting blood sugar can go up to over 100, but 90-100 is not considered to be pathological if it is due to the lower carb content of the diet.

One amazing realization was that a low carb diet does not make you more insulin sensitive. It also does not require less insulin from the pancreas because the pancreas has to put out insulin to deal with fat and protein as well. It pretty much takes the same total amount of insulin to manage the same number of calories, but the breakdown between basal and post prandial (post meal) insulin may be different. Lower carb diets do tend to produce more stable blood sugar, a tighter range.

Interesting. Are we talking total of basal plus bonus or basal only? Most days I hit 17 bolus in addition to the 17 basal, making a total of 34. It all depends on the food that day of course

Total for both basal and bolus. If you are under 6.0 and under half a unit per kilogram then you are considered to have significant help especially coming into range for breakfast. Do you get consistent good morning blood sugar?

When the honeymoon period is over you will not correct at night at all. If you go to bed at 140 you will wake up at around 140, and people often have to start adding corrections in the morning. Plus my son is still running about 100 through the night getting help from the self correction, but when his honeymoon is over, if he goes to be at 170 he will stay there. If he gets a night time hormone surge that shoot him up to 170 at night he might stay there (sometimes hormone related rises correct themselves because the hormones that raise blood sugar get depleted from the body for the following hours).

So eventually the goal of Lantus is to keep your blood sugar “flat”. If it is 180 it will stay 180, if it is 70 it will stay 70. type IIs get help from their pancreas and so they will take enough lantus to get their fasting number optimal, usually around 95, but it doesn’t work like that when all of your beta cells are gone. People will actually set the CGM to alarm at 130 or 150 if they rise during the night so they can give themselves a correction bolus. And when Lantus levels get THAT high, you become low much more easily at night after intense training I have heard. I know kids who play sports and have evening games like basketball and they wake up every night at midnight and have a box of juice on the stand in case their activity has resulted in a low. This is part of my fear with my son coming out of the honeymoon. Lantus doesn’t get you to a good morning blood sugar anymore, it just makes your blood sugar flat wherever it is, but it also has a little peak between 2-6 hours, so you may find that you go to bed at 130 and drop 40 points by 3:00 am.

I had been training for about 5 years before dx. Though I must say my nutrition was casual powerlifter style “enough protein and whatever”. Now a days it’s way more structured, both diabetes and training supporting each other (the better I eat the better my training and diabetes, makes me feel efficient, ha!)

As for the doctors advice the “1 unit/10 pounds” is what is taught also here for us patients. …other than that the advice is pretty basic since most people have no idea about proper diets etc. Unfortunately it seems that at least my doc is pretty dogmatic and likes being the-person-who-knows-better. Point being that if one wants to really take good care instead of okay-ish care of the D, you have to be proactive in figuring stuff out and educating yourself.

Big props to mertdawg for his research on the subject, there’s alot to digest for me!

Does either one of you have a source where I could read about liver and diabetes? My knowledge is really basic level stuff about the pancreas, and I’m confused about liver’s role, especially when approaching hypo levels.

I can tell you this from my research. Most people, including type 1s in the first few years will have their liver put out glucose to help stop low blood sugar caused by too much insulin/activity. The hormone that causes the glucose to be put out is glucagon. It is put out by the alpha cells of the pancreas, cells that don’t get destroyed by the autoimmune attack. Unfortunately when the beta cells that put out insulin and amylin are gone, the alpha cells start to act dysfunctionally. They will spit out glucagon and raise blood sugar when you eat even before the carbs from the food hits your bloodstream. They will even spit out glucagon if you eat low calorie large mass vegetable matter like a lot of lettuce. The second problem is that you no longer have amylin to tell the stomach to delay emtpying its contents and also to tell the liver not to release stored glucose from glycogen. The third problem is that the pancreas STOPS working to release glucagon when you get low blood sugar, so after about 5 years most type 1s loose the ability to have their liver help in a controlled way to bring up blood sugar when needed. It is believed that this may be a neuropathy of the alpha cells caused by high blood sugar (so good control can help you keep this ability longer, and therefore keep good control longer). It COULD be that the disfunction is due to the pancreas not having self made insulin, and so it gets out of whack in knowing how much glucagon to make or when to release it because the insulin levels in the body help regulation.

