Retrospective #349: Yoga for Diabetes

I woke up the other day, with the TV still on, during the last minute of a “Yoga for Diabetes” TV program, so I missed it. Dang! Fascinated by the idea, though, I decide to Google it. I found a gazillion sites, with videos. Whoda thunk it?

No offense (intended), folks, but this idea made me laugh. It reminded me of the time in the 1970s when, after 5 years of working on a high-profile project with one of the best solar architects in the country, I opened my own architectural practice specializing in active and passive solar energy design. Unfortunately for me, without the benefit of experience, so did everyone else in my practice area. Everyone wants to be on the “diabetes solution” bandwagon, without regard to whether they are qualified.

Yoga is no doubt a useful activity for meditation, stress reduction, and even stretching. I hesitate to call it exercise, but if you are old or unfit, it may be good fitness training for you. I’m not knocking it, but to suggest that yoga has real benefit for “treating” or even “curing” Type 2 Diabetes as many of the TV sites do, well, give me a break! Type 2 Diabetes is a Dietary Disease, and the only effective treatment is a low carb or very low carb diet.

But if that isn’t enough for you, you could add Metformin. Metformin will slightly increase your Insulin Sensitivity (i.e., reduce your Insulin Resistance), and it will suppress unwanted glucose production in the liver. But a low carb diet alone, with fasting, will result in a reduction in A1c (as well as weight loss) such that, for many people diagnosed with Pre-Diabetes or even long-term Type 2 (like me), your disease will go into remission.

You will not be cured (you will always be Carbohydrate Intolerant), but nobody will know it – not even your doctor – if you don’t tell him or her. That’s because a doctor is trained to treat symptoms, and you won’t have any symptoms detectable by any lab test (s)he will likely administer. So, from your DOCTOR’s perspective, you will be “cured.” If there is nothing for him or her to treat (because you are treating yourself with a low carb diet and intermittent fasting), what other conclusion could he or she reach?

It’s that simple folks. Don’t waste your time looking for a miracle cure, or trying to re-invent the wheel. And don’t think you can cheat Mother Nature. Your body is a very complex biological organism and is much smarter than even you! You can’t fool it. And even though you might talk yourself into thinking it will only cost you a little to cheat, kachung, the “cheat” will register in your blood glucose. Every carb will wind up “under the curve” and have to be absorbed eventually. If not burned for energy, your liver will use these extra carbs to make fat, via a process called de novo lipogenesis, another good reason to take Metformin. Didja know that?

In basic science, the funding continues to flow from government sources (NIH, etc), for an understanding of what causes Insulin Resistance (IR), Type 2’s underlying metabolic dysfunction. It is the first in a galaxy of related metabolic disorders (Metabolic Syndrome) and the one that appears to cause, first, Impaired Glucose Tolerance (IGT), and then Impaired Fasting Glucose (IFG), the two blood measurements that characterize incipient diabetes.

They are reflected, respectively, in the blood tests used by clinicians to diagnose Type 2: Fasting Blood Glucose (FBG) originally, and today the hemoglobin A1c test. The latter is a better test because, like Impaired Glucose Tolerance, it incorporates postprandial (after meal) excursions and thus catches the rise and fall of your blood sugar after eating. Another test, the Oral Glucose Tolerance Test (OGTT), usually administered over 2 hours in an outpatient hospital setting, is the gold standard, but it’s more expensive.

In applied science (pharmacology) the search continues for a miracle drug – to treat the SYMPTOM: an elevated blood sugar. What did you expect? That’s how Big Pharma got to be big. It’s their raison d’être. And that’s because they can’t patent the cure for the CAUSE; because Insulin Resistnce is caused by CARBOHYDRATE INTOLERANCE!

But YOU can treat the cause. YOU CAN EAT LOW CARB. It will put your Type 2 Diabetes into full REMISSION, and you’ll lose a lot of weight to boot.

Retrospective #348: Nervous Eating

In Retrospective #342, I asked, “Is cheating okay?” I answered (to myself) “no,” with an explanation. I stipulated:

“So long as I remain in a state of mild ketosis (remember: that’s 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 (an open bag or box in the pantry), d) social pressures (when 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 reply: I ask myself, “Am I hungry?” The answer, of course, is “no,” and that is almost always sufficient.”

It occurred to me afterwards, however, that the most common “other” occasion for my non-hunger driven eating is “nervous eating”: eating (alone mostly) and for no good reason! How could I have overlooked this!

Since writing #345, I have managed somehow to stick (mostly) to plan. It has gotten easier and easier, because so long as I eat mostly foods that are protein and fat, I’m never hungry. Day after day, week after week!

