Glucotoxicity and Double Diabetes- T2D 36

posted in: Diabetes, Health and Nutrition | 41

The glucotoxicity paradigm

The Prime Directive of Diabetes Management

For as long as I have practiced medicine, the mantra of excellent diabetic care was tight blood glucose control. All the diabetes associations, the university professors, the endocrinologists, and diabetic educators agreed. The prime directive was “Get those blood sugars down into the normal range at all costs, soldier!” The only acceptable response was, “Sir! Yes, Sir!” Insubordination was not tolerated.

At first glance, lowering blood glucose as the primary therapeutic target seemed fairly logical. The underlying premise assumes that high blood glucose is the major cause of morbidity. But remember that high blood glucose is only the symptom. In Type 1 diabetes, insulin levels are very low and in type 2 diabetes insulin levels are very high. The symptom is the same, but the diseases are essentially opposites. So how could the exact same treatment be beneficial in both cases?

It’s hard to imagine that the same solution exists for opposite problems. For example, we don’t use the same treatment for both underactive and overactive thyroids. We don’t use the same treatment for both over-eating and under-eating. We don’t use the same treatment for both fever and hypothermia. We don’t wash clothes by soaking in water and then dry clothes by soaking in water.

Type 1 diabetes is caused by lack of insulin, so logically, the cornerstone of management is the replacement of the missing insulin. Type 2 diabetes, however is caused by excessive insulin, so logically the cornerstone of management should be the reduction of the high insulin. Further, being predominantly a dietary disease, the cure must be dietary rather than pharmaceutical. Drugs can’t cure a dietary disease. Only fixing the diet can. These inconvenient facts were simply ignored.

For most of the early and mid 20th century, much of the research focused on type 1 diabetes. Insulin replacement therapy effectively cured type 1 diabetes, the severe lack of insulin. Untreated patients, usually children, experienced unrelenting weight loss until they died, emaciated and skeletal. With exogenous insulin injections, weight stabilized and this formerly fatal disease became manageable. But injecting exogenous insulin came with its own complications.

Symptoms of Hypoglycemia

In order to avoid too high or too low blood glucose, it is essential to match the insulin dose with the amount of food, predominantly carbohydrates, being eaten. Underdosing caused high blood glucose and overdosing of insulin caused low blood glucose, called hypoglycemic reactions. Patients would become sweaty, tremulous and if severe, could suffer from seizures, loss of consciousness and death.

These hypoglycemic reactions are immediately life threatening. Even over the longer term, they are strongly associated with a wide range of adverse outcomes including heart disease and death, particularly in older adults. In 2014, nearly 100,000 emergency room visits and 30,000 admissions to hospital are directly related to hypoglycaemia. From 1999-2011, an estimated 404,000 patients were hospitalized for low blood sugars compared to 280,000 hospitalized for high blood sugars. There’s also a steep fiscal cost associated with these reactions. Over 5 years, the estimated cost of this care is $600 million.

Because of the immediate severity of hypoglycemia, until the mid 1990s, researchers and physicians argued back and forth whether high blood sugars were even all that dangerous. Extremely high blood glucose could cause diabetic ketoacidosis in type 1 diabetes and non-ketotic hyperosmolar coma in type 2 diabetes, but these complications were relatively uncommon. On a typical blood glucose-monitoring device, the levels would literally need to be off the scale.

Moderately raised levels of raised blood glucose were not obviously detrimental to long-term human health. In the short-term, there were no symptoms whatsoever. Normal blood glucose levels vary depending upon what and when you last ate. Fasting blood glucose is considered normal below 6.1 mmol/L. It goes up after a meal and typically peaks approximately two hours after the meal at less than 10.0 mmol/L.

The renal threshold for glucose, the level where glucose begins to appear in the urine, is approximately 10 – 11 mmol/L. In the normal situation, glucose is completely reabsorbed by the proximate tubule of the kidney so that no glucose spills out into the urine. Above the renal threshold, this re-absorptive mechanism is overwhelmed and progressively more and more glucose spills out into the urine and symptoms may appear. Patients may notice increased urination as the excreted glucose pulls water along. Patients become dehydrated and then will also notice increased thirst. This excessive drinking and urination is a classic sign of diabetes mellitus.

At blood glucose levels below 10 mmol/L, there are no noticeable symptoms of hyperglycemia. Insulin could tightly control blood glucose but inevitably resulted in more hypoglycemic episodes, and this tradeoff was not obviously beneficial. For many decades, the standard medical practice was to keep the blood glucose levels slightly high but below 10 mmol/L. This avoided both hypoglycemia and the symptoms of high blood glucose. Yes, the blood glucose level was higher than normal, but there were far fewer episodes of hypoglycemia. Nobody had yet found definitive proof that the slightly high blood glucose was injurious.

Things completely changed in 1993 with the publication of the Diabetes Control and Complications Trial (DCCT). This large randomized trial was designed to answer this very question by comparing intensive insulin therapy in type 1 diabetes to conventional treatment. The high dose group successfully lowered the A1C but, as expected, there was a price to be paid. The incidence of hypoglycemia was three times higher in the intensive control group. Was it worth it?

