This Causes Type 2 Diabetes Not Just Glucose or Fats

welcome to one more show today I have a beautiful uh lecture that I'm presenting it is Dr Barbara Barbara e Corky's lecture it is called Banting lecture 2011. where she presented this hypothesis that I've discussed about it a few times before I wanted to go a little more in detail so I'm going to give you the the sneak peek now the components in our food which may be for food colors preservatives or other components that allow the foods to not have the oil and water separate from each other surfactants or emulsifiers these are called monolorin is actually one such product but that is not used in the food iron calcium and other monoglycerides again emulsifiers these are the products that can increase insulin levels without increase in glucose levels the reason for saying this statement is that normally insulin levels increase after we have glucose or carbohydrates ingested here even if you eat food that doesn't have a lot of carbohydrates that does not add a lot of glucose but the other preservatives and other products are present insulin levels will still go up then to generalize this she says that any product any food product that will increase reactive oxygen species above the normal required level for our body will cause pancreatic beta cells to produce higher levels of insulin and she says out of all the other for example iron calcium and reactive oxygen species producing products those products that produce reactive oxygen species are the most potent in stimulating or triggering insulin secretions so this is a summary this is a sneak peek and now I want to go a little more in its papers uh detail one more thing if I can share she also said in her in vitro tests she also said that when they used those ski Ventures that will pick up reactive oxygen species for example an acetyl cysteine or NSE then even when the products that caused reactive oxygen species were placed on the cells and were supposed to increased increase insulin these products did not increase insulin when Ross were picked up so that's a very important proof at least in vitro that the Ross are also responsible for triggering insulin in addition to Fuels for example glucose so this is the discussion now I'm going to go in the detail of it but this is what this basic discussion is all right so let's start foreign .com and there are hundreds of videos over here similar lectures if you would like to have access to them there is a link in the description of this video with this enormously low price so you can take advantage of it this is Dr Barbara e Corky professor emeritus medicine I believe that she's in Boston University this is her paper Banting lecture 2011 hyperinsulinemia cause or Consequences or consequence and then a little bit about monoglyceride so with this I'm gonna go to this is her paper as well I have shown it once before too and I'm going to go to my drawings I think with these drawings we can do a better job so let's start these are gifts for Humanity they're continuing and if you would like to support for these gifts there are links in the description that you can use to buy me a coffee or use PayPal or subtract or patreon there are many ways this is the Banting lecture it is called Banting lecture because it is an award given by American Diabetes Association to someone who has done this so let's read it the Banting medal for scientific Achievement Award is the American Diabetes association's highest scientific award and honors an individual who has made significant long-term contributions to the understanding of diabetes its treatment and or prevention so she is the receiver of this award so let's start from here the first concept she presents in her paper is the following she says there have been many studies where the researchers have found connection or link between various living or environmental setups genetics and diabetes and obesity they found associations for example air quality for example air temperature for example we control we do air conditioning some countries do not have as good air quality as others then for example activity levels the environment and then the fungi and other things in the environment allergens and so on activity levels of various people and then relating that to obesity for example saying that somebody who is not very active becomes obese so she says there are many such studies however she believes that these studies haven't yet found the actual reason for example environmental factors let's say clean air it is present in many countries clean air and then many countries do not have clean air however the pandemic of obesity and diabetes is prevalent almost worldwide so regardless of the air quality people are obese and diabetic or they are becoming obese and diabetic you can't say that this bad air quality country has more obesity and diabetes versus this good air quality country has less similarly air temperature so air conditionings effect so there are studies that have actually linked air conditioning at an air temperature with the association with diabetes similarly activity levels for example let's say you go to one country let's say you go to U.S so air quality and other environmental factors are controlled now if you say that people are becoming obese or diabetics because of activity levels then within the same country there are children there are farmers there are office workers there are different kind