Retrospective #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, bariatric means “relating to or specializing in the treatment of obesity.” Well, non-surgical bariatric medicine is what Yoni Freedhoff, MD, an Ottawa, Canada, family doc practices.  He also founded Ottawa’s Bariatric Medical Institute, “a multidisciplinary, ethical, evidence-based nutrition and weight management centre.” He quips in “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 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) 2014 issuance of “Sugar, Heart Disease and Stroke” – what Yoni calls a “world leading sugar statement” -- she gave me a heads up.

Yoni described the HSF position statement “as hard hitting as any I’ve read,” providing “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 thrust. It was what enabled the HSF to make their recommendations possible in the first place: HSF’s decision to “divorce themselves from their throngs of food industry partners.”

Yoni’s exhilaration is palpable. 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 continues, “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 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.”

OTTAWA IS very LUCKY TO HAVE YONI FREEDHOFF SERVING THE “NON-SURGICAL BARIATRIC” POPULATION.

Muckraking is a messy business, though. Many a good researcher and clinician has in the past had their career ruined by going against the flow, unable to get research funds or be published in a peer-reviewed journal, by advancing an alternative hypothesis or clinical approach to practicing medicine. Two names that advocated such views that come to mind while I have been writing are Kurt Harris, MD, (The Archevore Diet) and Kris Gunnars, (Authority Nutrition).

I wrote about Dr. Harris several times, beginning in 2011 with “Retrospective #19.” Dr. Harris is today a radiologist in Sturgeon Bay, WI, but he figured it all out way ahead of everyone. If I ate today (or then), from “the beginning,” the way he advocated and I related in #19, I could not have improved on it. I daresay, the same goes for all of us.

Kris Gunnars usually blogged about healthy eating, but occasionally he went off on a tangent into the politics of nutrition. One of my favorites was, “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’ – the ones in charge of licensing Registered Dietitians in the U.S.”

Another withering Authority Nutrition post was “15 Million Reasons for Low Fat Diets.” That’s the amount of food industry funding the American Diabetes Association (ADA) receives, while still recommending that “people eat a low-fat, high-carb diet. According to the ADA, diabetics should eat 45-65 grams of carbohydrates PER MEAL.”

Then there’s this Gunnar’s post: “Six Reasons I Do Not Trust Mainstream Health Authorities”. You can’t find any of these stories at the hyperlinks I provided in the original #257 but you can still read them by title search. Do you still trust your government, your medical associations (who guide doctors and Medicare) and your food ‘manufacturers’?

Retrospective #256: Prediabetes: An Existential Question?

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

This is not the legendary John Ludkin, 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, and was promptly ostracized by academicians and ridiculed like Atkins in the U.S. He died in 1995. Neither is this John S. Yudkin a son of the famed MD; he’s probably a nephew.

The arguments in the BMJ piece read like the “con” side of an Oxford debate. The Medscape author concluded, “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. When I was tested back in the 80’s, it was as a hospital outpatient.

That procedure was supplanted in 1997 by simply drawing blood and sending it to a lab. This new “intermediate hyperglycemia” procedure was called “Impaired Fasting Glucose.” It was revised in 2003 when the diagnosis of diabetes was dropped from 140 to 126mg/dL and the new category of “prediabetes” created (100 to 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. It allows 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, in 2010, an upstart group suggested a more aggressive standard: ≥6.0% (eAG:125mg/dL). The ADA, however, as well as the WHO/IDF, now still define T2DM as an A1c of ≥6.5% and A1c’s of 5.7% - 6.4% as “intermediate hyperglycemia” and thus “prediabetes.”

The second issue that should be recognized in “the case against considering elevated but sub-diagnostic 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 half…” surprised me.

“Another important question is whether treatment for prediabetes can prevent diabetes onset,” Both Medscape and the BMJ say “yes,” the “diabetes risk among high-risk individuals can indeed be reduced, but “…only among a subset of the intervention groups.” This last sentence is critically important for my readers. YOU want to be a member 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 glucose metabolism is broken. If you’re “prediabetic,” YOU ARE INSULIN RESISTANT, ergo CARBOHYDRATE INTOLERANT.

Afterword: The best part of this hyperbolic debate over the “risks and harms” of overtreatment were the “comments” in the BMJ. The first two were 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 are related to your glucose levels. Takeaway: Control your blood sugar!

