Sunday, September 18, 2016

Type 2 Diabetes, a Dietary Disease #347: Lowering glucose in T2D is largely useless, unless…

If my last post (#346 here) left you, dear reader, in a quandary, that was not my purpose. Nor do I think it was Dr. Jason Fung’s intention. The title of his blog post, “Futility of Blood Sugar Lowering in T2D,” was an accurate reflection of this premise: lowering blood glucose by using medications that cause weight gain (such as insulin and sulfonylureas), is demonstrably harmful to the patient. So, lowering blood glucose by that method, as is still the standard of practice, is worse than useless; it is malpractice. There, I said it (if he didn’t).
To see that conclusively, you have only to read #346, or Dr. Fung’s blog, or acquaint yourself with the cardiovascular outcomes of the UKPDS and ACCORD studies. On the other hand, Metformin does suppress unwanted hepatic (liver) glucose production and improve insulin sensitivity/glucose uptake, and thus lower blood glucose, without weight gain. Dr. Fung concludes his blog, however, with the lamentation: “Yet, here we sit in 2016, with no better idea of how to treat type 2 diabetes than to lower blood sugars.” However, his implication goes further.
Dr. Fung’s point was that lowering blood glucose alone, as practiced today by most clinicians, though well-intentioned, has negative consequences and is insufficient; it must instead be in conjunction with lowering blood insulin levels. “It only makes sense to reduce BOTH glucotoxicity and insulin toxicity,” he says here in an earlier blog post. “Drugs such as SGLT2 Inhibitors do this, but diet is obviously the best way. Low Carb diets. Intermittent Fasting.” For the mechanism of action, see here or read Dr. Fung’s book, “The Obesity Code.”
Why is an elevated blood insulin (from the ingestion of carbs) considered “toxic”? Because it is the impetus for a constellation of metabolic disorders, starting with Insulin Resistance, that have come to be known as Metabolic Syndrome. They have all been precipitated by the changed dietary practices of the last century, during which we have seen the introduction and proliferation of highly processed carbohydrate “foods” and vegetable oils.
These two developments have been abetted by an officialdom who, in a misguided effort to protect our arteries from foods containing saturated fat and cholesterol, has encouraged us, since 1977, to avoid them and instead eat more highly processed carbs and vegetable oils. The Dietary Guidelines for Americans were first published in 1980 and have changed little since. Recently they dropped the limitation on total fats, and are struggling with the guideline on dietary cholesterol, but they have doubled down on replacing saturated fat with vegetable oils. And the Nutrition Facts panel on processed foods is still based on 60% carbohydrate, 30% fat and 10% protein.
The effect of these guidelines has been an accelerated introduction of manufactured food products to conform to them and a mass movement in the culture to adopt them. The outcome, as we develop the markers of metabolic disease – obesity, hypertension, type 2 diabetes, hypercholesterolemia, dyslipidemia, and NAFLD – is a growing body of evidence that this nationwide dietary experiment has, tragically, gone awry (see chart).
All of these chronic metabolic disorders are related, and all of them can be traced back to a chronic elevated blood insulin, i.e. Insulin Resistance (IR). They are caused by what we eat. Carbohydrates start the process by signaling the pancreas to secrete insulin. Insulin is required to transport the glucose (digested carbs) and to open the door to the cells that take up the glucose for energy. While more and more insulin is circulating, trying to “open the door,” it signals our other source of energy, stored body fat, that they are not needed. They are in fact blocked from use. So, while the glucose and insulin circulate, we do not burn body fat for energy. And any glucose from overeating that is not needed for immediate energy is converted by the liver to more body fat.
An elevated insulin starts it: insulin resistance, obesity, hypertension, type 2 diabetes, hypercholesterolemia, ED and NAFLD all follow. So, as Jason Fung says, “It only makes sense to reduce BOTH glucotoxicity and insulin toxicity,” and “diet is obviously the best way” to do it. “Low Carb diets. Intermittent Fasting.”

