Keto Confidential EP013: Insulin Resistance
Terms In This Episode (0:45)
Pancreas – The pancreas is a unique organ that has two distinct bodily functions. It is both and exocrine glad that secretes pancreatic enzymes that helps in the digestion and metabolism of foods, as well as an endocrine glands which regulates blood sugar levels by producing and secreting the hormone insulin. Because of this dual purpose, the pancreas is made up of two distinct types of tissue. The exocrine tissue that secretes pancreatic enzymes makes up about 90 – 95% of pancreas. The other 5 – 10% is comprised of endocrine tissues that secrete the hormones insulin and glucagon. This particular area that contains beta and alpha cells is known as the isle of Langerhans.
Alpha Cells – Alpha cells are a specific type of cell in the islet cells of the pancreas that produce the hormone glucagon. These alpha cells make up 40% of the total cells in the islet of Langerhans. Glucagon keeps you from becoming hypoglycemic during times when food and or glucose is in short supply. It does this in two ways, the first is by stimulating the liver to convert or breakdown stored glycogen into glucose through the process of glyco-neo-lysis which is the Latin term for breaking down a sugar molecule into glucose. The second is by actually causing your body to produce endogenous glucose from amino acids and fats a process known as glyco-neo-genesis, which is the Latin term for the creation of glucose. For the remainder of this podcast we will only by examining the secretion of the hormone insulin. I will address the hormone glucagon in another podcast.
Beta Cells – Beta cells are a specific type of cell in the islet cells of the pancreas that produce the hormone Insulin. These beta cells make up 50% of the total cells in the islet of Langerhans. It is primarily though the production of the hormone insulin that our bodies regulate our blood sugars.
Insulin – Insulin is the hormone that is produced by the beta cells the islet cells in the pancreas in an area known as the ‘islet of Langerhans’. It is the hormone that regulates carbohydrate, protein, and fat, metabolism. It drives the cells in our body to take up glucose that is circulating in our blood stream reducing blood sugar levels. It is the hormone that signals the muscle cells in our bodies to take up and use amino acids to promote the growth of muscle tissue. Insulin prevents the release on endogenous glucose that is produced by the liver, and it inhibits the release of stored fat from the cells in our body.
Endogenous – Simply means produced from within. In the case of insulin when I refer to endogenous insulin I am referring to insulin produced by the beta cells in your pancreas.
Exogenous – Simply means produced from without or from outside sources. When I refer to exogenous insulin I am referring to pharmaceutical grade insulin that you inject into the subcutaneous tissues of your body to help lower blood glucose levels.
Glucose Toxicity – Glucose toxicity is a state in which the beta cells of the pancreas have decreased the production of insulin due to an increase in insulin resistance. This state of glucose toxicity then worsens the condition of type 2 diabetes by causing beta cell damage and or death due to chronic hyperglycemia. This cellular damage and death reduces the pancreas’s ability to produce insulin and leads to even higher levels of circulating blood glucose, a vicious and dangerous cycle.
Main Topic (4:15)
- Diabetes is a problem of hormone dis-regulation.
- In T1D, the majority of beta cells that produce endogenous insulin are either destroyed or die off generally from an autoimmune response. Not enough Insulin production.
- T1D need to inject themselves with the hormone insulin multiple times a day to maintain safe blood sugar levels.
- For T1D, then the question is not whether they need insulin, but rather how much insulin do they need.
- In T1D, the majority of beta cells that produce endogenous insulin are either destroyed or die off generally from an autoimmune response. Not enough Insulin production.
- In T2D, the beta cells are damaged or destroyed generally by the over production of insulin due to the stimulation of gross amounts of glucose in the blood stream.
- When the beta cells become damaged and or destroyed, insulin production falls off and blood sugar levels rise.
- Once this happens, T2D, are generally prescribed subcutaneous insulin or oral anti-diabetic medications and may soon have to contend with the same risks of hyperglycemia and or hypoglycemia that T1D have to deal with on a daily basis.
- When the beta cells become damaged and or destroyed, insulin production falls off and blood sugar levels rise.
