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…..

Sunday, August 7, 2016

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. 

Sunday, July 31, 2016

Type 2 Diabetes, a Dietary Disease #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, but that’s a secondary or “side” effect. Of course, you might make this change with the purpose of losing weight (as my doctor suggested I do), but even if that’s your primary motive, the effect on your general health, in many respects beyond weight loss, will be a much broader benefit than the lost weight: e.g., lipids (cholesterol), blood pressure (hypertension), and inflammation markers like hsCRP.
It’s worth noting, however, that in “prescribing” Very Low Carb (VLC) my doctor didn’t know this. He must have had an inkling 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 morbidly obese and had been a diagnosed Type 2 diabetic for 16 years. That was 14 years and 140 pounds ago. And within a day of starting VLC, I had a hypo. I called him and he took me off the 3rd oral med that I had just started. The next day, after another hypo, he cut the other two “maxed out” oral meds 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 it or I agreed 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 point of fact, as many doctors and others “in the know” now understand, insulin resistance, the condition that leads to Type 2 diabetes, is what causes obesity, as I’ll explain in a moment.
If it makes sense to you that eating low carb is a safe and effective way to lose weight, as is now generally accepted by most “establishment” medical researchers, clinicians, food writers, pundits and TV personalities, doesn’t it make sense that eating a high carb diet is how that weight got on our bodies in the first place? Surely you’ve heard it; it’s been reported ad nauseum. And everyone knows how they fatten feed-lot beef; they feed them corn from a trough for weeks on end! So, why does our government still push a high carb diet on everyone – one size fits all – even the overweight, obese, insulin resistant, pre-diabetic and Type 2s among us?!!!
If you’re genetically predisposed, a diet very high in carbohydrates (say 60%, the amount on which the % Daily Value is based on the USDA’s Nutrition Facts panel), especially carbs that are refined and thus “pre-digested,” leads to overload on the liver and on insulin receptors on the surface of cells that take up the glucose. The overload results in backup which results in resistance (in the destination cells) and conversion (in the liver).
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 of glucose (glycogen 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 gets the message that it doesn’t need to break down body fat for fuel. It can run on all that glucose “going around.”
Eventually, with all that insulin circulating, the glucose gets taken up and your blood sugar crashes. Your body now needs, indeed craves, more fuel to maintain a steady energy state (homeostasis). But with your insulin still elevated, the signal to break down body fat for fuel is blocked, so your body tells you to eat. Your chance to burn body fat is lost. When you then eat or drink to satisfy your hunger, this overloads your already full liver, which converts the carbs to fat (de novo lipogenesis).
If you’re lucky, you’ll just get fatter; you won’t get non-alcoholic fatty liver disease (NAFLD).

Sunday, July 24, 2016

Type 2 Diabetes, a Dietary Disease #338: MoĆ­? 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 of one of the papers and the publisher of the other invited me to write a weekly column. The editor actually suggested it be called, “The Country Curmudgeon.”
I declined. I didn’t think of myself that way, and 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, 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, “Implications of Reaven's Unified Hypothesis, Part 2.” With titles like that, nobody’s gonna read them, so do yourself a favor and click on those links. You won’t regret it, and you’ll thank Dr. Noakes for his courage.
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 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 the entire 1-page preface (#151, here). It’s an homage to her husband, the famed explorer-anthropologist Vilhjalmur Stefansson. I wrote about him in “Stefansson and the Eskimo Diet” (The Nutrition Debate #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 staff 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, I by eating a diet of mostly fat, moderate protein, and very low carb. I’ve been doing it for 14 years now, and I feel great!

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

Sunday, July 17, 2016

Type 2 Diabetes, a Dietary Disease #337: Facts and Fallacies About the Nutrition Facts Panel

Probably more than half my readers are women, but I’ll venture that almost all (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 “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 8g of fat, 15g of protein and 16g 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%. I inferred that 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 can that be? Well, for starters, 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 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. USDA’s Nutrition recommendation is one-size-fits-all.
The % Daily Value then – the % that appears on the label on the Nutrition Facts panel – is a percentage of our government’s horribly flawed dietary regimen that is WHOLLY UNHEALTHY FOR ANYONE, much less someone with Insulin Resistance who has been told they are pre-diabetic. What matters is the percentage of calories by macronutrient in the product in hand. 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.
I do these in my head to get a rough number, which is always 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 new changes coming in the Nutrition Facts panel will reshuffle the numbers and change the font size and where they appear on the label. They will not, however, make any substantive changes in the content, and they will not change the % Daily Value of the macronutrients. A “mostly plant based” diet that is 60% carbohydrate is still the USDA’s/HHS/FDA’s recommended “eating pattern” – with the same macronutrient distribution that has made many of us sick. Does this sound to you like rearranging the deck chairs on the Titanic? It does to me.
* 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.)