Type 2 Diabetes, a Dietary Disease #308: Introduction to What Causes Type 2 Diabetes

Google “type 2 diabetes” and, in one third of a second, you get 118,000,000 “hits.” On my search the very first, after a brief description of the biological condition, asks, “What Causes Diabetes?” Their answer: “Usually a combination of things cause [emphasis added by me] type 2 diabetes,” What follows is a list of 6 symptoms, effects and parallel conditions associated with type 2 diabetes, none of which is a cause of type 2 diabetes. Only the first “cause” listed, “genes,” is relevant in that it is a precondition, but not a cause of this disease.

I am not a microbiologist or geneticist, but geneticists will tell you the genetic aspect of the science of Type 2 Diabetes is in its infancy. Although some genes associated with Type 2 Diabetes have been identified, no one has yet deciphered the complex combination of genes that have been modified by our Western diet to express themselves in a way that compromises the ability of our cells to accept glucose. This modification is called “insulin resistance.” Insulin carries glucose through the bloodstream, delivering it to cells throughout the body. If glucose can’t enter the cells, it continues to circulate. The pancreas releases still more insulin to solve the problem and eventually (after years) it wears out.

Elevated blood sugar, again over time, causes the complications of diabetes. And elevated insulin in the blood signals that there is glucose (energy primarily from carbs) circulating in the blood so there is no need to burn fat reserves for energy. So the body keeps our fat in storage, and the liver converts excess dietary carbohydrates (and fats) to triglycerides (fat) and adds them to our stores. Insulin resistance, resulting in high levels of circulating insulin in the blood, is thus the cause of diabetes and obesity, not the other way around. IR causes diabetes, IR causes obesity.  And obesity is usually a signal that your blood glucose is not under control.

What then is the “treatment” for type 2 diabetes caused by insulin resistance? The website cited lists 18 generalized “risk factors:” 3 are “things you can’t control,” and 11 others are “related to your health and medical history,” things that are epidemiologically associated with those who develop Type 2 Diabetes. That may be helpful to your doctor if he or she is otherwise clueless about whether to diagnose you as “pre-diabetic” or a frank Type 2. But let’s face it: they are history. There’s not much you can do to change the past.

Then the website lists 4 “Other risk factors (that) have to do with your daily habits and lifestyle.” It suggests, “These are the ones you can really do something about.” The site’s advice (amid pop-ups for anti-diabetic drugs): “Take medications and follow your doctor's suggestions to be healthy.” The site’s suggestions: “Lose weight, Get active, Eat right, Quit smoking.” Not bad advice, but not an effective treatment plan for IR.

The best way to think of Insulin Resistance is that you have become intolerant of dietary carbohydrates, i.e., you are Carbohydrate Intolerant. So, an “eating pattern” that reduces dietary carbohydrates to a minimum, or as few as you are willing to eat, will reduce the levels of both glucose and insulin circulating in your blood. This will, by lowering your blood glucose, 1) minimize your risk of pre-diabetes, frank type 2 diabetes and later complications, and, by lowering your blood insulin, 2) enable your body to access fat stores. You’ll lose weight and, in the bargain, avoid diabetes. Why doesn’t your doctor tell you this, instead of writing a prescription?

* If you’ve been wondering if you are one of those who is genetically predisposed, there is no genetic test as yet, but if you are overweight there is a very strong likelihood (true, just an association) that you have developed a degree of Insulin Resistance sufficient to cause that buildup of adipose tissue (body fat). This is particularly true for those with a waist/hip ratio greater than 1.0.

Type 2 Diabetes, a Dietary Disease #307: A Personal Story (N = 1)

I was diagnosed with type 2 diabetes in 1986. The standard at the time was 2 consecutive fasting blood sugars ≥ 140mg/dl. The standard today is ≥126mg/dl, so I had probably been diabetic for many years. I weighed 300 pounds at that point, up from 250 in 1974. So my doctor told me to lose weight. He also began to treat me with a sulfonylurea, an oral antidiabetic medication that called upon my pancreas to produce more insulin whenever it was presented with simple sugars and other carbohydrates that I had eaten.

I tried many times to lose weight on the “balanced, calorie restricted” diet recommended by my doctor and his staff nutritionist, a registered dietitian (RD). I was always hungry. And from time to time when I did lose weight, I always gained it back. Over the years I continued to gain weight, and my diabetes worsened. In the mid 1990s, after I was “maxed out” on the sulfonylurea (glyburide), my doctor prescribed metformin, a new medication (in the U.S.). In a few more years I was maxed out on that drug too, and my doctor started me on a third class of oral diabetes medication. Soon, I feared, I was going to be injecting insulin directly into my veins.

By August 2002, I was the heaviest I had ever been. In fact, for several previous appointments I had been too heavy to be weighed on my doctor’s office scale. So before my next appointment, I weighed myself (with permission) at the Fulton Fish Market. The commercial scale told me the truth: 375 pounds. That was really scary. When I walked into the doctor’s office later that day, I was motivated to lose weight.