- Insulin resistance can occur in as little as a few years or it may take as long as 10 – 15 years for your body begins to build up a resistance to this over production of insulin.
- The beta cells have to produce even more insulin in order to try and keep your blood sugars within a normal range.
- Over production of insulin or stress that the beta cells have to withstand that causes them to become damaged and start to die off. A process know as apoptosis.
Insulin Resistance and Beta Cell Damage/Death
According to the article ‘Mechanisms Of Pancreatic B-cell Death in Type 1 and Type 2 Diabetes’ “Chronic exposure to elevated levels of glucose and fatty acids causes beta cell dysfunction and beta cell apoptosis (or cell death) in type 2 diabetics. Exposure to high glucose has dual effects, triggering initially glucose hyper-sensi-tization and later cell death via different mechanisms.” The article ‘Apoptosis In Pancreatic Beta Islet Cells in Type 2 Diabetes states “In T2D, insulin resistance with visceral obesity leads to a glucose toxicity effect (or highly toxic levels of blood glucose), which accelerates beta cell death.” Later in the same article it states “Glucose is the main fuel, which stimulates insulin secretion….and chronic hyperglycemia causes beta-cell glucose toxicity, and eventually leads to beta cell death”.
High levels of circulating blood glucose causes the beta cells to produce extra amounts of insulin to try and decrease your blood sugar levels a process known as hyperinsulinemia. Over time, chronic hyperinsulinemia leads to insulin resistance. In simple terms our bodies cells build up a tolerance of sorts to insulin. So in order to lower the circulating blood sugar levels, the beta cells in the pancreas kick it up a notch and produce even more insulin. The problem is, your beta cells can only do this for so long before they start become damaged from being in this hypersensitive state in which they are over producing insulin. As your Hgb A1c increases, so does your insulin resistance.
- Hgb A1c of 6.5 – 7% had an increased insulin resistance of 9%.
- Hgb A1c of 7.1 – 8% had an increased insulin resistance of 14%.
- Hgb A1c of 8.1 – 9% had an increased insulin resistance of 18%.
- Hgb A1c greater than 9% had a 29% increase in insulin resistance.
So you can see as your Hgb A1c becomes higher than 6.5% you become increasingly insulin resistant which means the beta cells in your pancreas have to work harder. Unfortunately, over time, the harder they have to work, the less efficient they become. So where does the ADA recommend that physicians maintain their patients Hgb A1c levels. That’s right, about 7%. So if your physician keeps your Hgb A1c somewhere in the 6.5 – 7.5% range, then their goal is to keep you in an insulin resistance state of about 9 – 12%.
Reduction of Beta Cell Function Related to Cellular Damage/Death:
- Hgb A1c of 6.5–7% increases beta cell function, increasing insulin production.
- Hgb A1c of 7 – 7.9% promotes a marked decrease in insulin production must likely due to damaged cells and the beginning of beta cell death.
- Hgb A1c of 8 – 9% reduces beta cell function by 37% due to damage and or beta cell death.
- Hgb A1c of 9% or greater had a 62% decrease in beta cell function due to glucose toxicity and
beta cell death.
Think of this way. If you owe more more money than you make you have two options. You can increase your income or decrease the amount of money you spend. To increase your income, maybe you take on extra hours at work, or you get a second part-time job. So instead of working 40 hours a week, you are working 60 or 80 hours a week. Now you may be able to handle this extra work load for a limited amount of time, but eventually you begin to become overloaded, tired, and cranky. As you become more fatigued, your immune system becomes weakened due to lack of sleep and rest. You become less productive and eventually, the continued physical and emotional stress makes you sick. In other words you are literally working yourself to death. So while working extra hours or taking on another part-time job may be a viable option in the short-term, in the long-term it can cause irreparable damage. A second or better long-term option would be to increase your workload temporarily, while decreasing your expenditures before you work yourself into an early grave.