Type 2 Diabetes, a Dietary Disease #346: “Glucose lowering in T2D is largely useless”

Okay, I’m a big fan – a devotee you might say – of Jason Fung, MD, a Canadian nephrologist, blogger, and author. His very good book, “The Obesity Code” (2016), appears to be targeted to medical professionals but is equally comprehensible to the lay reader. He is also a frequent blogger, and his recent, “Futility of Blood Sugar Lowering in T2D,” like a previous one, “Obesity is Protective,” is getting attention. It certainly got mine (#341).
All reasonably well-informed students of diabetes – including clinicians who treat diabetics, endocrinologists, diabetologists, as well as Certified Diabetes Educators (CDEs) and Registered Dieticians (RDs), are familiar with the large, long-term UK studies, the DCCT and the UKPDS, and the US follow-up, the ACCORD study. What Fung did in his recent blog post was succinctly summarize the findings of those studies and posit, in conclusion, “…that blood glucose lowering in type 2 diabetes is largely useless.” That’s a pretty stunning conclusion.
His logic, however, is impeccable. “The DCCT study…had already established the paradigm of tight blood sugar control in Type 1, but whether this held true for Type 2 remained to be seen,” he said. In UKPDS33, he went on, a large cohort of “newly diagnosed T2D patients who failed a 3 month lifestyle therapy trial were enrolled into an intensive group of sulfonylureas or insulin vs. conventional control.”
“The drugs certainly were successful in lowering blood sugars” [to 7.0% vs. 7.9% in the diet group], he said, “but there was a price too. Weight gain was far worse on the drug group….” But over the 10 years of the study, they found no “benefits for the end points that everybody was interested in – cardiovascular disease. Despite reducing blood sugars, CV disease showed no benefits,” he averred. “Since the majority of deaths are due to CV disease, the primary goal of therapy was reduction in deaths and CV disease, not microvascular disease.”
In a sub-study called UKPDS34, overweight patients with T2D were randomized to either metformin or diet control alone. “Once again, over the space of over 10 years, the average blood sugar was lowered by metformin to 7.4% compared to an average A1c of 8% in the conventional group,” he said, but, “In contrast to the previous study, intensive control with metformin showed a substantial improvement in clinically important outcomes – there was a 36% decrease in death (all cause mortality) as well as a 39% decrease in risk of heart attack.”
“Metformin performed far better than the insulin/SU group despite the fact that average blood sugar control was worse,” Dr. Fung concluded (emphasis his). “What’s the major difference between the two medication groups,” he asked? “Insulin! Insulin and sulfonylureas (SU) increase insulin levels. Metformin does not.”
Refrain, all together now: “Because it does not raise insulin, and insulin drives obesity, metformin does not cause weight gain.
Troubled by the failure of the original UHPDS study to show a benefit from reducing high blood sugar in Type 2s, the U.S. National Institutes of Health (NIH) undertook “an ambitious large trial called the ACCORD study (Action to Control Cardiac Risk in Diabetes).” Two groups with an average A1c of 7.5% were randomly assigned, the 1st to “standard therapy,” the 2nd to “intensive drug therapy,” “…with the goal of seeing whether this intervention would reduce disease.” They were successful in lowering their A1c to 6.5%.
But that was not the primary end point. They “wanted to know whether this made any difference. It sure did,” Dr. Fung says. “When the trial results broke, there was a media firestorm. Why? Because the intensive treatment was killing people! The risk of death increased by a horrifying 21% in the intensively treated group,” he wrote. Then, with 17 months before the scheduled end of the trial, “the safety committee looked at the available data and forced the premature end of the [ACCORD] trial.”
Was the study design flawed because there was no specification of which medications to use to intensify treatment, and the drug Avandia, which was very popular at the time, was included? I took Avandia briefly before I began to eat VLC. Avandia now carries a black label warning that it may cause heart attacks, angina, and heart failure. “Yet, here we sit in 2016, with no better idea of how to treat type 2 diabetes than to lower blood sugars,” Dr. Fung concludes.
(Read Part 2 next week to see what Dr. Fung suggests be done about it.)