“Have I got a diet for you!” my doctor said as he greeted me from the nurse’s station in the lobby of his office. Serendipity had created a moment where my doctor had a specific recommendation for me, and I was totally receptive to his suggestion. He told me that he had personally tried a diet that he had read about in The New York Times! It was the July 7th Sunday magazine cover story, “What If It's All Been a Big Fat Lie?” by Gary Taubes, an award-winning science writer. This was a ground breaking story that was to change countless lives.

Both my doctor and I were interested in this diet because we both wanted me to lose weight – a lot of weight. But as my doctor walked me down the hall to schedule my next appointment, he put his hand on my shoulder and said, “Dan, this may help your diabetes too.” Boy was that an understatement!

The first day on this new diet, in the late afternoon, I experienced a “hypo” or hypoglycemic episode – a low blood sugar with “sweats.” I knew something was wrong so I tested my blood and then went to the news stand in the lobby and bought a candy bar. I then called my doctor, and he told me to stop taking the 3^rd oral medication. But the next afternoon I had another hypo. I ate another candy bar and called the doctor again. This time he said to cut the other 2 oral meds in half, and the next day, when the scene repeated itself, to cut them in half again. In only a few days of strictly following this diet I was taking just 1/9^th the meds as before.

On this diet, as is manifest, I didn’t need to take all these antidiabetic medications. And in time I was able – correction, I had to eliminate the sulfonylurea completely to avoid hypos. And all this happened before I lost weight. Of course, I did lose a lot of weight on this diet (170 pounds at my lowest), but more importantly my type 2 diabetes went into remission – so long as I continued to stay on this diet. I’m not “cured.” I never will be, but neither is my Type 2 Diabetes still “a progressive disease.” It is, quite simply, A DIETARY DISEASE.

* My lipid profile also improved dramatically: My HDL more than doubled and my triglycerides dropped by 2/3rds. My ratios (TC/HDL and TG/HDL) are now stellar, and my inflammation markers have plummeted. My blood pressure, of course, also improved (on the same meds). And my type 2 diabetes is in total remission!

The Nutrition Debate #306: My New Manifesto: “Type 2 Diabetes, a Dietary Disease”

You may have noticed I took some time off for R & R.  The 305 archived columns, however, saw frequent visits.

The hiatus gave me an opportunity for introspection. It enabled me to re-examine my purposes and the best methods of achieving them. As my visitors know, I d­­o this for eleemosynary purposes. I have no pecuniary interest: no advertising, no dietary supplements to sell, no book to promote; there’s nothing in it for me. I do this, with the help of a great volunteer editor, for purely educational purposes.

As I said in The Nutrition Debate #114, “My Insulin Dependent Type 2 Pharmacist,” I started writing this column because a friend in my community – who was a registered pharmacist – died, unnecessarily and tragically. He was a Type 2 Diabetic. In 1986 when I was first diagnosed a Type 2, he helped me pick out my first blood glucose meter, and he filled my first prescription for an oral anti-diabetic medication.

That’s when my pharmacist told me that he was an insulin-dependent Type 2. He followed his doctor’s orders – and the advice our government has dispensed for half a century – and his disease progressed to its inevitable conclusion. His death was a waste. It didn’t need to happen that way. And that’s my motivation and my message.

With that in mind I have decided to focus my efforts on a large underserved segment of the diabetic population.  I want to explore an aspect of Type 2 Diabetes care that is little understood and generally ignored by the medical and pharmaceutical communities: the self-management of Type 2 Diabetes by the patient and how best to do it.

I am especially interested in reaching what the medical community calls the “treatment-naive” patient, that is, someone who is newly diagnosed (as Pre-Diabetic or Type 2 Diabetic) and has never been subject to any “treatment.” Such patients are at a critical juncture, and denial is an extremely tempting option. Typically, the patient just defaults into a dependent state and accepts their doctor’s ministrations (as we usually do in healthcare matters). However, a diagnosis of Pre-Diabetes or Type 2 Diabetes is actually a great time to look into what this disease is really all about and learn what you, the patient, can do about it. As a well informed patient, you can self-manage your diabetes care under your doctor’s watchful eye and “supervision”? 

Self-management of Type 2 Diabetes is a mutually beneficial arrangement. Doctor’s know that Type 2 Diabetes is largely a patient managed disease. They call it “patient-oriented” care, but that still leaves the impression that patient care is a collaboration that the doctor manages. I’m sorry, but as far as dispensing dietary advice is concerned, most doctors and conventionally educated and certified Registered Dieticians aren’t qualified to manage the care of Type 2 diabetics. So, in the days, weeks and months between doctor’s appointments, you will manage your diabetes care, and at the office visit your doctor will order tests and monitor (not manage) your improvement. Alternatively, if you default to medical management, after initially getting your blood sugar under control with drugs, your doctor will simply manage, and record, the progressive worsening of your condition.

You, the patient, know full well that “doctor’s orders” to “try hard to diet, exercise and lose weight,” aren’t easy to follow and aren’t enough. You’ve seen friends and relatives struggle. Something must be wrong with the “prescription,” you’re thinking. The doctor knows it too, but the only arrow in the quiver of the otherwise uninformed or, sadly, misinformed clinician is, “More medications could be used.” That’s the road my poor pharmacist took, and look what it got him – progressively worsening disease… and then a slow, premature death.