In the morning I have cream in my coffee. That’s it. Enough to take pleasure from it, and swallow a few pills.

For lunch, I have a small meal, a snack really. Just a can or small tin of kippered herring in brine, or 2 hard boiled eggs with some homemade mayo. Sometimes, I eat a can of sardines in EVOO. Why do I eat lunch? (I’m still not hungry, and therefore I’m breaking Retrospective #319, Rule #2, “Eat only when hungry”). My rationale? Habit? Boredom? A break from morning activity? Who knows… but I rationalize that it’s a small meal, and it’s all protein and fat.

Then, for supper, my wife prepares a small plate of protein/fat and a low-carb vegetable. Last night it was two small New Zealand grass-fed lamb chops and cauliflower pureed with full-fat cream cheese and pecorino Romano. Delicious! I wanted more, but not because I was hungry; it was that good! My supper was accompanied by a 2^nd red wine spritzer, to wash down my evening pills. The first one preceded supper – a “happy hour” of sorts.

And then as we settled in to watch Jeopardy, I got “restless.” I say “restless” because it was an urge of sorts or thought. I was tempted to eat, but not because I was hungry. I was in a “fed” state; my stomach was not the source. It was “nerves.” I wanted something else? Was it an emotional need? Hey, I’m not of a mind for “the couch” – too much there to explore, and way too dangerous (LOL). But if my need was not alimentary, then the gastrointestinal tract was not the road to fulfillment. If the need lay elsewhere, I reasoned, I would need an alternate way to satisfy it.

I recall that when I addressed this issue originally in Retrospective #63, “Impulse Control and Metacognition,” I relied on a substitution approach, using an alternate thought (to the urge to eat) to replace and distract me from the urge or temptation. This usually worked. It replaced one thought (the “temptation”) with another. such as reading novel with an engrossing narrative. The approach advocated in #319, #342 and reprised above and again here is, “To all these things [temptations or urges] I have – in fact, I need first only to ask myself: ‘Am I hungry?’ The answer, of course, is ‘no,’ and that is almost always sufficient.” It really is. It completely eliminates the emotional or “nervous need” to eat. It is entirely rational, and it’s working for me.

I have been helped in this direct approach by insights I’ve obtained from Daniel Kahneman’s brilliant book, “Thinking Fast and Slow.” It is premised on his concept of System 1 (fast) thinking which operates automatically, intuitively, involuntary, and effortlessly, and System 2 (slow) thinking, which requires slowing down, deliberating, solving problems, reasoning, computing, focusing, concentrating, considering other data, and not jumping to quick conclusions. Nervous eating is System 1. Not eating when not hungry is System 2.  

Of course, slow thinking is made easier if you are “keto adapted.” When you are mildly ketogenic, with low serum insulin, and a stable blood sugar that is normal for the fasted state, your body is breaking down stored body fat for energy. Your metabolism is “pumped;” it’s in a happy balance, called “homeostasis.” It’s “the normal state of man.”

Retrospective #347: Lowering glucose in T2D is largely useless, unless…

If yesterday’s post left you, dear reader, in a quandary, that was not my purpose. Nor do I think was it 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 (such as insulin and sulfonylureas) that cause weight gain, is demonstrably harmful to the patient. So, lowering blood glucose by that method, as is still the Standard of Care, is worse than useless; it is malpractice. There, I said it (if he didn’t).

To see that conclusively, you have only to read Retrospective #346, or Dr. Fung’s blog, or acquaint yourself with the cardiovascular outcomes of the UKPDS and ACCORD studies. On the other hand, the drug 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.” If you haven’t guessed it, this statement is just prelude. He goes much 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 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 #328 or read Dr. Fung’s very good book, “The Obesity Code.”

Why is an elevated blood insulin considered “toxic”? Because it is the lynch pin and impetus for a constellation of metabolic disorders, starting with Insulin Resistance, that have come to be known as Metabolic Syndrome. An elevated insulin leading to Insulin Resistance has been caused by the changed dietary practices of the last century, in which highly processed carbohydrate “foods” and vegetable (seed) oils have proliferated.

These two developments have been abetted by an officialdom who, in a misguided effort to protect our arteries, has encouraged us, since 1977, to avoid foods containing saturated fat and cholesterol. Instead, they have replaced them with more highly processed carbs and vegetable oils. The Dietary Guidelines for Americans were first published in 1980 and have changed little since. In 2015 the DGA did however drop the limitation on total fats, and the 300mg/day cap on dietary cholesterol, but they doubled down on replacing saturated fat with vegetable oils. And the % DV on the Nutrition Facts panel on food boxes and bags is still 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, high cholesterol, dyslipidemia, and non-alcoholic fatty liver disease (NAFLD) – is a growing body of evidence that this nationwide dietary experiment has, tragically, gone awry.

