Retrospective #226: Improved Glycemic Control and CV Risk

A Medscape Medical News story on a Poster Presentation at the American Diabetes Association (ADA) 2014 Scientific Sessions in San Francisco made an important, but unstated, point. The “new, real-world study,” the report said, “based on real clinical practice,” demonstrated “a very strong effect” of glycemic control on cardiovascular outcomes.” The lead author of the study was a professor of epidemiology and biostatistics at University College London.

The lede for the Medscape piece was, “Among patients with Type 2 diabetes who start taking insulin, those who attain good glycemic control are less likely to have a major adverse cardiac event (MACE) in the medium term than those who fail to achieve this.” But the unstated point was that “it doesn’t appear to matter how you get to (glycemic) control; it’s getting to control that matters.” The message was to “achieve improved HbA1c…by whatever means.”

“The study covered nearly 3,000 patients who had had diabetes for about 9 years but had hyperglycemia despite generally receiving oral antidiabetic agents.” That’s like me, before starting a low-carb diet. “The patients had a mean age of 61, about half were women, and at baseline they had a median body mass index of 28.6.” Despite taking up to 3 oral antidiabetic agents [again, like me], their median HbA1c was 9.3% (range 8.1 – 10.7%). These patients were relying solely on their doctors to manage their Type 2 diabetes. The result: their disease had progressed to the point where their doctors HAD to start them on insulin.

So, what happened? “Patients whose HbA1c levels remained high had worse outcomes.” How much worse? 25% worse. “Specifically, a 1% higher HbA1c increased the risk of a major adverse cardiac event (MACE) during a 4-year follow-up by 25% compared with an otherwise similar patient with a 1% lower A1c.” The “1% increase in HbA1c above the mean was associated with a significant 36% increased risk of a first stroke, and a significant 31% increased risk of cardiovascular death. During the study follow-up, there were 44 nonfatal MIs (myocardial infarctions, or heart attacks), 57 nonfatal strokes, and 60 deaths from cardiovascular causes. There were 148 deaths from all causes.”

Seven percent were not taking any oral antidiabetic agents when they began insulin therapy. About a quarter were taking 1, half of the patients were taking 2, and a fifth were taking 3 orals. Two thirds of the patients were taking Metformin, three-quarters a sulfonylurea (!), twenty percent were on a TZD, and the rest on other diabetes meds.

“The patients made substantial gains in glucose control,” the lead author said. “The median HbA1c dropped to 7.4% (range 6.7% – 8.4%) at 1 year and remained around that level at years 2, 3 and 4.” “The results confirm that people with better blood glucose control have better cardiovascular outcomes,” the author said.

The guided-poster-tour moderator told Medscape Medical News, “This study suggests (that) getting glycated hemoglobin down with low-dose insulin in combination with other therapies is safe and might be beneficial by reducing CV events.” That’s a safe conclusion! He added, “Although it was not a prospective study with a comparator arm, nevertheless it reinforces that ‘good glycemic control is important to prevent cardiovascular events.’” Duh!

Not surprisingly, this study was funded by Sanofi, a manufacturer of insulin (Lantus and Apidra), So, the outcomes benefited them by promoting the use of “low-dose insulin in combination with other therapies.” But remember the takeaway: “It doesn’t appear to matter how you get to (glycemic) control; it’s getting to control that matters.”

Unfortunately, this study did not consider dietary choices as part of their diabetes care. But neither did it exclude diet. It doesn’t matter how you get control; it’s getting control that matters. In this study, the patients relied on their doctors to take care of them, and they “had had diabetes for about 9 years but [still] had hyperglycemia [high A1c’s].

My Fasting Blood Sugars, after 16 years of letting my doctor prescribe progressively more anti-diabetic meds (3 total), and doing nothing on my own behalf, was still in the 150s. Like these patients, I was on the verge of injecting insulin. But here’s the critical difference: instead of insulin, my doctor started me on a Very Low Carb diet. I not only lost a great deal of weight, I had to discontinue most of my antidiabetic meds to avoid hypoglycemia (low blood sugar)!

Retrospective #225: Diet and Type 2 Diabetes Risk

I keep hoping that someday I will read in the scientific or mainstream media that eating a low-carb diet will reduce the risk for Type 2 diabetes. I mean, it’s so obviously true that I am at a loss to explain why I don’t read it all the time. Then, a recent Diabetes in Control headline gave me renewed hope, until I saw the source and read the story.

The headline, ADA: Improving Quality of Diet Reduces Risk for Type 2 Diabetes, had me hopeful. The sub-title, “Consuming healthier foods improves risk independently of other lifestyle changes such as weight loss or physical activity,” gave me further encouragement. Then, my hopes crashed.

The story began, “Researchers at the Harvard School of Public Health have found that patients who ate more whole grains, fruits, vegetables, and less sweetened beverages and saturated fats improved their diet quality index scores by ten percent over four years. This reduced their risk for developing Type 2 diabetes by about 20% when compared to those who made no diet changes.” The “control” ate the Standard American Diet (SAD), which is filled with junk food.

