The Nutrition Debate #257: Non-surgical bariatric medicine

Does this sound like an oxymoron to you? It did to me, until I looked up the definition of “bariatric.” According to Merriam-Webster online, it means “relating to or specializing in the treatment of obesity.” And non-surgical bariatric medicine is what Yoni Freedhoff, MD, an Ottawa, Canada-based family doc and Assistant Professor at the University of Ottawa, practices.  He is also the founder of Ottawa’s non-surgical Bariatric Medical Institute, “a multidisciplinary, ethical, evidence-based nutrition and weight management centre,” according to his Blogger website, www.weightymatters.ca. He quips in his “About Me” that, “Nowadays I’m more likely to stop drugs than start them.” He sounds like my kinda doc.

What brought Dr. Freedhoff (I’m gonna call him Yoni) to my attention, I think, was an email from my editor. “Sugar” has been one of her long-time “faves.” So, when Yoni heralded Canada’s Heart and Stroke Foundation’s (HSF) issuance of what he calls a “world leading sugar statement,” she gave me a heads up with this link. And within Yoni’s post, he provides this link to the HSF new position statement, “Sugar, Heart Disease and Stroke.”

Yoni describes the HSF position statement “as hard hitting as any I’ve read….” It provides “a slew of recommendations” for consumers, the Federal and Provincial Governments, and other regulatory bodies such as school boards. Some of the recommendations, such as taxing sugar sweetened beverages and “Bloomberg style” drinking cup size bans, I do not favor. Likewise they would have little chance of enactment in the more individualistic, civil-libertarian political environment of the U.S., but that’s not Yoni’s main thrust. It was what enabled the HSF to make their recommendations possible in the first place. It was the HSF’s decision to “divorce themselves from their throngs of food industry partners.”

Yoni’s dual exhilaration is clear. He begins, “Huge kudos for Canada’s Heart and Stroke Foundation,” and then he adds,

“Whether or not you agree with the HSF’s recommendations, one thing’s incredibly clear, the HSF is no longer the food industry’s partner – and that news is tremendous for Canadians as it’s amazing how forceful and broad-sweeping public health organizations’ recommendations can be when there’s no worry about upsetting industry partners.”

Yoni goes on, “While reading this position piece and in it the HSF’s clear unadulterated-by-industry voice, I couldn’t help but wonder what sort of forces Dietitians of Canada and the American Academy of Nutrition and Dietetics [formerly the American Dietetic Association] could be were they to divorce themselves from the throngs of food industry partners, for as it stands now, they’re both rather toothless and certainly not describable as drivers of change or true champions of health.” Boy, the Ottawa community is lucky to have this kind of doctor serving the “non-surgical bariatric” population.

Muckraking is a messy business, though. Many a good researcher, and practitioner as well, has had their career ruined by going against the flow, unable to get research funds or publication in a peer-reviewed journal, by trying to advance an alternative hypothesis or clinical approach to practicing medicine. That hasn’t deterred, among others, one of my favorite bloggers, Kris Gunnars, a medical student who blogs regularly at Authority Nutrition, an evidenced-based approach. His posts are always backed up with citations in the medical literature, and he’s got a big following.

Kris usually blogs about healthy eating, but occasionally he goes off on a tangent into the politics of nutrition. One of my favorites was http://authoritynutrition.com/big-food-is-much-worse-than-big-tobacco/ in which he takes off on the same American Academy of Nutrition and Dietetics, the “professional” organization that is “the ‘biggest organization of nutrition professionals in the world’ – they are the ones in charge of licensing Registered Dietitians in the U.S.,” he says. Take a look at that link and open the links he provides to see what a mess – what a disgrace, really – our situation is.

Another post of Authority Nutrition is http://authoritynutrition.com/15-million-reasons-for-low-fat-diets/. This one takes off on the American Diabetes Association (ADA), which still recommends that “people eat a low-fat, high-carb diet. According to them, diabetics should eat 45-65 grams of carbohydrates per meal.” Kris calls that a “crime against humanity.”

Still not convinced? Impossible, but here’s another anyway: http://authoritynutrition.com/6-reasons-i-do-not-trust-mainstream-health-authorities/. Tell me you’re read these three Kris Gunnars’ posts at Authority Nutrition and still trust your government, your medical associations (whom doctors and Medicare use for guidelines) and food ‘manufacturers.’

The Nutrition Debate #256: Prediabetes: An Existential Question?

“As part of a series in the British Medical Journal on overdiagnosis, which looked at the risks and harms to patients of expanding disease definitions, Yudkin and Montori analyzed the concept of prediabetes,” began a Medscape Medical News article. The lead author of the BMJ essay is John S. Yudkin, emeritus professor of medicine, University College, London.

This is NOT the legendary John Yudkin, founding professor of the department of nutrition at Queen Elizabeth College, London, who advocated for a low-carb dietary and lobbied against sugar in the 60’s and 70s. That John Yudkin retired in 1971, published “Pure, White and Deadly” in 1972, was promptly ostracized by academicians and ridiculed like Atkins in the U.S., and died in 1995. Neither is this John S. Yudkin a son of the famed MD; he’s probably a nephew though.

