The Nutrition Debate #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 an eponymous story from Medscapemedicalnews.com. The study (involving just 143 people) doesn’t support the headline, but what made this story interesting to me were the stories that ran with and mostly against it. The Reuters Health story, about a research study at the University of South Australia, appeared online August 13^th in Appetite.

The recommended upper limit for salt intake for Australians is 6g/day. Six grams of salt a day seems like a lot, but it’s essentially the same as the U. S. Dietary Guidelines (2010) recommendation for “healthy people,” which is 2,300 mg/day of sodium, or about 1 teaspoon of sodium (over 2.5 tps of salt). Six grams of salt x 0.393 (the % sodium in NaCL) = 2,358 mg of sodium. For adults with high blood pressure, the recommendation is no more that 1,500 mg/day of sodium. According to Medscape, in Australia today men eat more sodium (2,907 mg/day) than women (1,962 mg/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 1.5 g/d limit. I reported on this “The Nutrition Debate #153”here.

How does one decipher this conundrum? 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 this August 26^th post addressed “Dear Medscape Readers.” You really oughta read this piece. “This is important stuff that the public wants to know about,” Dr. Topol says. Even more compelling is this chart that Dr. Topol describes as “the most striking evidence of the relationship of sodium and cardiovascular events…”

Dr. Topol’s analysis of the chart: “Although there was a trend of higher adverse cardiovascular events with sodium excretion greater than 5 g/day, this was much more pronounced at levels less than 2 g/day. In other words, consumption of too little sodium is as harmful as consumption of too much sodium. In fact, the AHA guidelines would lead – according to this latest research – to about a twofold risk for major adverse events.”

Dr. Topol then cites “the real coup de grace: the Wall Street Journal’s editorial column, ‘The Salt Libel’ (subscription required, unfortunately), which highlighted this conclusion: ‘[T]he illusion that science can provide some objective answer that applies to everyone…is a special danger.” He then quips, “I believe that adequately sums up all there is to say about sodium, at least for now.” But he notes, “The AHA… isn’t backing off from its 1.5 g/d sodium 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? Some people are exquisitely sensitive to salt intake, while others are remarkably resistant. Average is over” (emphasis added by me).

Well, the “average” Australian male’s sodium intake, if they are ignoring salt warnings at 2,907 mg/day (sodium), is in my view still on the low side. And the Australian woman, who it appears to me is trying hard to comply with sodium guidelines, and whose intake is 1,962 mg/day, does so at their own great peril! The optimum intake of sodium, from my reading of the chart, is between 4 and 5 grams a day. That is 10.2 and 12.7 grams of salt (3½ to 4 tablespoons of salt).

The second thing that caught my attention in this Medscape piece is that Lauren Graf, a New York dietician who was not involved in the study, but who was interviewed for 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.” She works for the Montefiore-Einstein Cardiac Wellness Program in New York. That’s pretty good advice coming from a cardiac wellness program.

“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 increase the intake of beneficial antioxidents and fiber.”

Really good advice! It sounds like the message about eating more real food and less processed food is starting to get out there. Huzzah! Huzzah!

(Salt intake, btw, is measured by how much sodium you excrete in your urine. I guess sweat doesn’t count, or can’t be easily collected.)

The Nutrition Debate # 247: Age-Based Universal Screening for T2DM

In The Nutrition Debate #244, “Diabetes on Rise but Complications Decline,” I explained what I believe is the primary explanation for the percentage decline in complications from type 2 diabetes mellitus. It is the dramatic increase in the denominator of the fraction, i.e. the number of cases reported, due to changing standards in diagnostic criteria, not that “preventive care for adults with diabetes has improved substantially in recent years,” as the doctors claimed.

 In my opinion, while attention to diabetes – the number diagnosed in particular – has increased, preventive care has not improved. I would make the case that while the number of cases being treated (with better pharmacological agents, I admit) has increased, the medical establishment in general, and the vast majority of individual practitioners 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 has been derelict, and I am angry about that.