The measurement tool that the Harvard “researchers” used was the “110-point Alternate Healthy Eating Index 2010” (AHEI). Harvard’s Walter Willett and colleagues developed the AHEI in 2010 to “improve on” the Healthy Eating Index (HEI) that was originally developed by the USDA in 1990 and updated every five years to conform to the changes in the USDA’s Dietary Guidelines for Americans. It measures diet quality as a function of conformance to the Guidelines.

A comparison of Harvard’s AHEI and the USDA’s HEI can be viewed on Yahoo. The Yahoos site’s main value, however, is that it provides links to both the 2010 AHEI and the HEI. In my view, obviously, the AHEI and HEI are both deeply flawed, not least for their views about fats, especially liquid fats (refined “vegetable” oils) made from polyunsaturated sources (corn, soy bean, sunflower, peanut, canola and others). In addition, both Harvard’s AHEI and the USDA’s HEI regard a “move to a plant-based diet” an “important step in the right direction,” according to the AHEI link. They would have you view “solid” (saturated) fats as harmful, and severely curtail your consumption of egg yolks, butter and red meat. Harvard is still hopelessly hamstrung by its Hammurabian bias. This latest “study” simply seeks to promote the “ancient” (50-year old) and totally erroneous bias against saturated fats.

The USDA’s Center for Nutrition Policy and Promotion [note the undisguised use of ‘promotion’ here] uses data collected via 24-hour recalls of dietary intake in national surveys to construct the HEI score. The methodology of Harvard’s 110-point AHEI uses “a scoring system similar to the USDA’s index…using information about daily diets collected from more than 100,000 female nurses and male health professionals taking part in two long-term studies.”

Harvard can’t be faulted for wanting to improve or replace the “one-size-fits-all” Dietary Guidelines for Americans. But just tweaking it, as Harvard does, is not the solution. Neither, however, do I fault some of Harvard’s tweaks. My main gripe is with their confounding of “more whole grains, fruits, vegetables,” with “less sweetened beverages and saturated fats.” And, in this last phrase, the conflating of “sweetened beverages and saturated fats.” Elsewhere, they (and the USDA) consistently conflate “saturated fats” and “trans fats.” These are egregious examples of using a rhetorical device to confuse and mislead the public. And it is downright damnable. Damnable, I say.

With respect to this particular “study” and public policy press release, how can Harvard say that the 10% improvement in diet quality index scores (over those who made no self-reported diet changes), and which lead to a 20% reduction in developing Type 2 diabetes, was attributable to reporting eating “more whole grains, fruits, vegetables,” or eating “eating less sweetened beverages and saturated fats.” Perhaps the 10% improvement in scores was attributable to the (self-reported) elimination of sweetened beverages without any change in saturated fat intake or whole grains, fruits and vegetables. Or eating more whole grains, fruits and vegetables and fewer sweetened beverages, but the same amount of saturated fat. Or any combination. But that’s epidemiology, a very weak “science,” at best.

But that’s about what I expected when I read that this “study” was a product of the Harvard School of Public Health. It is simply a promotional piece to advance their idea of a “healthy diet.” A perfect example of confirmation bias.

Retrospective #224: Diabetic Foot: A Cinderella Condition?!!!

The full title of this Medscape Medical News story is, “Diabetic Foot: A Cinderella Condition, Needs a Team Approach.” The simple title, “Diabetic Foot Needs a Team Approach,” would have been much better, but would get fewer “clicks.” It was actually a good story. The findings were reported at the ADA’s 2014 Scientific Session. The key takeaways:

●     There is a need for a “uniform, multidisciplinary approach,” with a “national treatment plan” for diabetic foot. To this end, a U.S. National Diabetic Foot Registry is now being established. (All four commenters agreed).

●     At one large “safety-net hospital system that serves a diverse patient population,” in “2000 there was nearly a 50-50 chance that if you came in with a diabetic-foot infection, you would lose your foot.” As a result of their establishing a limb-salvage program, there has been a staggering reduction in the number of amputations.

●     The average age of the amputee population was 55.9 years, 72.5% of the patients were male, and the average H1c was 9%. Seventy percent of the patients had coronary artery disease, and 14% end-stage renal disease.

●     Amputation was “a robust independent predictor of death, associated with a significant, almost 85% increased risk for mortality,” with “most of the deaths – just under 50% -- due to cardiovascular disease.”

●     “Even minor amputations were associated with an almost 50% increased mortality risk, a somewhat surprising finding.” And, “Once you have an amputation, you go down a not very healthy road.”

The session moderator told Medscape Medical News, “It was…disappointing... to see that minor amputations had no better outcome – you would expect that they would do better, but apparently not.” “But I think that if you look at the natural course of the disease, these patients die of cardiovascular disease – it doesn’t matter what you do to their extremity. They all die of CVD. I guess we should expect it, but we would hope it would be better,” he said. Wow!

