Recently,for some reason,I had to shift my regular evening walk to morning walk.But to my shock,my sugar level after exercise, still fasting,was exceptionally high.Sugar level after exercise should be lower,right?In my case, it spiked. I was intrigued and did some searching on the net.I got following understanding.
I am on insulin and after dinner at 9.00 pm,the insulin supply would be near zero by next morning.So,while I walk for about 35 minutes,the body releases glucose into the bloodstream to meet the increased energy demand.Sugar levels shoot up due to absence of insulin.Is my understanding correct? If so,what is the remedy?
I thought of having some nourishment before I start walking,but due to fear of adding additional calories,I desisted.
Forum,please share your similar experiences and advise.
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ramana42
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I have somewhat similar experience. At bedtime, my blood sugar level was 96 and in the morning it shot up to 122 although fasting whole night. Even after the morning walk, the blood sugar level remained high. Eventually, it does come down few hrs after breakfast.
There can be one of the two reasons for this - 1. Somogyi Effect 2. Dawn Phenomenon.
One has to first confirm which factor is responsible for the rise in blood sugar.
If your blood sugar level around 3 to 4 am becomes lower than bedtime level, it is Somogyi effect.
If your blood sugar level around 3 to 4 am remains more or less same as bedtime level, it is Dawn Phenomenon.
In the first case ( Somogyi) eating some snacks at bedtime which releases sugar slowly may help.
The second case ( Dawn phenomenon) is more difficult to control at least in my experience. One can use slow acting medication which prevents lever to release glucose, but I am trying to fix it by natural means. Still, work in progress. In my case, it is not very high.
The dawn phenomenon can be managed in many patients by avoiding carbohydrate intake at bedtime, adjusting the dosage of medication or insulin, switching to a different medication, or by using an insulin pump to administer extra insulin during early-morning hours. In most of the cases, there is no need to change insulin dosing of patients who encounter the dawn phenomenon.
Thanks. I have been trying my luck with some of the home remedies - taking vinegar (ACV) before bed but of no value and such a bad taste, so stopped it.
Yes, it can be up to 5 am. I monitored twice around 3.45 to 4.00 am and found the blood sugar around same as bedtime and then I went to sleep and in the morning at 8.30 am BS was much higher as mentioned in the above post.
Read at various places that taking ACV before going to sleep reduces FBS but not for me.
I will try to understand this subject properly by monitoring sugar levels at several stages in the coming days.If I fail to understand and tackle the issue,maybe I should switch back to evening walks.
Hi bade bhaiya. My best wishes for the year 2018 to everybody here.
Dawn phenomenon is a natural occurence in every body. Due to circadian rhythm of the hormones. But we as t2d can't clear carbs.
Fbs is a mystery. I get high numbers even when I fast or take low carb diet and sometimes in normal range when have taken a bit high carbs in dinner. I have still not been able to understand and control fbs effectively despite very low carb keto range diet. Response to the dawn varies from person to person and time to time in the same individual.
I had stopped all my medications for a few days, but my fbs kept rising and one day reached 207. 😳 My one hour pp was 120. I restarted metformin.
Once on keto / lchf and reasonable control of blood sugar, getting rid of IR I think liver heals by itself. Liver is a victim and a servant and not a master in causation of Diabetes.
Absolutely. I also think and experience that even with keto diet blood sugars may not be controlled. I'm practically on zero carb or very low carb diet but fasting blood sugars can't be controlled. When i stopped medicines my blood sugar started shooting up. That showed my inability to cope with de novo glucose synthesis. Medications help me control my blood sugars. I don't know if in the long run those medication free friends will continue to be medication free and control blood sugars effectively.
ramana42 typically there could be numerous factors that can cause this to happen. Any form of exercise including walking there is a caloric requirement that is typically more than what the body uses in a rested state. Even when walking there is some amount of energy that is coming from the muscles coming into action (legs/hips etc) and typically muscle glycogen is being used along with energy that is typically a combination of fat/glucose depending on the heart rate at that instant and hence oxadative stress.
Essentially that means a few things. If muscles is expending glycogen and there is glucose available in the liver, it is released both for energy expenditure and for uptake in the muscles and hence the spike.
Always the effect is a net positive, if one were to look at it from a A1C perspective as that much of glucose and hence carbs is expended as energy from liver and also sent to the muscle and enters into the muscle( its a one way street, glucose one enters the muscle cannot reenter the blood stream). This could be the temporary spike.