Now, Medscape.com reports that researchers at Palo Alto Medical Foundation Research Institute, in an online paper in the American Journal of Preventive Medicine, have yet another idea on how yet to identify even more patients with diabetes: screen everyone 35 years old and older for type 2 diabetes. They argue 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, my new doctor, who had a Registered Dietician on staff, added metformin and tirelessly urged me to lose weight (on a balanced, one-size-fits-all, government recommended diet). The diet didn’t work.

Sixteen years after diagnosis, by which time I was maxed out on 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 LC diet” himself. It worked. He lost 17 pounds, and his lab tests were stellar. He then suggested I try “the low-carb” (Atkins Induction) too. I did, and over several years, I lost 170 pounds (from a starting point of 375). I still follow it (sort of), and I’ve kept off 125.

Would lowering the screening age (and vastly simplifying the screening criteria to age alone) help to identify more cases of undiagnosed type 2 diabetes? Undoubtedly it would. I was probably a full blown diabetic for years before I was diagnosed. But diagnosis is not prevention or an effective treatment. It would simply lead to earlier treatment, which is good if the treatment works. But if the only arrows in the physician’s quiver are pharmacology, and the one-size-fits-all government recommended “balanced [high-carb] diet,” that will not lead to an effective treatment. It will simply mean that, as the ADA acknowledges, the disease will “progress” (as they admit) and require progressively more medication, as it did for me.

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

When my doctor started me “cold turkey” on Very Low Carb, he had to take a telephone call from me every day for several days, as I had hypos (symptoms of low blood sugar). He told me to cut back on the meds: eliminate the TZD; then, cut the sulfonylurea and the metformin in half, then cut them in half again. For a year he saw me monthly. He just took blood and did a physical. Eventually, I (we) eliminated the sulfonylurea altogether. Today, I just take 500mg metformin with dinner.

So, my “Practice Pearl” for any physician readers: It is possible – I would say easy – to “cure” your patient of this chronic disease, with “patient support.” And universal age-based screening may be an effective way to identify undiagnosed cases of type 2 diabetes, but preventive care requires an effective treatment. Diet is an effective treatment for type 2 diabetes.

The Nutrition Debate #246: “Sugar Substance Reduces HDL”

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

The Diabetes in Control lede: “The substance, methylglyoxal (MG), was found to damage ‘good’ cholesterol, which [HDL] removes excess levels of ‘bad’ cholesterol from the body.” MG is formed during glycolysis, the utilization of glucose to eventually make ATP, the little energy furnaces in our cells. Wikipedia explains that “Why methylglyoxal (MG) is produced remains unknown, but it may be involved in the formation of Advanced Glycation Endproducts (AGEs). ... 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 [#27: "...the strongest predictor of a heart attack"], 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…,” they say.

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 body. (Sounds a bit like sugar isn’t a very clean “fuel” for your body, doesn’t it?) Well, what can be done about it, the researchers ask? Not surprisingly, they have 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 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 have both new drugs and new foods [somehow a “food supplement” becomes a “food”] 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:

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

“Practice Pearls” from Diabetes in Control 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 their 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 carb = lower trig -> increased HDL (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1950669/). The British Heart Foundation, which funded this study, should request a refund. 

My doctor, since deceased, first suggested that I eat very low-carb. It worked. I lost a lot of weight, my health improved and I felt much better. Then, when I started writing about my success, he read my blog regularly. A few years ago he emailed me suggesting I write a column, “Foods that Raise HDL.” So I did (#34)   Nine months later I wrote a sequel, #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. Since writing that column, my average of the most recent 7 HDLs is 78; median 77, range 58 to 91. Wanna double your HDL? And reduce your triglycerides by 2/3rds (#68)? You can do it by diet.

The Nutrition Debate #245: “…in patients on sulfonylureas.”