The results were nothing short of revolutionary. Diabetic eye disease decreased by 76%, kidney disease decreased by 50%, and nerve damage was reduced by 60%. Clearly, long-term hyperglycemia was causing end-organ damage. Insulin treatment to tightly control blood glucose could preserve organ function.

In 2005 the Epidemiology of Diabetes Interventions and Complications (EDIC) study was published. This followed the original DCCT patients out to seventeen years. The results were, once again, revolutionary. Intensive insulin treatment had reduced cardiovascular disease by an astonishing 42%. This clearly established the paradigm of glucotoxicity (toxicity resulting from high blood glucose) in type 1 diabetes.

Other than the increased hypoglycemic reactions, there is another cost to intensive insulin treatment. The incidence of substantial weight gain increased significantly. Over nine years, almost thirty percent of subjects developed ‘major weight gain’, far in excess of the conventional insulin group.

By the late 1990s, as the obesity epidemic gained momentum and the type 2 diabetes epidemic was starting its run, some inkling of concern percolated amongst some physicians about the excessive weight gain. One quarter of the intensive treatment group increased their Body Mass Index from 24 (normal weight) to 31 (obese). The well-known propensity of insulin to cause weight gain is not some trivial problem of trying to fit into your swimsuit, but had significant health consequences.

There were other danger signs, too. This weight gain concentrated in the abdominal area. Blood pressure and blood cholesterol increased. The combination of central adiposity, hypertension and dyslipidemia is the hallmark of the metabolic syndrome that is more typical of type 2 diabetes, characterized by insulin excess. This could not be good news, but there was worse to come.

Weight, waist circumference, and insulin dosage continued inexorably higher. Blood pressure and cholesterol followed the upward trend. Intensively treated type 1 diabetic patients were developing the metabolic syndrome, the problem of hyperinsulinemia.

The coronary artery calcification (CAC) score and carotid intimal medial thickness (CIMT) are both well accepted measures of atherosclerosis – the buildup of plaque in the artery that leads to heart attacks and strokes. Heavy calcification and thickened blood vessel walls are subclinical markers of atherosclerosis and sure signs of bad things to come. Type 1 diabetic patients with the most weight gain also developed higher CIMT and CAC scores. High insulin dosage reliably predicted advanced atherosclerosis. While type 1 diabetes is originally a disease of too little insulin, over time, these patients are all developing the problems of too much insulin.

There are two types of toxicity – glucotoxicity and insulin toxicity. At the time of diagnosis, type 1 diabetic patients have extremely low insulin levels, so the dominant problem in the short term (<10 years) is glucotoxicity. Taking insulin to reduce blood glucose improves clinical outcomes.

But over time, heavy handed dosing of insulin produces all the problems of excessive insulin – obesity, metabolic syndrome and atherosclerosis. Hyperinsulinemia leads to insulin resistance causing the same exact problems seen in type 2 diabetes. The heavy dosing of insulin in type 1 diabetes was creating type 2 diabetes!

Double Diabetes

The Dietary Guidelines for Americans had, since the late 1970s recommended a diet low in total fat and high in carbohydrates. Since refined carbohydrates such as bread raise blood glucose significantly more than dietary fat, this required higher insulin dosing in type 1 diabetics to keep blood glucose control. This wasn’t so bad. Was it?

It is well established that type 1 diabetics have a four fold higher risk of death compared to non-diabetics. Most believe this is caused by glucotoxicity, but the evidence points to the contrary. Multivariate analysis of the EuroDiab study revealed the stunning conclusion that glucotoxicity, as measured by Hemoglobin A1C was not a significant risk factor. The one factor everybody assumed was critically important turned out to be almost irrelevant. Instead, the most important modifiable risk factors were Waist to Hip Ratio (a measure of visceral fat), blood pressure, and cholesterol.

These are all the usual culprits found in metabolic syndrome, caused by insulin excess, not insulin deficiency. Type 1 diabetics patients suffered all the disease as type 2 diabetics, but high blood glucose was not the causal link, as had always been assumed.

Multiple other studies confirmed the EuroDiab results. The Golden Years Cohort Study followed 400 type 1 diabetic patients who lived over 50 years managing their disease. This group had beaten the odds and survived. What was their secret? One thing became clear. The secret was not tight blood glucose control.

The Golden Cohort’s average A1C was 7.6% – well over the standard recommended target of 7.0%. This level could only be described according to standard management as ‘poor’. Some had A1C measurements in the 8.5-9.0% range, yet still far out-lived the average. Strikingly, no Golden Cohort patient had an A1C in the normal range! Clearly, glucotoxicity was not the major player here. The entire Golden Cohort of survivors had ‘sub-optimal’ blood glucose control and it didn’t matter. Their health was excellent.

The common bond shared within this group was not low blood glucose, but rather a low insulin dosage. Obesity, high blood pressure, and the other manifestations of hyperinsulinemia were notably absent. Elevated HDL (good) cholesterol was associated with lower insulin doses. Since long-standing type 1 diabetics have no insulin production of their own, all insulin must be injected from prescribed doses of medication.

Another paper wonders, “Why do some patients with type 1 diabetes live so long?” Blood glucose control plays a minor role. Only a reasonable, but not necessarily ‘ideal’ blood glucose is needed for longevity. Glucotoxicity is a not a major player.

