Sunday, July 15, 2018

Type 2 Nutrition #441: Have I cured my type 2 diabetes?

“You’re cured,” the clinician told me. “You no longer have type 2 diabetes.” You’d think I would greet this news with a sigh of relief since I was diagnosed 32 years ago; but I did not, because I didn’t believe it.
I was not, however, surprised with that doctor’s response. I had just told her that, because I changed my Way of Eating (WOE), my A1c was now 5.0% and my average FBG in the mid-80s. From the clinician’s point of view, as one who treats patients according to the ADA’s Standards of Medical Care, her goal would be to manage my diabetes to get my A1c to ≤7.0%, or even ≤6.5%, the diabetes threshold. Thus to her, clinically speaking, I am “cured.” I asked her, “Would you then write on my chart that I no longer have diabetes?” She replied, “Yes.”
When I shook my head in dismay, she asked me why I wouldn’t accept this “good news.” I replied, “Because I will always have Insulin Resistance and therefore will always be diabetic.”  She just smirked, not wishing to get into an argument. We were, after all, just chatting in a social setting after a panel discussion in NYC with Gary Taubes. Nevertheless, she said dismissively, and with authority, that what I said was untrue. I left it at that. The divide between us was too great. In her view, unlettered dotards like me shouldn’t be taken seriously.
This doctor wasn’t my doctor and wasn’t going to be. Except for my MD friends who read this blog – and there are a few – I leave the one-on-one re-education of the trained professional to others. But, as the Heal Clinic's Dr. Eric Westman sadly said to me recently (in #402 here), “Ignorance is the biggest problem. Gary Taubes expressed a corollary sentiment to me that night. He said the Low Carb “movement” has increased 100 fold in just a few years from 1/100th percent to 1 percent. That’s a huge relative improvement…yet still an abysmal state of affairs. There is yet so much work to be done to overcome the entrenched positions in the political, agribusiness, big pharma, public health, medical, and other special interest establishments.
But I digress. Insulin Resistance is a genetic expression of a bundle of genes, in those genetically predisposed, such that the insulin receptors on cells that ordinarily open to allow glucose energy to enter and nourish them, no longer function properly. When these insulin receptor cells “resist,” and the uptake of glucose is impaired, the pancreas secretes more insulin to help out. Type 2 diabetes is thus a disease of too much insulin in the blood stream. Characteristically, type 2s have both an elevated blood glucose and an elevated blood insulin.
The elevated blood glucose is what clinicians use to detect the presence of incipient pre-diabetes or type 2 diabetes. Today the hemoglobin A1c (HbA1c) blood test is used for diagnosis. Previously, an elevated fasting blood glucose (FBG) was used. The gold standard, still used by endocrinologists, is the Oral Glucose Tolerance Test (OGTT). It takes at least 2 hours and is thus more expensive. It is, nevertheless, still the best. The easiest test is to measure your waist/hip ratio; anything over 1.0 (male) or .8 (female) signals insulin resistance.
The elevated blood INSULIN  causes obesity. While insulin is elevated, the body must rely on food by mouth for energy. Most people eat carbs in every meal and frequently between meals. So, if you have a little Insulin Resistance, your blood INSULIN level stays high. That’s why we are always hungry and why, when we eat more and more often, we get fat. Only when your blood INSULIN level drops will  the liver look for an alternate energy source and turn to breaking down body fat for energy. But to do this, a person either must eat VERY LOW CARB most of the time, or FAST for a day or two, or BOTH.
So, while I have no clinical signs of type 2 diabetes, and a doctor may regard me as “cured,” I know that I am still Insulin Resistant. I know that it is only because I eat Very Low Carb most of the time, and fast a few days most weeks, that my Insulin Resistance is not expressed. But my Insulin Resistance will always be there, and that is why I will always be a type 2 diabetic – a (thin) type 2 in remission, but only because of the way I eat.