Lots of type 2 diabetes patients are on sulfonylureas. They were the first class of oral anti-diabetic medications approved in the U.S. (1955) and remained so until 1995 when metformin (Glucophage) was added. Metformin eventually took over and became the first-line drug, used even for the treatment of “pre-diabetes.”  (Note I put pre-diabetes in quotes since it was only defined by the American Diabetes Association in 2002, and the definitions of both clinical type 2 diabetes and pre-diabetes are both controversial. See the last few paragraphs of #244 here for a fuller explanation.

The second generation of sulfonylureas, approved in 1984, includes the familiar generics (and trade names) glyburide (Micronase, Diabeta) and glipizide (Glucotrol). They act by increasing insulin release from the beta cells in the pancreas. For that reason, “Some diabetes experts feel that sulfonylureas accelerate the loss of beta cells from the pancreas, and should be avoided, ^[1]” according to Wikipedia. Ralph A. DeFronzo, MD, in his 2008 Banting Award lecture at the ADA convention, said, “Sulfonylureas are not recommended because, after an initial improvement in glycemic control, they are associated with a progressive rise in A1c and progressive loss of ß-cell function” (emphasis mine). See #86 here for more info on this.

There is also some evidence, again according to Wikipedia, that sulfonylureas “decrease lipolysis (breakdown and release of fatty acids by adipose tissue) and decrease clearance of insulin by the liver.” Thus, “like insulin, sulfonylureas can induce weight gain…” (emphasis mine). In addition, “All sulfonylureas carry an FDA-required warning about increased risk of cardiovascular death.” You think that’s all? It’s just the beginning.

Wikipedia continues, “First line therapy with sulfonylureas significantly increases the risk for death in patients with type 2 diabetes when compared with treatment with metformin. Additional research showed that the combination of metformin and a sulfonylurea was also associated with a significantly increased risk for death when compared with combination therapy with metformin and a dipeptidyl peptidase-4 (DPP-4) inhibitor.” For more, see “Side Effects and Cautions” here.

“Sulfonylureas are potentially teratogenic [think 2-headed calf] and cannot be used in pregnancy or in patients who may become pregnant. Impairment of liver or kidney function increases the risk of hypoglycemia, and are contraindications.”

And then there are the Interactions. Wikipedia: “Drugs that potentiate or prolong the effects of sulfonylureas and therefore increase the risk of hypoglycemia include acetylsalicylic acid [aspirin] and derivatives, allopurinol, sulfonamides, and fibrates. Drugs that worsen glucose tolerance, contravening the effects of antidiabetics, include corticosteroids, isoniazide, oral contraceptives and other estrogens, sympathomimetics, and thyroid hormones. Sulfonylureas tend to interact with a wide variety of other drugs, but these interactions, as well as their clinical significance, vary from substance to substance.” Sympathomimetics include caffeine, some decongestants.

Now there’s a brand new report in JAMA Internal Medicine regarding interactions of sulfonylureas and antibiotics resulting in hospitalizations or emergency department visits. The lede: “Use of certain antimicrobial agents is linked to an increased risk of hypoglycemia in older patients on sulfonylureas, according to a study of Medicare claims.” Older is defined as 66. The JAMA finding: “Physicians should definitely avoid using those antibiotics in patients on sulfonylureas,” Medscape advised. The sulfonamide class of antibiotics is already known to be problematic, but some of these antibiotics are outside that class. Bactrim was shown to have “particularly high risks,” and the number needed to harm for clarithromycin was just 71. Adding the NNH (number needed to harm), makes this study particularly useful. For an intro to NNH, see this YouTube video.

I was on a sulfonylurea (Micronase and then glyburide) from my initial T2 diagnosis in 1986. When Glucophage (metformin) was permitted the U.S., my doctor added it. As I continued to eat a “balanced diet” (“one-size-fits-all”) with “moderation- in-all-things,” and 55% to 60% carbohydrates as recommended since 1980 for everyone by the USDA’s Dietary Guidelines, my diabetes got progressively worse. Eventually, I was “maxed out” on both metformin and glyburide and starting Avandia, a TZD class of oral antidiabetic drug. (This was before the DPP-4 inhibitors came to market.) Of course, with my doctor’s and his RD’s help, I was trying to lose weight (I weighed 375lbs), but I knew in my heart-of hearts that my oral “cocktail” of antidiabetic meds was soon destined to be replaced by injected insulin.