All of these chronic metabolic disorders are related, and all of them can be traced back to a chronically elevated blood INSULIN, i.e. INSULIN RESISTANCE (IR) that is caused by what we eat. Carbohydrates start the process by signaling the pancreas to secrete insulin. Insulin is required to transport the digested carbs (as glucose) 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 the body’s other source of energy, stored body fat, that it is not needed. Body fat is, in fact, blocked from use. So, while both glucose and insulin circulate, we do not burn body fat for energy, we are in energy imbalance, we are hungry and we eat. And any carbs or fat we overeat is converted by the liver to more body fat.

An elevated blood insulin starts it: insulin resistance, obesity, hypertension, type 2 diabetes, high cholesterol, 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.”

Retrospective #346: “Glucose lowering in T2D is largely useless.”

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), has been hugely popular in large part because it is comprehensible to the lay reader. He is also a frequent blogger, and his 2016 post, “Futility of Blood Sugar Lowering in T2D,” like a previous one, “Obesity is Protective,” Retrospective #341, got my attention.

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 two 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 was 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, i.e., cardiovascular disease (CV). 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 1^st to “standard therapy,” the 2^nd 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.

But Dr. Fung doesn’t leave the matter there. Check in tomorrow to see what he suggests be done about it.

Retrospective #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 too many processed carbs and sugar for too many years.

Don’t blame yourself entirely. By 1961 the AHA 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 Retrospective #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 ADA 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 ACE 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 over half of the 34 years I have been a diagnosed Type 2. My doctor isn’t worried, though. He, like most, and the ADA, he considers anything under 7.0% “well controlled.”

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 A1c 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. [Jenny’s source:]

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, if your doctor is like mine (or anyone who follows the ADA Standard of Care), (s)he is going to consider anything under 7.0% to be “good control,” so you are pretty much on your own if you choose to strive to attain a lower A1c.

Fortunately, how diabetic you want to be is entirely within your control… as will be the consequences of your decision. Now you can see why I said in Part 1 (Retrospective #344) that my target A1c has been the “low 5s” (5% to <5.5%). My last lab report was a disappointing 5.7%. Too much cheating! Resolve: eat strictly Very Low Carb and take Metformin. 

Update: When I originally wrote this column in 2016, my "last lab report was...5.7%." For this 2020 Retrospective, my last lab report (12/19) was 5.3%.

Retrospective #344: How Diabetic Do You Want to Be? (Part 1)

Setting aside for a moment the definitions 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 various cancers. 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 too. IR comes first. Weight loss, unless the dieter is eating Low Carb as 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 (Glucophage).

To measure the degree of progressivity of the disease, the doctor will then do periodic follow-ups with A1c tests. A1c’s measure the percentage of glucose on the surface of your red blood cells, which have an average life of 2-3 months. It’s a marker for the average level of glucose in your blood 24/7. It’s a nifty surrogate, and inexpensive.

Here’s where it starts to get sticky. The Quest Laboratory reports say, “According to ADA guidelines, a hemoglobin A1c <7.0% represents optimal [my emphasis] control in non-pregnant diabetic patients.” It goes on to say, “Different metrics may apply to specific patient populations.” The ADA Clinical Guidelines counsel your doctor to consider an A1c of <8% to be “optimal” for 75 or 80 year olds!

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/ACE 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 American College of Endocrinology, the medical establishment’s metabolic specialists. Note: 6.5% is WELL BELOW the level the ADA considers “optimal” (<7.0% or <8.0%). What does that tell you about how confident the medical/pharmaceutical establishment are of their (and your) ability to effectively control your blood sugar to treat this disease? That’s why, by acknowledging the likelihood of failure to achieve permanent weight loss and good blood sugar control, Type 2 is considered “progressive,” IF YOU FOLLOW THEIR DIETARY ADVICE. Over time, you will take progressively more medication. Your diabetes will be progressive.

So, is an A1c of <7.0% (or <8.0% if you are “elderly”) the ADA target that you and your doctor have “negotiated”?

Or, is <6.5% your target, to avoid being officially diagnosed a Type 2 diabetic (by current ACE 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 34 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.”

So, HOW DIABETIC DO YOU WANT TO BE? Tomorrow I will show you the “multivariate-adjusted hazard ratios” (HRs) for the cardiovascular disease (CVD) risk of the choice you will make. It’s not complicated, as you’ll see.