The same is true for the beta cells in your pancreas. As your hemoglobin A1c rises into the 6 – 7% range, the beta cells start working overtime and secrete more insulin to try and lower your blood back into the normal non-diabetic range of less than 5.8%. As your blood sugars continue to rise above 7%, the productivity of you beta cells decreases, they can no longer keep up with the workload and they become damaged. Because the other cells in your body are becoming more resistance to the increased amount of insulin production, and the beta cells are less productive, your blood sugar levels remain high or actually increase. As your Hgb A1c climbs to the 8% range not only has your insulin resistance increased by 18%, but the function of your beta cells have decreased by 37% due to cellular damage and death. Now your body and endocrine system is being attacked from two fronts. Once your Hgb A1c becomes greater than 9%, your insulin resistance has increased to 29%, but the biggest problem is that high levels of circulating blood glucose has created a pool of glucose toxicity that has decreased your beta cell function by 62% due to damage or cellular death. Essentially the strain of increased blood glucose in T2D is working your pancreatic beta cells to death.
At this point, you are already on oral anti-diabetic medications, and most likely subcutaneous insulin. And in all likely hood your doctor has placed you on some form of American Diabetic Association (ADA) diet. Keep in mind that the ADA recommended goal is to keep your beta cells in a state of hyper-sensitivity or overdrive at around 7% (or about 150 – 155 on your blood glucose monitor). So at this point you have two options, you can maintain the status quo by adding more medications to lower your blood sugars in the form or more insulin, which guess what? Increases your insulin resistance even more. Or you can choose to try and attack T2D at the source and decrease the amount of circulating blood glucose in your body by decreasing the amount of carbohydrates you eat each day.
So the decision is yours. You have to chose your specific path, change you diet, or embrace that idea that you may need to take anti-diabetic medications for the rest of your life. No one else can make that decision for you. As for me I was on both oral diabetic medications and subcutaneous insulin. As my diabetes progressed and I ended up in the emergency room as a result of these medications I decided enough was enough and I embraced the ketogenic lifestyle. And just in case your wondering,I had my labs drawn on December the 12th, 2018 and my Hgb A1c is 5.2, and it has been at this level for more than 18 months. That’s the power of ketosis and the ketogenic diet.
Anyway, back to insulin resistance and glucose toxicity. Now that we know at which specific Hgb A1c levels are toxic to your beta cells, the next questions is can your beta cells recover from this damage? Can they be healed? Can we reverse the process of insulin sensitivity and glucose toxicity?
To find the answers to these questions we need to examine some more research. According to J.J. Meier in his article ‘Beta Cell Mass In Diabetes: A Realistic Therapeutic Target? published in Diabetologia magazine. When examining the effects of treatments designed to lower blood glucose and how they affect beta cell turnover, one key aspect determining the fate of your beta cells is the body’s demand for high levels of insulin secretion. It is this constant stimulation of insulin secretion due to either high blood glucose levels as well as the use of oral anti-diabetic medications such as Glyburide and , Glucotrol each of which are a class of medications known as sulfonylurea’s. While used to treat T2D, sulfonylurea’s can make the problem of hyperinsulinemia worse as they increase your endogenous production of insulin production. So if your beta cells are already stressed and over producing insulin adding a sulfonylurea which pushes the beta cells to produce even more insulin can cause even more beta cell damage and ultimately lead to increased rates of beta cell death.
The article goes on to say, that “while the increased demand of insulin secretion can lead to beta cell damage and potentially accelerate the loss of beta cells in type 2 diabetes, the induction of a rest period in which the beta cells are not overly taxed by insulin secretion appears to give them much needed protection. This rest period allows beta cells to recover from the stress of having to over produce insulin due to insulin resistance, and increasing beta cell longevity”.
Catherine Gleason and her associates at the Pacific Northwest Research Institute found that high levels of glucose increased insulin resistance, and that the quicker that glucose concentrations were lowered, the greater the recovery of insulin resistance. However, when it came to glucose toxicity which can result in beta cell death, their findings indicate that there is a small time frame in which full recovery from glucose toxicity is possible. In essence, the sooner that your hemoglobin A1c returns to a normal level of less than 6.5%, the better your chances are for decreasing or stopping beta cell destruction.