Sunday, September 11, 2016

Type 2 Diabetes, a Dietary Disease #345: How Diabetic Do You Want to Be? (Part 2)

That sounds like a stupid question, I know. Nobody wants to be diabetic. But once you’ve been diagnosed as Pre-Diabetic or Type 2, you have, for life, for better or worse, to one degree or another, a condition called Insulin Resistance (IR)). For all intents and purposes, that means you are to some degree Carbohydrate Intolerant. You got this way by 1) having a genetic predisposition and 2) eating a diet too high in carbohydrates for too long.
Don’t blame yourself entirely. By 1961 the AMA had come out against saturated fat and dietary cholesterol and in 1977, the Senate Select (McGovern) Committee issued their Dietary Goals of the United States, recommending we all eat a low-fat, high-carbohydrate diet. Both the medical and public health establishments were tragically misguided in these recommendations, and they were soon ably abetted by Agribusiness and Big Pharma.
So, if you’ve been diagnosed either Pre-Diabetic or Diabetic (Type 2), as I ask rhetorically in #344, using the hemoglobin A1c, today’s marker for blood sugar control, “How Diabetic Do You Want to Be?”
Is an A1c of <7.0% (or <8.0% if you are elderly) the target that you and your doctor are comfortable with?
Or, is <6.5% your target, to avoid being officially diagnosed a type 2 (by current medical standards)?
Or, is <5.7% your target, so you can comfort yourself with the phrase, “consistent with the absence of diabetes”?
Or, is an A1c in the “low 5s” your target? It has been for me for half of the 30 years that I have been a diagnosed Type 2. My doctor isn’t worried, though. He, like most and the ADA, considers under 7.0% “well controlled.”
Or, is an A1c ≤5.0% your target? I know several long-term type 2s who manage their disease this way; this is the true “optimal” or normal A1c. They do this with a combination of a strict Low Carb diet and insulin injections.
So, to be an informed consumer/patient, you need to be armed with some facts. The following is filched from one of, if not the best, on-line sites for Pre-diabetics, Type 2s and Type 1s: Jenny Ruhl’s “Blood Sugar 101.”
Risk Quantified For Non-Diabetic A1cs and Heart Attack Risk
The Atherosclerosis Risk in Communities study tracked 11,092 black or white adults who did not have a history of diabetes or cardiovascular disease for 15 years. It found no association between fasting blood sugar and risk of heart disease, but A1c was a different story. The table below summarizes the correlation of baseline A1c with the risk of developing cardiovascular disease. [CVD]
Multivariate-Adjusted Hazard Ratio [with my translation, for the statistically challenged].
5%:                    0.96 (0.74-1.24) [If you have an A1c of 5.0%, your chance of developing CVD is just                           below “even.”
5% to < 5.5%:  1.00 (reference) [In this range, your CVD risk is THE SAME AS ANYONE ELSE!]
5.5% to < 6%:  1.23 (1.07-1.41) [In this range, you are almost 25% more likely than if your A1c is                               5% to <5.5%.]
6% to < 6.5%:  1.78 (1.48-2.15) [In this range you are more than 75% more likely (range almost 1½                           to >2 times)].
≥6.5%:              1.95 (1.53-2.48) [If your A1c is ≥6.5%, you are almost twice as likely to develop                                   cardiovascular disease, and the range of risk is from more than 1½ times to almost                               2½ times.
Glycated Hemoglobin, Diabetes, and Cardiovascular Risk in Nondiabetic Adults. Elizabeth Selvin et al.NEJM Volume 362:800-811. March 4, 2010 Number 9.
Keep in mind that because these subjects were probably diagnosed as "non-diabetic" using a fasting glucose test many of those with the higher A1cs probably were diabetic at the study outset based on post-meal values. If you are recently diagnosed with diabetes and have no signs of heart disease, your risk/A1c ratio should be similar if not identical to those shown here.”
So remember, if your doctor is like mine (or any MD, DO, RD or CDE who follows the ADA Standard of Care), (s)he is going to consider anything under 7.0% (or maybe 6.5%) to be “good control,” or worse, “optimal,” so you are pretty much on your own if you choose to strive to attain an A1c lower than 6.5%, or <6.0% or even <5.5%.