Therefore, the new focus of “The Nutrition Debate” will be “Type 2 Diabetes: A Dietary Disease.” It will begin with this post (#306) by the eponymous title. Then, the next posts will be #307, “Preface, A Personal Story (n = 1),” and then #308, “An Introduction to What Causes Type 2 Diabetes.” The first is my bona fides – my “credentials,” as it were. The second post is an overview of the science, as I see it. These will be followed by #309, “Type 2 Diabetes Q & A: 20 Brief Vignettes,” each fewer than 150 words (4-pages total) in Q & A format.

Further posts will return to the manifesto that drives this new focus: that Type 2 Diabetes is a Dietary Disease. I welcome comments and “debate.” After all, I have taken a very strong position which, as I see it, is irrefutable. Of course, although I consider myself “informed,” mine is just “A Personal Story: n = 1,” and “Your Mileage May Vary (YMMV).”  But, if you read “An Introduction to What Causes Type 2 Diabetes,” it’s difficult for me to see how anyone could look at Type 2 Diabetes in any way other than that Type 2 Diabetes is a Dietary Disease.”

The Nutrition Debate #305: My Troubled Relationship with Food

This is a hard thing to admit, but easy to see, if you know me. While I am still 110 pounds lighter than I was in 2002, I am 60 pounds heavier than I was at my lowest in 2008, and that’s no accident. I ate myself that way, and today I am, in fact, still fat. Technically, with a Body Mass Index (BMI) of 37, I am considered obese. And even at my lowest weight (204 pounds), my BMI (28.5) was still at the high end of overweight! How did the weight regain happen? Well, I’ll tell you.

Before I do, though, I want you to know that I am, I think – and I think my doctor would agree – much, much healthier than I was in 2002. And I don’t mean just less fat. I have a much better and more stable blood sugar level, and I have been able to give up and stay off virtually all of the oral anti-diabetic medications I was taking back then. My Type 2 diabetes is still “in remission,” although my fasting blood sugars are usually “pre-diabetic” (>100mg/dl <126mg/dl), as are my A1c’s (high 5s). But my cholesterol profile has dramatically improved, with HDLs doubled and triglycerides cut by 2/3rds. See my popular blog posts # 281, #282 and #283 for a 35-year history with charts. And my hs CRP’s, chronic systemic inflammation markers, are very much improved (usually <1.0mg/dl, down from +/-6mg/dl). And – (drum roll) – my doctor took me off statins years ago.

And why is that? Why all the good news while I have re-gained 35% of my original weight loss? It is because I have fundamentally changed what I (usually) eat. I still follow a low-carb, high-fat (LCHF) Way of Eating most of the time. But I “cheat.” I’ll sometimes scarf down rolls (with butter) brought to the table in a restaurant. Sure, we could say, “no bread,” and sometimes we do, but at other times we don’t. I also raid the freezer at home occasionally to steal some of my wife’s ice cream. You see how easy it is to “blame” someone else for mytransgressions. At least I recognize the self-delusion.

It would also be easy to blame “habituation to rewarding neural dopamine signaling [that] develops with the chronic overconsumption of palatable foods, leading to a perceived reward deficit and compensatory increases in consumption.” For a good scientific roundup of why obesity is a vexing problem, see The Nutrition Debate #297: “Obesity in Remission.”

How things now stand: Because I eat LCHF, for the most part my Type 2 Diabetes continues to be in remission. But because I have lost a great deal of weight, I also have Obesity in Remission. As a consequence I need always to remember to “eat healthy” and at least 20% less than someone who has not previously been fat. “Elections have consequences,” and since I elected to eat carbs in excess and developed carbohydrate intolerance, I am foreverpredisposed to accumulate excess fat.

But 1) if I eat only the foods I have espoused and recognized as “good” for me, and 2) if I only eat when I am hungry, or alternatively just two small meals a day instead of the conventional three, I believe a) I would not have gained back any weight, and b) I might have continued to lose weight. After all, I probably shouldn’t weigh, at most, more than 175 pounds (BMI=24). But I did and I do, and so I confess it. Will that do me (or you, for that matter) any good? Well, the first step in making a change in your life is to acknowledge what you are doing that needs to change. And now I’ve done that.

So, we’ll see. I’m going to take a break now from writing this blog. I’ve written 305 posts over the last 4 years and 5 months. They have received altogether more than 150k page views, so it’s likely that someone (besides me) has benefitted from them. Readers who want to keep in touch, while I return to basics, can write to danbrown@thenutritiondebate.com. Or, visit the Bernstein Diabetes Forum, where I post from time to time and there’s lots of other friendly help and support and very good advice, especially for Type 2s and pre-diabetics who want to manage their condition with the aim of avoiding “the current treatment protocols (that) trap patients in a lifelong regimen of drug management, obesity and escalating diabetes.”