The arguments the BMJ piece read like the “con” side of an Oxford debate. The Medscape author concludes, “The existential question of whether prediabetes is a useful concept or should be abandoned is largely philosophical.” In this I agree, but the arguments presented by Yudkin and Montori do raise several issues that deserve consideration.

The first is that “prediabetes is a heterogeneous concept,” e.g., definitions “overlap” and from the start create confusion. The original concept of “intermediate hyperglycemia,” Medscape points out, was termed “impaired glucose tolerance” and was “based on the oral glucose tolerance test (OGTT).” While used today and still the “gold standard,” this procedure is time consuming and expensive. An endocrinologist I saw back in the 80’s had me tested in a hospital outpatient setting.

Then, in 1997 that procedure was supplanted by simply drawing blood and sending it to the lab like other blood tests. This new “intermediate hyperglycemia” procedure was called “Impaired Fasting Glucose” and was revised in 2003 “to expand the range of qualifying values.” That was when the diagnosis of diabetes was dropped from 140 to 126mg/dL and the new category of “prediabetes” created, defined as two consecutive fasting glucose readings between 100 and 125mg/dL.

“Only recently,” in 2010, Medscape continues, “a nameless intermediate category based on A1c was designated.” It is “nameless,” I suspect, to allow for the dust to settle. Since 2010 the medical profession, through disciplinary rivalries, has engaged in internecine battles on guidance to clinicians treating a likewise “heterogeneous” patient population, allowing clinicians to treat some elderly or intractable patients to an A1c of 8.0%.  Prior to 1997 the ADA defined DM as an A1c ≥7.0% (est.Aver.Glucose:154mg/dl), then in 2003 ≥6.5% (eAG:140mg/dL), then, if we are to believe this chart, in 2010, ≥6.0% (eAG:125mg/dL). The ADA, however, as well as the WHO/IDF, now still define DM as an A1c of ≥6.5% and A1c’s of 6.0% - 6.4% as “intermediate hyperglycemia” and thus “prediabetes.” N.B: Others define full-blown DM as low as 5.8%.

The second issue that should be recognized in “the case against considering elevated but subdiagnostic levels of glycemia a disease unto itself that deserves intervention” is whether such a diagnosis “can provide benefit by precisely identifying those who will develop diabetes…” That was a key question examined by the authors, Medscape says, and the surprising answer, Yudkin and Montori say, regardless of how pre-diabetes is defined, is “no.” “Less than one half of all such people develop diabetes within 10 years.” I knew it was less than 100%, but “Less than one half…” came as a surprise to me.

“Another important question is whether treatment for prediabetes can prevent diabetes onset,” Medscape says. The answer to this important question, both Medscape and the BMJ authors say, is “yes,” the “diabetes risk among high-risk individuals can indeed be reduced.” Whew!!! I haven’t been wasting my time for the last several years. But here Yudkin and Montori take the position that “diabetes onset was merely delayed by 2-4 years, at high cost and only among a subset of the intervention groups.” This last sentence – especially the last clause (“only among a subset of the intervention groups”), is critically important for my readers. YOU want to be a part of that subset that not only delays the onset of diabetes but reverses prediabetes. This exclusive club is a subset-of-the-subset exception, and YOU can be a member, really. But you have to change your diet. Stop eating the carbohydrate foods (sugars and starches) that raise your blood sugar. You have to recognize that your “sugar” (glucose) metabolism is broken. If you’re “prediabetic,” you are carbohydrate intolerant.

Afterword: The best part of this hyperbolic debate over the “risks and harms” of overtreatment were the “comments” in the BMJ. Click on this link if you’re interested. The first two are academic essays in themselves and, while good, got just one or two “likes.” The 9th down was from a practicing doctor who argued the “pro” prediabetes case. His short comment got 50 “likes” at last count (including mine). I hope the editors and readers of the BMJ take note. And besides, even if you never become diabetic, your heart disease and dementia risk closely correlate with your blood glucose levels. Control your blood sugar!

The Nutrition Debate #255: “Risk Prediction with triglycerides…”

Virtually everyone who has blood taken at the doctor’s office these days gets a standard “lipid panel.” The cholesterol test. Your doctor gets assayed values for Total Cholesterol (TC) and High-density lipoproteins (HDL), the so-called “good” cholesterol, and more recently a value for non-HDL cholesterol in lieu of very low density lipoproteins. It also has a related measurement, serum triglycerides, a fat molecule circulating in your blood. In addition to these measurements, the lipid panel also reports on low density lipoproteins (LDL), a calculated value using the Friedewald formula (LDL=TC-HDL-TG/5).

Your doctor will use the Total Cholesterol, if it’s over 200mg/dL, to try to persuade you to take a statin drug. Statins effectively lower LDL cholesterol, known as the “bad” cholesterol, and therefore lower TC. (TC=HDL+LDL+TG/5). This is a dubious benefit for virtually everyone except those with coronary artery disease (CAD). In patients with existing coronary artery disease, statins are indicated for secondary prevention, to prevent a heart attack.

