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 1^st 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.

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.

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…..

Type 2 Diabetes, a Dietary Disease #340: “Obesity is a hormonal imbalance…”

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

How is this relevant to those of us who are heavy, or fat, or obese? Answer: you became that way not because you were a glutton, but because you were hungry. You might even have eaten ravenously (with attendant guilt), or frequently, because your body told you that you needed food to maintain energy balance (homeostasis). You took that energy in by mouth (an external source) because that hormone, insulin, was preventing your body from gaining access to your internal source of energy: the food stores (fat) it put away for the purpose.

An elevated insulin blocks body fat breakdown because your brain gets the message (via other hormones) that you don’t need that energy; you have energy (glucose from carbs) flowing in your blood (with the transporter hormone insulin) from food by mouth, digested and circulating in your blood but not yet taken up by your cells. This other role of insulin is true for everyone, but it is especially relevant for people with a touch of insulin resistance, the hallmark of a pre-diabetic. It is even more relevant for the full-blown type 2, who is by definition insulin resistant. Insulin resistance results in the pancreas making more insulin to help push glucose into cells.

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. It 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, 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 his very good book, “The Obesity Code” (2016).

Then, there’s another important ramification of running on full energy, via fat burning 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) and (or) by blocking access to stored energy, it will adapt to this perceived 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 was also Jason Fung! He makes the analogy 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 is relatively new but 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 unknowingly 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. Eventually, when given the opportunity, it engorges itself to restore its natural metabolic rate.

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.