Retrospective #255: “Risk Prediction with triglycerides…”

Virtually everyone who has blood taken at the doctor’s office these days gets a standard “lipid” or cholesterol panel. Your doctor receives assayed values for Total Cholesterol (TC) and High-density lipoproteins (HDL), the so-called “good” cholesterol, and, nowadays, non-HDL cholesterol in lieu of very low-density lipoproteins. The panel also includes a related assay, triglycerides, a fat molecule circulating in your blood. In addition to these measurements, the lipid panel reports on Low-density lipoproteins (LDL), but it is a calculated value, not an assayed, direct measurement.

If it’s over 200mg/dL, your doctor will use the Total Cholesterol result to try to persuade you to take a statin. Statins do lower both TC and LDL cholesterol, the so-called “bad” cholesterol, because TC = HDL + LDL + TG/5). This is a dubious benefit for virtually everyone except those with diagnosed 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 HDL (TC/HDL), as a cardiovascular “risk indicator” for events such as heart attack, stroke, and death. However, in “Retrospective #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 eight years ago, applies to the general “healthy” population and has been one of the most popular I have written.

A 2014 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” (my emphasis). The aim of the 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 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 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.

“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. That is stunning.

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, i.e., 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) and significantly LOWERING THE CARBOHYDRATES in your diet. 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.

Your doctor is not likely to have seen this research from the German Cardiac Society. My intrepid editor found it.  Besides, current guidelines regard as “borderline” a fasting serum triglyceride from 150- 199 mg/dL, so your doctor will probably say something like, “We’ll have to watch that.”  But remember, the hazard ratio for TGs above 150 mg/dL, for people with CAD and taking a statin, was 1.79 (80% greater risk). Do you want to become a statistic?

Retrospective #254: Saudi Approach to Diabetes

At a 2014 European Association for the Study of Diabetes (EASD) meeting, Anne Peters, MD, for Medscape Medical News, interviewed Saudi MD and diabetologist Aus Alzaid. Dr. Peters asked, “…knowing the epidemic of diabetes that you are having in Saudi Arabia, can you tell us what diabetes care is like there?” Dr. Alzaid replied, citing International Diabetes Federation figures, “Saudi Arabia has the highest rate of diabetes in the world after the small island nations in the Pacific.” Citing previous studies, he said, 1 in 4 people after the age of 30 has diabetes.”

Dr. Alzaid explained: “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 a person’s perception of lifestyle modifications that must be made.” “I don’t know of any Saudi family that doesn’t have a member or two with diabetes.”

Dr. Peters replied 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.’” They make a good point. Resistance to change is strong, and fatalism commonly prevails. But would that be so if there were a “treatment” that worked?

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.” [They don’t know?! That’s money well spent…if it’s good research.]

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 has turned the conversation to “diet and exercise,” the Western meme that we are eating too much and exercising too little. Well, at least the conversation has begun to turn. Let’s see where it goes.

Dr. Alzaid continued: “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 interview. It’s all about calories-in/calories-out. True, there was no mention of “eating fat making you fat,” or anything about dietary cholesterol. But neither was there so much as a word about CARBS, just calories.

Newsflash, Dr. Alzaid: Dates and rice and fizzy [sugary] drinks are ALL CARBOHYDRATES! Sugar and starch! 4 Medjool dates, about 100 grams of pitted dates, are 277 calories, of which 266 (96%) are sugar. 100 grams of medium grain white rice, about 3.5 ounces, is 130 calories, of which 116 are carbohydrates. I don’t know what kind of “fizzy drinks” Saudis use to quaff their thirst, but I’ll assume (generously) it’s Coca Cola. A 12-ounce (370g) cola is 152 calories.

So, I think that Dr. Alzaid has identified the problem with the Saudi diet; he just hasn’t named it. 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 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.’ Fatalism. And, for both doctors, treatment means prescribing drugs to control high blood sugars.

And the Saudi Ministry of Health has launched a public-awareness campaign “to tackle the problem with the right lifestyle.” The right lifestyle? To both doctors, that means, “diet and exercise.” Eat less of the same carbohydrate-dominated diet and move more? THAT IS A LIFESTYLE CHANGE THAT IS GUARANTEED TO FAIL. Type 2 diabetics are CARBOHYDRATE INTOLERANT, by definition. The best treatment for Type 2 diabetes is a very low carbohydrate diet.