In taking leave of my readers I would be remiss if I didn’t heap praise on my editor. She has been a stalwart friend and helper throughout this period, always there with timely and helpful edits and links to scholarly resources. She is an inveterate professional, a tireless fact checker and my overall guiding support. And - no contest here – she always knew the subject better than I did. Thank you, thank you, and thank you, Laurie Weakley. (Too many “thank you’s,” Laurie?)

The Nutrition Debate #304: “I am not making this up”

“Novel differences in the glucose response to HP [higher-protein] vs. NP [normal-protein] breakfasts were observed and were influenced by the frequency of habitual breakfast consumption in overweight adolescents.” At 176 characters (with spaces), it might have made a good tweet. But, and I am not making this up, that was the CONCLUSION from the Abstract of a recent article in the European Journal of Clinical Nutrition (EJCN). I saw the groundbreaking news from Diabetes in Control: “Breakfast Habits Affect Overweight Teen Girls Metabolic Responses to Protein-Packed Morning Meals.”

“The primary aim [of the study] was to examine the daily glycemic response to normal-protein (NP) vs. higher-protein (HP) breakfasts in overweight adolescents who habitually skip breakfast (H-BS). The secondary aim examined whether the glycemic response to these meals differed in H-BS vs. habitual breakfast consumers (H-BC),” according to the EJCN. If this sounds elementary, Watson, I’ll generously assume the research was intended to educate overweight/obese late adolescent girls in an online chat line or similar social media or some teen-oriented supermarket magazine.

The unsurprising outcome was that “those who typically ate a high-carbohydrate breakfast had improved glucose control after they ate a high-protein breakfast.” No news there. But the researchers seemed surprised that “the habitual breakfast skippers experienced poorer glycemic control throughout the day when they consumed a high protein breakfast.” Hmmm. Ingested food affects your circulating blood glucose! It disrupts and destabilizes it! It causes glucose, from carbs and then from protein digestion via gluconeogenesis over 4 or 5 hours, to enter your bloodstream, resulting in peaks and crashes!

The Abstract (you have to pay to access the full paper) does not tell us what a “normal protein” breakfast is (as compared to a higher-protein breakfast) but you can bet it contains lots of carbs too: juice, cereal and/or some bread product.

“These findings may indicate an increased inability among habitual breakfast skippers to metabolize a large quantity of protein,” the corresponding researcher told Diabetes in Control. “However, our data would suggest that once someone begins to eat breakfast, they should gradually transition to a breakfast with more protein – or about 30 grams – to elicit improvements in glycemic control,” the researcher said. Wow! That (30g) is a lot of protein. They must be growing girls.

I think the education of the researcher is proceeding swimmingly. The paper stipulates, “Current scientific evidence shows that sustained elevations in post-meal glucose is a strong contributor of poor glycemic control and is associated with an increased risk for the development of Type 2 diabetes and cardiovascular complications. Because of the potential risk in the long term, identifying dietary strategies that individuals can begin when they are young to reduce post-meal elevations in glucose might prevent the occurrence of Type 2 diabetes and cardiovascular disease.” That’s a safe bet. And well said!

According to the Diabetes in Control write-up, the researcher suggested that “young women should routinely aim for a 350-calorie breakfast with approximately 30 grams of protein. To meet the recommended 30 grams of protein, [the researcher] suggests foods such as scrambled eggs, breakfast burritos with eggs and lean meats, or Greek Yogurt.” Interesting, my breakfast is 3 eggs, fried or scrambled, 1 strip of bacon, a large coffee with stevia powder and about 4 Tbs of half and half, and a 1 gram fish oil capsule. It’s 375 calories, but only 20 grams of protein, 31 grams of fat and 4 grams of carbs.

I also think the researcher needs to take another look at 1) gluconeogenesis and 2) the “standard lunch” the girls ate. But progress, progress.

The Nutrition Debate #303: Poor Dr. Walter Willett

The Nutrition Source, not to be confused with The Nutrition Debate (teehee), is the Harvard T. H. Chan School of Public Health’s website. Its aim is “to provide timely information on diet and nutrition for clinicians, allied health professionals, and the public.” I took a poke at their Alternate Healthy Eating Index last year in The Nutrition Debate #229 with “My Alternate Healthy Eating Index.” To their credit, they do bring to the table some gravitas, in my view, because they deign to criticize the USDA’s Dietary Guidelines, as the HSPH’s Alternate Healthy Eating Index amply demonstrates.

Much of that gravitas is attributable to Dr. Walter Willett, Professor of Epidemiology and Nutrition and chairman of the HSPH; he’s also professor of medicine at the Harvard Medical School’s teaching hospital, Brigham and Women’s. Willett is “the principal investigator of the second Nurses' Health Study, a compilation of studies regarding the health of older women and their risk factors for major chronic diseases. He has published more than 1,000 scientific articles regarding various aspects of diet and disease and is the second most cited author in clinical medicine,” according to Wiki.