Retrospective #343: My “No-Cheat” Week

My doctor’s appointment was coming up soon, so I decided to do a “no-cheat” week. Doctors know that patients try to be on their best behavior before their appointment (while “cheating” the rest of the time). That has to be one of the reasons that the Standard of Care transitioned a few years ago from the Fasting Blood Sugar to the Hemoglobin A1c as a diagnostic tool for Pre-diabetes and Type 2 Diabetes. The main reason, though, was that A1c also includes post-prandial (after meal) spikes and measures blood sugar 24/7 over roughly 3 months.

I decided to “go straight” because my average Fasting Blood Sugars for the three previous weeks had been 104, 107 and 106mg/dl. Your doctor would probably tell you that these averages, which are low on the Pre-diabetes scale (100-125mg/dl), are okay. Your doctor will probably tell you he or she will continue to monitor your blood sugar periodically, but they’ll not be very concerned for you, in order to relieve your anxiety. They should be, though.

Also driving my “no-cheat” motivation was the change in my Metformin prescription. Early in 2016 I had requested that my prescription for Metformin be increased from 500mg daily to 1,500mg daily. I had been on 500mg since 2002, within a week of starting 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, in a drug class later associated with increased heart attacks. I had to stop taking these other 2 anti-diabetes oral meds completely to avoid “hypos” (hypoglycemia, a dangerously low blood sugar).

I asked to have my Metformin increased because I had just attended a conference on Metabolic Therapeutics at which many normoglycemic attendees (body builders and fitness buffs, mostly) were eating low carb and taking maximum doses of Metformin to induce ketosis and fat-burning. Metformin does this by suppressing hepatic 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 a daily 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. THIS WAS VERY LIBERATING. My editor suggested I do a follow-up column in a few months. She didn’t say why, but I said I would.

I thought about the follow-up, though, and two reasons came to mind: 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, that 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 reading was a morning after a restaurant dinner.) So, did the metformin effect wear off over time? It did, a little. (87mg/dl vs. 79mg/dl). 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, NON-DIABETIC 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 Retrospective #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.

Retrospective #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 on yourself! But there are two ways to look on cheating on yourself: 1) the momentary “cheat,” and 2) the lifelong cheat of being deprived of good health.

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 diabetic. Or you could be just a little overweight because you are Insulin Resistant and probably on the road to becoming a Type 2 diabetic.

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 eating habits and patterns to address the inevitable “cheat”? These are my prerequisites:

1.      We all say, “Our health is the most important thing,” but is that just an empty axiom? Not if you know that by close adherence to a Very Low Carb WOE over the years you have seen and will see mega improvements in your health. And not if you know that to “cheat” 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 HUNGER, avoiding fat storage and enabling fat burning.

3.      In this state, with hunger virtually never present (honestly), 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. I have plenty of them. But if I’m not hungry, I must 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 therefore do not eat, 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. A few hours later, you feel hungry. But when you are in a state of mild ketosis, the absence of hunger is not a delusion. It’s a fact. It’s not about will power. My body is not asking me to eat because it is eating; it is eating my body fat. That breakdown of body fat, while in ketosis, is “the normal state of man.” Ketosis is the way our biology 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.

Retrospective #341: “Obesity is Protective,” says Jason Fung, MD

“Obesity is not widely considered a protective mechanism,” Jason Fung began a 2016 blog post. “Quite the opposite,” he says. “It’s usually considered one of the causal factors of the metabolic syndrome and insulin resistance.” Lamentably, most physicians think this way. In large part it is what government research, insurance reimbursement and medical association Clinical Guidelines are predicated upon. And so it is the Standard of Care of most physicians. Who can blame them for believing it?

Jason Fung, however, is a thinker (and a Canadian nephrologist), and he boldly has freed himself from those constraints – like south African Tim Noakes, and Australian Gary Fettke both of whom fought and won in court, and John Ludkin (UK) and Robert Atkins (U.S.), who were cast out by their profession. The list of heretics is long, including Vilhjalmur Stefansson from the 1920s.

Science writer Gary Taubes started it all again in 2002 with his “What If It’s All Been a Big Fat Lie,” and later his seminal tome and magnum opus, “Good Calories, Bad Calories” (2007), whose audience was medical professionals. But Jason Fung also deserves singling out because he is a trailblazer. And unlike Gary Taubes’s GC-BC, Jason 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 a 2016 New York Times article by Gina Kolata about a rare case of a genetic disorder called lipodystrophy (a lack of fat cells). Fung 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 bottom line – these excerpts from Fung 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.”