Most lipid panels also include a ratio, Total Cholesterol to triglycerides (TC/TG), as a cardiovascular “risk indicator.” Doctors use this to evaluate the risk of cardiovascular events such as heart attack (Myocardial Infarction or MI), stroke, and death, among other outcomes. In The Nutrition Debate #27, I presented the case that “the strongest predictor of a heart attack” is the ratio of triglycerides to HDL cholesterol, or TG/HDL. That column, written three years ago, applies to the general “healthy” population and has proved to be one of the most popular I have written. It’s also one of my editor’s favorites.

A more recent study, published in Clinical research in cardiology: official journal of the German Cardiac Society, provides a fresh look at “Risk prediction with triglycerides in patients with stable coronary disease on statin treatment.” The aim of this prospective study was “to analyze the role of fasting and postprandial triglycerides (TG) as risk modifiers in patients with coronary artery disease (CAD).” The trial used standardized measurements of oral triglyceride and glucose tolerance in 514 patients with stable CAD, confirmed by angiography, 95% of whom were treated with a statin.

After 48 months follow-up, using both fasting and postprandial measurements and primary outcomes of cardiovascular death and hospitalizations, the researchers sought to determine if either fasting and/or postprandial serum triglycerides were a risk indicator and could predict the primary outcome. The results were surprising – indeed, startling, in my opinion.

“CONCLUSIONS: Fasting serum triglycerides >150 mg/dL independently predict cardiovascular events in patients with coronary artery disease on guideline-recommended medication [statin drugs]. Assessment of postprandial TG does not improve risk prediction compared to fasting TG in these patients.”

The RESULTS were unequivocal. For fasting TG >150 vs. <106 mg/dL, the hazard ratio (HR) was 1.79. Translation: If you have CAD and are taking a statin, and your triglycerides are over 150 mg/dL, you have an ~80% greater chance of dying or being hospitalized for CAD over 4 years than if your triglycerides are <106/mg/dL.

The analysis then concluded, “Risk prediction by TG was independent of traditional risk factors, medication, glucose metabolism, [and] LDL- and HDL-cholesterol. Total cholesterol [and] LDL- and HDL-cholesterol concentrations were not associated with the primary outcome [cardiovascular death and hospitalizations].”

MY TAKEAWAY: If you have been diagnosed with coronary artery disease (CAD), your doctor will surely prescribe a statin, the guideline-recommended medication, and you should take it. But remember that your fasting serum triglycerides are an independent risk factor. Fortunately, they are also a modifiable risk factor, which is to say, one that YOU can change. But there’s no magic bullet. Prescriptions for Niacin and fibrates work for some people, and may be indicated for very high TGs, but the best way to lower your fasting serum triglycerides and to keep them low  is with Omega 3 fatty acids (2g fish oil/day) (http://www.nlm.nih.gov/medlineplus/druginfo/natural/993.html) and lowering the carbs in your diet.

Your doctor is not likely to have seen this research from the German Cardiac Society. My intrepid editor found it for me.  Besides, fasting serum triglycerides from 150- 199 mg/dL are currently regarded as “borderline” in the medical guidelines, so your doctor will likely says something inane like, “We’ll have to watch that,” or “Cut back on your drinking.” But remember, the hazard ratio for “primary outcomes” for TGs above 150 mg/dL was 1.79. Do you want to become a statistic?

Take a look at The Nutrition Debate #68, “Triglycerides, Fish Oil and Sardines,” to see my n=1 odyssey with triglycerides. I started out “borderline,” but my most recent TGs have been 51, 55, 34, 49, 47, 58, 54, 56, 65, 53, 31, 38, 52, 49, 50 and 34.

The Nutrition Debate #254: Saudi Approach to Diabetes

In this video interview with transcript from the recent European Association for the Study of Diabetes (EASD) meeting, Anne Peters, MD, at medscape.com, interviews Saudi MD and diabetologist Aus Alzaid. Dr. Peters asks, “…knowing the epidemic of diabetes that you are having in Saudi Arabia, can you tell us what diabetes care is like there?” Dr. Alzaid replies, citing International Diabetes Federation figures, that “Saudi Arabia has the highest rate of diabetes in the world after the small island nations in the Pacific.” Citing previous studies, he says, 1 in 4 people after the age of 30 has diabetes.”

But that it seems is part and parcel of the problem, Dr. Alzaid avers: “That part of the Middle East is steeped in history and tradition and culture, which means a lot to people. Then we have diabetes as a condition, which has to do with the person’s perception of the lifestyle modifications that must be made.” “I don’t know of any Saudi family that doesn’t have a member or two with diabetes,” he adds.

Dr. Peters replies by relating how she “work(s) with the Latino population in East Los Angeles where everybody just shrugs and says, ‘Everyone in my family has diabetes, so of course I have it too.’” In this respect I think the good doctors make a point. Resistance to change is strong, and fatalism commonly prevails. But would that be so if there was a “treatment” that worked? I read on in hope of enlightenment.

Dr. Peters: “Most healthy 30-year olds don’t go to the doctor. Are you making a push to convince young, healthy people to be checked earlier?”