One again, low daily insulin dosage is the key to survival, leading to lower body weight, lower blood pressure, and improved cholesterol. High daily dosage of insulin leads to the metabolic syndrome, a disease of hyperinsulinemia. This puts them at the same risk of cardiovascular disease that all the type 2 diabetic patients develop. The over-exuberant treatment of type 1 diabetes leads, in essence to type 2 diabetes. They have what can only be called ‘double diabetes’.

The conventional dietary advice of the past 30 years to eat a low fat, high carbohydrate diet requires more insulin to keep blood glucose levels normal. This ‘carb up and shoot up’ strategy, requires decades of chronically high insulin levels, eventually leading to increasing insulin resistance and the precursor to type 2 diabetes as well as the rest of the metabolic syndrome. As type 1 diabetic patients develop double diabetes, factors like cholesterol, high blood pressure and central adiposity all become increasingly important.

There are two toxicities at work here. Early on, glucotoxicity is the main concern. But over time, insulin toxicity becomes increasingly important and the key determinant for survival. The optimal treatment strategy reduces both.

While we acknowledge the damage caused by glucotoxicity, we ignore the insulin toxicity. Raising insulin to lower blood glucose simply trades insulin toxicity for glucotoxicity. Sledgehammering patients with high doses of insulin to reduce blood glucose was not improving the health of patients. Blood glucose and insulin must be lowered simultaneously.

 

 

41 Responses

  1. sten bjorsell

    It is well put at the end: “Blood glucose and insulin must be lowered simultaneously”.
    But how can that be achieved on a Standard American Diet, S.A.D., the for health recommended low-fat high-carb diet?
    That diabetes and obesity explosions started just after SAD was introduced in the late 1970’s does not look like a coincidence anymore. It seems now obvious that the new dietary advice is the direct cause of the epidemics, as it is impossible to keep blood glucose low with a high carb intake without producing or taking more insulin.
    The recent video talk by Nina Teicholz from Breckenridge goes deeper. https://www.youtube.com/watch?v=FXjB-5-uzuw

  2. Wow! Stunning post. I have a 22 year old nephew with T1d. Through lifestyle changed he has not needed ANY insulin for 7 years now, but his recent 7.5 hgb A1c signals an end to his honeymoon period, and the introduction of insulin. I’m reading that we need to modify his carb intake more tightly than we have done in the past. He was allowed to have an occasional bun with his burgers, and a half order of french fries (his parents did not want him to be singled out as that kid who could not eat the same as his friends). But I see now, like T2’s, my T1 nephew will need to minimize carbs. Dr. Fung, you have changed my life!

    • You should take a look at Dr. Richard Bernstein as to tight managment of T1D. He is on YouTube, and has a book.
      https://en.wikipedia.org/wiki/Richard_K._Bernstein

    • The issue with the low carbohydrate diet is that when you reduce your insulin levels at all times of the day week after week, and month after month, you also greatly impact your lean body mass (muscle). Insulin is an anabolic hormone and is absolutely required to build and maintain muscle. Body composition is of just as much importance, if not greater importance than total body weight. By eating a balanced diet of healthy carbohydrates, including ample exercise (especially some form of strength training), and tapering the insulin dose to “just enough to get the job done” not excessive nor inadequate, you are able to see much more pronounced benefits vs a lifelong low carbohydrate diet alone. Also carbohydrate deprivation causes lots of intracellular stress setting in motion for weight regain in the form of fat tissues when you cycle on & off the low carbohydrate diet (which is what young kids, teens, and college students will often do). Most importantly, the are of the body where this weight gain post low carb diet is generally located is the abdominal region (visceral fat) which is bad news for insulin sensitivity in the long run. Either extreme of the diet is bad (too little carbs or too much carbs). I encourage you to find a good dietitian to help figure out what your nephews’ daily nutrition needs are for growth and get the dose to precisely to match those needs. As we learn more about the microbiome (gut bacteria), yes we see that excess animal protein in the diet is strongly associated with poor immune system function and colorectal cancer, as well as irritable bowel disease. Berstein’s book on the diabetes solution was written ALONG time ago before this recent research from 2010 and newer was published. Always follow the latest research on health, not outdated schemes or diet fads.

  3. RIchard Fish

    Great information Dr. Fung! Thank you.

  4. Well as a T2D I’m glad I have been reducing my insulin injections as they were going higher and higher as the years went by and no doctor told me to just cut the carbs. I was told you doing okay this is just what the disease does. Funny I was actually paying for this advice never has the term buyer beware more appropriate in my opinion. Here a while back I stumble upon your blog started to follow your advice and now I have gone for injecting 2 different insulins daily to using one. I’m hoping that by early to mid July to be off that one also. Thanks Dr Fung for telling it like it is.