Their findings also indicate that glucose toxicity happens over time rather than happening at a specific blood glucose level. Because of the gradual ongoing process, the shorter the period of glucose toxicity, the greater the degree of recovery. Overall their findings indicate that while beta cell damage and exhaustion occur during the early stages of T2D, it is more likely to be reversible, whereas glucose toxicity which occurs later is less likely to be reversible. Therefore, early recognition and effective treatment of hyperglycemia in T2D’s is vital in preserving residual beta cell function.
So yes, insulin resistance and glucose toxicity are reversible. As with most things, the sooner the better, especially when it comes to glucose toxicity. The bottom line, reducing the amount of glucose circulating in your blood is the easiest way to give your beta cells a needed break so that they can recover from all the damage related to the overproduction of insulin and glucose toxicity.
So, what happens when you reverse your insulin resistance and bring your Hgb A1c back to normal levels? Will your beta cells recover from all of that cellular damage? What about the beta cells that have died off due to glucose toxicity? More importantly, can your body produce new pancreatic beta cells to replace those that you have lost? The good news is that you do not have a finite amount of beta cells in your pancreas. A healthy pancreas not bogged down with hyperinsulinemia or glucose toxicity will continue to produce pancreatic beta cells throughout your lifetime. Or that is at least the current consensus among researchers. What they cannot seem to agree on is the overall frequency of beta cell replication in the adult pancreas. However current thinking is that beta cell replication is extremely low in adults and it continues to slow as we age. Because research on human pancreatic cells is difficult, determining the specific number or the speed in which your beta cells replicate as you get older is inconclusive. Your best option is to adopt preventative measures to try and reverse the damage that has already been done to your pancreas and preserve as much of your beta cell function as possible while you still can. The strategies you can use to help preserve your pancreatic beta cell functions on is what we are about to discuss next.
Now that we know at which specific Hgb A1c levels are toxic to your beta cells, and that your beta cells can recover form this damage. How can you reduce your circulating blood glucose levels without the addition of more medications to reverse your insulin resistance? Or is that even a possibility? That is what we are about to discover.
Most researchers agree that from a clinical point of view, one of the simplest ways of inducing beta cell rest is to reduce the bodies insulin demand by either improving insulin sensitivity or by lowering blood glucose levels. One of the easiest ways to reduce the bodies key demands for insulin production is through dietary measures. Primarily by limiting or eliminating foods which cause a substantial rise in blood sugar levels after they have been consumed. Foods that contain a large amount of carbohydrates such a simple sugars, and starches such as bread, rice, pasta and other grain by-products should be restricted. In addition, starchy vegetables such as corn, potatoes, and other tubers should be eliminated or severe restricted.
Initially, diet alone may not give the body enough time to recover from insulin resistance or cellular damage. Physical activity can also increase the effectiveness of the bodies ability to absorb and utilize circulating blood glucose thereby reducing the need for additional insulin production. Studies have also shown that moderate physical activity also increases insulin sensitivity which enhances the effectiveness of endogenous insulin production. Having said that sometimes, dietary measures and increased physical activity alone are not enough. Especially if you have elevated Hgb A1c levels greater than 8%.
I realize that for some of you physical exercise may not be an option. Whether it is related to obesity, or declining health is irrelevant. In such cases you may initially need to be placed on oral anti-diabetic medications such as metformin or exogenous insulin until you are able to implement proper dietary measures. However once you adopt a ketogenic diet in which dietary carbohydrates are restricted to less than 20 grams of net carbs per day, you will start to see a substantial decrease in the daily blood sugar readings. In fact, many type two diabetics find that their insulin resistance quickly diminishes, and they are often able to substantially reduce or totally eliminate the use of subcutaneous insulin injections just as I did.