Sunday, September 4, 2016

Type 2 Diabetes, a Dietary Disease #344: How Diabetic Do You Want to Be? (Part 1)

Setting aside for a moment the definition of “Diabetic” and “Pre-Diabetic” (It’s a can of worms.), each person who has been diagnosed with a degree of Insulin Resistance (IR) has to decide, with their doctor in most cases, the method and degree of “countermeasures” that they think is prudent to avert “the dreaded complications.”
The complications are an increased likelihood of the familiar microvascular complications: retinopathy, (leading to blindness), peripheral neuropathy (ending in amputations) and nephropathy (ultimately, end stage kidney disease with dialysis), not to mention Erectile Dysfunction (ED). They also include macrovascular complications like heart attack and stroke…and a significantly greater chance of dementia, including Alzheimer’s Disease (AD). And overall, a reduction in life expectancy of up to 10 years.
 The American Diabetes Association describes Type 2 Diabetes as a “progressive” disease. To delay (not avert) the progression, most physicians employ the “usual care” Standard of Practice and advise diet (to lose weight) and exercise (175 minutes a week). Weight gain is associated with Prediabetes and Type 2 Diabetes and falsely viewed by most doctors as a “cause” of Type 2. In truth, Type 2 diabetes is caused by Insulin Resistance , and Insulin Resistance causes weight gain. IR comes first. Weight loss, unless the diet is Low Carb and eating Low Carb becomes a “lifestyle change,” will not be permanent. And, knowing that “diet and exercise” will fail, within 3 months of a Type 2 (or Pre-Diabetes) diagnosis, most doctors will prescribe drugs, starting with Metformin.
Depending on the patient’s age and other health conditions, the doctor will have in mind a marker of glucose control. Today, the A1c blood test has become the new marker. It measures the percentage of glucose on the surface of your red blood cells. These cells have an average life of 2-3 months, so it’s considered the average level of glucose in your blood, 24/7, over that period. It’s a nifty surrogate, and inexpensive.
Here’s where it starts to get sticky. The Quest Laboratory test reports say, “According to ADA guidelines, a hemoglobin A1c <7.0% represents optimal [emphasis added by me] control in non-pregnant diabetic patients.” It goes on to say, “Different metrics may apply to specific patient populations.” This is meant to imply that as you get older (say, 75 or 80 years old), the ADA counsels your doctor to consider an A1c of <8% to be “optimal”!
Important note: the ADA considers a <7.0% A1c “optimal” for a patient already diagnosed as a full-blown Type 2. For the not-as yet-diagnosed Type 2, the Quest report gives the ADA guidelines for screening for diabetes:
<5.7%              Consistent with the absence of diabetes
5.7-6.4%          Consistent with increased risk of diabetes (Pre-Diabetes)
≥6.5%              Consistent with diabetes
The 6.5% level is the level adopted by the medical establishment’s metabolic specialists, the American College of Endocrinologists. Note how 6.5% is well below the level that the ADA considers “optimal” (<7.0 or <8.0%). What does that tell you about how confident your doctor and the medical/pharmaceutical establishment are of their (and your) ability to effectively control your blood sugar to treat your disease? That’s why, acknowledging the likelihood of failure both in achieving permanent weight loss and blood sugar control, Type 2 is considered “progressive.” You will, over time, if you follow their dietary advice, need to take progressively more medication.
So, is an A1c of <7.0% (or <8.0% if you are elderly) the target that you and your doctor have “negotiated”?
Or, is <6.5% your target, to avoid being officially diagnosed a type 2 (by current “official” medical standards)?
Or, is <5.7% your target, so you can comfort yourself with the phrase, “consistent with the absence of diabetes”?
Or, is an A1c in the “low 5s” your target? It has been for me for half of the 30 years since I was diagnosed a Type 2 Diabetic . My doctor is much more relaxed, though. He, like most, considers the ADA’s <7.0% “well controlled.”
Or, is an A1c under 5.0% your target? I know many long-term Type 2s who manage their disease this way, to their advantage, as you’ll see. Most of them do this with a combination of a strict Low Carb diet and insulin injections.
So, just how diabetic do you want to be? Next week, I will explore, by multivariate-adjusted hazard ratio (HR), the cardiovascular (CVD) risk of the choice you will make. It’s not complicated, as you’ll see.