Retrospective #253: The “Diabetes Plateau”

“Diabetes rates among adults in the United States are finally leveling off, new data from the Centers for Disease Control and Prevention suggests,” a 2014 Diabetes-in-Control piece leads. The headline of the piece is less speculative. It simply declares, “Diabetes Rates in the US Have Finally Plateaued.” It grabbed my attention, and with the primary audience being clinicians, the Diabetes-in-Control also had a self-congratulatory tone that I think is unwarranted.

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 (T2DM) in the population. In the NHIS survey, both were self-reported. 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. Percentage change in 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 and wrongly suggests obesity is causal. The author notes that a statistical adjustment) “reduced the annual percent change in incidence by about a third…” with the 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.”

Searching for another explanation, 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.” 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 evidence she offers for this association – the decline in incidence of Type 2 diabetes with an assumed decline in obesity, contrary to every other study I’ve seen – is “improvements in diet and activity levels, and changes in diagnostic criteria.” Oh, how I wish that were so. That we could realize an actual result by just saying it over and over: 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 their condition? Could that 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 [for a Dx of T2DM] may have increased the diabetes incidence…,” the CDC study author noted. I love it! “May have,” she says. Whereas, “the 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 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. 

Retrospective #252: “400 Calorie Meals for Fall”

“400 Calorie Meals for Fall,” the email from FITDAY proclaimed. Exciting! Small meals. I’m always looking for ideas for small meals that are very low carb. The reason, besides the fact that I have been a Type 2 diabetic for 33 years, is that if they are very low carb, moderate protein and high fat, I won’t be hungry between meals. I will be able to eat just 3 small meals a day, without snacks, and always feel satisfied. And I will lose weight, which is what I need to do.

So, I opened the FITDAY link 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. Not thinking, it seemed promising, since FITDAY is known for helping people, who need and want to lose weight, keep track of the macronutrients of the foods they eat. Macronutrients are carbohydrates, protein and fats; together, total calories.

 So, I started reading the FITDAY write-ups. 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 narratives. There was no mention of carbs or protein. Okay, I thought, that’s “old thinking.” Most dieters still think that only calories count, and dietary fat makes you fat. But, for the broader readership, and the enlightened reader in particular, a fuller nutritional analysis is needed and surely would be included with the actual recipes. So, I looked further.

Each link opened to a different site that provided the ingredients and steps 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 41grams for recipe #4; 45g for #5; and 47g for #10. Those numbers were so large that 1) “fat burning” (body fat) would be impossible (the body will burn dietary carbs first), and then 2) when the carbs were burned, the body would crave more calories (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 Prediabetics. But it’s safe to say that virtually all of them are overweight or obese, and overweight correlates very highly with Prediabetes and Type 2 diabetes. It is the leading “risk factor” for a diagnosis of Type 2 diabetes. Eighty-five percent of Type 2 diabetics are overweight or obese, and the percent of U.S adults (≥20 y.o.) who are overweight or obese is 69 percent. So, why would FITDAY advocate that its users “incorporate [these] delicious healthy meals into [their] daily diet”? That’s worth pondering about, isn’t it.

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

Besides, can we really blame FITDAY if their users believe that only total calories and fat grams count? So, until the pendulum swings toward using macronutrient distribution 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 might lose members. We would have discovered what foods 1) cause us to gain weight (carbs, not dietary fat), 2) feel hungry a few hours after eating, and 3) spike our blood sugars. And that wouldn’t be good for FITDAY’s business model, i.e., their advertising revenues.

Ask yourself, when you learn “how great it feels” to eat “healthy meals” that are LOW-CARB, and you lose weight, and are full of energy, and your doctor is pleased with your weigh-in and lab reports, why would you need FITDAY?

Retrospective #251: High-fat dairy ‘good’; low-fat dairy ‘bad’

Good news from Sweden, via Vienna, site of the 2014 European Association for the Study of Diabetes meeting. According to Medscape Medical News, epidemiologists from Lund University Diabetes Center in Malmö, Sweden reported, that “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, heavy cream and whole-fat milk fans. People the world over should be rejoicing.