Then, after reading Gary Taubes’s “What If It's All Been a Big Fat Lie,” the NYT Magazine cover story on July 7, 2002, my doctor suggested I try Atkins Induction. I did. The first day I had serious hypoglycemia. I ate a candy bar and called the doc. He said, “Drop the Avandia.” The second day, as the severe hypoglycemia continued, he said, “Cut the glyburide and metformin in half. I did, and the next day, he said, “Cut them in half again.” Over time I eliminated the glyburide altogether and today, and for the last 10 years, I take just 500mg of metformin, with dinner, in case I eat too much protein! And I lost and have kept off 125 pounds, and my triglycerides have been cut by two-thirds and my HDL doubled. My A1cs are now usually in the high 5s (up from mid 5s when I was losing weight), and my blood pressure is “normal” (on the same “cocktail” of meds as before). And my hsCRPs, a systemic inflammation marker for heart disease risk, are in the low-average range.

So, for patients still on sulfonylureas – itself hard for me to believe, that a doctor would still prescribe them – I ask myself, in view of all the downside risks, why don’t patients just change the foods they eat? They won’t need to take a sulfonylurea.

The Nutrition Debate #244: Diabetes on Rise but Complications Decline (Duh!)

“Diabetes on the Rise but Complications Decline” was the title of a video with transcript on my Medscape Alert recently. The subtitle was “Diabetes on Rise as Waistlines Expand.” (That’s an association or “correlation,” not a cause of the rise. Obesity is a symptom of Metabolic Syndrome that includes a broken fat metabolism – but I digress.)

Both conclusions headlined above are based on epidemiological analyses of “sentinel indicators of outcomes” in diabetes collected from several very large public databases. According to the narrator, Henry R. Black, MD, from the New York University School of Medicine, “They examined 5 complications of diabetes – acute myocardial infarction (MI), stroke, lower extremity amputation, end-stage renal disease (ESRD), and death from diabetic ketoacidosis (hyperglycemic crisis)…” The “they” referred to above is Gregg EW, et al., whose ABSTRACT from their New England Journal of Medicine article can be viewed here and which is also listed as Reference #5 in the Medscape piece.

“We are all aware that we have epidemics of diabetes and obesity in the United States,” Dr. Black says, so he doesn’t attempt to explain that. Indeed, the NEJM article presumes that too, then postulates that “preventive care for adults with diabetes has improved substantially in recent decades,” and concludes that “rates of diabetes related complications have declined substantially in the past two decades.” Dr. Black’s comments and speculations are about the causes of the decline in complications. In that respect, in my opinion, both Dr. Black and the NEJM authors err in several fundamental ways.

But before I tell you how, let me first relate the specific “findings” of declining complications: “The diagnosis of diabetes increased from about 6.5 million in 1990 to almost 21 million in 2010, but the rates of major complications actually fell in all 4 age groups [studied].” There was a 69% reduction in MI cases, a 53% reduction in strokes, “but the rates of MI and strokes were about the same” (“when expressed as rates for the overall population”). According to Dr. Black, there were also fewer cases of amputations (“a reduction of more than 50%”) and fewer cases of end stage kidney disease (“a reduction of about 28%”), and hypoglycemic (sic) crises declined by 65%. (Gregg, et al. reported on hyperglycemic crises.)

Pandering to get published, or worse, maintaining an unquestioned acceptance of “perceived wisdom” to get “research” funding, is commonplace in today’s medical establishment. So saying, “Preventive care for adults with diabetes has improved substantially in recent decades” is nothing to get worked up about. I can give Gregg et al. a pass on that. But Dr. Black takes it to a new level with his myopic meanderings. “It is hard to pick any particular factor,” he says, but notes that “studies have shown that risk factor control, how you organized your healthcare system, and patient support for issues such as smoking cessation are all important in improving care, but certainly new drugs (e.g. statins) and such cardiovascular procedures as revascularization might help as well.” [Did he really call statins “new drugs”? He must be living under a rock.]