  5. Harry Kanis

    Yes Jason, I Fully agree, except for the Low Carbohydrate with High Fat Diet.
    I myself, 70 years old, have now a history of 16 years of DM 2, it is a family problem.
    Starting off with A1c of 6.1 % and ending now at present with 5.5 %. Initial BMI 25.4
    Right from the beginning I lost 14 kg weight in 1 month from my 70 kg at diagnosis date.
    Just by adjusting my diet and walking Daily 10.000 steps. Med Rx Gliclazide MR half A tablet & Pravastatin & an ACE inhibitor.
    Two years later I discovered Joel Fuhrman book “EAT to Live” and have Since followed his Diet of Low Caloric Density but High Nutriënt Density. Full of Fruits & Vegetables with kots of bioactive Polyphenols and dietar fiber and no bread or potatoes.
    But with Low GI High cereal fiber – 20 % fiber – rye WASA crackers.
    One year ago I had gradually gained weight again during Many years, I started the Circadian Time Restricted Diet of Professor Panda. Every Day according to the book the 8 hour Diet. This provided me with A Fasting period of 14 hours every Day during the evening and night!
    The results were amazing in 5 weeks I lost 7 kg resulting now in a BMI of 20.4 and still
    walking daily 9000to 10.000 steps.
    High Fat Diet is A risk for your Microbiome and gut Barrier I think and nowhere are there so Many Healthy Phytochaemicals to be found than in fruit and Vegetable and High fiber cereal Foods, but not in fat I think.
    I am interested in your Comment on my personal story.

    Harry Kanis, MD, MPH
    The Netherlands

    • From his book, his low carb does not exclude fruit and vegetables, but instead refined carbohydrates and sugars, both natural and unnatural. I think he would encourage you to eat fresh fruits and vegetables, with more emphasis on the vegetables. I thoroughly enjoyed the Obesity Code and would highly recommend it. Being a doctor, you would likely appreciate the biochemistry and physiology descried in good detail. Ultimately, my take away has been to incorporate regular fasting with a whole food diet that focuses on vegetables, nuts and seeds, legumes, some full fat dairy, low processed meats, and fruit, with occasional whole grains during your feeding times. Adjust your whole grains and fruit consumption to address elevated glucose or increase fasting periods.

    • Im interested with your writing , may i contact you via email ?

    • First of all, fruits and vegetables are not of “high” nutrient density. Meat is.

      http://www.zoeharcombe.com/2014/04/the-perfect-five-a-day/

      Moreover, fruit is very high in sugar. It’s just as healthy to eat a chocolate bar:

      http://www.zoeharcombe.com/2015/12/sugar-in-fruit/

      Finally, what evidence do you have that fat somehow “damages” the microbiome AND that damage will cause some negative effect? I want randomized, controlled trials over years. I’ll give you hint: there are no such studies.

      What I’ve found is the less fiber and vegetables I eat (I avoid eating fruit, as it causes my blood sugar to skyrocket), the better I feel. I’m going more and more toward a meat-based diet, with some offal.

  6. Kimberly

    Dr. Fung’s post is especially timely for me. After 12 years of T2D, I went into DKA, make virtually no insulin, and am insulin-dependent. My doctor and I are still working on my insulin protocol, but it looks like I will be taking approximately 21 – 22 units of Lantus (basal insulin) daily and most likely 6 – 10 units of Humalog (fast-acting insulin) daily to cover meals. How many units of insulin per day would be considered “low” for a 125 pound, 60-year old woman in my situation?

    • I think he is referring to low doses of naturally produced insulin. If you are taking insulin as a type 2 then you are flooding the body with insulin and injecting it too, just not using it well. If you have reached the point where you no longer produce insulin, then that is different. My guess is that he would recommend monitored fasting, elimination of refined carbs and strict limiting of whole unprocessed grains during feeding periods with extra exercise to reduce or avoid the insulin. I hope he responds to you I would be interested too!

      • Kimberly

        Aaron,

        I was referring to Dr. Fung’s comments on the Golden Years Cohort Study of Type I diabetics and their use of low doses of insulin. I am essentially being treated as Type I as I no longer make any insulin of my own. I MUST inject to survive. I have been eating low-carb for 12 years and a few years back added significant amounts of healthy fats. I also did intermittent fasting until the diabetic ketoacidosis episode. I will fast again once my blood sugars normalize and monitor to avoid hypoglycemia. I am wondering if 27 – 32 units of insulin per day is considered “low” and if longevity could be in my future simply due to the dosage.

    • Kimberly,

      I would recommend that you look into Afrezza, ultra-rapid inhaled insulin, for your bolus needs. Much faster acting than Humalog and much shorter tail by 3 to 4 times. Minimizes both prandial spike and hypoglycemia risk. Fast in, fast out, and no needles is a bonus.

  7. Possible the theory of glycation and oxidative damage is over-sold by bad pharma, and thus the need for tight management of glucose. In my research of diabetes for my website http://healthfully.org/rg/, I have come across hundreds of journal articles on low ascorbate, and in a few a causal connection for damage to collagen. Some of the articles point out that serum ascorbate is a measure of recent dietary intake; thus levels of ascorbate in cells that have stores very high levels of ascorbate are revealing of this health issue. Typical of the body, there are many functions and variation of a protein, and of many of the hormones, collagen is the principle protein in the body and has 7 forms, and many functions. Given the many roles of collagen and the low ascorbate connection to deformed collagen, I reasoned that the oxidative theory related to high serum glucose as the major cause of the conditions associated with diabetes are wrong. I reasoned, given ascorbate as an antioxidant, that low ascorbate is the main cause. One journal article criticized the glycation theory of tissue damage. What is your opinion on this causal relation to the comorbidities of diabetes?