of roles and people who all have distribution of diabetes amongst them and I'm talking about type 2 diabetes mellitus so she says that worldwide expansion of metabolic disorders especially obesity and diabetes is not really understandable by these factors so then what is it it is according to her paradigm the common aspect worldwide is food she's saying that worldwide processed food preserved food packaged food is becoming more and more prevalent this is one unique aspect almost similar throughout the world whatever is the environment and air qualities and the activity levels and so the food especially the processed food may be linked to diabetes and obesity the question is what is that link and what in the food is doing that and that is a paradigm she is presenting you would actually see that many of the modern diabetes management clinics and doctors who are talking about them they talk about hyperinsulinemia they talk about the need for fasting or intermittent fasting or ways to reduce insulin levels before looking at diabetes and obesity they talk about reversing diabetes and of course in 2021 American Diabetes Association said that here is the criteria for diabetes remission so that means diabetes remission is possible then there are proofs which I have discussed at bariatric surgery and after the bariatric surgery within 9-10 days when the patient has not really lost a lot of weight patient becomes euglycemic or their they become insulin independent they become normal glycemic so food and the ingredients of the food there are more possible cause so she says that in the the current food is very different from the food that was out there 400 years ago I think that even 100 200 years ago so the current food that we have if you brought someone from 400 years ago and said that this is the food they would probably say what is this really a food so she then says that there are 4 000 new ingredients new agents that have become part of our Foods in more modern times four thousand new agents that are in our food then the food animals their body weights have changed they have actually become bigger and their composition is changed poultry for example excuse me the poultry is changes that age of the poultry from 112 days has reduced to 42 days the federal weight has more than doubled the feed efficiency is more than tripled decrease immortality has occurred similarly mineral content in fruits I I wrote food here this is fruit fruit and vegetables changed over the past 40 years the point of saying this all there are lots of changes some intentional for example preservatives and colors and so on some unintentional for example we know that there are insect Parts in our food we know that nowadays the Plastics are finding their ways in our food so there are intentional and unintentional newer Parts ingredients or agents as she calls them in the food and these may be related to hyperinsulinemia so the question is do we have someone who will try these newer agents and figure out if they cause reactive oxygen species and then come back and say here are some possibilities and that is what she did so she says that growing the packaging and preparation of our food have also changed leading to an increase in non-edible packing material in the food many foods have contained preservatives emulsifiers flavor enhancers food colorings and other fillers that have not been previously consumed in significant quantities keep an eye on these preservatives emulsifiers emulsifiers for example monoloring like things so not monolorant but emulsifiers are those surfactant like things what they do is emulsifiers if there is some food item that has water and oil both usually if you place them the water and oil would tend to separate these emulsifiers keep the oil emulsified or broken up into microscopic smaller chunks and stay mixed with the water emulsifiers flavors coloring and other fillers virtually now this is an important statement virtually none of these non-food compounds have been carefully assessed for a potential impact on Obesity or diabetes then she says many treatments for and much of the research in obesity have focused on the role of diet and physical activity right so for obesity we say well don't eat carbs and and more exercise more most pharmacological research focus on the control of food intake increasing energy expenditure or improving insulin action these focused efforts were based on excellent models but despite evidence to support their utility they have not yet slowed the growth and rate of obesity or diabetes this is a very important statement that there are many agents that have been used there are many Therapeutics or interventions or exercises or methods or processes or habits that are being cultivated they haven't really reduced the rate of obesity and diabetes so she says we need an alternative model so her model then says she says my model proposes that environmentally induced elevated background levels of insulin environmentally induced elevated background levels of insulin superimposed on a susceptible genetic background or basal hyperinsulinemia is the root cause of insulin resistance obesity and diabetes just this much of this statement is sufficient to change our thinking about diabetes or management approach towards that and I am seeing some doctors doing it and are very successful what is she saying here she's saying if we just observed or thought or agreed that it is the