Repeating himself near the end of the video, Dr. Black says, “realizing how much we are estimating using these numbers, it could be better care, and the idea of using team-based care is promoted and probably an important factor. Medications are better (especially for lowering cholesterol), as are treatment of risk factors and patient education. Competing risks for ESRD might explain why that statistic didn’t decline as much – people live longer when they are not having heart attacks.” (Wow!)

What Doctors Gregg and Black fail to mention in either the abstract or the Medscape piece is that the increase in the number of patients with diabetes is in large part due to the changes made in the diagnostic criteria for type 2 diabetes.  In 1997, in the middle of the 2-decade study period, the threshold for diagnosing type 2 diabetes mellitus changed from a fasting glucose level of 140mg/dl to 126mg/dl. Then, in 2002, the American Diabetes Association defined prediabetes for the first time. People with prediabetes are at increased risk for developing type 2 diabetes and for heart disease and stroke.

Prediabetes is described as impaired fasting glucose (IFG,) defined as a fasting blood glucose of 100-125 mg/dl. But an IFG does not recognize insulin resistance which causes impaired glucose (carbohydrate) tolerance (IGT), defined as a glucose level from 140 mg/dl – 199 mg/dl two hours after consuming a glucose-rich drink. So, the ADA then introduced in 20XX the Glycated Hemoglobin A1c test (A1c for short) which measures (as a %) the glucose on the surface of your red blood cells (which have a life of +/- 3 months), thereby accounting for the postprandial, i.e. after meal, excursions your blood sugar took. This percentage converts into an estimated Average Glucose (eAG) value which sometimes now appears on your lab test results. And then the major medical societies, starting with the endocrinologists, lowered the level for diagnosing type 2 diabetes from an A1c of 7.0% to 6.5%. Now, an A1c between 5.7%and 6.4 is defined by the ADA as prediabetes. Note, however, that an increasing number of diabetologists now define an A1c of 5.7 as full-blown T2DM.

So, if you want to define changing standards for diagnosing type 2 diabetes as “preventive care for adults with diabetes has improved substantially” or “our care of patients with diabetes is getting better,” so be it. But changing standards for screening for and treating type 2 diabetes are the reason why the ratio of complications (numerator) to number of cases diagnosed (denominator) is improving. As the denominator gets larger, the fraction gets smaller. That’s 5^th grade math.

The Nutrition Debate #243: New York Times good; Fox News bad (coverage)

I was pretty excited to read several links in my email feed about a study just published in The Annals of Internal Medicine. Funded by the National Institutes of Health, it was (yet) a(nother) randomized controlled trial (RCT), the gold standard of studies, showing the superiority of low-carb over low-fat dieting for losing weight. For another – and this was the hypothesis to be tested – it showed the superiority of low-carb over low-fat in improving heart disease risk, using all the classical markers for determining that risk.

The study, “Effects of Low-Carbohydrate and Low-Fat Diets: A Randomized Trial,” was performed at the Tulane University School of Public Health in New Orleans. The lead investigator was Lydia Bassano, MD, PhD. It enlisted a diverse population of 148 men and women without either clinical cardiovascular disease or diabetes. The study DESIGN: “A randomized, parallel group trial. The OBJECTIVE: “To examine the effects of a low-carbohydrate diet compared with a low-fat diet on body weight and cardiovascular risk factors. The ABSTRACT can be view here. Full access will cost you (and me) $29.95.

The study participants were randomly selected to be placed in one of two diet groups and had no restrictions on calories. They were also told to make no changes in physical activity. The target for the low carb group was to eat less than 40 grams of carbohydrate a day. The target for the low-fat group was to eat less than 30% of daily energy intake from total fat and less than 7% from saturated fat. Both groups received dietary counseling from an RD and were tested at baseline, three months, six months, and twelve months. About 80% of the participants finished the one-year study.