Dr. Alzaid: “Absolutely, and there are messages going out about lifestyle modification. In our institution, we have Diabetes Awareness Day in November. [Whoopee!] It is still an overwhelming issue, and we are doing research to find out why we have such a high rate of diabetes.” [There’s money well spent…if it’s good research. Read on and you decide.]

Dr. Peters: “Have diet and rates of physical activity changed? What have you seen over the course of your career?”

Dr. Alzaid: “Decades ago, people were more mobile. Very little food was available in years gone by, but over recent decades, with the dividends of good fortune [oil revenue], there has been a ‘constant feast.’

Okay, the well-meaning Dr. Peters is turning the conversation to “diet and exercise,” the Western meme that we are eating too much and exercising too little. Well, at least the conversation is beginning to turn to diet. Let’s see where it goes.

Dr. Alzaid continues: “There are cultural things that we adhere to as part of our social etiquette. Food items such as rice and dates are very popular in our part of the world, and they are obviously very heavy in terms of calories. Fizzy drinks are commonly consumed.” That’s it, folks. That’s the good Saudi doctor’s understanding of nutrition, as captured in this Diabetes-in-Control piece. It’s all about calories-in/calories-out. True, there’s no mention of eating fat making you fat, or anything about dietary cholesterol. But neither is there so much as a word about carbohydrates (think ‘rice’ and ‘dates’).

Newsflash, Dr. Alzaid: Dates and rice and fizzy [sugary] drinks are all carbohydrates! Sugar and starch! 100 grams of pitted dates, about 4 Medjool dates, are 277 calories, of which 266 (96%) are sugar, 7 protein and 1 fat, plus a little indigestible fiber and ash. 100 grams of medium grain white rice, about 3.5 ounces, is 130 calories, of which 116 are carbohydrates, 10 protein and 2 fat. I don’t know what kind of “fizzy drinks” Saudis use to quaff their thirst, but I’ll assume (generously) it’s a Coca Cola. A 12 ounce (370g) cola is 152 calories, all sugar. That’s ten (10) teaspoons of sugar in one can of “fizzy drink.”

So, I think that Dr. Alzaid has identified the problem with the Saudi diet; he just hasn’t named it correctly. The “constant feast” he refers to is a carbohydrate feast, not a calorie feast. The fact that Dr. Alzaid describes “rice and dates” (part of the Saudi social etiquette) as “obviously very heavy in terms of calories” implies to me that it is his understanding that it is the calorie content of these foods, not the carbohydrate content, that is the cause of the Saudi diabetes epidemic. But what is there to do about it? It’s a cultural thing, and “that part of the Middle East is steeped in history and tradition and culture, which means a lot to people.” To which Dr. Peters replies, empathetically, ‘Everyone…has diabetes, so of course I have it too.’ Of course, it is a problem of education, which both doctors point out emphatically.

And the Saudi Ministry of Health has launched a public-awareness campaign “to tackle the problem with the right lifestyle.” The right lifestyle? Diet and exercise? Eat less (of the same carbohydrate-dominated diet) and move more? That is a lifestyle change that is guaranteed to fail. Diabetics are carbohydrate intolerant by definition. The best treatment for type 2 diabetes is a very low carbohydrate diet. The ‘right lifestyle’ to prevent type 2 diabetes is a reduced carbohydrate diet.

The Nutrition Debate #253: The “Diabetes Plateau”

This Diabetes-in-Control news piece begins, “Diabetes rates among adults in the United States are finally leveling off, new data from the Centers for Disease Control and Prevention suggest.” The headline of the piece is less speculative. It simply declares, “Diabetes Rates in the US Have Finally Plateaued.” Headlines often do that. They try to grab your attention. In this case, with the primary audience being clinicians and other health care providers, it also has a self-congratulatory tone that is entirely unwarranted, as the “fine print” of the article makes clear.

The Diabetes-in-Control piece is based on “findings from a National Health Interview Survey (NHIS) on both prevalence and incidence of diabetes from 1980 to 2012” published online in the Journal of the American Medical Association (JAMA). Prevalence refers to its widespread, existential presence while incidence, in the epidemiological sense, relates to the initial appearance of a new condition (diabetes) in the population. Both, in the NHIS survey, were self-reported by the patient. The findings which led to the headline are a reduction of the incidence of type 2 diabetes in the general population.

Among the 664,969 adults aged 20 to 79 who responded to the NHIS survey, the prevalence of diabetes was 3.5% in 1990, 7.9% in 2008, and 8.3% in 2012. The incidence per 1000 people was 3.2 in 1990, 8.8 in 2008 and 7.1 in 2012. The annual percentage change in both prevalence and incidence was not significant in the 1980s; however, both jumped significantly from 1990 to 2008. Then, from 2008 to 2012, prevalence plateaued and incidence diminished significantly.

“However,” Diabetes-in-Control highlighted, “both diabetes incidence and prevalence continued to increase at a significantly greater rate for young adults aged 20 to 44 years compared with older adults and for black and Hispanic adults compared with white adults.” In addition, “The rate of increase in prevalence was higher for those with a high school education or less compared with those with more than a high school education.” Hmmm. Another sociodemographic disparity. I wonder if dietary choices had anything to do with that. (Catch the sarcasm, pullese.)