Sunday, August 28, 2016

Type 2 Diabetes, a Dietary Disease #343: My “No-Cheat” Week

My doctor’s appointment was coming up soon, so I decided to do a “no-cheat” week. As doctors know, patients try to be on their best behavior before these periodic events (while “cheating” the rest of the time). That’s got to be one of the reasons that the medical establishment transitioned a few years ago from the Fasting Blood Sugar to the A1c as a diagnostic tool for Pre-diabetes and Type 2 Diabetes. The principal reason, however, was that A1c also incorporates post-prandial blood sugars and measures blood sugar 24/7 over roughly 3 months.
 I decided to “go straight,” for a week anyway, because my average Fasting Blood Sugar for the three previous weeks had been 104, 107 and 106mg/dl, respectively. Now, as your doctor will no doubt tell you, these averages are relatively low on the Pre-diabetes scale (100-125mg/dl). Your doctor will probably tell you they will continue to monitor your blood sugar periodically, but they’ll not be very concerned for you. They should be, though; just read the 1st sentence of this page from Jenny Ruhl’s updated “Blood Sugar 101.”
Also driving my “no-cheat” motivation was the change in my Metformin prescription. Six months ago I had requested that my prescription for Metformin be increased from 500mg daily to 1,500mg daily. I had been on 500mg since 2002, when I started to eat Very Low Carb. Before that I had been on a maximum dose of Metformin (2000mg) plus a maximum dose (20mg) of Glyburide, a Sulfonylurea, and I had just started on Avandia, a drug later associated with increased heart attacks. I had to stop taking these other 2 anti-diabetes oral meds completely to avoid hypos (dangerously low blood sugars), but have continued for the last 14 years on the quarter-dose Metformin.
I asked to have my Metformin increased because I had just attended a conference on metabolic therapeutics at which many normoglycemic attendees were eating low carb and taking maximum doses of Metformin to induce ketosis and fat-burning. It did this by suppressing hepatic (liver) gluconeogenesis and improving cellular glucose uptake, thus lowering serum insulin. With both low blood sugar and low blood insulin, fat burning is activated.
So, seeing no harm or stigma from increasing Metformin, and to get the unrealized benefits, I wanted to try taking more Metformin. Wow! Was I surprised with the result! My blood sugar control, as measured by fasting blood glucose, improved overnight and very dramatically. All of a sudden, my fasting blood sugars were all in the 70s and 80s, with two concurrent weekly averages of 79mg/dl. As I said in #329 and #330), THIS WAS VERY LIBERATING. My editor suggested I do a follow-up column in a few months. She didn’t say why, but I agreed.
Two reasons for the follow-up, though, came to mind immediately: 1) the body will adjust to the meds and the effect, over time, will wear off; 2) the “liberating” effect will result in my becoming less stringent in following my Very Low Carb Way of Eating. I would become a “libertine,” taking advantage of the benefit accorded me by the higher level of medication to eat more carbs. In other words, to cheat more often! So, this is the reason that I have decided to have a no-cheat week now, coincident with my upcoming doctor’s appointment next week.
Result: My fasting blood sugar the day before I started the no-cheat week was 111 (weekly average 106, range 100 to 119). The next 7 days were: 93, 82, 88, 79, 85, 83, 100; Weekly average: 87mg/dl. (The last 2 readings were mornings after restaurant dinners, the last with a few cheats) So, did the metformin effect wear off over time? Perhaps, a little. Did the higher dose have a liberating effect? Definitely! I cheated a little every day, and my weekly averages rose to 104, 107 and 106mg/dl. When I didn’t cheat, my FBGs were mostly in the healthy 80s, considered normal for young, non-insulin resistant people. It is definitely the best place to be for both my diabetic and general health.
The choice is mine, of course. How much risk to my general and diabetic health should I take? Do I want to live on the edge? Or do I want to continue to reap the benefits of a low blood sugar? And if I only eat when hungry, and remain at all other times in a mild state of ketosis, will I lose weight (which I still need to do)? Can I do it? The answer is TBD (to be determined). If I stick to the maxim espoused in #342, “Is Cheating Okay?” I think I can. I must simply ask myself, “Am I hungry?” If the answer is “no,” that is almost always sufficient to not eat.