The CONCLUSION was two sentences. The first is declarative and absolute: “The low-carbohydrate diet was more effective for weight loss and cardiovascular risk factor reduction than the low-fat diet.” The second, “Restricting carbohydrates may be an option for persons seeking to lose weight and reduced cardiovascular risk factors,” is couched with the word “may.” Perhaps this is more palatable to conventionally trained physicians (who are not trained in nutrition) and to the nutritional professionals who are but have been misled, along with the physicians, by half a century of poorly performed research and pure propaganda from public health policy makers and the perfidious players in the processed food business.

The results, in layman’s terms, have now been broadcast widely. Jimmy Moore (Livin' La Vida Low-Carb) and Andreas Eenfeldt (The Diet Doctor) were among the first. But The New York Times, The Wall Street Journal (by subscription), National Public Radio, Time Magazine, CBS News, and the Washington Post, were quick to follow. By now the story is so widely disseminated that in some media it has been reinterpreted to the point that it is hardly recognizable. So before or in case a distorted version of this story reaches your ears and eyes, let me apprise you of the principal findings.

●     Triglycerides – the type of fat that circulates in your blood – “plunged” on the low-carb diet (NYT)

●     HDL – the so-called good cholesterol – rose more sharply than it did for people on the low-fat diet (NYT)

●     Total Cholesterol/HDL ratio – an important maker of heart disease risk – improved (NYT)

●     Chronic systemic inflammation – as measured by hs-CRP (C-reactive protein) also “plunged.” (NYT)

●     Blood pressure, total cholesterol and LDL, the so-called bad cholesterol, showed little change in both groups. (NYT)

 

The NYT article was clearly open-minded and its view of the results positive. Dr. Allan Sniderman, a professor of cardiology at McGill University in Montreal and not associated with the study, was quoted as saying that the decrease in [heart disease] risk on the low-carbohydrate diet “should translate into a substantial benefit.” He added, importantly,

“One important predictor of heart disease that the study did not assess was the relative size and number of LDL particles in the bloodstream. Two people can have the same overall LDL concentration, but very different levels of risk depending on whether they have a lot of small, dense LDL particles or a small number of large and fluffy particles.”

In contrast to the very well reported and balanced story in the New York Times, the Fox News Channel had a cardiologist on the “Fox and Friends” program in the morning who failed to mention the first four clearly beneficial outcomes of the trial, in terms of heart disease risk, listed above. He did begrudgingly acknowledge, with genuine surprise it seemed to me, that total cholesterol and LDL (the so-called bad cholesterol) stayed about the same for people in each group. Maybe the more conservative Fox News Network was interviewing a more conservative cardiologist. Frankly, it seems to me that he (and most of the conservative medical establishment) has plaque on the brain, not in their arteries.

The Nutrition Debate #242: God Favors Animal Fat

About one-third through The Big Fat Surprise, possibly the best book yet on nutrition and healthy eating for the whole human race, I came across a reference I had never seen before. Nina Teicholz, the author, describes herself as a tireless researcher with a nine-year obsession reading thousands of scientific papers, etc. She does not explain, however, how she came upon this citation from the Old Testament, Genesis, Chapter 4, Verses 1-5 (New International Version):

[1] “Adam lay with his wife Eve, and she became pregnant and gave birth to Cain. She said, ‘With the help of the LORD I have brought forth a man.’ [2] Later she gave birth to his brother Abel. Now Abel kept flocks, and Cain worked the soil. [3] In the course of time Cain brought some of the fruits of the soil as an offering to the LORD. [4] But Abel brought fat portions from some of the first born of his flock. The LORD looked with favor on Abel and his offering. [5] but on Cain and his offering he did not look with favor. So Cain was very angry and his face was downcast.”