hyperinsulinemia that is the root cause of insulin resistance obesity and diabetes then we'll be on the right path excuse me so the question is why is this such a dramatic change what is different here what is different here is that in the traditional or classical model what we say is that there is something that happens that causes insulin resistance then when the insulin resistance or peripheral insulin resistance occurs then insulin is not able to open the doors for the glucose to go into the cells which causes glucose to sit outside and then cause its damage Plus get converted to fats fats in turn then produce free fatty acids which in turn cause further aggravation of the situation fat cells also produce the inflammatory mediators which further aggravate the situation so that is a classical model here the hyperinsulinemia does not come first it comes after the resistance and then hyperglycemia and then the fats and obesity in her model hyperinsulinemia comes first which then causes insulin resistance and then the remaining Cascade and she gives proofs for that so she says she has a few studies in her paper I just took one of them in one study they took rodents mice may be and they infused them with insulin they gave them lots of insulin and guess what happened you would have thought that if you give lots of insulin the the animal would die because insulin would cause glucose to enter the cells and hypoglycemia would occur glucose that is present in the tissues and blood circulation will be pushed in the cell forcefully not forcefully but because of insulin's action and there'll be less glucose out in the circulation that would cause hypoglycemia that can cause the animal to have severe outcomes or even die but instead they saw that the animal became insulin resistant so can I say then and this is what she says that this was the becoming insulin resistant is an Adaptive response it is a protective response of the body so she presents studies for that and then she talks about this she says and I can read this over here first B studies suggest that hyperinsulinemia can cause insulin resistance and that lowering insulin secretion in hyperinsulinemic individuals may be beneficial so what she's saying is when the insulin levels are high these higher levels can cause adaptive response and cause insulin resistance very different model now of course the question that should be in your mind is what is causing this insulin I've given you some ideas so once again over here as well if I can inject that idea once more in your mind that is anything that would cause reactive oxygen species anything that is pro-inflammatory which includes glucose as well but we are talking about anything non-glucose as well which has the potency capability of producing reactive oxygen species producing inflammation will cause hyperinsulinemia and then of course insulin resistance and then diabetes and obesity so in her model she says that imagine there is a factor x something anything iron or calcium or Emoji or or any other pro-inflammatory product I would add to this this is my addition anything that can cause inflammation for example let's say um an infection let's say vaccine let's say uh any other product that you took that could be pro-inflammatory for example is one is to imbalance so anything that would cause beta cells hypersecretion right so of course when the question becomes what is that thing and so we'll talk about it then beta cells will produce more hyper insulin and they'll produce more insulin which will then cause an Adaptive response of insulin resistance in this process the patient will become or the person will become obese and diabetic as well this is how Prime model in this model he then further talks about the controller the master metabolic regulator of this model and that is redox redox is reduction oxidation so right we we know that our body our cells have chemical actions in which oxygen becomes radicalized oxygen becomes charged and then so reduction and oxidation occurs she says that redox operations when they go above their normal limit above the needed so we need redox operations to operate and function normally we actually need to produce reactive oxygen species for successful function of our body then there are cells for example neutrophils that need extra reactive oxygen species to produce to kill the pathogens however when this goes above the normal levels then our cells all of our cells in our body behave differently to them if you increase reactive oxygen species for example in the liver then liver start saving glucose and producing glycogen if you go to the fat cells they start doing lipid storage if you go to the pancreas and increase the redox operations or reactive oxygen species they start producing insulin so various parts of our body various tissues respond differently to the redox abnormality so then of course that question would become okay fine we understand that there can be things that would that would cause redox imbalance meaning increased reactive oxygen species above the limit that we should have which would cause insulin levels to increase which would cause insulin resistance and now diabetes and obesity would occur the question is how do we know so for the classical model of diabetes we know that we can go and check blood glucose levels we know that we can check hemoglobin A1c levels What do we do here so she proposes she proposes that in our body the redox