    • sten bjorsell

      To Jerome Kahn.
      You also have the same receptors for taking up glucose and the very similar ascorbate molecules.
      “Uptake time” is after meals. High glucose generating foods like fast carbs raise blood glucose often to twice the fasting level, while blood ascorbate usually remains at same levels as before meals leaving the relative ascorbate/glucose ratio in blood to drop to half what it was set to before the meal, the body set level, probably resulting in half the uptake as intended/required. Only because of unnaturally high after meal blood sugar from foods, that we never adapted to. Low glycemic meals that also keep insulin low is, of course, a double advantage.
      Subclinical Scurvy is probably a much more common problem today than we think, also thanks to the new high carb recommendations brought in based on fake science and “consensus” in the late 1970’s. Who wants to risk weakened collagen in blood vessels, apart from diabetes-2 and/or heart disease?
      In summary, there is no good reason to keep blood glucose down by means of medicines when a double whammy is available through food.

    • Victoria V.

      You state: “One journal article criticized the glycation theory of tissue damage.”

      Can you please provide a link to this journal article? Thank you.

      Victoria V.

  8. Sascha Heid

    OMG a Captain Picard meme, i love you.

  9. Abdulaziz A. Alnawfal

    I love you
    This is logic
    This is poem
    This is melody
    This is intellectual art
    This is why I believe in you Dr.
    If your information is not correct, at least you give us HOPE.. ❤️

  10. BernardP

    “Fasting blood glucose is considered normal below 6.1 mmol/L. It goes up after a meal and typically peaks approximately two hours after the meal at less than 10.0 mmol/L.”

    — Quick question: What is the definition of “two hours after a meal”. Is it two hours after one has started eating, or two hours after one has finished eating?

    • dr denis

      It is 2 hours after finishing. Also fasting blood glucose is considered normal if not above 5.5 mmol/L [ = 100 mg/dL] in some sources. 6.9 mmol/L [ = 125 mg/dL ]is considered diabetic.
      There are different ideas about the top end of fasting normal. I believe in the 5.5 mmol, or 100 mg/dL limit.

    • BernardP, I’ve read many different opinions on this. I usually try to hit the peak after my meal. I usually use 1 hour after the end of the meal. Some people use the beginning, others suggest the end. /The two hour peak is simply one estimate. There are many more.

      This suggests a peak anywhere from 20 minutes to 2 hours after eating (which I think means the end of the meal?):

      http://www.livestrong.com/article/448193-how-long-after-eating-does-blood-sugar-peak/

      The best advice I saw was to test your own response to a meal by taking many blood samples over the course of a few hours. I did this and took a sample every 15 minutes. The problem is that I eat very low carb. I don’t get much of a peak. And, the blood glucose monitors are have poor accuracy. Thus, if your blood sugar goes from 100 to 115, that’s not much of a rise, given that your blood sugar monitor could easily have 10% random error. So, my test did not work that well. I’d like to redo it one day, with potatoes or some type of sugar, but have not done so. It’s a lot of pin pricks to your fingers and I try not to eat high carb meals.

      Even with such a test, it’s unclear your body reacts the same way each time. Here, they tried to reproduce the glycemic index using volunteers. The same food given to the same person on different days caused different responses. Between people, there were vastly different responses. They concluded that the glycemic index is useless:

      http://now.tufts.edu/news-releases/high-variability-suggests-glycemic-index-unreliable-indicator-blood-sugar-response

      I’ve found that I can get anywhere from -3 to +15 or more about an hour after eating a very low carb meal. A lot of that is probably the variability in the crappy blood sugar monitors, but some of it is my own variability, even though I’m eating the same meals.

      • BernardP

        Thanks. I read the article on TUFTS. I would not conclude glycemic index is worthless, but rather that it has a larger than expected margin of error.

  11. Dr Fung, a couple of questions for you:

    1. I’ve been reading Rob Thompson’s book The Low-Starch Diabetes Solution and he says that in T2 the beta cells are”burnt out” to a degree by the high blood sugars and don’t produce enough insulin, which is why you reach the point in insulin resistance when the blood sugars start climbing. That if you have T2 long enough they eventually don’t produce ANY insulin and you have both T1 and T2. Drugs that force the beta cells to pump out more insulin just accelerate the burnout. IIRC Dr Bernstein says much the same. Is this your experience with T2 that the beta cells are permanently impaired or do they recover with your fasting protocol?

    2. What do you think about the theory that many of the complications of diabetes are the result of thiamine (B1) deficiency, also known as beri-beri? Diabetics are chronically low in B1, and the symptoms of beri-beri include peripheral edema, neuropathy and nephropathy, all of which are also typical of diabetes. The usual medical response to diabetic edema is to prescribe diuretics, but diuretics (particularly furosemide) cause further excretion of B1, intensifying the deficiency! It’s Catch 22!