So there you have it, three specific strategies to combat insulin resistance and glucose toxicity. Adopting a ketogenic lifestyle, increasing the amount of daily or weekly physical activity, and finally, adding or increasing the amount of anti-diabetic medications. Dietary management. Of the three, the adoption of the ketogenic diet and lifestyle is the easiest and requires the least amount of physical work. No matter your age, health, or economic status or you can embrace the ketogenic lifestyle for very little cost. Physical activity helps, but not everyone is able to participate. In fact, for people who are morbidly obese, physical activity may actually have a negative impact on their health. And finally medications. It would be better if we did not have to take them, but you may need to need them especially when you first start tackling insulin resistance and glucose toxicity. By adopting a ketogenic way of living you may quickly find that you can start incorporating some light to moderate exercise in your daily or weekly routine. Doing so will only increase your rate of success. As you get further along in your ketogenic journey, like me you may be able to get off of your insulin because you have reversed your type 2 diabetes and are no longer insulin resistant or suffer form glucose toxicity. Just keep in mind that the ketogenic lifestyle is indeed just that. If you have type 2 diabetes and you go back to eating a high carbohydrate diet, then all of the problems that you have just eliminated will come crashing back down upon you.
Some things to consider about this episode. 1) In T2D, as your Hgb A1c rises, the beta cells in your pancreas become more susceptible to damage due to increased demand. Over time, this damage leads to a decrease in the number of beta in the pancreas due to cellular death. 2) A decrease in the number of beta cells means the remaining cells have to work harder in an attempt to produce even more insulin to combat your high blood sugar levels which leads to more cellular damage and death. A vicious cycle that is hard to break while eating the high carbohydrate diet(s) such as those recommended by the ADA. 3) Let’s be honest, as we age our beta cell production may naturally decreases, but for T2D this risk is elevated due to the long term complications of an increased demand for insulin production. The sooner you can decrease the workload of your pancreas, the more and healthier your beta cells will be throughout your lifetime. Possibly keeping you from having to increase your use of subcutaneous insulin. 4) For type 2 diabetics, a ketogenic diet in which you consume less than 20 grams of net carbohydrate per day will not only decrease your insulin resistance, but help you to lose visceral fat. 5) As you begin to feel the benefits of the ketogenic diet such as improved energy, weight loss, and increased stamina. You will be able to become more active which will in give you another valuable tool to help you decrease your insulin resistance.
As always, you can find additional information regarding this topic in the show notes on my website at www.ketoconfidential.net. You can also find links to all of our podcasts by clicking on the Podcast Archives link located on the home page.
You’ve Got Mail (30:00):
On December 17, 2018 in response to KCP005 ‘The LCHF Diet’ podcast Deva writes: “Thank you a bunch for sharing this, you actually understand what you’re speaking about!” Well thank you Deva, I appreciate your kind words, and I hope that you continue to enjoy the podcast.
If you have any feedback regarding anything you have heard in this or other episodes, or you just want to drop us a line with a question or two, or you just want to share your success story with us, you can send me an email at email@example.com. Please note that any questions you have, may be answered in one of the upcoming episodes of the ‘Keto Confidential’ podcast. If you do not want to send me a email, you can call and leave me voice message at 469-526-3665. Just keep in mind that I will be playing your voice mail in the podcast during the ‘You’ve Got Mail’ segment in the podcast. So if you do not want your name used in the podcast, please make sure you mention that in your message.
Recipe Of The Episode (32:45):
Wow, it’s only five days to Christmas, so I wanted to share with you one more of my keto holiday recipes. Today’s holiday keto recipe is for my keto eggnog. This recipe is very similar to the custard recipe that I use to make to my keto crème brulee. The only difference is the addition of almond milk which makes it, well a drink as opposed to a cooked custard. In addition, I will be sharing with you another salad dressing recipe, this time it’s my keto version of Ranch dressing.
Even though we raise our own free range chickens and I am not at all concerned about salmonela, I cook or temper the eggs for my eggnog. It is quite a bit easier to make if you use raw eggs, but as I make a virgin version (no alcohol) for the kiddo’s, I go with a cooked eggnog. To make our eggnog you are going to need the following ingredients:
12 egg yolks (carbs 7.2 grams)
¼ teaspoon liquid sucralose or other keto sweetener to equal ½ – 1 cup sugar
1 quart Heavy Cream (carbs 28 grams)
1 quart of almond milk, unsweetened
3 – 6 ounces of rum, whiskey, or brandy (optional)
1 tablespoon vanilla extract (carbs 1.6 grams)
¼ teaspoon ground nutmeg
¼ teaspoon ground cinnamon
Separate the yolks from the egg whites and combine the egg yolks, vanilla, and sucralose, or other low-calorie sweetener in a metal bowl and whip with a wire whisk until light and fluffy.