operations oxidation reduction operations are occurring all the times and when these operations occur there are byproducts that are made that leak out of the cells and these can be measured to understand the level of redox operations going on and she gives an example for example let's say in muscle and reduction oxidation action occurs the muscle produces lactate and pyruvate and then we ratio reflected to pyruvate tells you how much redox operations are occurring so this could be a test similarly in liver for example when the redox operations occur liver produces lactate and pyruvate as well and once again that can be seen in addition to that the beta hydroxybutyrate and we acetoacetic acid I believe these can also be measured the point is that if you're going to go with this model then how do you know that I have hyperinsulin anemia how do I know that redox operations are above or let me say how do we how do we know that we are in inflammatory state so remember today we do c reactive proteins and d dimers and lots of other antibodies and various T cells and B cells here she's saying to see that redox operations are higher bodies generally in reactive oxygen species abundance in in an inflamed State look at LP ratio and B beta and a ratio so continuing she then says that there are factors that can cause the beta cells of the pancreas to directly or indirectly trigger them to produce more insulin and directly means that factor x whatever that factor is calcium iron reactive oxygen species these would directly enter the cell beta cell and cause the beta cell to produce more insulin or it is also possible that this factor x goes and bothers some other cell that cell in response produces inflammatory mediators those inflammatory mediators and go to beta cell and cause beta cell to become triggered and produce more insulin remember we are talking about components that will produce insulin that would bother um using bother more Loosely that would trigger the beta cell to produce insulin while the glucose levels are normal so glucose is at basal level it is not glucose that is doing it it is some other thing that is doing it this is the ground Breaking part we always thought it is always glucose that would cause this this meaning really is insulin from the pancreatic beta cells she comes in and she says in her team that no there can be more things that would do it and actually those things those products those factors are more important to look at diabetes and obesity than a current model so she then says that to test this model right so she has a complete Paradigm so today you're listening to and you can please read that as well you are listening to a complete paradigm of diabetes and obesity with how to test that and with how to experiment for that and with what products to test for so here she says to test a model of hyper hyper insulin insulinemia as cause of obesity Associated type 2 diabetes it is necessary to find a way to induce insulin secretion at non-stimulatory glucose levels she says if I am right if this Paradigm is right then we should have some substances that would trigger insulin secretion while the glucose levels are normal so then she says one such thing is free fatty acids free fatty acids or ffas when produced and they act on the beta cells they would actually cause beta cells to produce more insulin but it takes 18 hours for them to do that so free fatty acids are not a very good product to test with but keep in mind that free fatty acids do it so this is why we say when somebody becomes obese and they have free fatty acids their their diabetes can become aggravated now continuing then she says what she did was her team did was she and her team they tested substances that have entered our food supply so they wanted to see what things so of course remember she said there are 4 000 such ingredients or not ingredients agents ingredients mean part of the food agent is maybe it didn't have to be part of the food but it is just there intentionally or unintentionally so here she said we started testing these things so what did she find he used in vitro cells that were insulin release capable cells and here is what you found less diagram than more reading now but it is very important this is the foundation of our health all of our health so first she says they found they identified the common lipid food additives that increase insulin secretion these are mono-ethyl glycerides these are surfactant like things these are emulsifiers she says they are formed and degraded in the gut and by lipoprotein lipase in peripheral tissue so on the peripheral tissue cells there is an enzyme called lipoprotein lipase that can break them down and are commonly added in small quantities as emulsifiers and preservatives the ability of mono oil Olio glass glycerol to stimulate insulin secretion at basal glucose again look at the condition stimulate the insulin but glucose is not going to be more you're going to work without glucosa so that glucose is not the one that is causing it so stimulate insulin secretion at basal glucose was concentration dependent and significant at a concentration as low as 25 millimole per liter all wolf says surfactants are causing inflammation and then diabetes so she found that these are one type of agents that are able to trigger insulin she then says the physical physiological relevance of monoglycerides is not established because there appear to be a few measurements