Given this dismal, if no longer abysmal outlook, I would hardly call this a “Cinderella Condition.” Even having the amputation rate fall from 36% to 11%, after the limb-salvage program was implemented at that particular safety-net hospital system, “They all die of CVD” is not a story-book ending. It’s not like “they lived happily ever after,” unless it is to be inferred, that the prospect of going forward with a “uniform, multidisciplinary approach” and a “national treatment plan” for diabetic foot has the potential for “a Cinderella ending.” I’ll try to imagine that that is what was intended by the title.

I haven’t written about diabetic foot before except to mention that diabetic neuropathy (the cause of “diabetic foot”), along with nephropathy and retinopathy, are the three major classes of diabetic Microvascular Complications, as well the seldom mentioned erectile dysfunction (ED). Cardiovascular disease (CVD) – as in “They all die of CVD” – is the major Macrovascular Complication of Type 2 diabetes. Hopefully, your A1c is much, much lower than 9%. That average glucose (eAG) of 212mg/dl requires drastic action on the part of both the physician and the patient.

Of course, if you’ve somehow just been diagnosed with diabetes and have an A1c as high as 9% (or higher), you can do something dramatic to lower it. One thing you undoubtedly will do, and are doing, is your homework. If the doctor hasn’t scared the bejesus out of you, reading about the progressive nature of this disease, if you follow “usual care,” is scary enough. Reading about the complications and the likely prognosis is ever scarier. Reading the five bullets above is downright terrifying. But you can do your homework and choose a course of action to avoid all of this.

The first A1c that I ever had, long before that test was common, was given to me by an endocrinologist 26 years ago in 1993. My A1c was 8.9%. Curiously – inexplicably, really – I didn’t have another A1c test for 10 years, and by this time I had already been on a Very Low Carb diet (20 grams a day) for almost a year. My A1c was then 5.4%. I would love to have known what it was just before I began to eat Very Low Carb. It would certainly have been “out of control.” My FBS’s were in the 150s and I was maxed out on 2 oral anti-diabetes meds and starting a 3^rd.

My editor says that I was very lucky. I sometimes forget. Many people develop early signs of complications in just a few years of “uncontrolled glucose control.” Others not. I guess I was, and continue to be, lucky. Do you want to take a chance that you’ll be lucky too? Are you a gambler? Just be aware: Diabetes Foot is NOT a Cinderella Condition.

Retrospective #223: Adding Insulin to Metformin for Type 2s questioned.

“Adding Insulin to Metformin for T2s May Increase Risk of Death,” was a scary headline of a 2014 Diabetes in Control article about a JAMA paper: “Association between Intensification of Metformin Treatment with Insulin vs. Sulfonylureas and Cardiovascular Events and All-Cause Mortality Among Patients with Diabetes.”

Both the Diabetes in Control piece and the JAMA paper were qualified and raised more questions than they answered. In my mind, so did the objectives and design of the study. Why, for example, would anyone today want to compare adding insulin to adding a sulfonylurea? Haven’t the sulfonylureas as a class been thoroughly discredited? I cite Dr. Ralph DeFronzo’s Banting Award keynote address to the 2008 ADA Convention in San Francisco and his paper published in Diabetes in which he wrote, “Sulfonylureas are not recommended because, after an initial improvement in glycemic control, they are associated with a progressive RISE in A1c and a progressive LOSS of ß-cell function.”

The “Adding Insulin…” study took place in the Veterans Administration (VA) hospital system in Nashville.  The Vanderbilt University researchers reported more patients in the sulfonylurea cohort than in any other. (“Among 178,341 Metformin monotherapy patients, 2,948 added insulin and 39,990 added a sulfonylurea.”) That reminds me of the story of the person who lost a ring in a dark alley and was looking for it under a street light. When asked why, he replied, “There’s more light here.” But couldn’t they have used a more current treatment modality than a sulfonylurea, like a GLP-1 (or today a SGLT-2), rather than one that causes more harm than good to the patient?!

The Objective of the study was alarming in itself: “To compare time to acute myocardial infarction (AMI), stroke or death in a cohort of metformin initiators who added insulin or a sulfonylurea.” They quickly dispel this most alarming outcome objective: “Acute myocardial infarction and stroke risks were statistically similar.” Whew! That’s the good news. The bad news? The Conclusion (from the full-paper): “Among patients with diabetes who are receiving Metformin, the addition of insulin compared with sulfonylurea was associated with an increased risk of a composite of nonfatal cardiovascular outcomes and all-cause mortality.”

Of course, this finding of an “association” was followed by, “These findings require further investigation to understand risks associated with insulin use in these patients…” Okay, that’s pretty much pro-forma these days. It also just a plea for more taxpayer funding for further investigations (a medical school’s research department jobs program). But that final sentence of the Conclusions section has a compound predicate; it continues, “…and call into question recommendations that insulin is equivalent to sulfonylurea for patients who may be able to receive an oral agent.” Okay, okay, but even in 2014 sulfonylureas weren’t the only oral agent available! And they overwork the remaining working beta cells that you have, leading to their destruction! Go back and read Dr. DeFronzo’s speech/paper.