Staying “King of the Hill” can be a rough game. Ancel Keys, despite numerous attempts to dethrone him, stayed King until long after he was smoldering in the grave. In fact, his ghost still casts a ghoulish pale. And Walter Willett has recently managed to do so too, using the same type of rough play as Keys used. This 2013 piece in Forbes tells the story of how the “Top Science Journal Rebukes Harvard’s Top Nutritionist.” The Nature story and accompanying editorial were both scathing. Willett’s offense was to say on NPR that a research piece in JAMA by Katherine Flegal, that showed people who were overweight (but not obese) lived longer than those deemed normal weight, was “a pile of rubbish, and no one should waste their time reading it.” He then organized a conference at Harvard expressly to discredit the JAMA piece.

More recently, Nina Teicholz, author of “The Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy Diet,” wrote a New York Times op-ed, “The Government's Bad Dietary Advice.” In it she says, “…the primary problem is that nutrition policy has long relied on a very weak kind of science: epidemiological, or “observational,” [i.e. “cohort”] studies in which researchers follow large groups of people over many years. But even the most rigorous epidemiological studies suffer from a fundamental limitation. At best, they can only show an association, not causation.”

“Epidemiological studies can be used to suggest hypotheses but not to prove them,” Teicholz said. “Instead of accepting that this evidence was inadequate to give sound advice, strong-willed scientists [ahem] overstated the significance of their studies.” Then, she zeros in: “Much of the epidemiological data underpinning the government’s dietary advice comes from studies run by Harvard’s school of public health.” Teicholz doesn’t pull punches. She also takes a hit at the Guideline’s advice on salt by citing a blistering and “authoritative Institute of Medicine study.” I cite it in #153: “Salt: Friend or Foe.” See also Medscape Medical News Editor-in-Chief Eric Topol’s report in #248, “Salt Warnings: Confusing and Contradictory.”

Now, Dr. Willett has used his quarterly, “Ask the Expert” interview to address the cholesterol issue. (Note: the draft 2015 Dietary Guidelines, for the first time since 1980, states that “cholesterol is not considered a nutrient for overconsumption.”) Largely responding to the Teicholz guest op-ed (that he inexplicably calls the NYT “story” or “article”), Willett says,

“The important point is to have the best possible evidence, and we shouldn’t be basing dietary guidance on just guesses or beliefs. In the case of both the egg issue and the total fat issue we were basically starting with virtually no direct evidence. When the evidence did start to come in – and there were different lines of evidence from our studies based on large cohorts and also short term studies investigating metabolic changes – it showed that people who consume more eggs did not have a higher risk of heart disease even after adjusting for any other factors, and that total fat in the diet was not related to heart disease risk or cancer risk. So it took those long term studies to show that those were not important factors, and that allowed us to modify the recommendations. We were really in a state 35 years ago in which we had very little direct evidence and we were basing guidelines on guesses and indirect evidence from very small, short term studies.”

Mea culpa? Mea culpa!!!!! But I think the best rebuke of Willett is from the Forbes piece. You have to read the story for context, but this sums it up well. This is “piling on,” of course, but sometimes that’s the best way with King of the Hill.

“Science is complex, and Willett’s message to his fellow scientists appears to be that the public can’t be trusted with this complexity (except, as noted, when it might be something that he thinks is worthy of research); the question, which the public might ask in turn, is whether Willett can be trusted with complexity given his apparent intolerance for it in other scientists?”

The Nutrition Debate #302: Another pill to prevent Type 2 Diabetes?

As everyone who regularly reads this blog knows, I am not a pill pusher. I once was a big-time pill-taker, however, until I tried an alternative “treatment plan” for my Type 2 diabetes. I was a passive victim of “the current treatment protocols (that) trap patients in a lifelong regimen of drug management, obesity and escalating diabetes” (see #292 here). 

That stopped when my doctor “prescribed” a total change of diet, to lose weight,which had the added effect of putting my diabetes in clinical remission. I went from being maxed out on 2 oral diabetes meds and starting a 3rd (with an out of control FBG) to where I am today, taking 1 low-dose Metformin and good glucose control. My A1c’s are always in the 5s.

But this blog is not about Very Low Carb dieting. It is about an interesting new idea (for me) from some Danish researchers, according to this Diabetes in Control story. It is based on “a large study population of adults (lean and obese, men and women) with normal and impaired glucose regulation.” They are from the Steno Diabetes Center, a Danish hospital and research organization owned by the drug maker Novo-Nordisk, “working in partnership with the Danish healthcare system.”

The FINDING, which could prove to be significant: “Reduction in the glucose-regulating hormone glucogon-like-peptide-1 (GLP-1) appears to occur before the development of type 2 diabetes and obesity," according to the abstract in Diabetes.

The lead investigator told Diabetes in Control, “We found that GLP-1 is reduced by up to 25% among people with pre-diabetes and up to 20% among obese people compared to normal-weight people. This indicates that the reduction in GLP-1 is not a consequence of type 2 diabetes, but appears much earlier in the disease development and may predispose people to type 2 diabetes.” These results were all in response to an oral glucose tolerance test (OGTT).

The Diabetes in Control piece also noted, “And what is surprising is that they have also found pronounced differences in GLP-1 secretion between men and women. They observed a higher GLP-1 response among women than men, but when glucose tolerance worsens, the decline in GLP-1 secretion is more pronounced in women than in men.”