Sunday, July 8, 2018

Type 2 Nutrition #440: The Drinking Man’s Liquid Fasting Diet

As a drinking man, this post is my approach to eating, drinking and fasting. Last week’s, Type 2 Nutrition #439, describes the original 1964, “The Drinking Man's Diet.” The premise of both is that, as Robert Cameron wrote in 1964, “Most everyone has a drink now and then.” My contention is that it is not necessary, when either dieting or fasting to give up alcohol completely. This should allay the fear, or excuse, for not trying it.
In this 2004 Forbes Magazine piece, commemorating the 40th anniversary of its original publication, Cameron was described as a bon vivant. It’s hard to know at this point whether he was or not, but his little pamphlet is replete with humorous references to various spirits in conjunction with the “high-life.” Reading it today it sounds more like a parody of the ‘50s, but in context, it could very well have been the way some people lived.
In any case, while today’s business man or woman no longer indulges in a 2-martini lunch, it is fair to say that “most (sic) everyone has a drink now and then,” many at home before or with dinner. It has been justified, or rationalized, as a way to relax and relieve stress. There’s a social aspect to it: a chance to sit down with one’s spouse and “communicate” (LOL). As a result, perhaps based on today’s mores, medical advice websites tout the “health benefits” of “light drinking,” usually defined as 1 alcoholic drink per day for women and 2 for men.
Okay, so that’s my set-up. I like a drink. I consider myself a light drinker, fitting the guideline above. I drink spirits (scotch, bourbon, vodka, etc) on special occasions. We go out for dinner on average once a week. In a restaurant I will often have one or sometimes two cocktails, depending on the bartender (the amount of the “pour”). We entertain at home much less often these days, but if we have people over for dinner, I will make just one for me and any guests who will join me. When I make the drink, one is always enough. LOL
On a daily basis, I drink wine at home. When I am NOT fasting, my Way of Eating is generally to eat Very Low Carb: to have just coffee with cream for breakfast, to have, if any, a very light lunch – usually a can of kippered herring – and then to have a small supper. Supper is a portion of protein with a low-glycemic vegetable, either roasted in olive oil or tossed in butter, or a salad. Daily food intake is about 1,200 kcal: 100g fat, 60g protein, and 15g carbs. In addition, I have two 5-ounce pours of red wine, the glass then filled with seltzer: a “spritzer.”
I describe my non-fasting daily eating routine as Very Low Carb, One Meal a Day, or VLC/OMAD. When I am “fasting,” I have the same “breakfast,” I skip lunch, and for “supper” I have just one red-wine spritzer.
If I am working at “hard labor” (in the garden), I will drink diet ice tea sweetened with liquid stevia. For electrolyte balance, I will supplement it with pickle juice, or a large cup of bouillon.  For any oral fixation impulses, especially after supper, I will make a “cocktail” of 1 Tbs of Bragg’s Apple Cider Vinegar (ACV), a few dashes of bitters, and 5 drops of liquid stevia, stirred (not shaken), the glass filled with ice and then seltzer.
The ACV cocktail is satisfying and is said to be good for blood glucose control too. Who knows? I’ve been a type 2 for 32 years and my A1c is now 5.0%, so I would say that I have my “progressive” disease under control. I do it with just a Very Low Carb diet, intermittent fasting, red wine and Metformin (750mg twice a day).
My “Drinking Man’s Liquid Fasting Diet” is about 300 kcal/day, equally divided between “breakfast” and “supper.” Macronutrient Distribution is detailed in Type 2 Nutrition #410. It is Protein: 1.2g; Fat: 16g; Carbs: 5.7g and ethyl alcohol: 18g. Last year, I lost about 60 pounds following this “Liquid Fasting Diet.”
I have been losing weight eating Very Low Carb since 2002. I weighed 375 pounds at the start and twice got down to 205, then stalled and regained some. In early 2017 I started my “Liquid Fasting Diet” to break the log jam. It was not a “water-only” fast, though. It was thisDrinking Man’s Liquid Fasting Diet,” as described. I generally ate 4 days and fasted 3 days a week. So, this would make my WOE a VLC/OMAD/4-3 DIET. Cheers!

Sunday, July 1, 2018

Type 2 Nutrition #439: “The Drinking Man’s Diet”