Sulfonylureas have been in use in the U.S. since the late ‘40s. Metformin was introduced in Britain in 1958, in Canada in 1972, and finally permitted by the FDA in the US in 1994. Now, it is the preferred first course of treatment both in Europe and the U.S. for pre-diabetes and is used as a monotherapy by many T2s (like me), who rely primarily on diet for blood sugar control. But if I needed a 2^nd therapeutic, I WOULD NEVER AGAIN AGREE TO TAKE A SULFONLUREA (Micronase, glyburide, glipizide, etc.), just as I would never agree to take a statin to lower my Total Cholesterol and LDL-C. Both my doctor and I are very happy with my lipid (cholesterol) levels as they are, thank you very much.

So, where do we go from here? It’s confusing. The first “Practice Pearl” in Diabetes in Control raises a very good issue: “Many variables were not considered in choosing the participants in this study.” Their takeaway: “These findings require further investigation to understand risks associated with insulin use in these patients.” Yes! More studies!

But it comes as no surprise to me that the VA is still administering sulfonylureas; or that the researchers at the Vanderbilt University Department of Medicine, Department of Biostatistics, and Department of Health Policy continue to advocate for that particular “oral agent” (a sulfonylurea). It is dirt cheap. And insulin, especially since this was originally published in 2014, has become really expensive. But isn’t that what drives our national health policy today?

Retrospective #222: Better Diabetes Self-Management with Cognitive Therapy

The day after the 2^nd of the last two bombs dropped in my inbox (see Retrospective #221), another one “exploded.” “Better Diabetes Self-Management with Cognitive Therapy,” is a Medscape Psychiatry Minute by Dr. Peter Yellowlees. As my readers know, I believe that self-management of Type 2 diabetes should be advocated by physicians and in the medical literature. Patients should be more involved in their own Type 2 diabetes care. So, what was this all about?

The video synopsis, with accompanying transcript, “A randomized controlled trial of cognitive behavioral therapy for adherence and depression (CBT-AD) in patients with uncontrolled Type 2 diabetes,” appeared in Diabetes Care. Note: “adherence and depression.” The work, with 87 adults, was done at Massachusetts General Hospital in Boston.

It was an expensive, randomized controlled intervention in a hospital environment, with a “usual care” component and a predictable outcome: the intervention group (depressed patients with uncontrolled Type 2 diabetes), received CBT and, after 4-, 8-, and 12-month follow-up time points, “maintained 24% higher medication adherence, 17% greater adherence to self-monitoring of blood glucose, and lower A1c values.” The “better” adherence outcome was not surprising, but what interested me was the outcome that, “…both groups being less depressed.”

Hmmm. Both groups took their pills, monitored their blood glucose and had A1c tests, and both groups ate the same horrible hospital food, so presumably the adherence end-points and A1c improvements of the intervention group were a result of their CBT treatment therapy. And because both the intervention and control groups saw themselves as receiving this expensive “care,” both groups came out less depressed! Well, that’s good for both patients and the psychiatrists who, after all, needed to feel that they’re helping patients, not least to justify the cost of the study.

Not to put too fine a point on it, in the ABSTRACT the only mention about depression was this: “For depression, there was some evidence of continued improvement post-treatment, but no between-group differences.”

I don’t mean to be critical of Cognitive Behavioral Therapy. I actually think CBT is good. My main frustration with this study is that these seriously-ill, hospitalized patients, all with uncontrolled Type 2 diabetes, were being taught, through CBT, “adherence:” Take you pills and test your blood regularly to see how sick you are AND HOW MUCH SICKER YOU’RE GETTING. No wonder they’re depressed! Isn’t everyone depressed when the medical therapy prescribed, including weight loss advice, isn’t working?

I guess it never occurred to these docs (they’re psychiatrists) that Type 2 diabetes is a disease of hormonal disregulation caused by insulin resistance arising from impaired glucose tolerance: in other words, carbohydrate intolerance. And the most effective treatment protocol, rather than “adherence” to a pharmacotherapy treatment regimen, is to dramatically curtail intake of dietary carbohydrates! (Good luck with that on hospital food!)

But that’s what I did. When, at my doctor’s suggestion, I started to eat a Very Low Carbohydrate diet (just 20 grams of carbs a day!), I was on three different classes of oral anti-diabetic medications, and maxed out on two. The first day I had a hypo, and I called my doctor. He carefully (and very quickly, all in the first week) drastically reduced my meds. It left me with only one, a small dose of Metformin (500mg, once a day). That was 17 years and 150 pounds ago.

Dietary “adherence” with Very Low Carb, is, for me, easy because on Very Low Carb, you’re never hungry. Medication and self-monitoring adherence will improve too as you will look forward to daily and weekly improvements.