The sub-head in the article asks, “Is It All About Obesity?” Phrasing it as a question, of course, begs the answer. The author notes that a little mumbo-jumbo (a statistical adjustment) “reduced the annual percent change in incidence by about a third…” with the study author telling Diabetes-in-Control, “This suggests that the leveling off of obesity that occurred over the same period explains a large part of the diabetes plateau, but not all of it.” The knock-out punch was, “The BMIs in the NHIS study were self-reported and therefore most likely underestimated.” Do ya think? Do you even know your own BMI?

Searching for another explanation for “the diabetes plateau” the Diabetes-in-Control author speculates, “Beyond obesity, other possible influences on the reduction in diabetes rates include improvements in diet and activity levels and changes in diagnostic criteria.” Wow! If I read this correctly, the author implies that we are getting obese at a lower rate than before; that she adduces this from the finding of this epidemiological study that since the incidence of diabetes diminished significantly from 2008 to 2012, that obesity associated with the incidence and prevalence of type 2 diabetes did as well.

The only evidence she offers for this association – the decline in incidence of type 2 diabetes with an assumed decline in obesity, contrary to all other studies of the population known to me – is “improvements in diet and activity levels.” Oh, how I wish that it were so. That we could realize an actual result by just saying it over and over: Improve your diet and activity levels (eat a balanced, USDA recommended one-size-fits-all diet and exercise more), and abracadabra you will become thin.

Maybe the explanation for “the diabetes plateau” lies instead in the “changes in the diagnostic criteria.” Do you think this could affect the way that 664,969 people self-reported on their condition? Could that alone have “confounded” the study results to the point that all the other “statistical adjustments” were totally insignificant by comparison? Do ya think?

“The 1997 lowering of the fasting plasma glucose cutoff from 140 mg/dL to 126 mg/dL may have increased the diabetes incidence…,” the CDC study author noted. I love it! “May have,” she says. Whereas, “… the more recent [2010] shift to use HbA1c for diagnosis may have reduced it, since HbA1c detects fewer cases of hyperglycemia,” she said. Interesting indeed, and contrary to my own understanding. The reason the medical establishment has shifted from “fasting” to A1c is for the express purpose of capturing blood glucose postprandial “excursions,” i.e. hyperglycemic spikes due to impaired glucose tolerance (IGT) over a 3-month period. Fasting glucose testing does not do that. It just captures impaired fasting glucose.

The Nutrition Debate #252: “400 Calorie Meals for Fall”

“400 Calorie Meals for Fall,” the email from fitday.com proclaimed. Exciting, I thought. Small meals. I’m always looking for ideas for small meals that are very low in carbs. The reason, besides the fact that I have been a type 2 diabetic for 28 years, is that if they are very low carb, moderate protein and high fat, I won’t be hungry after eating it. I will be able to eat just 3 small meals a day, without snacks, and always feel satisfied. And I will lose weight, which it seems we all always need to do.

So, I opened it to find 10 more links to recipes that promised “delicious healthy meals.” “Try any of these low-calorie dishes and see just how great it feels to eat well while still staying healthy,” FITDAY urged. Sounds promising, I thought, since FITDAY is well known for helping people who both need and want to lose weight keep track of the macronutrients of the foods they eat. Macronutrients are the carbohydrates, protein and dietary fats that add up collectively to total calories. Carbs and protein each contain 4 calories per gram, alcohol has 7, while fat contains 9 calories per gram.

 So, I started reading the FITDAY descriptions to check them out. And sure enough each of the 10 small meals was 400 calories or less. I noticed, however, that only the total calories and fat grams were provided in the FITDAY write-ups. There was no mention of carbs or protein in the FITDAY narratives. Okay, I thought, that’s “old thinking.” Most dieters still think that only calories count and that dietary fat makes you fat. But, for the enlightened reader, a fuller nutritional analysis is necessary and surely would be included with the recipes. So, I looked further.

Each link opened to a different website that provided the ingredients and preparation needed to make each meal. Of the 10 links, however, only 5 provided a nutritional analysis, usually as a sidebar. And of those, the carb counts per serving for these small meals were humongous, including 41g for recipe #4; 45g for #5; and 47g for #10. Those numbers were so large that 1) fat burning would be impossible (the body will burn the carbs first), and 2) when the carbs were “burned,” the body craves more carbs (the sugar burner’s “hunger syndrome”). If I ate these meals, my blood sugar would spike like crazy and then crash (leaving me both tired and hungry). Is this what FITDAY means by “how great it feels” to eat “healthy meals”?

Okay, not all FITDAY users are type 2 diabetics, or even pre-diabetics. But it’s safe to infer that virtually all of them are overweight or obese, and overweight correlates very highly with pre-diabetes and type 2 diabetes. In fact, it is the leading “risk factor” for a diagnosis of type 2 diabetes. Somewhat over 85 percent of type 2 diabetics are overweight or obese, and the percent of U.S adults (≥20 y.o.) who are overweight, including obesity, is 69 percent (2011-2012). So, why would FITDAY advocate that its users “incorporate [these] delicious healthy meals into [their] daily diet”? That’s worth pondering.