Sunday, August 21, 2016

Type 2 Diabetes, a Dietary Disease #342: Is “cheating” okay?

Hey, nobody’s perfect…and I suppose we all “cheat,” but is it alright to say it is okay to cheat? I think not. Is it to be expected? I think so. But then, if we do it, why is it then not alright to say it is okay? The answer is simple: it is wrong. Okay, that is a moral judgment but, are we humans not moral beings? Do we not make moral judgments? Is there not a right and wrong in this world? Do we have to see everything through a lens of moral relativism? I say the answer is “no.” It’s not okay, but it is to be expected. No one is perfect.
To be clear, “cheating” means that someone is being unjustly deprived of something that is rightfully theirs. That someone, in this case, is not someone else; it is you. You are cheating yourself!
You are rightfully deserving of good health. You were probably born with it and, if you are reading this column, you managed somehow to lose it. You lost it to the degree to which you have become 1) pre-diabetic, by your doctor’s observation of your fasting blood sugars or A1c’s, or 2), later in the progression of this metabolic disorder, you became a diagnosed Type 2. Or you could be a little overweight (and insulin resistant).
So, I don’t consciously give myself permission to cheat. That would be too permissive. It would lend it an aura of acceptance – that it was in some way permissible; that is was an acceptable practice that somehow wormed its way into my daily or weekly routine and had a legitimate role in my lifestyle. That’s not what I want it to be. How, then, can I control my Way of Eating (WOE) to address the inevitable “cheat”? These are my prerequisites:
1.      We all say, “Our health is the most important thing,” but is it just an empty axiom? Not if you know that by close adherence to a low carb WOE over the years you have seen mega improvements in your health. And not if you know that to eat otherwise would put all that at risk. I put the thought of my health first.
2.      I try to stay is a state of mild ketosis most of the time. This will keep 1) my blood sugars both low and stable and 2) my blood insulin level low, disabling both hunger and fat storage and enabling fat burning.
3.      In this state, with hunger virtually never present (really), cravings (from low blood sugars) are non-existent. So, eating becomes optional. If you’re not hungry, this legitimate reason to eat is off the table. There are, however, lots of triggers for eating besides hunger. And if you’re not hungry, you have to decide how to respond to each of them. Each opportunity to eat is an opportunity to cheat. Here’s how I deal with it:
I simply ask myself, “Am I hungry?” The answer, of course, is “no,” and that is almost always sufficient.
If I’m not hungry, and I do not avail myself of the opportunity to eat for that reason, I have succeeded. Contrast that with the compelling urge or craving you feel when you eat the standard American carb-loaded meal that shuts down fat burning. You feel hungry afterwards. The absence of hunger when your body is in a state of mild ketosis is not a self delusion. It’s a fact. It’s not about will power. My body is satisfied and is not calling on me to eat because it is eating; it is feeding on my body fat. That breakdown of body fat, so long as I am in mild ketosis, is the normal state of man. Ketosis is the way our biology was adapted to feeding ourselves for millennia prior to the Neolithic era only 500 generations (10,000 years) ago. This natural state of ketosis gave us the strength to hunt and gather. It is a healthy state. It is a high-powered, full-energy state, emblematic of an active metabolism.
So long as I remain in a state of mild ketosis (remember: without hunger), if I eat it is for another reason, and there are many: a) the sight or smell or food, b) the thought of food, c) rationalizations (open bags or boxes in the pantry), d) social pressures (when as a dinner guest, food is offered), e) unsolicited food (bread at the restaurant table, hors d’hoeuvres at a party), e) thoughts of deprivation (everyone else is eating dessert at the pot luck), and habit, such as eating two or three meals a day. To all these things I have – in fact, I need, only one response:
I simply ask myself, “Am I hungry?” The answer, of course, is “no,” and that is almost always sufficient.