I don’t need expensive therapy, although I don’t knock it. Do whatever works for you. The important thing is to choose the right dietary therapy for treating Type 2 diabetes. If you’ve been diagnosed with pre-diabetes or Type 2, Learn what carbohydrates are. Test your blood sugar regularly. “Eat to your Meter.” Your doctor and you will both approve of the weigh-in and lab results, and you won’t need a psychiatrist (for this), because as you lose weight and get better lab results, you will be less depressed. Your medication (if required) and self-management adherence will improve, at minimal cost to you and society. And your mood will be permanently elevated.

Retrospective #221: Medscape dropped 2 bombs in my inbox last week

Medscape Medical News dropped 2 bombs in my inbox last week. My post-bombing analysis is that they both missed the target. The first was due to a navigational error and the second due to cloud cover. That’s my analysis, anyway.

“Congratulations! We’re Making Strides in Diabetes Care, “by Dr. Anne L. Peters, MD, CDE, a respected, establishment diabetologist, is simply a cheerleading piece timed for the ADA convention. She provided three links to recent articles in 1) the Journal of the American Medical Association (JAMA), 2) the Annals of Internal Medicine, and 3) Diabetes, the Journal of the American Diabetes Association, summarizing, “This is great news. We are doing a better job than ever.”

Would that her audience, comprised largely of “treating” physicians (like herself,) agree? But then, maybe that’s the point of her getting ginned up to deliver this Pollyannaish piece. I suppose the treating physicians convened at the Annual ADA Convention are in need of a morale boost. She and her colleagues primarily treat uncontrolled diabetics.

In spite of the “strides” claimed, I feel there must be among the vast majority of practicing physicians a frustration, a frantic despair, in fact, a feverish frenzy over the utter failure of the “usual care” treatment protocol, dictated by their medical associations and their government overseers. Dr. Peter’s problem, and that of the entire medical and public health establishment, is that they simply are using the wrong treatment protocol (and many of them know it).

The 2^nd bomb, which appeared 2 days later, was titled “Diabetes Prevention Programs: A Waste of Money.” This was a Medscape Interview of Richard Kahn, PhD, Professor of Medicine, University of North Carolina, Chapel Hill. A controversial counter message, it focused on “lifestyle modification programs geared for weight loss,” since these programs have been shown to “delay or prevent the onset of Type 2 diabetes.” The Medscape Editors’ note that “as many as 82 million Americans are thought to have prediabetes.” “These people” (referring to people who had completed a “usual care” Diabetes Prevention Program) had an enormous amount of attention given by health professionals.” “Those interventions – almost every one – were expensive,” Dr. Kahn asserted. And they failed.

Dr. Kahn adds: “The first thing you see is that the overwhelming number of studies didn’t even go out to one year,” and “the assumption the authors make” is “that that amount of weight can be lost forever. That has simply never been seen except in bariatric surgery.” “From a medical point of view, it doesn’t look like that initial weight loss does much, if anything. For some clinical effect you have to lose substantially more weight – 20%, 25% of your body…,”and, Dr. Kahn continues, “it would have to stay off for a long time” to be a cost-effective program worthy of “society pay(ing) for the intervention,” given “how difficult it is to keep weight off.”

So, Dr. Kahn’s “after bombing assessment” confirms that the “usual care treatment protocol” you are likely to receive in your clinician’s office is ineffective and the reason why so many physicians and patients feel frustrated. Dr. Kahn said, under such “diet and lifestyle” diabetes prevention programs, “the assumption that the weight will be lost and held off for life… is unrealistic.” Dr. Kahn isn’t asked about what he meant by that, but I think I understand: his analysis of the data shows unproven tenets and assumptions; his conclusion: the present modus operendi (a low-fat, “balanced” diet protocol) is simply not cost-effective because it doesn’t work long-term.

But Dr. Kahn does leave a door open. I suspect he knows anecdotally (as I know personally), that long term, permanent weight loss is indeed possible – if we re-program our sights and target carbohydrates. He says, “Some people decide, ‘I’m going to do it. They’ve invested nothing. That’s great for them, but we’re not arguing about whether people should be encouraged to lose weight. What we’re arguing against is having society pay the bill for this when it hasn’t been effective.” Yeah, he does know. But, alas, the good professor can’t afford to say it. Too bad, really.

Medscape then asks, “What’s the main takeaway for clinicians, then?” Dr. Kahn’s final remarks, “People who are overweight or obese should be strongly encouraged by their healthcare provider to lose weight and keep it off. If a provider feels that there is a good resource in the community, he or she should refer the person to that resource.” Hello. Anyone listening? Check out how I lost and keep off 40% (150 pounds)of my body weight. See Retrospectives #213 & #214.

Retrospective #220: “Eat protein to lower stroke risk”

“Eat protein to lower stroke risk” is the title of a piece in The Telegraph. The article is based on a study in Neurology, “Quantitative analysis of dietary protein intake and stroke risk,” from the Nanjing School of Medicine in China.