    • Hi Stuart, I am not Dr Fung but your Q1 is incorrect. Can’t address Q2. The following is a video presentation by Dr Taylor in Newcastle, Eng credited with proving T2D was, in fact, reversible. This means, and he categorically proves, Beta cells are not burned out, not dead, that was a myth he busted. Here’s the link:

      https://campus.recap.ncl.ac.uk/Panopto/Pages/Embed.aspx?id=c3bef819-e5f4-4a55-876f-0a23436988ed

      Secondly, it is my experience Dr Fung, if he reads these blogs after publishing, does not respond. Two choices I believe you have available are: 1) join Diet Doctor site, advertised on this page, Dr Fung is often on it answering questions or
      2) subscribe to the FastingTalk podcasts. This is a weekly podcast where Jimmy Moore (coauthor of Complete Guide To Fasting), Dr Fung (once per month) and Megan Ramos, Dr Fung’s assistant/director discuss topics and answer questions submitted. I hope these references help.

      • Hi Walt, yes I answered my own question after posting the above by reading some of Jason’s earlier posts and viewing Prof Taylor’s video. My interpretation of Taylor’s findings is that in early T2 the beta cells are inactive but not dead and can wake up when you clear the pancreas of fat. This is consistent with Jason’s observation that 3 weeks fasting will return a patient to a normal BG state ie the pancreas has returned to pushing out high levels of insulin. But you’ve still got the problem of elevated insulin. This says to me that you’ve got to keep going at reducing your IR through IF and a ketogenic diet, maybe do another long fast. Incidentally the 800 calorie diet is based on the assumption that people can’t do water-only fasts. Actually a no-calorie diet is easier, no need to count calories, and should work faster. Re beta cell burnout I note that 2 of Taylor’s patients showed no improvement on the diet. Either their beta cells have burnt out or they just have a lot more fat in the liver than the others and would have improved if they’d fasted longer. Remember Taylor shows that the body metabolises liver fat first, then pancreas. This is consistent with Jason’s finding that longterm diabetics take longer to recover on his program.

        I had noticed that Jason had stopped replying to comments, at least directly. I can quite understand why, as with this volume of comments it would be enormously time-consuming, time that could be better spent in posting a blog entry which would be visible to many more people than a comment reply. I was hoping that I could prompt a future blog post or two. Re the B1 deficiency hypothesis, a search of PubMed turns up a 2005 paper proposing it as a major cause of diabetic complications, unfortunately the full text is behind a paywall.

        • Yep, funny you should mention that Stuart, I ran into that as well. Pay as you go!. And you are correct Dr Taylor has not had 100% curing of T2D but he does state he has seen in all his trials, with larger # of people and longer duration of T2D, 100% improvement. He didn’t elaborate that I saw but for instance, going from high insulin to metforman or some other non-insulin drug. As you said, maybe it takes more than 8 weeks for some. After I started my diet I didn’t have another A1C for 6 months and it was below 6 (literally ‘not diabetic’ was stamped in the comment section of the result. Now, about a year and half later it’s mid 5s. I am hoping in Aug it will be mid 4’s. Oh, I discovered that this friday is last FastingTalk with Jimmmy Moore and Megan Ramos (Dr Fung’s sidekick). But they do have the recordings you can listen to (for free).

  12. What are the repercussions of eating only fat, in conjunction with fasting? Like hard cheese, coffee with cream, when hungry, else fasting as much as possible. I’m on day 5 of a “fast” that has included about 1000 calories (total over 5 days) of hard cheese, probably about 10-15g of carbs total from these cheeses during this “fast”. Beneficial?

  13. I have a serious number of complications over and above Diabetes, which I suspect are all making this diabetic condition far worse: food allergies and sensitivities; celiac, tonsillar cancer (being treated and doing extremely well), enormous anxiety and stress and I believe candida overgrowth.
    > I take no vitamins etc.
    > I have been checking my blood first thing in the a.m. for a little over a week and the readings have not gone below 15!!!
    > For the past week I have missed a midday meal almost every day as I have been on the road and finding a right, inexpensive thing to eat (out there) is impossible.
    > I’ve been trying to fill up on more vegetables, but is this even right?
    > I have been cutting out (whatever I believe to be harmful) carbs wherever possible, using more olive and avocado oil but then I’m left with hardly anything that I can eat.
    > Breakfast is a tough meal – I am celiac so I use gluten free bread at breakfast – is this all wrong?
    > I am not a good cook and my food is disgusting, I find it hard to eat it.
    > I know that I am not getting enough exercise – at this time last year I was doing so much better, working in my garden and jogging everyday. Today again, I am indoors, competely covered even with socks on.
    > I do not have a family doctor (I’ve been trying, it’s a bit hard to find a new doctor in Scarborough) who can send me to an endocrinologist to find out what is really happening on the inside, BUT is an endo. really the right practitioner or is there another direction I should actually be going in?
    There is a lot here but someone must know the answers.