Everyone of a certain age has heard of “The Drinking Man's Diet.” But what do you know about it? I asked a friend recently if she knew what kind of diet it was. She shrugged and said something like, “It’s a diet in which you drink alcohol?” I said I thought so too, but we both missed the gist of it. It was the first (modern) low carb diet!!! And at 60 grams of “carbos” a day, it was pretty low carb! It might even be called a Very Low Carb diet.
First published in 1964, in 2 years “The Drinking Man’s Diet” sold 2.4 million copies at $1 apiece.  On the jacket of the 50th Anniversary Edition, it proudly proclaims, “THE ORIGINAL LOW-CARB DIET.” The subtitle is, “HOW TO LOSE WEIGHT WITH A MINIMUM OF WILLPOWER.” These are still both accurate claims!
On the occasion of the publication of the 40th anniversary edition (2004), Forbes Magazine did a column on the book and its author, Robert Cameron. Forbes described Cameron (who wrote using a nom de plume), as a San Francisco bon vivant whose brilliant title explains the book’s success, as well as how we were misled by it. The drinking aspect of the contents and title was just a gimmick. The diet works just as well for “teetotalers.”
The following quotes are taken from “The Drinking Man’s Diet,” 50th Anniversary Edition:
“This really is a simple diet. It can be summed up in one sentence: Eat no more than 60 grams of carbohydrates a day. That’s all there is to it.”
So what is a carbohydrate? As you will learn in this book, “Carbohydrates are concentrated in starches and sugars. They are almost absent from hearty foods like meat, fish, poultry, cheese and salads (yes, even the usually forbidden salad with Roquefort dressing is okay.)”
“Now, is it hard to count grams of carbohydrates? No, with the aid of tables at the back of this book you will find it very easy. The tables are derived from publication (sic) of the U. S. Department of Agriculture.”
“What makes this kind of counting more enjoyable as well as easier than calorie counting is that most of the things you like best don’t have to be counted at all: steak and whiskey, chicken and gin, ham, caviar, paté de foie gras, rum and roast pheasant, veal cutlets and vodka, frog’s legs and lobster claws, all count as zero.”
“Remember, you must count everything. A few innocent-looking dates or raisins in the afternoon can fill up your quota for the day. A slice or two of French bread might make your daily carbohydrate ration, but half a dozen slices would be a disaster. But with the great bulk of your diet – the meat and fish, the eggs and fats – counting at very close to zero, you really shouldn’t have much trouble keeping the total down around sixty.
The Forbes piece recounts how Dr. Frederick Stare, who in 1942 founded Harvard’s School of Public Health, had decried Cameron’s diet as unhealthful –calling it “mass murder,” which he later retracted. The accusation, however, ran everywhere on Page 1 and, as Forbes quipped, “…the drinking man’s goose was cooked.”
Robert Cameron wrote this pamphlet nine years before Dr. Robert Atkins’s (in)famous, “The Diet Revolution.” Atkins faced similar charges from the public health establishment. The American Medical Association, in public testimony at a congressional hearing, ridiculed and humiliated him, calling his diet “a dangerous fraud.”
But the diet worked. In two months, Cameron says he lost 18 pounds, “…was never hungry, and never missed a martini.” Cameron wrote, “Most everyone has a drink now and then,” and “alcoholic beverages such as gin, whiskey and vodka do not contain carbohydrates. Therefore, it allowed them to lose weight without giving up a daily cocktail.” Thus his 1964 pitch: “Did you ever hear of a diet that was fun to follow? A diet that would let you have two martinis before lunch (how 1960s!), and a thick steak generously spread with Sauce Béarnaise?”
The carb tables in this book, like the word “carbo,” are dated and unreliable, but the principles are still good.