Dr. Jason Fung has really nailed it here. 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…

Retrospective #340: “Obesity is a hormonal imbalance…”

“Obesity is a hormonal imbalance, not a calorie one,” is probably a quote from an online post by Jason Fung, MD. I scribbled it down on a Post It^©. I’ve written about this imbalance – specifically the way that an elevated blood insulin level blocks fat breakdown (lipolysis) and results in fat build-up (de novo lipogenesis) – many times, most recently in Retrospective #339 and #328. To my constant readers, it must seem like a tired refrain, but to everyone else – basically the entire rest of the world – it’s new information, so it bears repeating.

How is this relevant to those of us who are overweight or obese? We became that way not because we were gluttons, but because we were hungry. We might even have overeaten (with all its attendant guilt), or eaten over frequently, because our bodies told us to – that we needed food to maintain energy balance (homeostasis). We took that “energy in” by mouth (from “food”) because our hormone insulin level was elevated and prevented our bodies from gaining access to our internal source of stored energy: the food stores (fat) that it put away for that purpose.

An elevated insulin level blocks body fat breakdown because our brain gets the message (via other hormones) that we don’t need to use stored energy; we have energy (glucose from carbs) flowing in our blood (with the transporter hormone insulin) from food by mouth, digested and circulating in our blood but not yet taken up by your cells. This other role of insulin is especially relevant for people beginning to get insulin resistance, the hallmark of a pre-diabetic. It is even more relevant for a diagnosed Type 2, who is by definition Insulin Resistant. Insulin resistance is where the pancreas makes more insulin to help push glucose into cells…and the insulin level stays high a long time.

So, what are the implications of this for someone who is maybe heavier than he or she wants to be? To draw from Jason Fung again, “Fasting is about reducing insulin.” With a reduced level of insulin circulating in your blood, your body can now switch naturally to burning body fat for energy. Your body now has access to your energy stores, and since it is being fed by them, you will not be hungry. Your body will be in energy balance. And it will remain in balance so long as you refrain from eating, (fast), or eat Very Low Carb, and you have body fat to burn. As Jason Fung says, “If you don’t eat, you’ll lose weight, guaranteed!” Pithy, huh? Jason Fung has a way with words. I’m not sure where I found these other scribbles, but it was probably also in his blog, “Intensive Dietary Management,” or in Jason Fung’s very good book, “The Obesity Code” (2016).

Then, there’s another important ramification of running on body fat, via fat-burning mode made possible by a lowered blood insulin level: Your metabolism doesn’t slow down. Why is this important? Because if your body (at the cellular level) senses that you have restricted “energy in”, either by eating less (by mouth) while blocking access to stored energy, it will adapt to this calorie restriction by reducing your energy expenditures. Your metabolism will slow down. I’m not sure where I first read about this important point, but I think it preceded Jason Fung! He does makes the analogy, though, of a household budget. If you have less to spend, the rational thing to do is to spend less. The body is a rational mechanism.

The scientific insight into this physiological phenomenon has been around for a while and is widely accepted by medical researchers. It is also widely understood by dieters. People who restrict their food intake by mouth, and eat a balanced diet, by so doing restrict their access to body fat stores. As a result, they are always hungry because there IS an energy deficit. They ARE literally starving themselves. And the body slows down to compensate. Then, when given the opportunity, it engorges itself and restores its natural metabolic rate, and you regain the weight.

Conversely, when you are fasting, or you eat Very Low Carb, your blood insulin level lowers and your body has full access to and feeds on its fat stores. Thus, the body’s energy level remains high. Your metabolic rate is constant and you have full energy. You’re not hungry, because your body is being fed. It’s a nice place to be.

Retrospective #339: Low Carb? “It’s not a diet,” I blurted

Those in the know – the cognoscenti – know that eating Low Carb, or Very Low Carb, is not a diet; it’s a Way of Eating (WOE). And in the parlance of the medical establishment (skewed to my purpose), it’s a lifestyle change.

It’s also true that if you make this lifestyle change – that is, follow this WOE – you will lose weight – lots of it – but that’s only a secondary or “side” effect. Of course, you might, as happened when my doctor suggested I try Very Low Carb, make this change for the purpose of losing weight, but, even if that was your primary motivation, the effect on your general health, in many respects beyond weight loss, will be much broader than just the lost weight: e.g., lipids (cholesterol), blood pressure (hypertension), and chronic systemic inflammation markers like hsCRP.