The Telegraph’s story begins, “Eating a high protein diet [emphasis added] significantly lowers the risk of stroke and could prevent 10,000 deaths in Britain every year, a study has suggested.” A high protein diet? Maybe some hyperbole by an eager reporter, combined with bad editing. The lesson here: stories in the popular press are not peer reviewed.

“The (total) amount of protein that led to the reduced risk was moderate – equal to 20 grams a day,” it says. Moderate? That’s a small amount (by American standards). The Standard American Diet (SAD, ironically) on the Nutrition Facts Panel of manufactured and processed food packaging calls for 50 grams a day (10 percent of total calories), and most Americans eat a diet of more than 15 percent protein. Remember, the lower minimum percentage in the “Dietary Guidelines for Americans” only survives because they writers are heavily influenced by the vegan lobby who advocate a plant-based diet to save the planet from greenhouse gasses (caused by bovine flatulence), etc., etc.

The study RESULTS, from the ABSTRACT, however, are more specific: “The pooled RR [relative risk] of stroke for the highest compared to the lowest dietary protein intake was 0.80 (95% CI [confidence interval] 0.66-0.99 [range]).” That means the risk of stroke was 4/5s as great (0.80) for the highest compared to the lowest dietary protein intake.”

The ABSTRACT had another interesting result: In addition to the 20% relative reduction in stroke risk for overall dietary protein intake, they reported that “stratifying by protein type, the relative risk of stroke for animal protein was 0.71 (95% CI 0.50-0.99).” For the mathematically challenged, that translates to an almost 50% greater (29% versus a 20% reduction) in relative stroke risk. In simple terms, in the words of The Telegraph’s science correspondent, “The reduced risk of stroke was stronger for ANIMAL protein than vegetable protein.

“Consuming as little as one chicken breast, or a salmon fillet, -- the equivalent of 20g – reduced the risk of stroke by 20 per cent,” The Telegraph said. The study analysis does have a bias, however. According to the study’s lead author, “people should avoid red meat,” which has been associated with increased stroke risk, according to The Telegraph. “These results indicate that stroke risk may be reduced by replacing red meat with other protein sources, such as fish” Hmmm. Isn’t pork the “other white meat”? In any case, it appears the Brits have a vegan lobby too; Or, if this was part of the study’s conclusions, perhaps the lead author was pandering to the “perceived wisdom” to get published. 

The bias deepens, however, in the accompanying editorial in Neurology. The authors review what “many experts recommend”: “…a low-fat diet such as the AHA diet, formerly the National Cholesterol Education Program diet, based on the evidence for an atherogenic role for fasting cholesterol levels.” That means, you need to get Total Cholesterol (TC) below 200mg/dl (with a statin) regardless of the lack of hard evidence to support lower TC in CVD prevention.

“However,” they say, “evidence-based dietary recommendations for reduction of stroke risk are limited.” And then, interestingly: “The current recommendation for monounsaturated fat instead of saturated fat reflects the evidence that the source of dietary fat matters more than the proportion of calories from fat” (emphasis added). The worm turns (in 2014) in the UK. More evidence in the medical establishment’s thinking that the proportion of calories from fat now matters less than the type; still a lagging bias against saturated fat, but a green light for monounsaturated fat (olive oil, etc.) and no mention, and especially important, no advocacy for polyunsaturated fats (vegetable oils like soy bean and corn oil), which the American dietary establishment strongly advocated for in the 2015 Dietary Guidelines.

If this sounds like the Mediterranean diet, well, it is. The editorial then swings full speed into an incestuous vortex of “validating the expectations of the perceived wisdom.” “Therefore,” it concludes, “it seems invalid to focus exclusively on protein (‘Eskimo Diet’) or what we have done with lipids in the past.” [That sounds like a mea culpa ON FAT]. “In other words,” they say, “eating vegetables, fruits and protein every day will help to keep stroke away!” A not very clever attempt at drollery, to be sure, but to this skeptic, a sure sign of transition in the UK’s dietary establishment.

Retrospective #219: “Surgery Tops Usual Care in Obese Diabetics”

Not a surprising result but the term “usual care” caught my attention in this otherwise unsurprising Medscape Medical News piece in a special diabetes-themed issue of the Journal of the American Medical Association, timed to coincide with an annual American Diabetes Association (ADA) Scientific Session. These days the bariatric surgery business in on the rise, and self-serving articles like this one are all too common, even in peer-reviewed scientific journals.

“Usual care” is a “term of art” so commonly used that the Medscape reviewer did not define it. It was defined in the study itself and, I’m sure, in the practice guidelines of bariatric surgeons. Besides, this study was not about “usual care.” It was about promoting bariatric surgery as the preferred course of action for the treatment of obese diabetics.