Sunday, June 24, 2018

Type 2 Nutrition #438: Two Degrees of Separation

In Type 2 Nutrition #437, “Heading toward the cliff,” I described how standard clinical practice 1) treats type 2 diabetes as a progressive disease of insufficient insulin (not unlike type 1 diabetes) and 2) typically uses both oral and injected meds to “activate your body to release its own insulin.” This is still done with sulfonylureas, which should have fallen out of favor as documented in #437. However, a new once-a-week injectable medicine promises to do the same – to “activate your within” to “release its own insulin.” That’s a bad idea.
Why? Because it is a treatment that is designed to address a symptom of type 2 diabetes, an elevated blood sugar, and thus is a treatment TWO degrees removed from the cause of the disease: INSULIN RESISTANCE. This treatment increases insulin either from “your within” (your pancreas) or, with disease progression, direct injections of insulin. To be sure, increasing insulin will lower your blood sugar… but at what cost? You’ve beat up (wasted) your pancreas and become an “insulin dependent” type 2. That is the WORST thing you can do.
A better treatment, just ONE degree removed, would be to take a med that suppresses unneeded/unwanted glucose production by the liver and improves your insulin sensitivity (the opposite of Insulin Resistance). That medicine is Metformin. If the dosage is titrated (started low dose and slowly increased), the gut tolerates it well. It has virtually no other side effects and some salutary effects not yet fully understood.
By lowering glucose production and facilitating glucose uptake at the cellular level, this treatment approach accomplishes the same goal (lowering blood glucose) without putting any stress on your already overworked pancreas. This treatment is thus one degree closer to the cause of your type 2 diabetes: Insulin Resistance
The best treatment, a DIRECT treatment, then would be one that doesn’t cause your blood glucose level to rise in the first place. But, remember, you have Insulin Resistance. Because of a genetic predisposition and a diet very high (60%+) in carbs, especially refined and processed carbs and simple sugars for many years, your body developed resistance to high levels of blood insulin.
Refined and processed carbs are the worst; they’re almost all glucose. At least cane sugar is half glucose and half fructose. (Fructose is processed by the liver to become either glucose, or if your liver is full of stored glucose, via lipogenesis into body fat. Besides added pounds, this produces its own set of problems, not least of which is NAFLD, non-alcoholic fatty liver disease or worse, NASH, non alcoholic steatohepatitis.)
So, if you have Insulin Resistance, how do you prevent an elevated blood glucose? Clue: It’s NOT a drug, so your doctor can’t write a script. It’s a patient-directed treatment. Don’t eat foods that digest quickly and easily to glucose. If you don’t eat foods that convert to glucose, your blood “sugar” cannot become elevated!
Those foods would be 1) the refined and processed foods and the so-called “complex” carbohydrates (a criminal misnomer if ever there was one), which become virtually 100% glucose when digested; and 2) the simple sugars, like sucrose (cane sugar), lactose (as found in milk and yogurt), and maltose (as in breads).
As bad as table (cane) sugar is, (and honey and maple syrup and agave), most yogurts are worse, especially the non-fat ones. In place of fat, sugars and other carbs are added, and then fruit (nature’s candy bar) and fruit syrup. And breads! Besides, flour (a highly processed carb), and water, the third ingredient in almost every loaf of bread is sugar. Even those “sprouting” breads are maltose, a disaccharide (double sugar), all glucose.
So, you can (WORST: 2 steps removed) beat up your pancreas by taking a sulfonylurea or a once-a-week injectable that does the same thing, or you can (BETTER: 1 step removed) take Metformin to suppress unwanted glucose, or you can (BEST: directly address your IR), by eating fewer carbs, to keep your blood glucose level lower and stable, and avoid 1) having to take more meds and 2) “the dreaded complications.”

Sunday, June 17, 2018

Type 2 Nutrition #437: Heading for the cliff

The most memorable scene in the 1991 feminist comedy, “Thelma and Louise,” is at the end.  Let me set the scene: Being chased across the desert by a dozen cop cars, with a cliff in front of them, Thelma says to Louise, “Okay, listen; let’s not get caught.” Louise replies, “What’re you talkin’ about?” Thelma replies: “Let’s keep goin’! Louise: “What d’ya mean?” Thelma: “Go” [nods ahead of them]; Louise: “You sure?” Thelma: “Yeah.”
Now, juxtapose this dialogue, the action that follows, and the consequences, with a current TV commercial for a once-a-week injectable drug to “activate your within.” This drug works, they say, to “help activate your body to release its own insulin.” Why? Because “diabetes can be hard to manage. It’s important to remember that diabetes is a progressive disease, which means it usually changes over time. And when it changes, your doctor might have to change your treatment as well.” In other words, as Thelma said, “Let’s keep goin’!”
But, the pharmaceutical company counsels you, “You are not alone. Millions of people are living with diabetes and going through some of the same things you are.” Now, the image in my mind changes. Imagine you are among millions of lemmings heading for the cliff. “What are you talkin’ about,” you ask? “What d’ya mean?” Well, by the time you’re a candidate for this injectable medicine, you’ve already followed in the footsteps of the lemmings who take oral antidiabetic medicines, like sulfonylureas (see below) and have now “progressed.” Remember, in the ad, you’ve been assured: “Diabetes is a progressive disease,” and “You’re not alone.”
The medical dogma is that progression of type 2 diabetes from Impaired Fasting Glucose (IFG) to Impaired Glucose Tolerance (IGT), to frank type 2 diabetes is a gradual, decades-long continuum. Ralph A. DeFronzo, described it 10 years ago in his Banting Award keynote speaker at the 2008 American Diabetes Association meeting.  I chronicled DeFronzo’s remarks 5 years ago in this column, “Natural History of Type 2 Diabetes.” 
 A hyperlink in my old post will take you to the paper in the ADA’s “Diabetes” in which DeFronzo’s states, “Sulfonylureas are not recommended because, after an initial improvement in glycemic control, they are associated with a progressive rise in A1C and progressive loss of β-cell function  Why is this relevant? Because this new injectable drug “activates your body to release its own insulin.”
Sulfonylureas (SU’s) lower blood glucose “by stimulating insulin release from the Beta cells of the pancreas.” The current generation of SUs, still popularly prescribed, include the glimepiride (Amaryl), glipizide (Glucotrol and Glucotrol XL), and glyburide (Diabeta, Micronase, and Glynase). In the paper cited, DeFronzo says,
“Insulin resistance in muscle and liver and β-cell failure represent the core pathophysiologic defects in type 2 diabetes. It now is recognized that the β-cell failure occurs much earlier and is more severe than previously thought. Subjects in the upper tertile of impaired glucose tolerance (IGT) are maximally/near-maximally insulin resistant and have lost over 80% of their β-cell function” (all emphases added by me).
So, if (repeating myself), as Defronzo says in the first paragraph of his seminal paper in the ADA’s “Diabetes,”
“Sulfonylureas are not recommended because, after an initial improvement in glycemic control, they are associated with a progressive rise in A1c and progressive loss of β-cell function” (emphasis added), then…
Why, pray tell, if you may already have lost 80% of your pancreatic β-cell function on the drugs you have been taking for years, why would you “progress” to a drug that will ACCELERATE the loss of your remaining β-cells?  Wouldn’t that be like Thelma and Louise deciding to drive over the cliff? Quoting Louise, “Are you sure?”
Or could it be that the maker of this new medicine, Lilly, has you covered? It’s also makes and sells insulin, a drug with price increases at 10x the rate of inflation.  Now that’s acceleration!