Of course, as might be expected from a hospital research department “owned by Novo Nordisk, working in partnership with the Danish healthcare system,” the researchers casually said, “‘These results could have potential clinical implications as well,’ noting that GLP-1 analogs may help delay onset of type 2 diabetes,” Diabetes in Control noted. A GLP-1 analog would be a new drug designed “to prevent diabetes for those with prediabetes.” And…for overweight and obese patients too?

They may be on to something here. Preventing the destruction of GLP-1 would be a worthy area for further investigation. But, alternatively, developing a new drug, a GLP-1 analog, to treat the symptom rather than the cause – something that Big Pharma, working in partnership with the…healthcare system (government funding) does so well – is a sure fire hit. It sounds like a big money maker (for Novo Nordisk) to me. Think statins, or blood pressure medications, or any other of “the current treatment protocols (that) trap patients in a lifelong regimen of drug management.”

Hey, I believe in capitalism, and Novo Nordisk is not an eleemosynary enterprise. They have a pecuniary interest in this research. So, let’s hope the researchers are sincere when they say, according to their press release, “We should use the findings in prevention strategies for type 2 diabetes.” Sounds good. More studies. In the meantime, eat Very Low Carb! Preserve your GLP-1!

The Nutrition Debate #301: Healthy Food Choices

Unfortunately, this catch phrase has been co-opted and misused by our government’s “Dietary Dictocrats” to mean mostly things that I and like thinkers consider unhealthy food choices, like highly processed vegetable oils. It has also been used to denigrate saturated fat and, until the present iteration of the much anticipated 2015 Dietary Guidelines for Americans, dietary cholesterol. (In case you haven’t heard, cholesterol has been declared “no longer a nutrient of concern for overconsumption.”) If you searched for the USDA’s idea of “healthy food choices,” you should stop reading this now…or, maybe continue reading. You might learn something.

Healthy food choices, in the sense that I mean, are whole, unprocessed foods, including lots of animal-based proteins and fats, together with fresh, whole, low-carb vegetables (mostly of the above-ground grown type), and an occasional berry (with heavy cream) and a few nuts (added to salads, e.g.). It involves the almost complete avoidance of grains, and processed foods made from flour and sugars (cane, beet or corn) and all processed vegetable oils. So, among my healthy food choices, what other choices can I (we) make to be healthier?

Eggs from pastured hens: This was an easy choice. We have, at our farmers’ market, a farmer who raises hens in the manner of Joel Salatin’s Polyface Farm in Virginia, made famous by Michael Pollan’s “Omnivore’s Dilemma.” The hens roam freely and roost in a portable hen house that is towed around every week or two to pastures in which the farm’s ruminants (and pigs) had grazed and left “deposits” to fertilize the fields and nourish the hens. Chickens (and pigs) are omnivores, so the hens get a balanced diet including bugs and, from aged patties, larvae.

Butter from pastured cows: It stands to reason that cows that are fed, during part or all of the year, a diet of mostly silage, will produce milk, cream and butter that have fewer nutrients.  Is it not better for ruminants to eat natural forage instead of fodder? Laboratory tests of milk and butter have confirmed this. Grass-fed cows produce milk and butter that is higher in vitamins, minerals and other essential nutrients like Omega 3 fatty acids. Is it not then a better choice to choose butter made from cows that are grazed on forage all year round? I’m going to start buying butter made from grass-fed cows and ask my wife to use it instead of the store brand.

Wild Caught versus Farm Raised Fish: Of course, I eat wild-caught fish almost every day (a can of sardines for lunch), but choosing wild-caught fresh or flash-frozen fish from the supermarket or fish monger’s case is an easy choice to adopt. Some fish like North Pacific salmon must be wild-caught, but beware of farm-raised salmon from the North Atlantic or South Pacific (Chile). Other types of fish – cod, for example, one of the less expensive species, is always wild-caught and is a white, flaky, non-fishy tasting fish. I make a stove-top recipe with fennel and cauliflower. Halibut with celery, also stovetop, is another tasty wild-caught choice dish. Why not try them?

Lamb chops: Lamb chops, though expensive, are a very good fatty meat choice for a couple of reasons. Most lamb is raised in New Zealand, where they are grass-fed year round. They are not feed-lot raised. And they are ruminants, so they are a good choice for their fatty acid profile (better than chickens and swine). And, since lamb chops are small, they make portion control easy. My wife and I eat just two lamb chops each – about 4 to 6 ounces net – making a perfect protein portion for a supper where my “allowance” is just 25 grams of protein.

Heritage Pork: Supermarket pork, “the other white meat” has had all the healthy fats bred out of it. Supermarket pork chops taste like sawdust unless they are smothered in gravy (ugh!). You just can’t get away from how dry they are. The answer is to buy heritage breed pork. Breeds to look for are: Berkshire, Tamworth, and Red Wattle. Again, your local farmers’ market is the place to look for these superior tasting products, especially roasts. 