Well, we all know what happened next: Cain killed Abel. How prophetic! Cain, who favored “the fruits of the soil,” killed his brother who favored animal fat. And this in spite of the fact that God favored animal fat. When I read this passage from her copy of the NIV Study Bible to my wife, she said it sounded “paraphrased.” So, I went back to the pile of reference books next to my right shoulder as I read The Big Fat Surprise and found “The Revised Standard Version” of The Holy Bible. Verse 4 there reads thus: “And Abel brought of the firstlings of his flock and of their fat portions. And the LORD had regard for Abel and for his offerings.” When I read this to my wife, she had to agree it was essentially the same message: God favored animal fat.

But just to be sure, I searched online for the old King James Version of the Bible (the one I grew up with). Verses 4-5 read as follows: “[4] And Abel, he also brought of the firstlings of his flock and of the fat thereof. And the LORD had respect unto Abel and to his offering: [5] But unto Cain and to his offering he had not respect. And Cain was very wroth, and his countenance fell.” So, the Samaritan Pentateuch (Hebrew language version of the Torah), Septuagint, Vulgate, Syriac, and even the Masoretic Text all have the same ancient message: God looks upon fat, animal fat in particular, with special favor.

When my wife was satisfied that Nina Teicholz had accurately cited the passage from Genesis in The Big Fat Surprise, she got the message and then contributed the New Testament’s Parable of the Prodigal Son (NIV Luke 15: 11-31). For those unfamiliar with it, when the “lost” son, who had squandered his inheritance (while his father still lived), and returns home to humbly ask for his father’s forgiveness, the father instead celebrates the return of his “lost” son, with these words: [23] “Bring the fattened calf and kill it. Let’s have a feast and celebrate…” (emphasis added). Jesus also looked with favor on fat.

Could it be that animal fat has always been the preferred source of nutrients for optimal human health? That we evolved to select the “fat portions” of our “fattened” domesticated animals to eat first? We know, for example, that tribal peoples all over the world, who were neither Judeo nor Christian, also preferred the fat and viscera rather than the muscle meat. Teicholz writes (pg. 17) “…the Inuit were careful to save fatty meat and organs for human consumption while giving leaner meat to the dogs. In this way, humans ate as other large, meat-eating mammals do. Lions and tigers, for instance, first ravage the blood, hearts, kidneys, livers, and brains of the animals they kill, often leaving the muscle meat for vultures.”

Conversely, “(m)eat consumed without fat was commonly understood to lead to weakness. The Inuit avoided eating too much rabbit, because…these animals are too lean.” Vilhjallmur Stefansson, the Harvard-trained anthropologist, learned this during the year he spent living with the Inuit in the arctic.  He ate the same meat (marine and terrestrial) and fat, including organ meat, as the Inuit. And when he returned home and was ridiculed for reporting his observations, he submitted to a year-long experiment eating just “the Eskimo diet.” And “during the ensuing year,” Teicholz wrote, “Stefansson fell ill only once – when experimenters encouraged him to eat only lean meat without the fat.” “Diarrhea and a feeling of general baffling discomfort,” Stefansson said, “were quickly cured by a meal of fat sirloin steaks and brains fried in bacon fat.”

But lions and tigers and even “Eskimos” are not part of our experience. We (most of my readers) are products of what has come to be called Western Civilization. And we have become victims of our own prodigal past. We have abandoned our traditional ways of eating and have been led astray by “Cain” and a diet of processed vegetable oils and “mostly plants.”  

By some accounts, you can’t get much earlier in the history of the human race than Adam and Eve, who begat Cain and Abel. And, “(i)n the beginning” God looked with favor on Abel and on animal fat. So why did we go wrong?

Is The Big Fat Surprise on your reading list?

The Nutrition Debate #241: “HbA1c Increases with Age”

The headline in Diabetes in Control reads “HbA1c Increases with Age.” Headlines like this are often evidence of confirmation bias and are perilously misleading to the uninitiated. So, I had to read the digest piece and then the abstract in the medical journal Diabetic Medicine. If you register and pay a $$$ fee, you can get 24-hour online access to the full study from publisher Wiley.com. Such is the cost to society of dissemination of partially government-funded medical research.