Sunday, June 10, 2018

Type 2 Nutrition #436: “Science advances one funeral at a time.”

My subject’s photo, below the sub-header “Helped America Eat Better,” stares me in the face every day when I sit at my laptop. My computer shares a table covered with a NYT’s obituary page and a harpsichord keyboard I am fine tuning. It is both prophetic, and motivational; I am inspired to unload a little on “the state of things.”
My parents taught me to “never speak ill of the dead” so, while I’m going to violate that aphorism with this piece, I will not be hurtful to the departed personally. Before you say, “Bless your heart,” know that my feelings – my enmity, really – toward the myopic vision of my subject, heralded by the NYT with an 18-column-inch obit, is that society still viewed him in such an exalted status as late as 2017. This man, like so many of his colleagues, actually failed to lead us to “eat better.” But the NYT piece was an obituary, not an op-ed.
I am reminded of one of my favorite last lines in a movie. It is Joey Brown’s in “Some Like It Hot” (see this YouTube video excerpt). Brown proposes marriage to Jack Lemmon, cross-dressing to avoid a mafia hit squad. Lemmon replies in exasperation that he’s in fact a man, to which Brown replies, “Well, nobody’s perfect.”
From the obit: This doctor, a “surgeon, clinician, researcher, teacher and author, was pre-eminent in the study of obesity and nutrition.” Besides his medical degree, he held a doctorate in nutritional biochemistry from MIT and “largely spent his career at Harvard Medical School and Beth Israel Deaconess Medical Center in Boston.” He was professor of nutrition at Harvard, and at Beth Israel was the chief of Nutrition/Metabolism Laboratory and Director of the Center of Nutrition Medicine. He was at the apex of the “nutrition establishment.”
Yet, “what really put him and his colleagues on the world map were publications highlighting inadequate nutritional management of people in the hospital – so-called ‘hospital malnutrition,’” said a former colleague. How did he do that? “He helped develop nutritious liquid diets (Ensure, and others), supplementing them with protein…” In other words, he and Harvard profited handsomely from this misguided commercial collaboration.
He also correlated poor nutrition with obesity – a no-brainer there, but note again this habitual dependency of Harvard nutrition “experts” on epidemiology, or “correlation,” rather than a scientific interest in “causation.” His solution: “Advocate lower-fat diets and help develop gastric by-pass surgery and nutritional liquid diets.”
I’m not suggesting that this good doctor had a Mephistophelean streak; I’m sure he intended well, but like Ancel Keys before him, and others still in positions of  influence (e.g. Walter Willett at Harvard), he rose to power in the politics of the academy by buying into the “eat-less, exercise-more, a calorie-is-a-calorie” meme that is only now beginning to show wear at the edges because of the weakness of the scientific evidence.
His obituary writer noted that “weight loss benefitted patients with type 2 diabetes.” Now, there’s a scientific breakthrough! His obituary also described five strategies the good doctor “developed during four decades of encouraging patients to shed pounds: 1) Make time to prepare healthy meals, 2) Eat slowly, 3) Consume evenly sized meals, beginning with breakfast, 4) Do not skimp on sleep, and 5) Weigh yourself often.” Not bad advice, but pretty banal accomplishments, if you ask me. Forty years of “encouragement…to shed pounds.”
I also think that evenly sized meals sounds too much like “balanced” to me. And nutritious liquid diets like Ensure, even if supplemented to 15% protein, are still 60% highly processed carbohydrates. “Carbohydrates” are not mentioned even once in the entire 2-columned obituary. The emphasis instead is on calorie intake: “Even a small decrease in caloric intake could result in healthier weight,” he is quoted as saying. He summed it up: “Sustained weight loss requires a three-pronged approach: Cut the calories, eat quality food and exercise.”
As Max Planck, the German Nobel-prize winning physicist said in 1906, “Truth never triumphs; its opponents just die out.” Another paraphrased variant is, “Science advances one funeral at a time.” May he rest in peace.