Also keep in mind intensity of the walking (which is very relative, BS levels and stress levels again relative and individual based) can trigger lactic acid cycle etc which cause temporary spikes.
In my own case, when doing mild cardio, cycling for 15-20 mins or basic strength training in my early days took my BS from 105-100 (fasting) to 160-->180 post workout with absolutely no calories. The same with consistent practice and better fitness improvements has now resulted in 85-95(fasting) -->105-110 post exercise and then back to 90s in about 60 mins post exercise.
Trust your body and process and as long as the BS does not exceed 200-250 keep exercising. At those levels, there could be other negatives that outweigh the positives and hence reduce the duration and intensity of exercise even if walking or spread it over many sessions like Hidden is suggesting.
While Physiological IR is case to case and often only when on low carb and body is fat adapted, every diabetic as defined by western/Indian medical guidelines will dump glucose from liver if it is present and beyond what liver needs. How much , when and how it is handled is all a complex function.
If I may please ask, just to understand, how do you ascertain that you do not dump, as in my personal experience even those in stage 2-3 pf Krafts Insulin Assay or in modern terms "prediabetics" tend to dump unless of course there is pharma interventions. It has been extremely hard for most people i know to totally avoid it even on keto let alone LCHF.
If you could point to how you handle it and how you ascertain there is no liver dump and what you do, that might be very useful for folks like me. Thanks a lot.
Yes, everyone dumps and we diabetics have impaired negative feedback control. Liver has lost the fine-tune status of when to dump and when it dumps it never knows when to stop precisely so overshoots.
very rightly said bhai....impaired feedback to liver is the issue...
And therefore... I think ACV is useless....action of ACV is totally different... ACV will never help us against liver dump...
But sure... if we could concentrate of healing liver of fatty liver condition...it will help us...
Bottom line-Thanks to all the replies For my post and some searching on google,issue is clarified now.Today I visited one very important website and found a blog on the same subject with several posts.Based on all the inputs,I am switching back to my evening walks.Those who are on medication,particularly insulin may avoid morning workouts on empty stomach to avoid elevated sugar levels.Thank you all,once again.
The blood sugar rises following walking or exercise is a normal and natural phenomenon. Walking brings in glucogenic hormones like adrenaline, cortisol, glucagon and others to release / de novo synthesize glucose to provide energy to the muscles. We as t2d can't clear that glucose efficiently. So, we end up getting higher readings.
My dear friend. Somogyi effect is there. While dawn phenomenon is because of natural circadian rhythm whenever there is hypoglycemia in any individual - Diabetic or non-Diabetic, then there is a release of glucogenic hormones. That is somogyi. This is, as to my understanding.
Yes, the ketogenic diet is the answer at present and very helpful, too, but there are people like me who despite very low carb keto range diet can't deal with the de novo synthesized glucose and get at least high fbs. This despite exercise, may be many can become medication free.
suramo pardon my assumption but I am assuming you mean GNG which is Gluco Neo Genesis or synthesis of glucose from amino's / glycerol that is produced upon fat breakdown. De Novo Lipogenesis is the carbs-->triglycerides-->fats storing process.
Assuming it is GNG, GNG is a demand driven process and hence surplus of protein and hence amino acid pool / glycerol etc will not produce more than necessary etc. Given that is produced, the body will still struggle how to handle it. So for example if usually in deep ketosis my BS is around 75-85 on extended fasts (~40-96 hours) and the variation is because of the lack or response optimization as a type 2 and insulin deficient. Some or most type2's might not face that, if there is enough insulin production. Also on extended keto personally I have noticed my fasting insulin improve from 0.8--->1.5-2.5 as FBS settled from 100s to 85-95, showing some beta cell dysfunction reduction.
Keep in mind, the FBS variation can be due to numerous things, including how the previous day was, the sleep cycle, duration of sleep, time of sleeping and waking and that is critical as on a FGM(flash Glucose Monitor like CGM) I have often observed that measuring 30-60mins here and there messes my numbers by atleast 5-15 points.
Further, in all these circumstances, the A1C which is the area under the curve for BS is still advantageous and often the true indication if a very low carb or keto diet or if one is fat adapted is when FBS is always the highest BS reading of the day is the case for me most days. Hope this helps.
suramo a few things per my understanding and please do tell me what I might be missing.