26,930 Swedish people aged 45 to 74 years were included in the study. Swedes love their yoghurt with fruit, coffee and bread for breakfast. What interested me most about this study, though, was that both the Swedish scientists and the Medscape writer were both open to the findings. The Medscape banner was, “Big Intake of High-Fat Dairy May Be Protective for Diabetes.” That’s got to get the attention of the mainstream medical establishment.

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, founder of Diet Doctor, reported on that a long time ago. And he was among the first to herald the decision of the Swedish Government to change its official dietary recommendations. So, the Swedish scientists who initiated this study, declaring themselves to have “no relevant financial relationships,” were like the camel who stuck his nose under 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 polyunsaturated fatty acids (PUFAs) from vegetable oils have become the main dietary fat source for most Americans.

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 healthfulness of saturated fat 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 [just a 6 oz serving] …reduced the risk of developing diabetes by 20%.

As usual, the scientists, looking for new grant money, obviously, raised more questions than they answered. 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 raw 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…” That should clarify things.

“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. Among other reasons, meat is much more expensive there than here.

The Medscape article doesn’t mention any finding with respect to the other source of dietary saturated fat: fish. Fish such as herring and salmon are sacred to Scandinavians, and salmon is 29% palmitic acid, a very beneficial saturated fat. The last time we visited, Sweden to visit my wife’s relatives, in every home the gracious hosts served salmon with a crème fraiche and caviar topping, with aquavit and a beer chaser. Yum, yum. For breakfast, they offered muesli or full-fat yoghurt, fruit, bread, and coffee. It was a refreshing change from my usual eggs, bacon and coffee with HWC.

Retrospective #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 career, 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 2014 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 who need treatment for the progressive course of their 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? Or for confining their perspective to pharmacological treatments? New drugs? Surgery? After all, as a medical research journal, they only report on public health policy and nutrition research. But if 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 for the patient will be other than, “Whatever will be, will be.” Que será, será.

Retrospective #249: Type 2 Diabetics: You Have a Choice.

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

To illustrate the insulin treatment option, I will use an 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 Eli Lilly and Company’s fast-acting Humulin R (Insulin Regular). Why do I say that? Well, based on the advertising. As you scroll down the screen, the article is accompanied by 5 ads for Humulin R, 1 on top of the article, 3 on the side and 1 at the bottom. Then, I saw the hyperlink, “Humulin Insulin Special Edition September 2014.”

I have nothing against injecting insulin.  Exogenous 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 article are the Editor-in-Chief and Publisher of the Diabetes in Control “newsletter.” I didn’t know that because it was revealed in the “disclosures,” as is done in peer-reviewed medical journals. There were no “disclosures.” I knew it because I have been reading this “newsletter” for years.

I Googled the Diabetes in Control Editor-in-Chief and learned he “…speaks on diabetes, hypertension, and related co-morbidities for Abbott, Bayer, Pfizer, Novo Nordisk, Lilly, Sanofi, Sankyo, and Medtronic” (emphasis added). And, he “...is a non-physician member of the Lilly Primary Care Diabetes Advisory Board.” This guy has mega bona fides.

Nevertheless, the “Practice Pearls” for insulin as a treatment for Type 2s are very revealing, particularly the 2^nd one.

●     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 [like amputations, for instance].

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.  Your care giver can help on the amount of “basal” insulin you inject once a day, but only you can decide how much “bolus” to inject before each meal because 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 with each meal. As a result, many patients, and their caregivers including clinicians and CDEs, do not try for tight glucose control. They tend to inject too little to avoid the dangers of hypoglycemia, including hospitalization and death.

The 2nd 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” are started on Metformin. The dose is increased (as your disease “worsens”) until you are “maxed out.” Then a second agent, and probably a third will be added to the “cocktail.” Since, as we’ve seen above (in the 2^nd bullet), the accepted 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 eventually “progress” to insulin dependency.

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 you with drugs, your Type 2 diabetes WILL “progress” and “worsen over time.” Eventually, you are likely to develop some of the microvascular and macrovascular complications, like heart disease.

The 3^rd treatment option for Type 2 diabetes or Prediabetes: major dietary changes. Pros: no insulin (and no hypos), few if any oral meds (thus no side effects), and greatly improved (not worsening) glucose control, plus a bonus: improved BP and blood lipids (higher HDL, lower triglycerides, stable Total Cholesterol and LDL). And in addition to all this, you will lose lots of weight, have lots of energy and feel great! Cons: you have to give up all the highly processed foods and carb-loaded junk that made you sick in the first place. It’s your choice. And yours alone. 