Sunday, June 3, 2018

Type 2 Nutrition #435: Hungry or Undernourished?

“Hungry or Undernourished?” is what I would call a BIG question. It is way out of my league to propose a scientific answer or even describe the parameters of a proper study. I will venture, however, to tackle the matter as an opinion piece: I think it can be parsed into at least two different lines of reasoning, and I will attempt to posit and briefly explore them. I welcome informed comments from my erudite readers.
The first line of reasoning in the “hungry or undernourished?’” debate is that we will eat until our stomach is full. This is the “common sense” hypothesis; we have all experienced it. When we are “full,” hormones signal us to stop eating. Of course, there are exceptions. We sometimes continue to eat for other reasons. I’m a compulsive peanut eater. There’s also taste and palatability. See this link to carbohydrate-induced overeating (in rats). Lay’s potato chips captured this with the memorable meme, “Bet you can’t eat just one!”
There is a large body of new evidence that the “until full” hypothesis is hormonal. Hunger is regulated by the hypothalamus in the brain which gets signals to induce eating from ghrelin, a hormone produced in the lining of the stomach, and shuts down when another hormone, leptin, signals that hunger has been satisfied. Ghrelin was only discovered in 1999 and appears to have other functions as well. And “leptin resistance” as a cause of obesity is still a mystery. So, this is why the hormonal hypothesis of “eating until full” is also just a hypothesis.
The other line suggests that hunger drives eating until the body has met its requirements for essential nutrients. I know this sounds like a tautology and needs more explanation. It is, of course, more nuanced but at this point in the state of nutrition knowledge, the science is unknown. The theory is that what we eat, not how much, determines when the body is satisfied and hunger stops. Ergo, if your diet consists of nutrient-poor components, aka processed carbs, you will need to continue to eat until your body gets everything it needs.
These essential nutrients or components include the macronutrients and micronutrients. The macros are fats (fatty acids, SFAs, MONOs and PUFAs), proteins (and their 22 amino acids, into which protein breaks down), and carbohydrates, (none of which – repeat, none, are essential). The micronutrients are vitamins, minerals and phytochemicals, many as yet unknown.
My recollection is that this second line of reasoning is suggested in such very good books as “The Perfect Health Diet,” by Paul and Shou-Ching Jaminet, and Catherine Shanahan’s “Deep Nutrition.” It is a rational hypothesis, and I am biased in favor of it in part because the known science about the different fats and the amino acids has pretty well established how important they, or their absence, are to human health.
It also appeals to me because it supports the idea that all dietary carbohydrates, while a good source of quick energy, are not essential nutrients in the human diet. When carbs are not available to eat, our bodies are designed to make all the glucose it needs from protein and fat, through gluconeogenesis. The body also produces ketone bodies (brain food) from fat, and it gets glycogen, to make glucose, from storage and from the animal products we eat (intramuscular, subcutaneous, and from organ meats like liver). Admittedly there still isn’t a lot of hard evidence to support this hypothesis. Philosophically, though, it appeals to me.
If I had to guess, I’d hedge my bet by speculating that the answer ultimately will involve or combine these  hypotheses. In the meantime, we can be guided by what we “know” and eat with the knowledge that bodies will determine how much we need to eat and what a healthy diet is. I find my body likes it best when I eat mostly “healthy” fats (saturated and monounsaturated), and moderate amounts of protein from pastured meats and poultry and wild-caught fish. I try my best to avoid polyunsaturated fat (vegetable oil) altogether and since I am Insulin Resistant (32 years a diagnosed type 2 diabetic), I eat as few carbohydrates as possible.