Irrespective of insulin deficient or excess insulin, most mechanisms are triggered due to not adequate insulin to clear the glycogen. If there was adequate insulin, these would show up in Krafts Insulin Assays at a very early stage. Moment BS starts moving due to lack of insulin its T2D or even before when pancreas is being overworked without beta cell loss it happens.
GNG is always demand driven. Demand is metabolic and signaling based always and thats is a demand response but pathway could be hormonal, stress response, gene expression etc etc. Please do let me know when its not demand driven, i.e the specifics of instances that i might be missing
Dqan is hormonal signaling and liver response with glucose based on some individual homeostasis conditions. Not sure what you mean by kind of GNG. Please do clarify specifically
I need to understand what you mean by "most mechanisms ".
Gng in dawn phenomenon is not demand driven. It's natural circadian rhythm of the hormones. The purpose of which is still not understood or we don't know.
Insulin clears glucose and not glycogen. It's a typo I think. Diabetes has simple pathophysiology. High blood sugar is due to ir in type 2 diabetes and causes fluid to accumulate in the tissues due to osmotic effect. This tissue, which is called edema interferes with tissue oxigenation, production of more ros, which in turn cause oxidative damage to the body eliciting inflammatory response in the body. Most damage occurs to the organs supplied by end arteries because there is lack of collateral supply of blood. If the blood sugar is controlled, then the edema gets diffused. Tissues start receiving enough oxygen and if not damaged beyond a point, then they can recover completely. But this simple looking issue is not that simple. Controlling blood sugars may not always be possible even with strictest dietary measures.
By most mechanims I meant the insulin leptin signalling both phsyiological and intrecellular that impact overall energy balance hence metabolism and there fore the insulin-glucose axis in diabetics. Further the role of Grehlin signaling which happens within the pancreas and is involved in microcirculations with the pancreas has a role in regulating insulin release directly in the pancreas at the beta cell level. Of course you have talked about Cortisol which more commonly understood.
Please elucidate to me if you do not mind, references where GNG happens during dawn phenomena and how and even if does happen its demand driven only..not supply driven...
GNG pathway is facilitated by either glucogenic amino acids from protein or from glycerol derived from lipid breakdown when fat adapted. The other steps they can be generated is from the pyruvate and lactate pathways which typically are triggered in anerobic conditions when there is lack of oxygen typically when resistance training etc.
My own personal experience when fasting both shorter and longer fasts (44-96 hours) after hour 36 which is roughly the second morning fasted the FBS is in the 80s and typically that is maintained through day 3 and day 4. It doesnt drop below that in the absence of food and hence mostly through GNG. The same when am eating and my last meal is around 5:30-6pm, the FBS can vary anywhere from 95-105 and my blood ketone levels fasted in the morning is from 0.3-0.7 mmol.
"Ghrelin is a hormone that is produced and released mainly by the stomach with small amounts also released by the small intestine, pancreas and brain. Ghrelin has numerous functions. It is termed the 'hunger hormone' because it stimulates appetite, increases food intake and promotes fat storage."
Ghrelin is a recently discovered gastric peptide that increases appetite, glucose oxidation, and lipogenesis and stimulates the secretion of GH.
That's About ghrelin.
"The Dawn Phenomenon occurs in all humans regardless of whether they have diabetes. However, many people with diabetes also experience a rise in blood sugar. In people without diabetes, the body’s natural insulin response prevents the blood sugars from rising"
"Scientists have suggested that the Dawn Phenomenon experienced is mostly caused by a surge in nighttime growth hormone secretion. Other hormones secreted in this surge include cortisol, adrenaline and glucagon."
The difference is why the hormones are released. The Somogyi effect is caused by having too much insulin in the blood during the night. ... You wake up with a higher blood glucose that is out of target range. The dawn phenomenon, on the other hand, is not caused by low blood sugar.
It's well known that effects of these hormones are glycogenolysis and gng.
I appreciate your short 44 hr and long 96 hrs fast. I will try my best to follow your practice.
One doesnt need insulin for muscle growth. There are numerous pathways that the body uses and for a diabetic the mTOR is one such pathway that is extremely beneficial .
Afaik homa 2 doesn't calculate ir if s insulin is below 2.5 but yes if there is insulin in blood means all beta cells are not dead. Also i think beta cell dysfunction is a misnomer. In t2dpeople it's ir and beta cells produce more insulin.