Going to have to follow this thread. Thanks for all the info!

Thanks mertdawg, alot!

I’ve been trying to get the doctors tell me stuff like this, but they keep on yammering about “just measure often and eat healthy”.

Gotta start researching by myself too, thanks again!

My morning BS are usually in a range, 80-120, almost always depending on the previous day’s diet/training I think. So if we slightly reword the Lantus explanation to say the the amount of Lantus used establishes the “baseline” your body has (ideally around the 100 mark), depending on the amount used, and of course there is no ability to autocorrect anything, I theorize that if I go to bed at 120 and wake up at 80, then we have basically 3 options as to what happened:

  1. my body made some insulin to help out and try to correct itself
  2. my training or any physical activity the day/evening before made me somewhat more sensitive, OR my muscles soaked up a bit of the BS, being somewhat depleted, or both
  3. I am taking too much Lantus
    (or it could be a combination of any or all of these)

And two of these could be tested fairly easily. If BS is a bit on the low side each morning, whether I have trained or not, been sedentary or not, eaten carbs or not-whatever-just consistently on the low side, we can probably hazard a good guess that I am taking a bit too much lantus. This of course would mean also that my BS would tend to run on the lower end all day as there is basically too much insulin in my system and it would tend to have a lowering effect. If anyone that has taken too much Lantus can attest too, you would be fighting lows all day. When I was first dx, this became a problem for me big time as I was fighting all day to keep from going low. This was before I realized I had the power to fix this myself and was going with the doc’s original plan blindly. Now, this does not mean I am not making my own insulin to help though.

Now, my morning BS is usually dependent on training and diet the previous day. It may be helped out a bit, but the range does vary enough for me to suspect the help is fairly minimal, or intermittent at best. If I have not done any training, and carbs have not been restricted to any great degree, and I go to bed at, say, 100, it is a good bet I will wake up within a few points of that. If I train intensely the evening before, and “refill the tank” before bed and go to sleep with a BS of, say 110 (after training I almost never go to sleep under 100 (just in case there is a drop overnight), I may, or may not, drop overnight at all. If I have replenished enough, then all is good and I wake up in a good range. If my training was more depleting than I thought it was-cuz how can you really know other than “feel”- then there is some BS soaked up overnight and I wake up lower. We can call this an increase in sensitivity if we want and it will mean pretty much the same thing. Either the muscles soaked some up, or the Lantus worked more efficiently.
Interestingly, the type of training will affect this to a degree. If I have gone really heavy and intense-say a CNS intensive session, cortisol or whatever will be jacked up and I may run high as a result. This effect may run through the next day-or two. Soreness also plays in to effect-through hormones no doubt-but if I am SUPER sore from training- legs are the worst-then BS is pretty much guaranteed to be elevated for days. This is probably made worse by not being as mobile and just moving less as a result. I am interested in JonneKytola’s experience here too.
As another curiosity, if I eat hardly any carbs in the evening at all and just go with protein and veggies, and go to sleep with a perfect 100, I usually experience a small drop. This is not something I usually do, so it is not a huge deal, but it is a curiosity.

Either way, the hormones do their thing regardless and I can only try to keep them in control as best I can. This usually means a bit more rest from training, lower volume or at least not high volume for all bodyparts, etc. I can still push it, but any craziness will effect the system and make balancing BS a bit more difficult. Still the overall effect of training is on the positive side for everything just as JonneKytola said. Just have to learn to deal with it and adapt!

Good to see you in here. Are you a T1?

FAT loading and CARB loading-Is this how the anabolic diet works?

I mentioned that my son is small. There may be other issues that we haven’t been able to positively identify yet (type 1 diabetics have a much higher rate of celiac (gluten intolerance) and thyroid autoimmune disease. The Thyroid issue is considered to be the easy fix, just take synthetic hormones. Celiac is a problem because even a gram of gluten containing food can cause the intestines to wither up for weeks, and result in malabsorption and inflammation. You can’t just reduce gluten, you have to remove every speck every day.

Anyway, my son was negative for thyroid autoantibodies and considered in the “low likelyhood but borderline” range for celiac-though the only definitive test is an endoscopy. Enough of that, but I wanted to mention this because he felt bad eating larger amounts of carbs at diagnosis. He felt fine with a little starch, a little fruit and veggies and a little dairy, about 30-40 grams per meal, and so I really HAD to get him more fat in his diet because without it he was only getting about 1000 calories a day. I added fat from butter, olive oil, and high oleic sunflower, some egg yolks, some grass fed beef hot dogs, a little chocolate.