Well, FITDAY could still believe that only total calories and fat grams count. After all, the Dietary Dictocrats at the USDA still tell us all (EVERYONE) to “eat less and exercise more.” But the government will be the last bastion of misinformation in the cause of the “diabesity” epidemic. And they will be preceded only by the AHA and the ADA, whose corporate sponsorship by agri-business and big pharma are nearly as corrupt and/or misguided as the Federal Government’s approach to funding research. It’s just such a myopic view and dogmatic attitude towards obesity research and public health policy that has plunged the entire U.S. population into this 60-year dietary experiment, with the disastrous outcomes we see unfolding before us.

Besides, can we really blame FITDAY if their potential user population – those who are exposed to their advertisers since their site is “free” – itself believes that only total calories and fat grams count? That’s still the main message we hear from main-stream media, both print and TV. After all, total “members” are how FITDAY sells their site to advertisers. So, until the pendulum swings in favor of using macronutrient distribution as the means to determine whether a meal is “healthy,” we will continue to be blithely “misinformed” and not know that eating 400 calories meals that are low carb, not low fat, will lead to 1) losing weight easily, 2) feeling satisfied (full) longer, and 3) regulating blood sugar better with lower A1c’s.

But then, if we all learned to do that, FITDAY would lose “members.” We would have discovered 1) what foods cause us to gain weight (carbs, not dietary fat), 2) feel hungry a few hours after eating, and 3) spike our blood sugars (if we have impaired glucose tolerance). And that wouldn’t be good for (FITDAY’s) business, specifically their advertising revenues.

Ask yourself, when you have discovered “how great it feels” to eat “healthy meals” that are low-carb, and you lose weight, and are full of energy, and your doctor likes what he/she sees and pats you on the back, why would you need FITDAY?

The Nutrition Debate #251: High-fat dairy ‘good’; low-fat dairy ‘bad’

Good news from Sweden, via Vienna, the site of this year’s European Association for the Study of Diabetes 2014 meeting. This paper was presented by an epidemiologist from the Lund University Diabetes Center in Malmö, Sweden. According to Medscape Medical News, who reported on it here, “people who consume a large amount of high-fat dairy products… have a 23% lower risk of developing type 2 diabetes than those who consume lower levels…” That’s good news for full-fat yoghurt, cheese, cream and whole-fat milk fans. My Swedish relatives, and people the world over, should be rejoicing.

Admittedly, the portion size spread was large (>8 vs. <1), but that still accounted for 20% of the 26,930 Swedish people aged 45 to 74 years included in the study. Swedes do love their yoghurt with fruit and coffee and bread for breakfast. What interested me most about this study, though, was that both the Swedish scientists and the Medscape writer reporting on it were both open to the findings. The Medscape banner was, “Big Intake of High-Fat Dairy May Be Protective for Diabetes.” That has got to get the attention of skeptics, which is to say, the mainstream medical establishment. That in itself is news.

Of course, I am probably being naïve. A large cohort of the Swedish population is already eating LCHF (low-carb, high-fat). Andreas Eenfeldt, MD, The Diet Doctor, reported on that some time ago. And he was among the first to herald the decision of the Swedish Government to change its official dietary recommendations in this post. So, the Swedish scientists who initiated this study, declaring themselves to have “no relevant financial relationships,” were like the camel who stuck his nose into the tent. Their aim was, “to clarify the risk for type 2 diabetes associated with the intake of the main dietary [saturated] fat sources – namely, meat, fish and dairy. I added “saturated” because PUFAs (polyunsaturated fatty acids from vegetable and seed oils) have become the main dietary fat source for most Americans (86% vs. 14%, according to this 2008 USDA report, “Dietary Assessment of Major Trends in U.S. Food Consumption, 1970-2005,” page 12 and table 6).

In the cloak of pure, unbiased science, to the extent that is possible, they accepted certain tenets of “perceived wisdom” while opening the crack in the “growing body of evidence supporting the need to shift the focus of dietary advice away from nutrients like total or saturated fat to the differential healthfulness of food sources like dairy products or meat.”  The hazard ratios (HRs), after 14 years of follow-up, were striking. Most impressive was that high-fat fermented milk [yoghurt] consumption …reduced the risk of developing diabetes by 20%. The portion size here was just 180ml, or 6oz (3/4 cup!).

As usual, the scientists raised more questions than they answered, looking for new grant money, obviously. One of them said, “To place the observed beneficial association with high-fat dairy in context, it is important to tease out if the higher risk of no association of low-fat dairy products with diabetes was because low-fat products have extra added sugar instead, which we know from other research to be detrimental” (emphasis added by me). She also noted that, “Other beneficial health effects might be due to other beneficial compounds in dairy, such as probiotics [present in fermented foods like cheese and yoghurt] and other nonfat nutrients such as vitamins and minerals.”