You are right and they produce more insulin until fatigue sets in and they are whipped. At that point there is cellular dysfunction cause of excess usage and damage and there is modification in gene expression leading to some dying and some being dysfunctional. Often times dysfunction can be corrected through dietary changes. To understand this correctly a diabetic must track insulin responses in parallel with glucose numbers as that alone will give the true indication of demand-response system i.e insulin<->glucose
Genes modified due to uncontrolled diabetes is not certain. But, there is a gene defect that leads to Diabetes. Beta cells and for that matter, all the cells except a few of the body degenerate and regenerate. Beta cells also do that but the quantum of these cells degenerating and regerating can't be measured in vivo. In type 2 Diabetes, some beta cell function always remains. It's all theoretical that they die. Even if one controls blood sugar by diet, later a person may need to restart medicines.
Yes, "To understand this correctly a diabetic must track insulin responses in parallel with glucose numbers as that alone will give the true indication of demand-response system i.e insulin<->glucose."That's right.
Gng is the process by which glucose is produced from non-carb substances - fats and proteins.
Be it as demand driven or dp. Dp is peculiar phenomenon, so it's not clearly understood, but occurs irrespective of blood sugar levels as against demand driven gng. The same hormones play roles to increase the blood sugar levels.
But, in the case of demand driven instances, glycogen first degrades to provide instant supply of sugar until hormones exert their effects.
If at dawn there is hypoglycemia, then there will be acceleration of gng. If there is hypo., well before dawn and gng is going on, then I'm yet to learn if dp will play its role because hormones playing are the same.
In Diabetes, people even if blood sugar is high, pre-dawn because of food, dp will occur because gng hormones are suppressed due to high blood sugar due to diet.
I need to understand this, but what I say are physiological responses occurring in Diabetes and non-Diabetic people. I don't think it's insulin that has effect on glucagon secretion but glucose. Or glucagon would never be high in type 2 diabetic people. Maybe, the gng response vary individually. The blood sugar levels at which gng occurs might be different in different individuals.
Also, physiological responses are not static phenomena, but dynamic. There is constant interaction between sympathetic and parasympathetic systems. That's why we get different readings of blood pressure, blood sugar, pulse, etc. on both arms or at two different points of the body taken at the same time.
I beg to differ. Glucagon has no role in making us type 2 diabetics. Basically, it's ir due to some genetic defects. No hormone in our body ever directly causes or suppresses other hormone release, but indirectly by changing the body's milieu. There are releasing
" hormones" released by pituitary - brain which of course control hormone release, but then they don't have any effect on the body's milieu directly.
The insulin overdose is treated mainly by continuous glucose solution because glucose bolus would cause further release of body insulin. Glucagon, I'm not sure is the routine treatment, but steroids and adrenaline are used more frequently. These hormones get destroyed soon by the body and in such situations, any bolus treatment is not advisable. But, by continuous infusion. I'm talking about hypos.. Even in dka we need to give insulin by titration method that's in drip.
😃😃. The medication company 😜. Well. If a person with Diabetes becomes unconscious, then it may be hypo. or dka and by the time lab reports come, bolus of glucose should be given by an IV. If the person regains consciousness, it's hypo.. Yes, in dka there is a smell of rotten apple, but sometimes difficult to confirm.
According to the postulation 1) if hypo is due to high insulin dosage and 2) insulinoma - an insulin secreting tumour glucagon release will be suppressed. No. Glucagon will be released in both the situations. Glucagon has no role in generating Diabetes. And these medication companies 😱. Would push any theory to sell their products 😜. In hypos., glucagon levels are always high. Glucose is needed. Glucagon may be given empirically akin to injecting insulin in type 2 diabetics. Diabetes- the practice we have been opposing and challenging on this forum.
Blood sugar levels control glucagon or insulin releases. Sugar is the main force. Others if at all they have role to play has to be minor.
No we are not diverting from the topic. We must understand the pathophysiology of type 2 diabetes.
Well, it's said incretin suppress glucagon release, but incretin is released from L and K cells of intestine in response to the glucose in the food. This incretin causes insulin release from beta cells and dpp4 is the enzyme that destroys incretin. As far as glucagon release is concerned, high or rising glucose levels in the blood are more important and that's the prime factor. Neither insulin nor incretin can have significant role in glucagon suppression. Because there are many other hormones like adrenaline, thyroid hormones, growth hormones, etc. play a significant role in bringing sugar levels up.