REtrospective #248: Salt Warnings: Confusing and Contradictory

Here we go again. Another study about salt! It seems that Australians “pay little attention to salt warnings,” according to a 2014 story from Medscape Medical News. But what made this story interesting to me were the stories that ran with and mostly against it. The Reuters Health story about this research study appeared August 13^th in Appetite.

The recommended upper limit for salt intake for Australians is 6g/day, the same as the 2010 U. S. Dietary Guidelines recommendation for “healthy people.” That’s 2,300mg of sodium or 1 teaspoon of salt a day. Six grams (6,000mg) of salt x 0.393 (% sodium in NaCL) = 2,358mg of sodium. If you have high blood pressure, the recommendation is 1,500 mg of sodium a day. According to Medscape, Australian men eat more sodium than women (2907 vs. 1962mg/day).

The next day the prestigious New England Journal of Medicine (NEJM) published 3 major papers on the health effects of sodium consumption in 101,945 individuals in 17 countries, all QUESTIONING the science of salt restriction. And back in 2013, the Institute of Medicine (IOM) reviewed the evidence for the suggested guideline for sodium intake and reported that there was NO EVIDENCE to support the 1500mg/d limit. I reported on this “Retrospective #153.”

How does one decipher this confusing and contradictory advice? Well, Eric J Topol, MD, the Editor-in-Chief of Medscape Medical News, thought it was time to bring some clarity to the issue. In an August 26, 2014, post addressed “Dear Medscape Readers,” Dr. Topol said, “This is important stuff that the public wants to know about.”

Even more compelling is a chart which shows what Dr. Topol describes as “the most striking evidence of the relationship of sodium and cardiovascular events.” “Although there was a trend of higher adverse cardiovascular events with sodium excretion greater than 5g/day [vs. 2.358g], this [higher risk] was much more pronounced at levels lower than 2g/day [vis.1.5g]. In other words, consumption of too little sodium is more harmful than consumption of too much sodium. Following AHA guidelines would lead to about a twofold risk for major adverse events.”

Dr. Topol then cites “the real coup de grace, from a Wall Street Journal’s editorial, ‘The Salt Libel’: ‘The illusion that science can provide some objective answer that applies to everyone is a special danger.” He adds, “I believe that adequately sums up all there is to say about sodium.” But, “The AHA isn’t backing off from its 1.5g/d guideline.”

What followed in Dr. Topol’s rather rare editorial to his large, mostly doctor audience was the piece de resistance:

“But I think there’s a big lesson here about guidelines without adequate evidence. They can do harm. Hopefully this lesson will prove to be impactful, because that certainly has not been the case to date (as in cholesterol/LDL, BP, PSA, mammography and a very long list of poorly conceived non-anchored guidelines. Isn’t it about time to recognize that there shouldn’t be rules for populations? (emphases added by me). Some people are exquisitely sensitive to salt intake, while others are remarkably resistant.”

Well, the “average” Australian male’s sodium intake, currently at 2.9g/day of sodium, would then be still low. And the Australian (and American) women, who it appears to me is (are) trying hard to comply with U. S. sodium guidelines, and whose intake is 1.96g/day, do so at their own peril! From my reading of the chart, the optimum intake or sweet spot of sodium intake is between 4g/d and 5g/d. That is between 1.7 and 2.1 tsp (vs. AHA’s 1.0 and 0.64 tsp) of salt.

The second thing that caught my attention in this Medscape piece is that a New York dietician who was not involved in the study but who was interviewed by Medscape about the piece in Appetite, turned the whole discussion away from sodium intake and “hidden sodium in processed food.” She called the study “interesting and consistent with other research,” but moved quickly to say, “…but hidden sodium is only one of many unhealthy aspects of processed foods that have the potential to affect heart health directly and indirectly.” That’s really, really good advice.

“If a diabetic were to choose a low-sodium version of a highly-processed cereal or bread, they’re going to have a false sense of security in terms of doing something good for their health because they should be limiting a lot of those foods for a lot of reasons,” she said. “The focus,” she continued, “should be on shifting to eating real food and less processed food, which will automatically reduce the sodium content…”  And this dietician works for a cardiac wellness program.