Sunday, August 14, 2016

Type 2 Diabetes, a Dietary Disease #341: “Obesity is Protective,” says Jason Fung, MD

“Obesity is not widely considered a protective mechanism,” Jason Fung begins his recent blog post. “Quite the opposite,” he says. “It’s usually considered one of the causal factors of the metabolic syndrome and insulin resistance.” In this, I had to agree. It is lamentable that most physicians think this way, in large part because that is what government sponsored research is predicated upon, and the standards of practice of the various medical disciplines teach, and the medical associations preach. Who can blame the clinician for believing it?
Jason Fung, however, is a thinker (and a Canadian nephrologist), and he is free of those constraints – like Tim Noakes, MD (who is South African), and Jay Wortman, MD, and Vilhjalmur Stefansson (both also Canadians), and Gerald Reaven and Robert Atkins, both U.S. MDs cast out by their profession, and Gary Taubes, who started it all for many of us. The list of heretics is quite long – and growing daily – but Jason Fung deserves singling out. He is a trailblazer. Like Gary Taubes’s magnum opus, “Good Calories, Bad Calories” (2007), his target audience is medical professionals. But unlike Taubes’s book, Fung’s “The Obesity Code” (2016), is “accessible.”
“I think obesity is a marker of disease,” Dr. Fung continues, “but ultimately it serves to protect the body from the effects of hyperinsulinemia. Let me explain.” Fung then references this recent New York Times article by Gina Kolata, which I read when it was published. As a description of a rare case of a genetic disorder called lipodystrophy (a lack of fat cells), I thought it was interesting. Fung, however, calls this case “very interesting” and goes on to explain how it relates in a causal way to metabolic syndrome and insulin resistance. It’s a fascinating hypothesis. In an earlier blog post he calls it the new paradigm of insulin resistance.
“We need to understand the new paradigm of insulin resistance to understand how insulin resistance, obesity, fatty liver, and fatty pancreas are actually all the different forms of protection our body uses. But what is the underlying disease? Hyperinsulinemia,” Dr. Fung says.
Fung then elaborates further upon the physiological mechanisms of action that the body uses to protect itself from these manifestations. His writing style is easy to follow – just ignore the charts and figures and follow the prose. You’ll get it, I promise. And, if you seek this knowledge and understanding, it’s a worthwhile read.
However, if you want to cut to the chase – the so-called bottom line – these excerpts will spell it all out for you:
“There are many possible causes of too-much-insulin, but one of the major ones is excessive dietary intake of refined carbohydrates and particularly sugar.
“Insulin has several roles. One is to allow glucose into cells. Another is to stop glucose production and fat burning in the liver (gluconeogenesis). After this stops, then it stores glycogen in the liver and turns excessive carbohydrates and protein into fat via de novo lipogenesis. Insulin is basically a hormone to signal the body to store some of the incoming food energy, either as glycogen or fat.”
“There are two main problems with metabolic syndrome: Glucotoxicity and insulin toxicity. It does no good to trade the increased insulin toxicity to reduce glucotoxicity. That’s what we do when we treat people with insulin or sulfonylureas. Instead, it only makes sense to reduce BOTH glucotoxicity and insulin toxicity. Drugs such as SGLT2 Inhibitors do this, but diet is obviously the best way. Low Carb diets. Intermittent Fasting.
In the end, obesity, fatty liver, and type 2 diabetes and all the manifestations of the metabolic syndrome are caused by the same underlying problem. NOT insulin resistance. The problem is hyperinsulinemia. It’s the insulin, stupid.
“The power of framing the problem in this way is that it unveils the solution immediately. The problem is too much insulin and too much glucose. The solution is to lower insulin and lower glucose. How? Nothing simpler. Low Carb, High Fat diets. Intermittent Fasting.
I think Jason Fung has really nailed it. I wonder how long it will be before he is tarred and feathered and held in infamy by his chosen profession. As Richard Feinman says in “The World Turned Upside Down” (2016), being heretical is the price to be paid for being right. Or, has the profession begun to turn the corner…and seen the light? Naaaw…..