Interestingly, at first glance, only the digest is guilty of confirmation bias. The medical journal is just guilty of myopia. I say “at first glance” because that is the only look I can afford. The full study could disabuse me of my take (and my biases). That said, this study was a review of two-large datasets. The aim was “to determine whether using HbA1c for screening and management, in a “cross-sectional analysis in adults without known diabetes,” the effects of aging have an impact on diagnostic accuracy.” That’s a reasonable AIM, and the researchers produced some interesting, but unsurprising RESULTS.

My quarrel, therefore, is not with the researchers. It is with Diabetes in Control, and primarily with their headline writer in particular. It is not nit picking to point out that the headline and the story in Diabetes in Control are contradictory. Neither is the headline consistent with the AIM, RESULTS or CONCLUSION of the scientific paper, as reflected in the ABSTRACT. In addition, disparities like this just cause me to get a bit unglued and go off on a rant, so hold onto your seat. It’s a brief one.

The study adjusted for covariates for a multitude of factors, such as race, BMI, etc, but not for treatment modality. Here’s where the myopism, or maybe just ignorance comes in. Everyone in both datasets received the same or similar failed treatment plan that is the ADA Standard of Care of type 2 diabetes. So, naturally, everyone’s A1c increased as they got older! BREAKING NEWS: It was supposed to increase as they got older! The current medical definition of diabetes is that it is a progressive disease. That means: Your condition will get worse as you get older IF YOUR DOCTOR FOLLOWS THE ADA STANDARD OF CARE. And guess what, as your condition gets worse, your A1c will get worse. How could it be otherwise?!!!

So, that’s where the digest failed. It just saw this result the way it was predisposed to see it. Except it was also careless; it describes the datasets as “adults with known diabetes.” Maybe it was just a typo. But my editor would have caught it (LOL).

Another quibble I have is with the characterization that “the researchers found a remarkable decrement in the performance of the predictive value of A1c as compared with a 2-hour Oral Glucose Tolerance Test (OGTT), with age. Well, la dee dah. It shouldn’t come as news that the OGTT is and will always be the “gold standard” for screening for type 2 diabetes. I had one in the 1980s. Have you ever had one? Do you know anyone at all who ever has?

But my quibble is not with the obvious superiority of the OGTT; it is with the term “remarkable decrement.” The Abstract provides some specificity. In elderly subjects without diabetes, over 10 years, their HbA1c’s increased less that 1/10^th of one percent, whereas in an analysis of all elderly subjects, including those with diabetes on that failed treatment modality, their HbA1c increased by less than 1%. For reference, remember that the A1c Standard of Care for the general population of type 2 diabetics is 7%, but in the elderly the ADA now sets the bar as high as 9% to “lessen the burden” on the patient. In reality, it’s recognition and concealment by subterfuge of a failed medical policy.

Of course, the RESULT is that, when treated to the ADA Standard of Care, as all the patients in both large subsets of data presumably were, “both glucose tolerance and HbA1c levels increased with age.” I guess that’s what the Diabetes in Control headline writer saw first, and used to confirm their bias.

Another result was stated thus: “The HbA1c of an 80-year old individual with normal glucose tolerance would be 0.35% greater than that of a 30-year old with normal glucose tolerance, a difference that is clinically significant.”

Another: “The specificity of HbA1c-based diagnosis criteria for prediabetes decreased substantially with increasing age.”

Okay. One of the Diabetes in Control conclusions: “Age should be taken into consideration when using HbA1c for the diagnosis and management of diabetes and prediabetes.” Fair enough.

My conclusion: Everyone, who on the basis of 2 consecutive elevated Fasting Blood Glucose tests, or whose HbA1c is 5.7 or higher and is therefore suspected of prediabetes or type 2 diabetes, should have a 2-hour Oral Glucose Tolerance Test.

Can’t get one? Check your post prandial glucose readings.