and no standard for the level of circulating or tissue monoglycerides he just didn't have enough data available to tie them to say these are the agents that are causing problem but she observed them to be increasing insulin levels then the team moved on and they said okay how about other things how about other non-lipid things and they found out in artificial sweeteners second so there are many kinds of sweeteners okay she found out that sakurin was most potent and also inhibited glucose stimulated secretion interestingly only second stimulated basal circulation at concentrations that might be achieved by high levels of consumption for example in diet beverages so saccharine in diet beverages when present can cause secretion of insulin then iron she says iron consumption has increased as a lean content of food animals has increased although it is not clear that this has affected tissue iron content here we show that iron increased both basal and stimulated insulin secretion what does that that means when iron is added or when iron is part of a food it causes beta cells to increase insulin secretion but not only that if then you eat carbohydrates which are also going to cause insulin secretion that is a triggered stimulus then iron the beta cells would produce more insulin than they should have in the presence of iron so iron is another so again please realize that iron is actually very important for women it is important for men as well where there is a deficiency so we're not talking about deficiency we're talking about above that so that thus iron Emoji can be used as tools to study so she's saying to researchers that hey if you wanted to find how will cells behave and you wanted to induce more insulin secretion in in your Labs then use iron saccharins and emoji and she talks about reactive oxygen species so reactive oxygen species are oxygen molecules which have become radicalized so she says redox and draws are candidate signal for basal insulin secretion and we asked whether the putative signal was essential or sufficient said he found out that redox operations were the underlying phenomena of course redox are associated with reactive oxygen species so she said then we wanted to understand that is the production of reactive oxygen species a necessity to produce insulin and if it is sufficient to produce hyperinsulinemia or do we still need glucose with that so then she started doing those tests and she says here we show that emoji induced a robust increase in Ross peris can induce Ross finally we found that saccharine but no other artificial sweetener can produce Ross so she says ease data indicate that compounds that stimulate basal insulin secretion most effectively also generated Ros what a wonderful observation those things that were causing triggering of insulin they were also producing raws to test the notion that Ross generation was essential we used Ross scavenger to deplete intracellular Ros so in the in her tests they put an acetylcysteine to remove Ross and those cells from which Ross was removed they could not produce insulin and those cells where Ross was present they produced more insulin this not only prevented emerging induced basal insulin insufficient but also markedly decreased secretion from basal and six millimore per literal glucose so it actually inhibited insulin secretion so much that even with the glucose the insulin secretion reduced so then she says if the concept that redox-driven Ross generation is validated particularly in humans it may be possible to use this knowledge to prevent a Cascade from beta cell hypersecretion leading to diabetes now she gives a very important example the most striking example of rep rapid diabetes reversal in gastric by is gastric bypass surgery and if you see here there are many presenters who talk about insulin remission and they talk about intermittent fasting or other such methods you would see them to talk to give these examples and you would see them to talk about hyperinsulinemia here is the person whose basic paper is the foundation of this thought so for the bariatric surgery she says an apparent cure of diabetes following Roxanne why gastric bypass surgery so in which they kind of cut the stomach into a very tiny Walnut like size Plus they bypass their intestine as well so in these patients remember I actually discussed this study a few days ago within 10 days the patient becomes euglycemic the patient becomes normal glycemic they do not need insulin anymore before that they were insulin independent type 2 diabetics so the question is how come they became insulin independent and not diabetic anymore while their weight is still there you don't get all the weight off in 10 days and that is an example of how reducing insulin levels can actually help reduce the intensity of diabetes so she says an apparent cure of diabetes following Roxanne why gastric bypass surgery has been reported in the majority of patients with type 2 diabetes or impaired glucose tolerance there is no evidence for a sustained beta cell defect this is another part of the classical or traditional Paradigm to say that as the beta cells have to work more and more to produce more and more insulin because there is peripheral insulin resistance beta cells burn out and they stop producing insulin and so we have to then give external insulin and that is why we end up with type 2 insulin independent here she's saying there is no evidence for a