So he has ended up with about 1600 calories a day and about 100 grams of carbs (25%) with maybe 10-15% protein and around 60% fat. This does not actually concern me. I personally eat similarly-more protein, but add carbs around training and my wife is a cardiologist and even the ACA is moving to drop a fat limit from their dietary recommendations. I posted about this earlier this year.

What I found was that my son did not very easily get low blood sugar from exercise after injecting insulin. The exercise might keep his blood sugar peak down, and as he was using up energy he might be “lower” 4 hours later, say 70 instead of 110, if he ate and started to rise in blood sugar after breakfast and lunch he could be very active with little risk of hypoglycemia. He also has virtually zero adipose.

So I researched the main reasons why T1Ds get LOW during activity. I thought that the main reason was that insulin was holding glycogen locked in the liver and not letting it out to get to muscles, but that is not the main reason. When non-Ds get low on muscle glycogen they will mobilize fat from adipose which then travels to the muscle to supplement energy. When non Ds are have low blood sugar they actually have LOW insulin levels because blood sugar stimulates insulin. The same for type IIs who secrete a lot of insulin (in the early years after dx). Type 1s work utterly backwards. They have low blood sugar because they have high insulin. (this also can happen to some high endurance athletes who eat huge amounts of carbs and develop reactive hypoglycemia).

So anyway, it is hard for a T1D to burn adipose during activity because insulin is holding fat cells “closed” and not letting out fatty acids. High insulin also turns off hormone sensitive lipase enzyme that usually cuts fatty acids off of triglycerides to send them into the bloodstream for fuel. When a non T1D has low blood sugar (low insulin) they get more fatty acids in the blood, they get protein turned into glucose by the liver, and eventually they get ketones to suppliment for low blood sugar.

When a T1D has low blood sugar, insulin is high so all of those other energy sources are actually turned OFF! It is basically “all on” or “all off” with T1D rather than using one energy source when another is inadequate.

Anyway, I found several journal articles and other nutritional sources that discussed what is known as “physiological insulin resistance”. Basically when someone eats progressively less carbs, their body will become a little insulin resistant to preserve glucose for the brain. I will post some studies on this later, but as a rough guideline, if a person does not have pathology like progression to type II diabetes, typically individuals who eat over 50% carbs will have fasting blood sugars in the 80s, those who eat around 20-30% carbs will have fasting blood sugar in the 90s, and non diabetics who eat very low carb diets (10%) will tend to have fasting blood sugar gradually rise over the years to 100-110 or even as high as 120. Since it is not diagnostic of development of type II diabetes, it is not in and of itself a necessarily bad thing. Some studies have found that people are healthier with a fasting blood sugar in the 90s than in the 70s or 80s as long as it is not due to development of pathological insulin resistance.

SO anyway, when the carb content of diet gets under about 30%, as long as calories are not excessive, the body does not tend to store dietary fat in adipose cells. People who eat more carbs will have their muscles load up on glycogen if they are active, but people who eat lower carbs will have their muscles load up on fatty acids, and will also store fat right next to the muscle cells for energy. This means that their muscles can access the fat even if insulin levels are high because it is not locked away in adipose cells. Muscles can hold about 9x more energy per volume of fat than glycogen because 1 gram of glycogen has 4 calories, but is also bound to 3 grams of water, so 4 grams (or approximate milliliters) of glycogen has about 4 calories and 1 gram has about 1, but 1 ml of fat has about 9 calories. As a result, fat loading by eating more fat and less carbs for periods of time loads muscles with huge amounts of energy that they can access even if insulin is high.

Another thing is that as the carb content of diet goes down, muscles will make more fat burning enzymes and fewer glucose burning enzymes, but when people eat more carbs they will have more glucose burning enzymes.

Muscles use mostly fat at moderate steady state, unless it is for a very long time like over an hour. Even powerlifting type exercise using mostly fat as long as there are long rest periods followed by short periods of activity. (muscles will burn fat by beta oxidation, and this will reload their ATP and creatine phosphate so long as rest periods are adequate and exercise bursts are short, or as long as exercise is moderate enough in general to not deplete glycogen.

to be continued…


I apologize for being away for some time, real life getting in the way, ha!