It’s worth noting, however, that in “prescribing” Very Low Carb (VLC) my doctor didn’t know this. The idea may have crossed his mind, though, because as he walked me down the hall to schedule my next appointment, he put his hand on my shoulder and said, “Dan, this might even help your diabetes!” I was then, in 2002, morbidly obese and had been a diagnosed Type 2 diabetic for 16 years. That was 18 years and 150+ pounds ago. But within a day of starting VLC, I had a hypo. Doc immediately took me off the 3^rd class of oral meds that he had just started. The next day, after another hypo, he cut the other two “maxed out” orals in half, and a few days later he had to cut them in half again!

So, I guess it’s fair to say the Very Low Carb WOE did help my diabetes, as my doctor thought it might – even though that was NOT the reason either he put me on VLC or I agreed to try to do it. We both wanted me to lose weight – he because he thought (wrongly) that obesity was a “risk factor” and possibly a “cause” of Type 2 diabetes. In fact, as doctors “in the know” now understand, it is Insulin Resistance that causes both Type 2 diabetes and obesity.

If it makes sense that eating low carb is a safe and effective way to lose weight, as is now accepted by most medical researchers, clinicians, food writers and even, lately, the American Diabetes Association (ADA), doesn’t it make sense that eating a high carb diet is how we got fat in the first place? That’s how beef is “finished” (fattened) on the “feed lot.” Surely, you’ve heard that. They are fed corn from a trough for weeks on end! So, why does government still push a high carb diet on everyone – one size fits all – even the Insulin Resistant, Prediabetic and Type 2s among us?!!

If you’re genetically predisposed, a diet very high in carbohydrates –  say 60%, the exact percentage on which the % Daily Value recommendation is based on the USDA’s Nutrition Facts panel – especially carbs that are processed and refined – it will overload the liver and the insulin receptors on the surface of cells that take up glucose. The overload results in backup which results in Insulin Resistance in destination cells, and conversion of carbs to FAT in the liver.

How? The pancreas responds by secreting more insulin to help the destination cells take up the glucose, producing thus an elevated level of insulin circulating in the blood. In the liver, when it’s full glycogen (glucose in the storage form), it makes fat. And when the brain gets the signal that there’s an elevated level of insulin circulating (to help the resistant cells take up the glucose it is transporting), it sends the message that the liver doesn’t need to break down body fat for fuel. It can continue to run on all that glucose “going around.” Instead of burning fat, we add (store) fat.

Then, eventually with all that insulin circulating, the glucose gets taken up and your blood sugar crashes. Your body now needs, indeed it craves more fuel to maintain a steady energy state (homeostasis). But with your insulin still elevated, and access to body fat blocked, your hunger can only be satisfied by eating. Your chance to burn body fat to maintain equilibrium is lost. When you then eat or drink to satisfy your hunger, with your liver already full of stored glycogen, everything that is not burned for energy is converted to fat. The process is called de novo lipogenesis.

If you’re lucky, you’ll just get fatter. If you’re not, you’ll start to develop Non-alcoholic Fatty Liver Disease (NAFLD).

Retrospective #338: Moí? Grumpy or Grouchy?

“Claiming a math ‘block’ just doesn’t cut it with me,” I told a friend whom I’m mentoring…and she shot back, “You might have an empathy block.” Apparently, I had touched a nerve, and I deserved that riposte.

She wasn’t through with me, though. She then raised another issue. She said that I said that exercise “makes me ‘grumpy or grouchy.’” I replied that I had said no such thing. I said exercise makes me sweaty and hungry, to which she replied, ‘Okay, I’ll give it to you. I stand corrected and apologize,’… but then she added this zinger: “Why would I think of you as ‘grouchy and grumpy,’ I wonder?” Hmmm…That got me to thinking.

Years ago, I helped the circulation of a couple of local weekly newspapers by writing a “Letter to the Editor” every week during heated debates over issues like school district capital budgets and land use issues. One issue was a zoning change to permit quarrying in a rural residential district. Apparently, my letters were such a boost to circulation that the editor-in chief of one of the papers and the publisher of anther invited me to write a weekly column. The editor actually suggested a title: “The Country Curmudgeon.”

I declined. I didn’t think of myself that way, but I was dismayed that others thought of me as curmudgeonly. I was just trying to shine a light, I thought, on what was “wrong” for our community. My goal was to educate and thus influence the reader (and voter) on these issues. In the school district’s capital budget, I was a community member of the School Board’s Facilities Committee and faithfully attended weekly meetings to be informed and participate. My letters were pretty edgy though. One critic fairly and accurately called one of them “vitriolic.”