sustained beta cell defect this even occurs in individuals who were insulin requiring patients with diabetes before surgery it will be important to determine whether changes in redox accompany them so she's saying that in these studies they haven't actually looked at the redox because they were not suspecting that the Ross and redox will be underlying phenomenas so she says we should study that so she says in summary there is evidence that lowering basal insulin can be achieved through gastric surgery fat loss or drug inhibition of secretion this is a very very very important set of paragraphs it says we found that consistent with the direct and essential role of Ross Eventing with an acetyl cysteine NSE prevented insulin secretion beautiful you give antioxidants vitamin C is one such thing although she does not talk about vitamin C or they didn't use it and the C is another and taken together so she gives a more evidence then she says taken together these data suggest that Agents that increase redox or generate Ross Ross reactive oxygen species not the person Ross result in stimulation of basal insulin secretion result in stimulation of basal insulin secretion these data further indicate that hypersecretion of insulin can be caused directly by Ross and that raws are essential and sufficient signal this is the key statement again Ross reactive oxygen species by themselves are essential and sufficient to cause insulin secretion don't need glucose for them now if you say that well glucose does it too so of course glucose also produces ATP plus reactive oxygen species within the beta cell so glucose is its own mechanism that includes Ross as well but Ross Alone by any other method will also cause insulin secretion so this actually made me think and now this is my editorial part that means I can be completely wrong her paper is her paper and is accurate so this may be correct or not correct because it's a one person's hypothesis those patients of vaccine injury or long covet who are lean who who not to bees who are young and are becoming diabetics I guess in the Paradigm of this paper why are they becoming diabetic because they have an an inflammatory State going on because they have reactive oxygen species being produced and that is then causing hyperinsulinemia and moving them towards diabetes they didn't have to be obese to be diabetic so then she says however raws are not the only essential and sufficient signals there are more and she says calcium LC COA pre fatty acids however she says that Ross are the most important one so here she says Ross is so far the only documented signal essential for a basal hypersecretion in the absence of fuel stimuli fuel stimuli being glucoses or fuels glucose and others interestingly free others meaning protein and fats but primarily glucose interestingly free fatty somebody's gonna editorialize me further so glucose fructose these carbs and then protein to a lesser extent and fats to a lesser accent okay interestingly free fatty acids can contribute contribute to both lcqa and Ross free fatty acids fats actually contribute to LC COA plus Ros and they provide two signals for hyperinsulinemia so this is the last part of it in this conceptual model this is her conclusion insulin resistance is caused by hyperinsulinemia and is an appropriate adaptation to the increased need to store fat in a deposed tissue without causing hypoglycemia what is she saying here she's saying if we have more insulin as I said before that would cause more glucose to be pushed in the cells that would cause hypoglycemia and hypoglycemic outcomes which can be pretty bad so body kind of tries to get ahead of that by saying I'm not going to let insulin do all of this effect I'm going to become down regulated for insulin I'm gonna become insulin resistant thus insulin resistance is an Adaptive response so it's a normal physiological homeostatic response adaptive response that successfully maintains normal circulating levels of fat and glucose as long as the beta cell is able to maintain sufficiently elevated insulin levels so then who is who is at fault the components the agents in the food I would say environmental agents that do Ross even as you can see various interventions not necessarily Foods that can cause inflammation we'll do this as well so perhaps the time has come to expand our research Focus to carefully investigate the environmental changes that have accompanied the epidemic of obesity and diabetes this is the discussion I think this is a very very important paper 2011. and I believe the doctors who had seen them read this paper they actually became very very valuable they wrote books they helped people and they have reversed diabetes and others including me should learn more about these things so this is the discussion please like subscribe and share I know these are a little long videos but there is substance in them and if you would like to support this work as well there are links in the description you can actually get access to Dr Bean for a very very low price or you can use PayPal you can buy me a coffee you can use substack or you can become part of patrons you can actually become part of this YouTube channel as well so with this thank you very much and I would see you on Monday bye for now have a great weekend thank you

Channel: Drbeen Medical Lectures

Views: 26,573

Keywords:

Id: DNxUmB0AaB8

Length: 46min 22sec (2782 seconds)

Published: Sat Apr 15 2023