Retrospective #247: Age-Based Universal Screening for T2DM

In Retrospective #244, “Diabetes on Rise but Complications Decline,” I explained that the primary reason for the percentage decline in complications from Type 2 diabetes was, due to changing standards in diagnostic criteria, the dramatic increase in the denominator of the fraction from the number of cases reported. It was not that “preventive care for adults with diabetes has improved substantially in recent years,” as the doctors vaingloriously claimed.

In my opinion, while attention to diabetes – and the number diagnosed – has increased, preventive care has not improved. I would make the case that the number of cases being treated (with better drugs, I admit) has increased, but that the medical establishment in general, and the vast majority of clinicians in particular, have for the most part ignored the evidence that the best PREVENTATIVE care and the best TREATMENT for Type 2 diabetes, is a low-carb diet. In not recognizing that, the medical establishment and the clinicians have been derelict, and I am angry about it.

Now, Medscape.com reports that researchers at Palo Alto Medical Foundation Research Institute, in an on-line paper in the American Journal of Preventive Medicine, have yet another idea on how to identify even more patients with diabetes: screen everyone 35 years old and older for Type 2 diabetes. They argued [this was in 2014] that “guidelines on screening for diabetes are inconsistent with one another and complex for physicians to use.”

For example, “the U. S. Preventive Services Task Force (USPSTF) recommends routine screening of asymptomatic adults only if they have a blood pressure above 135/80 mmHg, while the American Diabetes Association (ADA) recommends screening for asymptomatic adults under 45 with a body mass index (BMI) of 25 or higher and at least one of 12 different diabetes risk factors, and everyone 45 and older regardless of their risk factors.” “It is cumbersome for physicians, and they may not adhere to that guideline,” the lead researcher noted in the Medscape interview.

I was diagnosed a Type 2 diabetic in 1986, at age 45. I don’t know the screening criteria my physician used, but I weighed 300 pounds and my blood pressure was 174/124. He started me on Micronase, a sulfonylurea, and I’m sure urged me to lose weight. When I moved to NYC in 1987, my new doctor, who had a Registered Dietician (RD) on staff, increased the Micronase ‘til I was maxed out and in 1995 added metformin. He and his RD tirelessly urged me to lose weight (on a balanced, one-size-fits-all, low-fat, high-carb Dietary Guidelines for Americans diet). The diet didn’t work.

Sixteen years after diagnosis, by which time I was maxed out on both Micronase and Metformin and starting a TZD, my doctor read Gary Taubes’s NYT Sunday Magazine cover story, “What If It’s All Been a Big Fat Lie,” and tried the recommended diet himself. It worked. He lost 17 pounds. He then suggested I try the very-low-carb diet too. I did, and over several years, I lost 170 pounds (from a starting point of 375). I still follow it, and I’ve kept off 150 pounds.

Would lowering the screening age and simplifying the screening criteria to age alone help to identify more cases of undiagnosed Type 2 diabetes? Undoubtedly. I was probably a full-blown diabetic for years before I was diagnosed. But diagnosis is NOT prevention NOR an effective treatment. It would simply lead to earlier treatment, which is good if the treatment works. But the one-size-fits-all government recommended “balanced [high-carb] diet,” will not work. As the ADA acknowledges, it will simply mean the disease will “progress” AND REQUIRE PROGRESSIVELY MORE MEDs.

An effective treatment does, however, exist. See Retrospective #239, “Low-Carb Diet Should Be First Approach for Diabetes.” But, the patient must be willing to do his/her part. But if the patient does, the doctor can just sit back and watch the patient’s health improve. How sweet that was, for both of us. No haranguing or hectoring. Just smiles from my doc and a pat on the back. I actually looked forward to my office visits, and I think he did too.

So, MY “PRACTICE PEARL” FOR ANY PHYSICIAN READERS: It is possible – I would say easy – to “cure,” i.e. put your patient’s T2DM “in remission,” make your patient’s clinical status “non-diabetic,” and develop a healthy lipid profile, all without or with only minimal drugs. It does, of course, require a willing and motivated patient. Universal age-based screening may be an effective way to identify undiagnosed cases of Type 2 diabetes, or Prediabetes, but preventive CARE requires an effective TREATMENT. A low-carb diet is a very effective treatment for Type 2 diabetes.