Artificial Sweeteners: I have finally weaned myself off artificial sweeteners. I used to take Splenda in my coffee and to sweeten the unsweetened Lipton’s ice tea we drink (instead of water!). Now I use pure stevia leaf extract, a powder with no bulking agents. I understand that stevia is also available as a liquid. I do not know the solvent.

The Nutrition Debate #300: ‘Sugar’ in Food and Blood: a primer on carbohydrates

I heard an ad on TV last night for a diabetes drug. The ad explains that, “It (the drug) removes some sugar from your body.” I asked (I think audibly to the TV), “How did the sugar (that the drug removes) get into your body in the first place!!!?” And that suggested the corollary question, “If you didn’t eat so many carbohydrates, wouldn’t you have less “sugar” to “remove…from your body”? And this brings me back to the basic question: What foods become “sugar,” in the sense of the ad, in the first place? What foods convert to glucose? The answer, basically, is all carbohydrates.

“Sugar” is in quotes because I am not referring to cane (or table) sugar; I and the ad copywriter are referring to “blood sugar” (glucose), the compound that most carbohydrates break down into by digestion. It’s true that some carbs break down into fructose and glucose, and a few (dairy carbs) into galactose and glucose, and starches are all long-chain glucose molecules, but it is the simple monosaccharide glucose, commonly called “blood sugar” or just “sugar,” to which we refer.

If you have been diagnosed with pre-diabetes or Type 2 diabetes, it is because you first developed a precursor condition called Insulin Resistance (IR). Insulin from your pancreas is required to move the glucose and “open the door” to your cells to “take up” the glucose for energy. IR means the ‘door’ is blocked; glucose can’t get into your cells. It continues to circulate and builds up to high levels, damaging your organs and small blood vessels. You are at high risk for a multitude of diseases.

Most people who are newly diagnosed pre-diabetics or Type 2 diabetics are surprised to learn the “sugar” (glucose) content of common foods. But how much “sugar” (glucose) do carbohydrates make? To understand the answer in context you need to know how much blood “sugar” is “normal,” that is, normally circulating in the blood of a person (before a meal) who has a normal glucose metabolism. The answer is surprisingly low; it’s 1 teaspoon (5 grams equivalent) of “sugar.” See The Nutrition Debate #232, “A spoonful of sugar,” and, for an explanation of the math, the blog of Michael Eades, MD.

As Dr. Eades points out, a diagnosis of Type 2 diabetes is having a “sugar” (glucose) level in your blood equivalent to just 1¼ tsp. Yet, a McDonald's“small” Coke (16oz) has 8 tsp of “sugar,” a Big Mac 9 tsp of “sugar,” a large fries 13 tsp of “sugar,” a large chocolate McCafé shake (22oz) 28 tsp of “sugar,” a bagel 10 tsp of “sugar,” a low-fat chocolate milk 5 tsp of “sugar,” a baked potato 7 tsp and an 8 oz container of low-fat fruit yogurt 9 tsp of “sugar.”  There are hundreds more examples here.

If the door to your cells is partially closed by Insulin Resistance, can you really afford to eat 30, 40, 50 times more “sugar” in one meal (carbohydrates → glucose) than your body can handle? Do you really want to become more and more dependent on drugs to take the “sugar” out of your body that you put into it? You really do have a choice, you know. Self management works. You don’t have to go crazy. You just need to be aware of what your body can handle (by testing your blood sugar), and then be guided accordingly in your food choices. If you don’t, the disease you have acquired by eating too many foods too high in carbohydrates for too long (on the government’s advice!) will surely damage your body, and shorten your life… 

That’s the choice you have to make. I’m not trying to scare you. I’m trying to educate and inform you about how you can make better choices. You probably know this. I hope you feel more empowered now to take the steps you need to take. 

If you’ve read this blog to the end, it’s a safe bet that you’re a neophyte to diabetes, or at least to diabetes self-management. If that’s true, welcome. You might also want to visit Jenny Ruhl’s website, Blood Sugar 101. It’s excellent.

The Nutrition Debate #299: The Set Point: Why Maintaining Weight Loss is So Hard

The excerpt from the Lancet Diabetes and Endocrinology comment in The Nutrition Debate #297, “Obesity in Remission,” brought to mind a segment from “Choices,” the 2^nd of four hour-long videos reviewed in The Nutrition Debate #275, “Weight of the Nation,” published on 12/31/14. You might have missed it. But if you are having trouble losing weight or, having been successful in the past, are now putting weight back on (as I am), you should read #297, and this blog post.

Starting at minute 17:00 in “Choices,” Rudolph Leibel, MD, Co-Director of the New York Obesity Research Center at the Columbia University Medical Center, says, “Individuals losing weight are NOT metabolically the same as they were before they lost weight.” “The weight reduced individual will be requiring about 20% less (sic) calories per day relative to what somebody of that weight who’s never lost weight would eat…in order to keep at that body weight,” he says

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“Consider two individuals – same gender, same age, exactly the same body weight – one of whom is at that body weight as a result of let’s say a 10 or 15% weight reduction, the other who’s been at that weight for their entire adult life. If that reduced weight individual goes out to lunch with her friend, and they both order the same meal, that will represent a 20% overeating for the weight-reduced individual, and be quite normal for the individual who’s not in that state. Twenty percent might seem like a little, but 20% excess calorie intake a year will account for the inexorable weight regain.”