Medscape quotes a JAMA editor who was also co-author of an accompanying editorial: “The study findings validate the expectations [LOL] of bariatric-surgery-associated weight loss and provide concrete numbers to cite.” She added, perfunctorily, “Diet and lifestyle measures will always be the cornerstone of diabetes therapy, but bariatric surgery is an option for patients who are unable to lose sufficient weight with diet and exercise and who are willing to accept the risk of bariatric surgery and comply with the lifestyle changes required after bariatric surgery” [all my emphases].

So, let’s see what we’re being told here: 1) “Usual care” usually doesn’t work, for most obese diabetics; The “usual” “diet and lifestyle measures,” a “balanced, low-fat diet and exercise,” as counseled by physicians who treat obese diabetics, are the “cornerstones of diabetes therapy.” And when this “usual care” is prescribed, and followed by the patient, with the resulting “insufficient” weight loss, the patient will then be counseled to consider the option of bariatric surgery. That is, if the patient is “willing to accept the risk of bariatric surgery and comply with the lifestyle changes required after bariatric surgery. Thanks a lot! Maybe a change before surgery should be thought about.

Okay, let’s review again: “Usual care,” as currently defined by the standards of medical practice, is such a hopeless cause as to be forlorn. And, of course, your failure to achieve sufficient weight loss with “usual care” is laid on YOU, the patient, who was obviously “non-compliant” with the diet and lifestyle measures your physician had “prescribed.” So, surgery to the rescue! The doctor takes charge AGAIN, providing the patient is “willing to accept the risk of bariatric surgery and comply with the lifestyle changes required after bariatric surgery.” Is this what you want?

And the “lifestyle changes” after bariatric surgery? Liquid meals only for weeks or months after surgery. Thereafter, only very small meals at frequent intervals because the stomach is no longer a large expandable storage pouch. And if you eat more than your greatly reduced stomach capacity: nausea, projectile vomiting, even dumping, i.e., where food gets “dumped directly from your stomach pouch into your small intestine without being digested.” Think about that!

Another point to bear in mind: These “lifestyle changes” are now life-long REQUIREMENTS, not options. In contrast, the “lifestyle changes” of a low-carb “diet and exercise” program are volitional. If you want to, you can take a “holiday” from them now and then, and the major downside is a temporary weight gain or loss of blood sugar control, and guilt. After bariatric surgery, you had better not try to take a break from your regimen; you will pay dearly for it. As a consequence of accepting the risk of bariatric surgery, you must comply with the lifestyle changes required after bariatric surgery. You are no longer “the master of your fate;” you are no longer “the captain of your soul.”

Of course, none of these consequences are necessary. You do not need to opt for bariatric surgery. You simply need to opt for A DIET THAT WORKS to achieve “sufficient” weight loss, permanently.  Admittedly, it is also a lifetime requirement, if you want to maintain the weight you have lost (and all the other improved health markers) for the remainder of your lifetime – a lifetime that will likely be longer if you do.

My regular readers know, of course, that I personally adhere to a Very Low Carb lifestyle. And I don’t exercise. I don’t enjoy it. You can, if you like it, or you can wait until you’ve lost 50 or 100 pounds to start an exercise program. You’ll enjoy it more and reduce your risk of injury when it isn’t so much work to lug around that extra weight. You could start (as I did) on a Very Low Carb regimen (20g/d), or you could just go Low Carb, at 50 or 100 or even 200g/d.

Retrospective #218: “Diabetes Causes Nerve Pain”

Misleading advertising riles me all the time, almost as much as grammatical errors by news anchors, talk show hosts and United States Senators. And I am especially riled by advertising that claims that others are being misleading while being themselves misleading. They must think we’re all dummies!

My current (2014) favorite is a teachers’ union advocating for the Common Core curriculum. In it, an actor playing a teacher says (I’m paraphrasing), “Those opposed to the Common Core are misleading the public”; she protests, “Common Core does NOT tell teachers HOW to teach” (emphasis mine). “THAT is misleading,” she says. What she DOES NOT say is that Common Core DOES tell teachers WHAT to teach! THAT’S ITS PURPOSE. Grrrrrrrrr!

Another TV commercial I’ve heard over and over says “Diabetes causes nerve pain.” I guess it’s a scare tactic. You’re supposed to rush to your doctor and ask him to prescribe the drug that is being advertised. It unnerves me (hehe) to hear it. Diabetes does NOT cause nerve pain. Uncontrolled diabetes causes nerve pain and will eventually damage the microvascular system, specifically the tiny blood vessels in the extremities (legs usually), the eyes (the retina), and/or the kidneys. These complications can lead to amputations, blindness and end-stage kidney disease.

The mechanism is that when the blood supply is cut off to the tiny blood vessels, they don’t supply the nerves with the oxygen they need to receive and send signals; thus, you become insensitive to pain or injury to your feet. A cut or some other undetected injury of an uncontrolled diabetic can thus lead to infection, then gangrene and amputation.

Uncontrolled diabetes is the culprit, NOT diabetes. The point is that uncontrolled diabetes – am I repeating myself? – is what needs to be avoided – and “treated” when it’s encountered. The worst thing you can do is ignore a blood sugar that is not in control. Over a period of years, it will manifest itself. And you will likely die from it. And that’s scary.

