Haha! Brilliant!
They say there is nothing new under the sun...
In answer to your point 2 though. Isn't that just the brain's tolerance to high levels of BS for prolonged periods of time & then going "cold turkey" when the levels come down into a safe range..Ah what most do not recognized is that
1) most T2D are still able to produce plenty of phase 2 insulin...10s of times higher then usual, in an effort to remove the carbs/glucose from the system. So at 2 hour mark, glucose reading is > 12 mmols, but with the massive amount of phase 2 insulin kicks in, and suddenly all the glucose have disappeared from the circulatory system. This can also be accelerated by strong tea... 10.3 mmol at 10:00pm to 3.7 mmol by 11:51pm (The Accuchek Performa date/time stamp was not in sync.)
2) There can be insulin resistance in the brain as being noted by the development of dementia. So the brain would now require higher level of glucose to feel normal or be adequatedly fueled. A relatively normal 4.5 mmol now is being sensed as a low and the brain starts to react in a hypo manner. It does not even need to go down to the 3 mmol range...
But if a T2D has been on a low carb, ketogenic diet, then there will be sufficient circulating ketone bodies to provide the brain with alternative fuel...and even if glucose is measure in the lower 4mmols or upper 3 mmols, There is no sense of hypo...
In answer to your point 2 though. Isn't that just the brain's tolerance to high levels of BS for prolonged periods of time & then going "cold turkey" when the levels come down into a safe range..
Think of an alcoholic going on the wagon? I've seen a detoxing drug addict quite literally look & act like she was having a hypo..
Brain insulin resistance and deficiency as therapeutic targets in Alzheimer's disease.However, growing evidence supports the concept that AD is fundamentally a metabolic disease with substantial and progressive derangements in brain glucose utilization and responsiveness to insulin and insulin-like growth factor [IGF] stimulation.
Can Ketones Help Rescue Brain Fuel Supply in Later Life? Implications for Cognitive Health during Aging and the Treatment of Alzheimer’s Diseaseyoung adults with mild insulin resistance or with a maternal family history of AD. (iii) Regional brain glucose uptake is impaired in AD and mild cognitive impairment (MCI), but brain uptake of ketones (beta-hydroxybutyrate and acetoacetate), remains the same in AD and MCI as in cognitively healthy age-matched controls. These observations point to a brain fuel deficit which appears to be specific to glucose, precedes cognitive decline associated with AD, and becomes more severe as MCI progresses toward AD
@Lamont D ,
Alway cool to have your input...
I've mentioned this before regarding RH.
I had a school friend tell me he had symptoms in his youth.. & my wife's old house mate (male nurse?)would quite often keel over with syptoms & fix it with something sweet to eat.. He wasn't a diabetic.
If you don't take insulin or any other drug, what makes you think you are ever anywhere near a danger zone from a hypo? Going hypo close to a meal time when taking no medication could be called being hungry.
You don't take insulin? Are you type 1?
If you are diabetic, T2, then you know what a hypo feels like
I'm a bit confused by this. Being diabetic doesn't cause or create a risk of hypoglycaemia more than anyone else in the general population. If anything being type two diabetic (a condition of high blood sugar) would make your risk of low blood sugar even less likely than the general population.
It's the drugs used to treat diabetes that can cause hypoglycaemia. If you aren't on any drugs where does the "danger zone" from low blood sugar come from? Your body will just survive with low blood sugar and take you back to where it wants your blood sugar to be by internal correction processes because there aren't any drug stopping that. Your body's just telling you to eat cos it's hungry.
Exercise might cause low blood sugar in a diet controlled type two diabetic. But is calling it a hypo medicalising something unnecessarily? Most marathon runners take glucose gels out with them as standard.
Sorry I guess it's one of the comments that really irritate me when people find out I'm diabetic the "oh I get low blood sugar" response. I do have to bite my tongue to stop from pointing out that would be the opposite of diabetes and that their low blood sugar, if they don't eat often enough, isn't quite the same as a low blood sugar caused by too much insulin. Maybe it's just because I've been woken up a 3am by an alarm to tell me I'm hypo though so probably I can be reasonably ignored.
Exogenous ketones will not work with T1. Yes, it might mean the brain functions with no issues (and believe me I understand how the brain functions whilst ketogenic and hypo having been down incredibly low, having my nervous system stop communicating with my legs properly, but having my brain fully aware the entire time, and not losing consciousness), but when exogenous insulin is involved, especially a lot of it, rarely does the body have the ability to counter the insulin, and it has to get to a very low blood glucose level to even start that. So while signalling may play an important part in managing hypos in non-medicated types of diabetes, while there are exogenous agents in play, I'd be surprised if that's all it took.Given the increased understanding/interest in ketone bodies and brain glucose uptake impairment, it is not inconceivable that a few years down the road, exogenous ketones/MCT/VCO may be the preferred treatment for hypos.
Exogenous ketones will not work with T1. Yes, it might mean the brain functions with no issues (and believe me I understand how the brain functions whilst ketogenic and hypo having been down incredibly low, having my nervous system stop communicating with my legs properly, but having my brain fully aware the entire time, and not losing consciousness), but when exogenous insulin is involved, especially a lot of it, rarely does the body have the ability to counter the insulin, and it has to get to a very low blood glucose level to even start that. So while signalling may play an important part in managing hypos in non-medicated types of diabetes, while there are exogenous agents in play, I'd be surprised if that's all it took.
http://diabetes.diabetesjournals.org/content/58/5/1237Medium-Chain Fatty Acids Improve Cognitive Function in Intensively Treated Type 1 Diabetic Patients and Support In Vitro Synaptic Transmission During Acute Hypoglycemia
CONCLUSIONS Medium-chain triglyceride ingestion improves cognition without adversely affecting adrenergic or symptomatic responses to hypoglycemia in intensively treated type 1 diabetic subjects. Medium-chain triglycerides offer the therapeutic advantage of preserving brain function under hypoglycemic conditions without causing deleterious hyperglycemia.
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