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.