    • Miriam Kearney

      I’m not a doctor, just a Diabetic patient but I have been following the Autoimmune Paleo protocol for a few months now and my body is responding by (a) losing weight – I’m down 13 pounds (b) I’m feeling better – no more nausea after eating. Basically I eat meat, poultry, fish and above ground vegetables i.e. no starchy vegetables at all. Breakfast is a pork chop and green vegetable or simply bone broth. I make a large pot of bone broth every week. I’ve stopped drinking coffee and tea in the morning but occasionally have one or the other when I’m out. I no longer eat any grains at all even if they are gluten free. I eat no beans or lentils, only have occasional dairy when I’m out (like cream in my coffee). I’ve also cut out nightshades (tomatoes, potatoes, peppers and eggplant). I don’t know which foods are doing the trick but after a couple of months I no longer miss the ones I’m not eating. I find if eat even the smallest amount of carbs I want more and it’s difficult to go back so I am leaving them out altogether. Don’t know if it would be the same with beans, dairy and nightshades but I’m trying to be absolute about it. I feel so much better that I’m rarely tempted to go off the program. Most morning we just have bone broth and lunch is either more bone broth or eaten around 2 pm. Dinner is around 6pm so limiting the number of hours during which food is being consumed. These are all suggestions I have found on Dr. Fung’s site and others. Seems to be working so I’ll stick with it. You don’t have to be a good cook to make a porkchop and steam some veggies.

  14. Interesting article. While I agree that insulin resistance is important to consider in DM1 and that it likely contributes to mortality in this group, it is not the only thing to consider. Solid data do exist that show a correlation between A1C in DM1 and the development of microvascular complications, so to ignore long term control would be foolish. However, the point is not lost to me that the SAD plus intensive control makes a near normal A1C almost impossible without flirting with weight gain/insulin resistance/metabolic syndrome. What I suggest, and I think Dr. Fung does to if you read between the lines, eat low carb with DM1 and get a solid A1C to avoid vascular complications as well as to reduce daily insulin requirements (to the individual extent possible) to avoid development of insulin resistance and it’s known complications.

  15. Miriam Kearney

    What Dr. Fung is saying about the liver and pancreas being clogged with fat as the primary cause of insulin resistance makes a lot of sense however it makes me wonder about people with Type 2 who are not overweight. Are there different types of Type 2 Diabetes?

    • The skinny T2 people are probably TOFIs – Thin Outside Fat Inside. The BBC medical journalist Michael Mosely was amazed when he was diagnosed T2 despite being skinny. An MRI revealed that he had high levels of visceral fat. Waistline is an indicator of visceral fat in most people but not all.

  16. I am continually amazed by the number of people who visit this site that think they (and their metabolism) are somehow special or unique. Yes, we are all unique.

    But the point(s) of Dr. Fung’s blog and various other postings he has produced are (as I see it) about statistics for all cause mortality AND the mistaken and harmful focus on curing the numbers, and not the disease. He also maintains, generally without exception, as I understand his posts, that the CAUSE of T2 Diabetes (and “metabolic disorders”…) is excessive insulin production, leading to insulin resistance, leading to weight gain and then various (premature) gross organ failures and death. At no point has Dr. Fung ever conceded, or promoted the idea, that in type 2 diabetes the body stops making insulin. The problem is precisely that the body doesn’t stop producing insulin, so long as the body is presented with an excessive amount of “sugars” in food. Insulin production is the body’s proper and necessary reaction to sugars in food. Carbohydrates are sugars in a longer chain form.

    Thus this latest post by Dr. Fung, as I see it, makes the point that T1 diabetics who take too much insulin (to fix the sugar numbers) effectively get T2 diabetes and, in the end (literally), die from the effects of too much insulin. Thus his conclusion was: Better to have the body with “too high” sugar levels and live a longer and healthier life than to (in effect) over-dose on insulin. This is a dismissal of the failed idea/paradigm of curing the sugar numbers. Numbers don’t kill you.

    Advice from a physician that the patient has stopped making insulin sounds simply wrong in terms of the paradigm presented by Dr. Fung. The point of this latest post by Dr. Fung is that the previous paradigm and advice to get blood sugar “numbers” controlled (by taking insulin) makes the problem worse, because insulin taken to do that (and insulin in that context is powerful “drug”) only increases the body’s resistance to insulin. As Dr. Fung says, the idea of taking drugs to “cure” a dietary disease is simply wrong. The way to fix a dietary disease is to fix the diet.

    One obvious fix is to eliminate carbs/sugars from the diet. That may work but for most people it is very difficult, and it is probably unnecessary in any event.

    The better answer seems to be to minimize carbs/sugar consumption AND to take longer periods between meals (fasting) where the body produces no insulin and thus instead of the body storing fat (because of the insulin) it burns fat and regains its sensitivity to insulin.

    This minimalist approach has several additional benefits: You don’t have to buy or take any drugs. You have “more time” because you don’t spend as much time preparing (or buying) food, eating food, and cleaning up after eating. You will lose weight, and you will feel better. Yes, the downside is that you will have some moments of feeling hungry. You can give in to those food cravings and die young (and fat), or you can learn that you can easily and happily live on one or two meals each day.

    It is also worthwhile to realize that Physicians who follow the normal protocol for fixing diabetes have the weight of “authority” on their side, not in terms of science necessarily, but rather in terms of the accepted medical dogma. That dogma is that diabetes is un-curable and progressive. The physician can therefor give advice (indeed they feel obligated to give such advice) that will likely kill the patient, with complete justification and no guilt. We also have to keep in mind the role of the drug companies in this accepted paradigm. Follow the money.