Pour the heavy cream into small saucepan and bring to the scalding point (just before it boils). Remove the saucepan form the heat and with a ladle, gradually add the hot cream into the yolk mixture about a ½ ladle at a time while stirring rapidly to keep the eggs from curdling. Once the eggs are tempered, add the egg mixture to the saucepan and bring up to about 160 degrees.
Remove the saucepan from the heat and pour the contents of the saucepan into a bowl or large container and place it in an ice bath to stop the cooking process. Once the cream and egg mixture have cooled, add the almond milk and mix thoroughly with a wire whisk. Cover and place in the fridge until ready to serve.
I tend to make this eggnog in one big batch so that they whole family can enjoy it and allow the drinker to add the alcohol to their individual glasses. The alcohol is optional, and while bourbon, brandy, rum, or whiskey do not contain any carbohydrates, some people believe that it can slow down ketosis. Anyway, no matter how you make it, just take care and please do not drink and drive during the holiday season. The life you save may not only be yours but that of your family as well.
Total Recipe (about 72 ounces, or Nine 8oz servings)
4069 Calories, 40.4 grams protein, 418 grams fat, 38.2 grams, net carbohydrates.
Per 8 ounce Serving
508 Calories, 5 grams protein, 52 grams fat, 4.7 grams net carbohydrates.
Made with ½ Gallon of Almond Milk
Total Recipe (about 104 ounces, or 13 8oz servings)
4189 Calories, 44.4 grams protein, 430 grams, fat, 42.2 grams, net carbohydrates.
Per 8 ounce Serving
322 Calories, 3.4 grams protein, 33 grams, fat, 3.24 grams, net carbohydrates.
Homemade Keto Ranch Dressing
Now there are two different approaches to making your own LCHF Ranch dressing. The primary difference is whether you use fresh herbs or dried herbs. I have made it both ways, but as I generally keep dried herbs on hand, I almost always use dried herbs in my Ranch dressing and in many of my vinaigrette’s as well. While it is true that fresh herbs have more essential oils and do taste fresher, I have found that most people have the necessary dried herbs and spices in their pantries. As dried herbs and spices are cheaper as well as being more shelf stable, I will be using them in this Ranch dressing recipe. To make this recipe you will need the following ingredients:
Homemade LCHF Ranch (Yield: 2 cups, 32 tablespoons)
1 cup LCHF mayonnaise or any mayonnaise with 0 carbs
1 cup heavy whipping cream
1 ½ teaspoons dried parsley, divided
½ teaspoon dried dill, divided
¾ teaspoon garlic powder
¾ teaspoon onion powder
½ teaspoon salt
1 drop of liquid sucralose (Optional)
1/8 teaspoon ground white pepper
1/8 teaspoon paprika
Combine all the ingredients in a bowl and mix well with a spoon or wire whisk until smooth. You can use more or less whipping cream depending on how thick you like the your Ranch dressing. Refrigerate for at least 1 to 2 hours before serving, although I find waiting 24 hours before using yields a better flavor. The dressing will thicken up a little after being in the fridge for a couple hours. If you wan to use this as a Ranch dip for vegetables, then use ¼ less heavy whipping cream. If you like you Ranch and little thinner, hen add ¼ cup of unsweetened almond milk. The great thing about using almond milk to thin the dressing some is that it only contains 0.25 grams of net carbs, so it does not impact the nutritional value of the recipe, and it has a neutral flavor profile. You could of course just use plain water or a ¼ cup of bone broth.
Anyway, you can keep this dressing in fridge for about 10 to 14 days if using homemade mayonnaise, up to 4 weeks for commercially prepared mayonnaise. You can use an immersion or traditional blender or food processor to make this dressing, but you will want to process the ingredients just until they are well blended. You do not want to over process the dressing or you will and end up with Ranch style heavy whipping cream.