Retrospective #246: “Sugar Substance Reduces HDL”

“Sugar Substance Reduces HDL,” Diabetes in Control reported on an August 2014 paper in Nutrition and Diabetes. Most people know LDL is the “bad” cholesterol and HDL the “good” cholesterol. That message has been pushed to promote the use of statins, which do lower LDL cholesterol (and thus Total Cholesterol). But how can you raise HDL?

The Diabetes in Control lede: “The substance, METHYLGLYOXAL (MG), was found to damage ‘good’ cholesterol, which removes excess levels of ‘bad’ cholesterol from the body.” MG is formed during glycolysis, the utilization of glucose to eventually make ATP, our cell’s energy furnaces. “Why methylglyoxal (MG) is produced remains unknown, but it may be involved in the formation of Advanced Glycation Endproducts,” per Wikipedia. “Due to increased blood glucose levels, methylglyoxal has higher concentrations in diabetics, and has been linked to arterial atherogenesis.”

“Low levels of High Density Lipoprotein (HDL) are closely linked to heart disease, with increased levels of MG being common in the elderly and those with diabetes or kidney problems.” “MG destabilizes HDL and causes it to lose the properties which protect against heart disease. HDL damaged by MG is rapidly cleared from the blood, reducing its HDL content, or remains in plasma having lost it beneficial function,” the researchers say. MG damage to HDL is a new and likely important cause of low and dysfunctional HDL…,” the researchers speculated.

To recap, when you eat carbohydrates, glucose (sugar) becomes energy (ATP) and along the way HG is produced. The HG damages the “good” cholesterol and prevents it from removing LDL, the “bad” cholesterol, from the blood stream. (Sounds a bit like sugar isn’t such a clean “fuel” for your body, doesn’t it?) Well, the researchers asked, what can be done about it? Not surprisingly, they had an answer: “By understanding how MG damages HDL, we can now focus on developing drugs that reduce the concentration of MG in the blood, but it won’t only be drugs that can help.” (That’s sounds promising, I’m thinking. Maybe they’ll mention a dietary intervention. Let’s see.)

“We could now develop new food supplements that decrease MG…” “This means that in future we will now have new drugs and new food supplements too that help prevent and correct low HDL, all through the control of MG.” To emphasize just how dangerous MG really is, and the importance of their “new” discovery, they add:

“MG is formed from glucose in the body. It is 40,000 times more reactive than glucose and damages arginine residue (an amino acid) in HDL at a functionally important site causing the particle to become unstable.”

Diabetes in Control “Practice Pearls” for the busy physician trying to keep up on the latest research in lipid chemistry:

●     Methylglyoxal (MG) was found to damage “good” HDL cholesterol.

●     There are currently no drugs that can reverse low levels of HDL.

So, what can a Type 2 diabetic or elderly person or a person with kidney problems or heart disease do now to raise HDL? Well, my answer is you don’t have to wait for a drug or a supplement to be developed. You don’t need a drug or a food supplement. You need to simply but substantially reduce the amount of “sugar” (carbohydrates) that you eat.

All carbohydrates, whether simple sugars or “complex” carbohydrates, become glucose in your blood. Carbs will raise your triglycerides, and there’s an inverse relationship between HDL and triglycerides. So, lower carbs = lower triglycerides →  increased HDL. The British Heart Foundation, which funded this study, should request a refund. 

My doctor, since deceased, first suggested that I eat very low-carb (to lose weight!) in 2002. It worked. I lost a lot of weight (170 pounds), my health improved and I felt much better. Then, when I started writing about my success, he read my blog regularly. Then, a while later, at my request, he emailed me suggestions for subjects to write about, and “Foods that Raise HDL” was first on his list. So, I did (Retrospective #34). Nine months later I wrote a sequel (Retrospective #67), HDL Cholesterol and the Very Low Carb Diet.” The table in #67 shows how before I changed my diet, my average HDL over 10 visits was 39. When I wrote that column the average of my most recent 10 HDLs was 81. After writing that column, the average of the next 7 HDLs was 78; median 77, range 58 to 91. Do you want to double your HDL? And reduce your triglycerides by 2/3rds (Retrospective #68)? You can do it by diet – a VERY Low Carb diet.