Anyways, first thing that I noted from your post is the comment about soreness. I’ve definitely noticed elevated bloodsugar due to soreness, especially legs (I suppose the bigger the muscles are, the effect becomes greater and more systemic).

But, I must say that I do not do bodypart-annihilation style training, 'cause I hate being sore. I do full body templates with moderate volume. Also, I do mobility/movement work everyday due to a very seated lifestyle. I do notice though - alongside reduced general wellbeing - that my blood sugars become more unpredictable if I’m not moving enough. But I can’t say if that’s because of inconsistency (moving daily --> not moving daily) or the positive effects of exercise: i.e. I don’t find it hard to believe that with a totally sedentary but consistent lifestyle I’d have any more irregularities than with a consistent active lifestyle. If anything, exercise does increase the variables to take care of, but it’s too good not to be done.

About the evening meals and morning sugars: currently it’s going well. On training days (I train around 6-9 pm, go to sleep around midnight) I eat a post workout meal of oats, milk, whey and honey (90 g carb, 50 g protein) with 2 IU, and 30-60 minutes before bed I eat usually a whole meal of rice + dead animals + some veggies. This has occasionally caused some nighttime highs, and it seems to me that during sleep insulin is less efficient/sensitivity is lower. For the rice (60 g carb) I need around 1.5 IU, previously I used only 1 IU which was enough (or not enough, ha) to cause the mentioned highs. No Lantus on training evenings.

Non-training days I obv. don’t eat post workout meal, and for my last meal I eat just a little carbs (10-20 grams), moderate protein (20-40 grams, depending on daily macros) and quite a bit of fat (20-30 grams). If my sugars were stable before this meal I don’t have to use any insulin for this meal, but I do need Lantus for the night, currently around 5 IU. If I am too low or high I just fix that with some quick carbs or small insulin dose (most likely just 0.5 IU), and I let the base meal take care of me during the night.

This is very case-specific and obviously long term physiological changes are most likely going to happen in the long run, but these are some notes from where I currently stand.

Wow. That’s some great info. This might be the best info I’ve seen on T-Nation in a long time. If you had to give an opinion, how do you think all of this relates to a person of normal physiology trying to lose fat?

Also, based on your thoughts about intramuscular fat storage…do you think carbs are necessary for muscle growth? I ask because my son (who’s still very young) was born with a genetic disorder in which his body doesn’t produce the enzymes necessary to break down Sucrose, Lactose or Starches. He’ll be able to take some enzymes to help, but he’ll likely be very very limited in terms of carbohydrate intake throughout his life.

Thanks again for all the great information

I realized this was directed at mertdawg with his great informational post, but I am going to give my opinion based on your question of how all of that relates to a person of normal physiology trying to lose fat.

Taking the principle laid out in mertdawg’s post that essentially high insulin = low levels of fatty acid mobilization, one would conclude that high insulin levels are not conducive to fat loss. Insulin being an anabolic hormone is going to act in a manner opposite of being catabolic, and fat loss is a catabolic process.

The debate for aesthetic minded people really comes down to a matter of maximizing muscle gain, maximizing fat loss, or preserving as much muscle as possible while synchronously losing as much fat as possible.

In simplistic terms, maximizing muscle gains would require overall periods of high insulin levels. This can lead to increased protein synthesis, and decreased catabolism of proteins. Concurrently though, it could lead to an increase in triglyceride synthesis and decreased catabolism of triglycerides.

Maximizing fat loss would require overall periods of lower insulin levels. This can lead to decreased protein synthesis, and increased catabolism of proteins. Concurrently though, it could lead to an increase in fatty acid mobilization and a decrease in triglyceride synthesis.

Preserving as much muscle as possible while synchronously losing as much fat as possible would require a mix of high insulin levels and low insulin levels. High insulin levels would be appropriate intra-workout to promote protein synthesis, and glycogenesis, while at the same time preventing catabolism of protein, glycogenolysis and high elevations of circulating cortisol. Low levels of insulin would then be appropriate for the rest of the day to allow an increase in fatty acid mobilization and a decrease in triglyceride synthesis.