So, I am continually wary of being overly negative about nutrition. I do, however, occasionally rant about a particularly egregious pitch for some so-called “healthy” processed food. And I am angry, most assuredly with good cause, at our government, especially the USDA/HHS and the ADA, the AHA and the AMA. The reason is simple, as Dr. Tim Noakes explains #334, “A Unifying Hypothesis of Chronic Disease, Part 1,” and particularly in his pithy #335, “Gerald Reaven's Unified Hypothesis, Part 2.” Almost nobody read them, but they were among the best I have published. Read them! You won’t regret it, and you’ll thank Dr. Tim Noakes for his courage in writing about Reaven.

So, if I occasionally express a little anger and use a little invective, or even if I’m at times “vitriolic,” and that equates with “grumpy and grouchy,” well, that’s a price I’m gonna have to pay. As Evelyn Stefansson, wife of the famous arctic explorer Vilhjalmur, said, in the preface to Richard Mackarness’s 1958 book, “Eat Fat and Grow Slim,”

“Stef used to love his role of being a thorn in the flesh of nutritionists. But in 1957 an article appeared in the august journal of the American Medical Association confirming what Stef had known for years from his anthropology and his own experience. The author of this book has also popularized Stef's diet in England, with the blessing of staid British medical folk.

“It was with the faintest trace of disappointment in his voice that Stef turned to me, after a strenuous nutrition discussion, and said: "I have always been right. But now I am becoming orthodox! I shall have to find myself a new heresy."

You should really read Evelyn Stefansson’s entire 1-page preface (Retrospective #151). It’s an homage to her husband, the famed explorer-anthropologist Vilhjalmur. I wrote about him in “Stefansson and the Eskimo Diet” (Retrospective #61). If you don’t know his story, that’s another link I encourage you to read. Stef was “right,” and after a year on a special diet of just fatty meat and offal, the medical doctors of Bellevue Hospital had to admit it.

Well, I haven’t gone to those extremes, but as Vilhjalmur did, I have improved my health tremendously, by eating a diet of very low carb, moderate protein, and fat (mostly saturated). I’ve been doing it for 18 years, and I feel great!

N.B.: Stefansson's "Eskimo diet" was 100% protein and fat, including lots of offal (organ meats). 

Retrospective #337: Facts and Fallacies about the Nutrition Facts Panel

Probably more than half my readers are women, but I’ll venture that almost all my readers (both men and women) are deceived – I believe intentionally – by the USDA’s design of the Nutrition Facts Panel on manufactured “food” products. Many women especially have been handicapped by their refusal to use their intelligence to do a little simple math. Claiming a math “block” just doesn’t cut it with me.

The most recent example came to light when my pre-diabetic friend (and new LCHF acolyte) thought she was in compliance with her announced plan to eat only 15-30g of carbohydrates per meal. For her convenience, she wants to continue to drink a meal replacement or “snack” beverage called Glucerna Hunger Smart Shakes, which, according to their website, is “specially designed for people with diabetes.” The Nutrition Facts Panel on the product says it contains 180 calories, with 8 grams of fat, 15 grams of protein and 16 grams of carbohydrate.

I told my friend that this beverage was 35% carbohydrates and that that was a higher percentage of carbs than I thought she wanted to eat (on her new LCHF 60/20/20 eating plan). She replied by sending me the percentages on the label that she apparently believed were the percentages of calories in that serving: FAT 12%; CARBS 5%, and PROTEIN 30%. SHE THOUGHT THAT THE PRODUCT SHE DRANK WAS JUST 5% CARBS. In fact, the actual percentages of calories in that serving are 40% FAT, 27% CARBS (see footnote*) and 33% PROTEIN. How do I explain that?!!!

Well, the percentages on the Nutrition Facts panel are the percentages of the USDAs catastrophic recommendations for “% Daily Values (%DV)”: That recommendation is CARBOHYDRATES: 300g a DAY for women and 375g A DAY for men; PROTEIN: 50g; and FAT: 67g. By percentage of calories, that’s a whopping 60% CARBOHYDRATE for both men and women, 10% PROTEIN AND 30% FAT. The USDA doesn’t care if you’re diabetic or pre-diabetic, young, old, active, or sedentary. The USDA’s Nutrition recommendation is ONE-SIZE-FITS-ALL.

So, the % Daily Value then – the % that appears on the label on the Nutrition Facts panel – is a percentage of the government’s horribly flawed DAILY recommendation, which is WHOLLY UNHEALTHY FOR ANYONE, much less someone with INSULIN RESISTANCE who has been told they are PRE-DIABETIC. My friend thought the drink was 5% carb; it was actually 27%. And this trap is easy to fall into, as I believe intentional. The USDA wants you to eat carbs.