Medscape also noted that while “previous epidemiological studies have indicated a high intake of dairy products is associated with a decreased risk of developing type 2 diabetes,” the Swedish scientists said, ‘but it has been suggested that mainly low-fat dairy lies behind the observations.’” However, Medscape concludes, “The findings presented here suggest only high-fat content is protective.” “In comparison with high-fat dairy products, a large intake of low-fat dairy was associated with increased risk for type 2 diabetes, but this association disappeared after additional adjustment for protein.”

Another interesting finding reported by Medscape was that “molecules with odd numbers of carbon atoms (15 and 17), which are found in dairy products such as yoghurt, cheese and milk, appeared to have a protective effect. This contrasts with evidence suggesting that even-chain saturated fatty acids, as found in alcohol and margarine [demonizing one by association with the other] are associated with a greater risk for type 2 diabetes.” More studies (money) needed here too.

“The results in relation to intake of meat and meat products were found to be in line with previous findings,” Medscape reported. “An increased risk for diabetes was found for meat and meat products regardless of fat content.” The camel’s nose knows not to go any further. But Swedes and Europeans in general love dairy and eat far less meat than Americans.

The Medscape article doesn’t mention any finding with respect to the other source of dietary saturated fat: fish. Fish is sacred to Scandinavians in general, and salmon is 29% palmitic acid, an even chained saturated fat. The last time we visited Sweden, in every home we visited the gracious host served salmon with a crème fraiche and caviar topping, with aquavit and a beer chaser, of course. Yum, yum. And full-fat yoghurt and fruit and coffee (no bread for me) for breakfast. Real food.

The Nutrition Debate #250: “40% of American Adults Will Develop Diabetes”

When I was growing up, I remember Doris Day singing “Que será, será.” I was 15 years old (in 1956), and I thought of it as an optimistic song that held the promise of a future of boundless opportunity and possibilities. Remember the lyrics?

When I was just a little girl	When I grew up and fell in love	Now I have Children of my own
I asked my mother	I asked my sweetheart	They ask their mother
What will I be	What lies ahead	What will I be
Will I be pretty	Will we have rainbows	Will I be handsome
Will I be rich	Day after day	Will I be rich
Here's what she said to me	Here's what my sweetheart said	I tell them tenderly
Que sera, sera	Que sera, sera	Que sera, sera
Whatever will be, will be	Whatever will be, will be	Whatever will be, will be
The future's not ours to see	The future's not ours to see	The future's not ours to see
Que sera, sera	Que sera, sera	Que sera, sera
What will be, will be	What will be, will be	What will be, will be
		Que Sera, Sera

At the time it never occurred to me that the actual message of the song, contained in the response, was “fatalistic,” which it clearly was. It just never occurred to me. I think that’s because I grew up in a privileged environment. I believed the answer to the question was, in large part, up to me. As I grew older, I often thought about how chance played a role in my destiny, but I still considered that I had free will and that I chose the path in life that I travelled and the things that came of it.

The title of this blog post challenges that premise. It is a simple declaration, from researchers at the Centers for Disease Control and Prevention (CDC), that “approximately 40% of American adults will develop diabetes in their lifetime.” And that, “In Hispanic men and women, and non-Hispanic black women, the projected increased risk is even higher, over 50%...” These findings came to my attention through a Diabetes-in-Control news item reporting on a paper in The Lancet.

The Lancet’s hypothesis was that since diabetes incidence has increased and mortality (in the total population) has decreased greatly in the USA, there would therefore be “substantial changes in the lifetime risk of diabetes.” So besides estimated “remaining lifetime diabetes risk,” the study also looked at “life-years lost due to diabetes” and “years spent with and without diagnosed diabetes.” “Because of the increasing diabetes prevalence, the average number of years lost due to diabetes for the population as a whole increased by 46% in men and 44% in women. Years spent with diabetes increased by 156% in men and 70% in women,” The Lancet’s statistical analysis concluded.

The Lancet’s INTERPRETATION of the CDC’s report and their (The Lancet’s) FINDINGS:

“Continued increases in the incidence of diagnosed diabetes combined with declining mortality have led to an acceleration of lifetime risk and more years spent with diabetes, but fewer years lost to the disease for the average individual with diabetes. These findings mean that there will be a continued need for health services and extensive costs to manage the disease, and emphasise the need for effective interventions to reduce incidence” (emphasis added).

The Lancet’s and the CDC’s projections are a dispassionate analysis of statistical trends - exactly what a study like this is supposed to do. And the call for “the need for effective interventions to reduce incidence” of diabetes should be a clarion message to the medical establishment. Instead, the message that I think the medical establishment gets is “that there will be a continued need for health services…to manage the disease.” In other words, job security for the medical establishment in managing (i.e., treating) the increasing numbers of diabetics and the progressive course of the disease.

Okay, I am cynical and maybe a bit unfair. I don’t doubt that The Lancet is sincere about “the need for effective interventions to reduce incidence.” Can they be blamed for a myopic view of what such interventions might be? To confining their perspective to pharmacological treatments? New drugs? Surgery? After all, they can report on public health policy and nutrition research, but the government only seems willing to support research in line with predetermined dogma of “good” public health policy and nutrition. What hope is there that the outcome will be other than, “Whatever will be, will be.” Que será, será.