This of course as I mentioned is a simplistic and more conceptual look at the overall physiology involving normal people. There are certainly more intricate details available for discussion.

Another note regarding the physiological insulin resistance when individuals eat a lower carb diet. I am not sure if that research was done on resistance trained individuals, I am going to assume not. Obviously, insulin resistance in muscle cells are not ideal for the aesthetic minded individual, however, I would speculate that any muscular based insulin resistance from low carb dieting would be offset by an increase in muscular based insulin sensitivity from resistance training. I am sure there is a threshold at some point, though.

Thanks for the detailed response. All very true. But it all really leads you back to calories in vs calories out. Your body will adjust to your macronutrient intake over time ultimately leading to a zero sum game. Your muscles can store fat or carbs to use for energy, your body can produce more or less enzymes necessary for breaking down certain macronutrients.

Mertdawg might be giving us the answers to questions I’ve had for a long time. I’m no anthropologist, but it always seemed odd to me that on one hand, you could have Eskimos living on a ketogenic diet and on the other hand have the Hunza, Q’ero or Okinawans living on a high carb diet… all healthy.

I’ve always assumed that it was genetics… different cultures thrive on different diets based on their genetics. This all makes me think differently. Our bodies will simply adapt the diet we give it. The thing that actually matters is the total load of calories, carbohydrates, fat etc. If you eat too much, you’ll get sick. Over time, high total intake of any macronutrient will lead to heart disease and diabetes.

This is obvious i suppose, but I think it’s important. Also, it seems unlikely to me that sugar, salt, white flour or anything else is inherently bad for you. The real problem is just that modern foods are engineered to drive your taste buds crazy making it impossible to “just eat one.”

Calories in vs calories out is certainly a very important principle. But, understanding the biochemical implications that micronutrients, phytochemicals, antioxidants, hormones, etc. have on metabolic functions, it is not as simple as calories in vs calories out. Calories are not created equal in this sense.

Lets look at a simple comparison of a meal that consists of equal parts protein, fats, carbs, and thus calories. But, the sources of foods are different. One is say a meal of hydrogenated vegetables oils, factory farmed beef, charred on a grill, and a highly refined wheat product like pasta. Contrast that with a meal that is baked fish, avocados, and other fruits and vegetables.

One is significantly going to add to the amount of free radicals and advanced glycation end-products while minimally contributing to the antioxidant pool. This could likely cause a net increase in the amount of oxidative stress and damage on the body. The other meal will significantly contribute to the antioxidant pool while minimally contributing free radicals and advanced glycation end-products. This could likely cause a net decrease in the amount of oxidative stress and damage on the body.

This is just one small, isolated example of food choices. There are obviously more complex interactions that happen, but I think it sufficiently shows that a calorie is not always a calorie.

So I wanted to give an update and also possibly get into the insulin resistance issue. My son just went in for his 1 year appt. with the endocrinologist. His A1C was 5.8 which is considered to be better than you should even shoot for at least with a 55 pound kid. Three months ago it was 5.9 and it was 6.0 and 5.9 before that at each 3 month check. So we have 4 three month A1Cs of 5.9, 6.0, 5.9 and 5.8. That is really an incredible year as it is better average blood sugar than many people without diabetes (about 120 for the year). He also has spend minimal time above 180 which is the point where sugar starts to spill out in urine (and this puts the kidneys at risk). The endocrinologist only wants us to try to keep A1C under 7.5 which is about a 170 average blood sugar. 10 years ago the goal was 8.5 or about a 200 average blood sugar. A few decades back type 1 diabetics took 1 shot a day and did not even check their blood sugar in any reliable way (there was a urine test that could get within 50-100 points! If you felt low, you ate. You spent most of your time in the 200-300 range (average A1Cs in the 10-12 range). If you missed your shot 1 day you would end up in the hospital with diabetic ketoacidosis for several days. The goal of insulin was to prevent you from dying from DKA, and NOT to give you normal blood sugar.

Anyway, here’s the bad news. My son’s endo is perplexed as to why I am worried, and also concerned that he is very low in BMI (about 5th percentile-always has been). He has grown in the last 9 months and he is eating 30-45 grams of carbs 3x per day. I also have been getting him about 1600 calories a day for the last 6 months but mostly by adding butterfat-whole reduced carb milk, beef, egg yolks and olive and safflower oil (high oleic).