“As far as we know, this phenomenon does not go away,” Dr Leibel says. “So, being successful for a year or two doesn’t mean that you’re going to be able to go back to eating what would be appropriate for a person who’s never lost weight.”

“Does that seem unfair?” an off-camera voice asks an overweight woman. “Sure, it does seem unfair. It’s unfair that, you know, I just can’t lose the weight and go back to the way a normal thin person lives their life, but that’s part of the price you pay for allowing yourself to get overweight in the first place,” the woman responds. Okay, that’s the thinking of this well-meaning and very well-funded, widely-viewed and deeply-flawed HBO series. Forget for a minute who funded it.

You can choose to blame yourself for following the Government’s Dietary Guidelines since 1977, and your doctor’s advice at least since 1961 when the American Heart Association started telling you to eat less saturated fat and cholesterol. That’s when Agribusiness starting making more “low-fat” manufactured foods with added sugars and processed carbohydrates.

Or you can choose to eat many fewer carbs and more fat – both saturated and monounsaturated, but not polyunsaturated fats (vegetable and seed oils). You will feel fuller when you eat fatty meats and fish and a few low-carb veggies. Fat satiates. Protein digests slowly. Your blood sugar will stabilize, your blood lipids will improve, your inflammatory markers will too, and as you lose weight, without hunger, your blood pressure should come down too. All these good things happened to me.

And when I regained some of the weight I lost, but continued to eat low-carb, high-fat – just too much of it – the only thing that went up was the number on the scale. Like many of my readers, I have a “biological predisposition for energy storage” and I live in “an environment that promotes high energy intake” (both carbs and fat). The RESULT: an obesity–promoting interaction between the two (weight gain). This condition is both chronic and, at times, treatment-resistant. I like to eat.

The Nutrition Debate #298: “Obesity in Remission” Part 2

My hopes were up in #297, “Obesity in Remission,” because the powerhouses in obesity medicine whose long comment in Lancet Diabetes and Endocrinology I partially excerpted, appeared to understand the mechanism. Most doctors do not. They also included phrases like “promotes energy overconsumption” (due to habituation and dopamine signaling, palatable foods and reward deficits, etc.), and “increases fat storage capacity” (suggesting the importance of the hormone insulin). I was soon to be disappointed. Apparently, these guys have first-class cabins on the Titanic, and they’re not giving them up

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They’re right of course about all the things that promote “energy overconsumption,” so long as the energy referred to is carbohydrates. But they do not mention that word even once in their long comment. Alas! Would that they explain why!

The human body has two main sources of energy, both in food ingested and stored: Carbohydrates and fat. Carbs can be eaten (to make glucose) or can enter the blood as glucose from glycogen stored in the liver from previously eaten carbs. Fat can be eaten or enter the blood from triglycerides broken down from stored fat when serum insulin is low either because of fasting or when blood glucose is low. This includes people with a disregulated glucose metabolism (Type 2 diabetics, pre-diabetics and carb addicts, i.e. people who have Carbohydrate Intolerance from years of over consuming carbohydrates).

Protein is not considered a primary source of energy for the body because it cannot be stored. But it is needed and used every day for essential functions. The amino acids that protein breaks down into, that have NOT been “taken up” within 4-5 hours of being eaten, go to the liver and are later used to make glucose (blood sugar) in a process called gluconeogenesis.

However, the authors of the Lancet comment do not mention dietary fat as an energy source, much less one to be used for weight reduction since they associate its caloric density (9 calories per gram vs. 4 calories per gram for both carbs and protein) with weight gain and thus advocate avoiding “calorically dense food” as part of a weight reduction strategy. Maybe they’re afraid of saturated fat and cholesterol. If so, they have been wearing blinders and are out of touch with the evolving world of nutrition, perhaps dining in the first class salons as the Titanic continues on its course in the frozen North Atlantic

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They get SO close. They say, “Because sustained obesity is in large part a biologically mediated disease, more biologically based interventions are likely to be needed to counter the compensatory adaptations that maintain an individual’s highest lifetime bodyweight.” Okay, a candidate biologically based intervention would be carbohydrate restriction, allowing serum insulin levels to drop and thus triglycerides (body fat) to be broken down, enter the blood stream, and be used for energy.

But no. They say, “Current biologically based interventions comprise antiobesity drugs, bariatric surgery, and…intermittent intra-abdominal vagal nerve blockade.” (I suspect this 3^rd method is so new it may have been what this is all about.) “These interventions do not permanently correct the biological adaptations that undermine efforts for healthy weight loss but do, during use, alter the neural or hormonal signaling associated with appetite to reduce hunger and caloric intake.” Well, that’s exactly what Carbohydrate Restriction does! “During use,” it “alters the neural and hormonal signaling associated with appetite” and “reduces hunger and caloric intake.” And improves lipid profiles and other CAD and CVD risk markers!

And it does all these things without risk of surgery or the side effects of drugs. What don’t these people understand?