Why are we complicating type 2 diabetes? There are many postulations like ominous octate, leptin resistance and all that, but no postulation can explain type 2 diabetes fully. Only genetic defect can make all the body cells insulin resistant. I'd keep glucagon out.
Well, hypo., too may have nausea and vomiting and IV glucose in a comatose Diabetic patient if lab reports are not readily available. In the present time, even general practitioners keep glucometers. So we can always get blood sugars done. Nausea and vomiting occurs due to metabolic causes - dka and neurological - gross imbalance in sympathetic parasympathetic interplays.
"Glucagon in diabetes. In people with diabetes, glucagon's presence can raise blood glucose levels too high. The reason for this is either because not enough insulin is present or, as is the case in type 2 diabetes, the body is less able to respond to insulin."
So, in type 2 diabetes, α cells might be as insensitive to the glucose as other cells in the body.
On the other hand, glucagon increases insulin secretion - so anti action of itself 😳. But, fair enough as insulin has to clear glucose from the blood so insulin is released and glucagon gets suppressed because of sugar and in a part by inhibition of release by insulin. But, insulin effect on glucagon has to be minor. Where's glucagon causing insulin release by providing glucose mainly, but may be minorly by direct action?
As far as i understand, we need not complicate issues. Our cure is as less carbs as possible. That's the only remedy as of now. Medications to be used as supportive measures. If there is anything that can increase insulin sensitivity of the cells of the whole body permanently that's our cure.
"The hormones produced by pancreatic alpha and beta cells also modulate insulin release. Whereas glucagon has a stimulatory effect on the beta cell,541 somatostatin suppresses insulin release.542 It is currently unclear whether these hormones reach the beta cell by traveling through the islet cell interstitium (thus exerting a paracrine effect) or through islet cell capillaries."
"I am explaining in a way that even an average Joe can understand." 😜😜😝😝
We are discussing dump with regards to Diabetics and NonDiabetic people who can take lots of sugar, but can control blood sugar well within normal limits. So, glucose loads get cleared effectively by them and not by us. Even if as you say glucagon has a role to play in Diabetes by putting loads of sugar into the blood and let's not forget negative feed back on glucagon by sugar and the insulinotrophic effect of glucagon it's primarily our inability to clear glucose efficiently. Also if not genetic reason how would one explain entire body tissues become refractory to insulin? What's common to all the tissues of our body is the genome/genes lying at the center of all the cells. Brain is spared because it can utilize glucose independent of the presence of insulin. Dump we are discussing is the result of our insulin resistance - failure to dispose of sugar from the blood.
I would love to know how we can measure β cell quantum directly in vivo. Only that will make it clear if we lose β cells or not and to what extent. Also it may be a part of the script written in our genome.
It's postulated that β cells have glucagon receptors that stimulate release of insulin by direct effect.
Also glucagon is not the only hormone that has glucogenic effect but are many hormones. Only insulin has bs lowering effect. My understanding is clear and different from yours and whatever causes postulated for type 2 diabetes may be minor or less important than the genetic defects and all other events may be subsidiary to it. It's not the cause of type 2 diabetes.
And yes. Fully agreed. Lchf is not cure but a mean to control / reverse our Diabetes.
"Basal glucagon secretion in type 2 diabetes is increased and this almost certainly contributes to fasting hyperglycemia by increasing fasting hepatic glucose output."
Yes, α cells too are refractory to glucose so "think " glucose is insufficient and in a way you are right glucagon is responsible for dump, but had we not been poor at clearing carbs our blood sugars would be wnl. NonDiabetics can clear loads of glucose, but we can't, or let the glucagon dump any amount of glucose and we would be clearing it. What I'm saying is, that primary cause is inability to clear glucose - be it insulin insufficiency or ir. 😝
And why only glucagon? There are other hormones too for the dump. 😃
Yes. You are right, but even after 16 hours of fasting my fasting blood sugar remains high. Also, the body conditions have a role to play. For example, c cold, lack of sleep etc. raises the blood sugar / fasting blood sugar.
I strictly follow what we advise others. Avoiding all the food including fruits. But, perhaps, ghee and paneer and cheese raise my blood sugar /fasting blood sugar.
Hidden suramo my experience and numbers of measuring FBS and BHB on waking 190+ out of last 310 days in Keto tells me there is a clear coorelation between those two numbers. I would wager that BHB has a causative effect on FBS in some sense. In the sense with a BHB>1 FBS is always <90, BHB >0.5 FBS<95 and BHB >0.3 FBS< 100 . This indicates that there have been instances where FBS is 86 and BHB is 0.3, but never an instance where FBS is 91 and BHB 1.1.