But if you disagree with the USDA’s bias in favor of carb, you need to know a little about how to find the truth. The Nutrition Facts panel doesn’t tell you that. You have to do the math.

●     Protein contains 4 calories per gram, so to get protein calories, multiply the protein grams by 4 and then divide that by the total calories to get the percentage of protein in the product.

●     Carbs also contain 4 calories per gram, so to get the carb calories, multiply the carb grams by 4 and then divide that by the total calories to get the percentage of carbohydrate in the product.

●     Fat contains 9 calories per gram, so to get the fat calories, multiply the fat grams by 9 and then divide that by the total calories to get the percentage of fat in the product.

The math is easy. I do these in my head to get a rough number, which is good enough. But if you don’t want to do that, you could just buy and eat real food. Real food doesn’t need a Nutrition Facts panel to tell you it’s good to eat.

The recent changes in the Nutrition Facts panel only reshuffled the numbers in the panel and change the font size. They did not, however, make any substantive changes in the content. They did not change the % Daily Value of the macronutrients. A “mostly plant based” diet that is 60% carbohydrate is still the USDA’s/HHS recommended “eating pattern” – with the same macronutrient distribution that, since 1977, has MADE US FAT AND SICK.

* The micronutrients listed on the label added up to 196 kcals (not 180) so I had an online chat with a Glucerna nutritionist who said “some sugar alcohols in the product contain fewer than 4 kcal/gram and some fiber is not absorbed.” So, I calculated that the number of carb grams contributing to the 180 calories was not 16 but 12.)

Retrospective #336: Noakes: “It’s the fatty liver disease, stupid.”

Continuing my theft of Dr. Tim Noakes' 2016 post on South African blogger Marika Sboros’s FOODMED.NET, Dr. Noakes relates how “more support for Gerald Reaven’s unifying hypothesis of chronic disease has come from an unexpected source – from those doctors, hepatologists, who specialize in…diseases of the liver.”

Dr. Noakes adds, “It has been known for some time that the added risks associated with obesity depend, in part, on where that extra fat is stored in the body. Thus, fat that accumulates under the skin – subcutaneous fat – is far less unhealthy than is fat that accumulates within and between the organs in the abdomen, so-called visceral obesity.”

“The hepatologists have now gone one step further to show that the real killer in visceral obesity is the fat that accumulates within the liver, causing NAFLD, a disease that is now reaching epidemic proportions” (bold added).

“Their work shows that it is NAFLD and not obesity per se that produces the abnormal metabolic state – the atherogenic dyslipidemia – that causes heart disease in those with insulin resistance and the metabolic syndrome.”

“The metabolic features of atherogenic dyslipidemia present in those with NAFLD and insulin resistance

●    Elevated blood glycated hemoglobin (HbA1c) levels

●    Elevated fasting blood insulin levels

●    Elevated fasting blood glucose levels

●    Hyperinsulinemia and hyperglycemia (elevated blood glucose levels) in response to carbohydrate ingestion

●    Low blood HDL-cholesterol concentrations

●    High blood triglyceride concentrations

●    Elevated numbers of small dense LDL-particles

●    Elevated blood Apo lipoprotein B concentrations

“The absolutely key point is that dietary carbohydrates and not dietary fat cause NAFLD. For when the insulin resistant eat excess carbohydrates including fructose found in sugar and fruits, they must convert into fat any extra carbohydrate they cannot either use as a fuel or store immediately as carbohydrate in liver or muscles.”

“Note that all these options are severely reduced in those with insulin resistance.  Instead under the action of insulin – the fat-building hormone – that fat is stored, initially as fat in the liver.  But as NAFLD develops, insulin resistance worsens, hyperinsulinemia increases, atherogenic dyslipidemia deteriorates and the seeds for the chronic diseases of obesity, diabetes, heart disease, NAFLD and perhaps cancer and dementia are sown.”

“Thus, it is that dietary carbohydrates and not dietary fat are the direct cause of this group of chronic diseases in those with insulin resistance.”

Noakes’s Summary:

●    The work of Dr Gerald Reaven is as revolutionary to the understanding of medicine as were the works of Newton, Galileo and Darwin to their disciplines.

●    By producing a unifying theory for perhaps six chronic diseases and by presenting the initial evidence that these conditions are initiated by high carbohydrate diets in those with insulin resistance, he has fundamentally changed our understanding of how these conditions develop and how best they should be treated.  And also how they might be prevented.

●    Our challenge is to incorporate this new understanding into our teaching and practice of medicine.”

If you read this in a hurry, please go back, print it out, and read it again…and again. And give a copy to your doctor. It should inform us all.