Total Recipe – Calories 2470, protein 3.8 grams, fat 271 grams, carbohydrates 10.5 grams
Per Tablespoon – Calories 77, protein 0.12 grams, fat 8.4 grams, carbohydrates 0.33 grams
The following are a few of the variations that I have made over the years. I am sure there are many other possible combinations so I encourage you to experiment and expand your palate.
- Bacon Ranch – Add 4 to 6 slices of crispy bacon chopped fine.
- Buffalo Ranch – Add 3 to 4 tablespoons Louisiana Hot Sauce.
- Buttermilk ‘Style’ Ranch – Substitute ½ cup sour cream for ½ cup of mayonnaise.
- Chipotle Ranch – Add one chipotle pepper (smoked jalapeño) and one teaspoon of the adobo sauce. Remove the seeds if you wish as they contain most of the heat and do not attribute to the flavor of the dressing.
- Fiesta Salsa – Add ¼ to ½ cup of your favorite LCHF salsa.
- Santa Fe Ranch – Add 3 to 4 tablespoons of salsa verde (green chile salsa) or Hatch green chilies.
I find that when making any of the variations that have solid ingredients such as the ‘Chipotle’, ‘Fiesta Salsa’ and ‘Bacon’ ranch etc. That combining the ingredients in a pint mason jar and pureeing them with my emulsion blender before adding the mayonnaise helps give the dressing a smoother creamier texture. That’s all there is to it, my delicious variation of Ranch dressing, the most popular salad dressing used in the United States.
For more information regarding any of the recipes from this podcast, you can check out my keto food blog ‘CulinaryYou’ at www.culinaryyou.blogspot.com where you can find step-by-step instructions as well as pictures of the recipe(s) featured in this episode.
Cnop, Mariam, et. al, Mechanisms Of Pancreatic B-Cell Death In Type 1 and Type 2 Diabetes: Many Differences, few Similarities, Diabetes, Vol 51, supplement 2, December 2005.
Gleason, Catherine, et. al., Determinants of glucose toxicity and its reversibility in the pancreatic islet B-cell line, HIT-T15, Pacific Northwest Research Institute, and Departments of Pharmacology and Medicine, University of Washington, Seattle, Washington, 2000.
Kim, Mi Kyung, et. al, The Effect of Glucose Fluctuation on Apoptosis and Function of INS-1 Pancreatic Beta Cells, Korean Diabetes Journal, 2010.
Lim E.L. et. al, Reversal Of Type 2 Diabetes: Normalisation Of Beta Cell Function In Association With Decreased Pancreas And Liver Triacylglycerol, Diabetologia, 2011.
Marlon E. Cerf, Beta Cell Dysfunction and Insulin Resistance, Frontiers In Endocrinology, March 27, 2013. Meier, J.J., Beta Cell Mass In Diabetes: A Realistic Therapeutic Target?, Diabetologia, 2008.
Misa, Siddhartha M.D. (2016). Reversing Diabetes: the High 5 Way, Educreation Publishing,
New Delhi, India.
Phinney, Stephen M.D., Volek, Jeff, Ph.D. (2011). The Art And Science Of Low Carbohydrate Living. Beyond Obesity LLC.
Phinney, Stephen M.D., Volek, Jeff, Ph.D. (2011). The Art And Science Of Low Carbohydrate Performance. Beyond Obesity LLC.
Stanojevic, Violeta, Habener, Hoel. Evolving Function and Potential of Pancreatic Alpha Cells, Department of Health and Human Services, 2015.
Tomita, Tatsuo, Apoptosis in pancreatic B-islet cells in Type 2 diabetes, Bosnian Journal of Basic Medical Sciences, 2016.
Weir, Gordon, Bonner-Weir, Susan, Glucose Driven Changes in Beta Cell Identity Are Important for Function and Possibly Autoimmune Vulnerability during the Progression of Type 1 Diabetes, Frontiers in Genetics, 2017.
Weir, Gordon, Bonner-Weir, Susan, Five Stages of Evolving B-Cell Dysfunction During Progression to Diabetes, Diabetes, Vol. 53 Supplement 3, December, 2004.