Yes. Cut the carbs. Even when I'm on noncarby vegetables cooked in co, cheese and ghee blood sugars remain high. Let me be still stricter. Trying, but can't become nonveg. 😜
Hidden its honestly not easy in the beginning, but when once is truly adapted, the cravings switch from sugar- fat . As you know and I have said many times I crave ghee/cream/nuts etc more than grains/sugar/processed. It also has to do with the biochemical adaptation and alternate pathways in action and hence signaling.
Hunger is a complex phenomenon. There are many factors affecting it, but mainly
1) hypoglycemia and 2) empty / stretching of stomach walls are most imp. The brain is not the primary organ to cause hunger pangs, but it's the reverse. Hunger pangs inform brain to look for food. Other factors causing or suppressing HP are humoral ( leptin ghrelin ), pschological
( stress and grief suppress and depression makes many to eat more and carby foods ). Gastric upset and fever kills hunger. There may be many more factors influencing hunger, but the brain controls many hormones by releasing hormones ( Ghrh, tshrh, acthrh, Gnrh and many others ), but not insulin and glucagon. Also, leptin and ghrelin. So, hunger primarily is controlled by peripheral forces.
In my understanding, rise followed by fall of insulin is the cause for HP. Low glucose levels are more imp. because if you eat bland diet like salad despite full stomach we don't get full-like feeling. Also, high sugar, but empty stomach don't stop HP. So, complimentary to each other.
1) It's abolition of insulin spikes rather than low triglycerides which come later on lchf diet is responsible for less or absent HP. Even on prolonged fastings initially there are strong HP, but gradually fade away. Also taking water may decrease hp temporarily sending false signals by stretching stomach walls. I think abnormal lipids are the result of ir and not the cause.
2) Agreed, but our body rather than adrenal gland gets fatigued.
3) No. Only temporarily because it's ultimately the sugar that's most imp. than the stretch.
And why should triglycerides make only hypothalamus / hunger areas of the brain refractory? What about other brain cells?
By tg, you mean long chain, right? I don't think lct can cross bbb easily and in large quantity. Bbb is a functional barrier and its anatomical existence yet to be found afaik. It prevents any large molecules from entering brain. But leave that aside. I'd love to know how tg causes resistance - in the brain and elsewhere? Also, the brain is not a fat storing organ though high in fat.
And yes. Agreed. Carnivorous people and animals make their own glucose. That's the basis of our lchf diet. Carvnivorous animals are strong and run faster requiring more energy. But high protein diet is not recommended for type 2 diabetics. Ketogenic ratio recommended is 3-4: 1.
Sct and mct are burnt off by the liver. Fat stored in the body is lct. Fatty acids are long chains and associated with phospholipids and lct can't cross bbb. The brain produces its own nonessential FAs. "Fatty acids do not readily cross the BBB as components of phospholipids or triglycerides ...".
"However, the brain, being composed of lipids in large part, has a high capacity for endogenous production and elongation of fatty acids, so given impaired degradation by peroxisomes (as in Zellweger’s syndrome) it is not surprising that they would accumulate there."
Brain doesn't need insulin for glucose utilisation or we type 2 diabetics would have been dumb, confused and disoriented. Insulin is a polypeptide and can't cross bbb.
Let me come straight and not beat around the bush.
1) What's first? Tg or IR ? Whatever hypothesis is put forward should be logical and reproducible. There are many people with high Tg and not D. There are many obese who go on eating but are not D. Why are they leptin resistant?
2) If tg first any remedy that lowers tg levels should remove IR permanently and we should be able to eat carbs freely. Why high tg in some like us cause IR and not others?
3) I still need to understand the mechanism how tg causes resistances - leptin IR or other.
Researches can be manipulated. IR first can answer almost all questions related to type 2 diabetes.
"However, fibrates such as PPARα-agonists are weak and their efficacy is limited (at least in part) by dose-dependent side effects such as elevation of levels of transaminases, homocysteine and creatinine20,21. Fibrates increase the risk of myopathy, and have been associated with rhabdomyolysis. In addition, the efficacy of fibrates on NASH in humans is not known.