So the problem is that he seems to have become physiologically insulin resistant. Not to the level of some very low carb dieters, but to the point where he requires MUCH more meal time insulin per gram of carbs than most kids who they have eating 200-300 grams of carbs a day. It seems that fat, especially palmitic acid on a low carb diet ends up filling up and surrounding muscle cells to give them energy. That is really not bad. Fatty acids just go through beta oxidation and then the pieces get put into the Kreb’s cycle just like pieces of carbohydrates. What you don’t get from fats is “fast glycolysis” which is needed to provide energy above a certain level for an extended period of time. Powerlifting uses basically ATP with long enough rest periods to refuel the ATP and creatine phosphate from burning fat. At a certain duration, or with short enough rest periods though the body has to turn to fast glycolysis because burning fat is just too slow to refuel the ATP. I know that in textbooks they suggest that you use carbs first, but that is a little misleading because it has to do with maximum power output.

Anyway, it seems that to upregulate the use and storage of muscle glycogen you have to train hard enough for a long enough stretch (about 60 seconds?) or with short rest periods so that ATP can NOT be restored by burning fatty acids.

When people train in this fashion they can actually have lots of intramuscular fat, but also have lots of glycogen and be insulin sensitive. So a big key here seems to be to MAKE your muscles insulin sensitive by training them in long enough hard bursts so that they have to use glycogen. This will tend to make the muscles insulin sensitive all the time. It may NOT make them so sensitive right after training because catecholamines reduce insulin sensitivity during intense training, primarily anaerobic.

So I speculate that a certain type of training, basically glycogen depleting training makes the muscles more insulin sensitive (but doesn’t make fat cells more insulin sensitive). From a training point of view, you have to make the muscles more insulin sensitive. When the muscles can hold more glycogen, glucose doesn’t get turned into fat so much because there is plenty of room in the muscles.

So it is possible perhaps to load muscles with both fat and glycogen.

Next post about my son’s problems.

My son is growing very slowly despite the fact that adding fats has put his calories over the mean level for a kid his size and age (55 pounds and about 1600 calories). His blood sugar again is considered to be “normal” non-diabetic except that he occasionally goes over 200 after meals (which is still very mild. On average, type 1 diabetics go over 300 at almost half of their meals.

But the fat itself raises his blood sugar, and it does so 2-4 hours after eating. The mechanism seems to be by making him less sensitive to his basal (long lasting) insulin after his meal time insulin has worn off. Now he is not gaining fat because the fatty acids are being used by his muscles, not stored in adipose. Again this was a change that occurred over a years time on a higher fat diet where he gradually needed more insulin to cover meals but he also has a strong resistance to low blood sugar because his muscles run mostly on stored fat. A muscle can store about 9 times more energy per volume of intra and intermuscular fat than it can store glycogen because glycogen is also bound to water 1:3. 1 gram/ml of glycogen has 4 calories, but also is bound to 3 grams of water which means that muscles store about 1 cal per ml of glycogen+water. They store 9 cals per ml of fat.

Anyway, the problems we have are that while my son has good blood sugar, his insulin will sometimes be in effect before his blood sugar even starts to rise. Most T1Ds who eat higher carbs have a hard time spiking high in the first 90 minutes after eating, but my son will run under 100 for 2 hours after dinner only to rise as his meal insulin wears off and the fat comes in and raises blood sugar by reducing insulin sensitivity.

It makes it hard to identify “lows” because he may have a blood sugar of 90 an hour after breakfast which for most kids would mean, look out for going low, but in his case he hasn’t even started to rise yet.

Also I think that the high palmitic acid in beef and butter/dairy fat has made his muscles somewhat insulin resistant and so he is not storing much muscle glycogen and his muscles don’t get the anabolic signal from insulin to grow. We will see, but I would caution against high saturated animal fat, especially butterfat, or high palmitic acid plant fats either unless you train in a glycogen depleting manner (higher reps, 60+ seconds all out) as it may make the muscles less responsive to the anabolic effects of insulin.

This obviously has interesting implications.

Anyway, the challenge now is to transition my son to less palmitic acid rich fats. It seems that palmitic acid is the primary fatty acid that causes muscles to become physiologically insulin resistant.