Glucotoxicity and Double Diabetes- T2D 36

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The glucotoxicity paradigm

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.

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.

 

 

2017-10-12T21:31:26+00:00 43 Comments

About the Author:

Dr. Fung is a Toronto based kidney specialist, having graduated from the University of Toronto and finishing his medical specialty at the University of California, Los Angeles in 2001. He is the author of the bestsellers ‘The Obesity Code’ and ‘The Complete Guide to Fasting’. He has pioneered the use of therapeutic fasting for weight loss and type 2 diabetes reversal in his IDM clinic.

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43 Comments on "Glucotoxicity and Double Diabetes- T2D 36"

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sten bjorsell
Guest
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… Read more »
Pete
Guest
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… Read more »
Jerome Kahn
Guest

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

Mari
Guest
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… Read more »
Tumblemark
Guest

@Mari Carbohydrates are not the only way to stimulate insulin release. Lysine can raise insulin even more than glucose. BCAAs and whey protein also boost insulin. There’s no reason to eat carbohydrates, and raising insulin certainly isn’t one. And there are plenty of references for this effect on PubMed. “I encourage you to find a good dietitian…”

RIchard Fish
Guest

Great information Dr. Fung! Thank you.

Joe
Guest
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… Read more »
Harry Kanis
Guest
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… Read more »
Aaron
Guest
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… Read more »
Luqman
Guest

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

Harry Kanis
Guest

Yes you may.

BobM
Guest
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… Read more »
Kimberly
Guest

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?

Aaron
Guest

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
Guest
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… Read more »
Robb
Guest

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.

Jerome Kahn
Guest
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… Read more »
sten bjorsell
Guest
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… Read more »
Victoria V.
Guest

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.

Sascha Heid
Guest

OMG a Captain Picard meme, i love you.

Abdulaziz A. Alnawfal
Guest
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.. ❤️

BernardP
Guest

“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
Guest

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
Guest

Thanks.

BobM
Guest
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… Read more »
BernardP
Guest

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.

Stuart
Guest
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… Read more »
Walt
Guest
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… Read more »
Stuart
Guest
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… Read more »
Walt
Guest
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… Read more »
Vbha
Guest

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?

LAAF
Guest
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… Read more »
Miriam Kearney
Guest
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… Read more »
Hnak
Guest
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… Read more »
Miriam Kearney
Guest

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?

Stuart
Guest

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.

Richard
Guest
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… Read more »
Stuart
Guest
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… Read more »
Walt
Guest

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.

Walt
Guest
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… Read more »
Ken Stephens
Guest
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… Read more »
Ken Stephens
Guest
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… Read more »
Rambabu Chippalapally
Guest
Rambabu Chippalapally

Sir you explanation is really excellent.
my question is if diabetic patients reversed his diabetes by changing food habits by eating hflc can he become a diabetic again??

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