The next generation of PPARα-agonists is called “selective PPARα modulators” (SPPARMα). They maximize the beneficial effects and minimize the adverse effects of fibrates27. Pemafibrate is the first of the SPPARMα to be developed, and has been shown to be safe and efficacious against dyslipidaemia in a phase-2 study28. Pemafibrate has not been associated with rhabdomyolysis in Caucasian or Japanese subjects.
Here, we investigated the effect of pemafibrate on rodent models of NASH (methionine choline-deficient (MCD)-fed db/db mice and amylin liver NASH model (AMLN)) in comparison with fenofibrate. AMLN is a diet-induced model of NASH and elicits obesity, insulin resistance, and the three stages of NAFLD (steatosis, steatohepatitis with fibrosis, and cirrhosis) without reliance on genetic mutations, use of toxins, or nutrient deficiency".
These studies are done on mcd fed mice and so artificially created nash in mice.
Ir is because of genetic defect/s. Ir is a mathematical calculation simply showing we need more insulin to push glucose into the cells. So even after reducing ir if we take carby food our bs gonna be high because our basic defect remains there. Drugs may bring down tg and lower ir. Some way ir and tg might be interrelated but can pemfibrates lower ir despite carby food in humans need to be investigated and researched. So again diet to reduce tg. But diet low in carbs as such are gonna reduce lipogenesis by reducing insulin requirement. The basic issue according to me is insulin refractoriness due to some genetic defect.
And don't get hurt. I have learnt from you so much but my detailed postings help others to understand.
"That explains that you are on wrong coordinates." No. If the primary cause is removed we get cured. If we could do away with insulin refractoriness we would be cured.
Actually,I have no issues with T2,TG,BP,KFT,LFT etc etc.I get into problems when age related issues disturb my routine.I am facing them but it takes too long to get back to normalcy.For example,most part of 2017 was spent by me fighting sleep disorders.Conflicting medical opinions did not help either.
Age related problems are dealt with by Geriatric Practitioners. A specialized branch in the US. Here, that concept has not yet come. For sleep related problems you can try
" ashwagandha " 1-2 tsf with luke warm milk at night. Dates with LW milk also can help. There are many means. You can try whichever is suitable to you. Organs wear and tear can be retarded by diet, exercise, reading, remaining active socially and otherwise.
"Again wrong coordinates. No cure. WE can never get cured. "
If we can get rid of insulin refractoriness. No cure because our genome can't be changed now. So even if tg is brought down we are not going to be cured.
Any specific questions i have not answered ?
Researches regarding drugs i'm saying not reliable as we have seen in case of statins.
Let them try and be another "statin scam ". If at all, it's effective and it'll certainly not be curative. I don't look into tg theory too much because it's not reproducible. There are many people including those having familial dyslipidemia who have high tg levels - far more than 100-300 range, but are not Diabetic. Whereas acc to the tg theory they should be. But, almost all Diabetic people if not on idm will certaintly have abnormal lipid profile including high tg levels. Finding of tg in csf can be incidental and may not suggest the cause of Diabetes or LR. Let's wait for some time to see what pemafibrate brings for us.
And when more logical and confirmatory measure - the lchf / keto diet - is available why should we fumble with medications? No medication is without side effects and the words like:
" less complications " don't convince me. If human trials were conducted ethically no medication would need to be withdrawn from the market.
"We are not discussing SCT/MCT. It's long known to me that MCT is shunted thru portal vein to be turned to ketones. So not a news to me. I think I have been talking about this since 2013."
You've used these words and i said, "don't get hurt ". Nothing absurd or personal.
This surprised me. I think I may have the same. I was fasting the from 11 PM to around 730 AM when my blood sample was taken. I was shocked that my blood sugar shot up 400+.
No surprise at all.To my knowledge, about 3 to 4 hours after dinner,you would have digested and absorbed what you have eaten during dinner.But ,you do not feel hungry and also do not feel like having another meal.This is because,the liver will start releasing glucose from it's stored reserves and sensing the presence of glucose in the blood stream,the pancreas will release requisite insulin to utilize the glucose and keep the vital bodily functions like breathing,heart,liver etc. keep going.In a normal person,proper equilibrium will be maintained and the FBS will be in normal reference range.Among diabetics,this will not be the case and FBS will be erratic depending on several factors.I think this process is not adequately understood by present day science.Our only choice is to take all necessary steps adequately and hope for the best.My understanding may not be correct, and so we have to keep learning and improve our understanding.
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