The Nutrition Debate #249: Type 2 Diabetics: You Have a Choice.

If you have been diagnosed a type 2 diabetic, your doctor (YOU actually) have a choice of long-term treatment options: 1) insulin injections, 2) oral antidiabetic medications, or 3) major dietary changes. I’ve oversimplified it, but this is an overview so the unschooled reader can see the “big picture.” Besides, I’m not without my own biases, as you’ll see.

To illustrate the insulin route, I cite a rather pedantic article, originally published in 2011 in Diabetes in Control, a source which bills itself as “News and Information for Medical Professionals.” It was re-posted on September 11, 2014, to promote the Humumin R insulin product. Why do I say that? From the advertising. The article is accompanied by ads for Eli Lilly and Company’s Humulin R,* as you scroll down the screen, 5 of them: top (1), side (3) and bottom (1). In fact, a hyperlink under the title reads, “Humulin Insulin Special Edition September 2014.” Maybe the whole article is just a paid advertisement.                                  * Specifically the U-500 version, a concentrated form for insulin-resistant patients requiring more than 200 units a day.

I have nothing against injecting insulin. Insulin is a good thing, and it works. And I have nothing against advertising. I do have a problem, however, when advertising and clinical practice advice get mixed together. I have an even bigger problem when the first two authors of the piece just happen to be Editor-in-Chief and Publisher, respectively, of the Diabetes in Control “newsletter.”  I didn’t know that, however, because it is revealed in the “disclosures,” as it is in a peer-reviewed medical journal. There are no disclosures. I knew it because I have been reading this “information source for medical professionals” for years.

But if you didn’t know, and care to go to the trouble, Google David Joffe (the Diabetes in Control Editor-in-Chief), and learn, “Dave speaks on diabetes, hypertension, and related co-morbidities for Abbott, Bayer, Pfizer, Novo Nordisk, Lilly, Sanofi, Sankyo, and Medtronic” (emphasis added). Or, “Dave is a non-physician member of the Lilly Primary Care Diabetes Advisory Board.” Admittedly, conflicts aside, reading his full curriculum vitae, the guy has mega bona fides.

Nevertheless, the “Practice Pearls” for insulin as a treatment for newly diagnosed Type 2s are a good “takeaway”:

●     By removing the glucolipotoxicity you can improve beta cell function.

●     Since Type 2 diabetes is a progressive disease and will worsen over time, by improving beta cell function the progression of diabetes can be slowed down to prevent complications

The 2nd long-term treatment option is also pharmacotherapy. Oral antidiabetic medications have evolved from the early days when insulin-secreting sulfonylureas were the only option. Today most newly diagnosed type 2 diabetics and even “pre-diabetics” (those that can “tolerate” it) are started on metformin. The dose is quickly increased (“titrated”) until you are “maxed out” and then a second agent, and even a third med is added to the “cocktail.” Since, as we’ve seen above (in the 2^nd bullet), the “perceived wisdom” is that “type 2 diabetes is a progressive disease and will worsen over time,” the assumption is that many type 2 diabetics who are treated with orals will “progress” to insulin dependency.

The major downside to injecting insulin is hypoglycemia, or low blood sugar. It can lead to coma and death. That is because you, the patient, has to decide on the amount to inject before each meal or snack.  Your care giver can help on the amount of “basal” insulin you inject once or twice a day, but only you can decide how much to inject before each meal ‘cause your doctor is not at your side 24/7. Even if you have a pump and continuous glucose monitoring (CGM), which few do, you have to figure the dose of mealtime insulin that you inject each time. As a result, many patients, and their caregivers including clinicians and CDEs, do not try for “tight glucose control.” They inject too little to avoid the danger of hypoglycemia.

The exception to this would be the pioneer on glucose meters, glucose monitoring, and low-dose insulin regimens, Dr. Richard K. Bernstein. His book, Diabetes Solution, is an authoritative source for all diabetics. And Dr. Bernstein’s Diabetes Forum (registration required), accessed from the same link, is a great place for learning about all aspects of diabetes.

The downside for oral antidiabetic medications is 1) all drugs have side effects and 2) if you do nothing else and just let your doctor monitor and treat your worsening glucose metabolism, your type 2 diabetes will “progress” and “worsen over time.” And if the progression of the disease cannot be slowed down, you run the risk of developing “the dreaded complications,” not to mention macrovascular complications like heart disease.

Now, the 3^rd long-term treatment option for type 2 diabetes or pre-diabetes: major dietary changes. Pros: no insulin (and no hypos), few if any oral meds (and no side effects from same), and greatly improved (not worsening) glucose control, plus a bonus: improved BP and blood lipids (higher HDL, lower triglycerides, stable Total Cholesterol and LDL). Less of that nasty MG (see The Nutrition Debate #246 here) stuff too. And another under recognized benefit: you will lose weight, have lots of energy and feel great! Cons: you have to give up the processed foods and carbohydrate-loaded junk that made you sick in the first place. It’s your choice. And yours alone.