    • I suggest you view the presentation by Professor Roy Taylor of Newcastle University in the UK titled “Reversing the Irreversible” of which Walt has posted the link above (Thanks Walt). Taylor’s blood testing clearly showed that T2 diabetics had much lower than normal Insulin despite their high levels of BG. After 8 weeks (?) of his 800 calorie diet – actually a partial fast – their insulin levels had risen to normal in all but 2 patients. This return of insulin production closely paralleled the reduction of fat in the pancreas as shown by MRI. The series of MRIs for each patient showed that the body metabolises the liver fat first and only then begins on the pancreas fat.

      This raises the possibility that Taylor’s 2 non-responders still had excess fat in their livers and hadn’t yet cleared enough of the pancreas fat. Taylor doesn’t say. Alternatively maybe their beta cells are burnt out. Either would be consistent with the observation that T2 diabetics treated via the medication-only route require more and more medication and eventually more and more insulin. By that point you are effectively both T1 and T2. The key question is can longterm diabetes be reversed? Jason’s success in reducing or eliminating his patients’ medications suggests that at least partial reversal is possible. Taylor’s study was done on short-term T2s, the next step is to repeat the study with longterm T2s. My take from all this is that the sooner you get rid of that liver and pancreas fat the better and fasting is the way to do it.

      The fact is that Bernstein, Fung and Taylor are not really in conflict. Bernstein’s primary focus is on T1s since he is one himself. He was one of the first to advocate a low carb diet for diabetics. Jason and Taylor both do likewise. A low carb diet as advocated by Bernstein, Michael Eades, Jay Wortman and others will also reverse fatty liver and diabetes. Taylor’s 800 calorie diet will do it faster and Jason’s 3 week water-only fast does it faster still. The differences are of degree, not absolute. Jason’s results show that his fasting protocols work, Taylor’s research shows WHY they work.

      • The other thing Stuart, in a recent clinical trial he had, as I recall, a person with T2D diagnosis of 30 yrs and it was reversed. The longer the duration the less likely a complete reversal but I don’t believe he’s hit a 0% yet.

      • One last thing. This is by no means an indictment. Jason Fung does an outstanding job of aggregating study data and synthesizing meta data from them. Dr Taylor Dr Hall, maybe Dr Bernstein, do original research. I don’t recall Taylor advocating low carb, well certainly not VLC (keto). His test subjects used Optifast which in the states is equivalent to SlimFast…lots of sugar, so lots of carbs. Dr Mosley, as you mentioned in 8 week blood sugar diet, used Mediterranean diet. Not sure if that’s naturally low carb but in his 5-2 fast I don’t believe that was carb level specific, only that the 2 ‘fast’ days were 25% of the calorie count of the other 5.

  17. There is always trickery going on when relative risk numbers are used. So someone for instance may have twice the risk of going blind than a so called normal person. Normal people rarely go blind though so this might sound scary but the absolute risk would be rather meaningless.

    So we do this with microvascular risk and avoid looking at macrovascular risk, and things like heart attacks and strokes are much more common, so a double risk for this stuff is something that really bears paying attention to.

    Most diabetics die of cardiovascular disease, and at a significantly higher rate per patient years than non diabetics, but the problem is that if we made too much of this then this is going to expose the fact that increasing insulin rather than decreasing it increases this risk markedly. Nothing to see here folks, let’s just keep our eyes on the donkey’s ass, the high blood sugar, and as long as we pretend this is the only thing that matters, don’t worry that we’re fattening you up like a pig, obesity is nothing, hyperlipidemia is nothing, hypertension is nothing, forget that we tell other people to worry about this, it really is all about the blood sugar with you.

  18. It’s actually just as bad with CVD management, they don’t tell you things like cut down on carbs to reduce your insulin levels, even though insulin levels are by far the highest risk factor for CVD when you consider that it just doesn’t damage blood vessels directly, it also causes all of the things that we worry about as far as risk factors for this, the obesity, the hyperlipidemia, the high blood pressure, and the other markers of metabolic syndrome.

    As it turns out, the worst thing about this is the lipotoxicity that excess insulin causes, this is what leads to the insulin resistance by damaging our cells, primarily by increasing ceramide. This is the stuff that does us in with diabetes and all other metabolic diseases.

    So what do they do? They give you the wrong diet and a bunch of meds that don’t help and make you worse. Sound familiar? There’s a lot of money made though and this is what it is all about, if you own shares in these companies you should be pretty happy as you can build a lot of wealth although if you listen to their advice you may not live long enough to enjoy it.

    I love Dr. Fung’s posts and this is one of the better ones on diabetes anywhere, as are a lot of his posts. I talk to people who think Dr. Fung is a true pioneer but I will tell you that all this stuff has been out there for years, it’s just that not many of us bother to look.

    We owe a lot of our understanding of metabolic disease to Dr. Roger Unger actually, whose groundbreaking experiments got to the root cause of diabetes, and by extension, other diseases caused by high insulin. Conventional medicine hates this stuff though, they hate any science that isn’t cooked up and distorted to help them sell toxic meds and steer people away from effective treatments, and that’s all they got really.

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