Getting your blood sugar to the point where it never exceeds 140mg/dl at any point after a meal and returns to under 100 mg/dl (if you are pre-diabetic or a diagnosed Type 2) should be your goal. Any after-meal spike above 140mg/dl are going to damage your microvascular system, slowly but surely. And remember that an A1c of 7.0% (the ADA target!!!) is equivalent to an estimated Average Glucose (eAG) of 154mg/dl. If you have an average blood glucose of 154mg/dl (7%), just imagine how much of the time your blood sugar is above 140mg/dl. Now, that’s, really scary.

So, how to you “treat” uncontrolled Type 2 diabetes? Your doctor will probably start you on oral anti-diabetes meds and tell you to lose weight, probably on a low-fat, “balanced” diet. You’ll probably also need blood pressure meds, maybe a cocktail of them. Oh, and of course, a statin, to lower your Total and LDL Cholesterol (because statins will do that, although the benefit of doing so has not been shown). You should know that under this regimen, your Type 2 diabetes will be a “progressive” disease. That is, your condition will worsen; you will take more and more medication, ultimately leading to injecting insulin. And don’t forget the complications. They’re in your future too, including Macrovascular complications (e.g., CVD). This is getting too scary even for me. But there is an alternative. Interested?

YOU could treat your Type 2 diabetes yourself. That’s right, YOU. YOU can control your blood glucose simply by controlling the things you put in your mouth. The foods (and drinks) that make blood sugar rise ALL contain carbs. Carbs, both the simple sugars and the more complex carbohydrates (both processed and unprocessed), when digested, all convert to glucose, or “sugar,” in your blood. The hormone insulin transports and facilitates its uptake.

If you have T2 diabetes (or are prediabetic), your body has over time become resistant to insulin, so the glucose continues to circulate. In essence, you have become carbohydrate intolerant. To control your diabetes, you only need to limit the amount of carbohydrates you eat and drink. It’s that simple.

I’ve been writing about this subject for 10 years. I’ve been a Type 2 diabetic for 33 years, the last 17 eating Very Low Carb, (mostly) healthy foods. My Type 2 diabetes has not progressed. In fact, it has been in remission for 17 years. I am much, much healthier today that I was 17 years ago. You can be too, if YOU take charge of your diabetes health.

Retrospective #217: Type 2 Diabetic says, “I can eat whatever I want.”

I was seated next to a Type 2 diabetic acquaintance at a church supper recently. As the plates of food were passed around, I took a nice portion of ham and then (guiltily) a serving of cole slaw. I knew it was loaded with added sugar, but I also knew my other choices would be limited. I passed on the scalloped potatoes au gratin and the peas, and the bread basket, and the sweetened ice tea, each time passing the dish to my friend, who took a regular portion of each.

I didn’t say anything, but I thought to myself, how can he do this to himself? This man is somewhere in his eighties, skinny as a rail and looks healthy. Maybe the question should have been, how does he get away with eating like this? Eventually, I managed to open the subject with him. He responded by saying, “I can eat whatever I want.” He then reached down to his belt and, out of a small pouch, raised his pump controller to show me how he does it. My friend, it turns out, is an insulin-dependent Type 2 with a pump that allows him to set the amount of basal and mealtime (bolus) insulin before each meal. So, he knew what was for supper – it’s the same every year – and had given himself a “shot” via the needle imbedded under his skin. Voila! He can now “eat whatever he wants” and “cover it” with insulin.

Managing Type 2 diabetes with injected insulin has heretofore always been the last resort of pharmacotherapy. Type 2s used to be started on a course of oral pharmaceuticals and told to continue to eat a “balanced diet.” As one drug failed to achieve the desired control (A1c’s within the ADA recommended range of ≤7.0%), the dose was increased and/or another class of oral introduced until the patient, still eating “a balanced diet,” maxed out on three classes.

Then, the dreaded insulin injection was employed for basal (slow acting for 24-hour control) and mealtime “boluses.” Today, the introduction of new classes of orals, and the (GLP)-1 receptor agonists, and more recently the new (SGLT)-2 inhibitor drugs, that work on eliminating sugar in the blood via the kidneys, have enabled some patients to delay multiple daily insulin injections. And “the insulin pump” has replaced them all, for those who use it.

Another approach has been the introduction of injected insulin as a first course of treatment. The rationale is that if you eat a low carb diet, and inject a low dose of basal insulin once a day, you can potentially achieve better control by reducing postprandial spikes (elevated blood “sugars” after meals), thus achieving much lower A1c’s vs. the 7.0%. Better control also means the surviving beta cells of the pancreas, that produce endogenous insulin, get a rest.

An A1c of 7.0%, by the way, is equivalent to an estimated average glucose (eAG) of 154mg/dl, but an A1c of 6.0% is an eAG of 126 and an A1c of 5.0% is an eAG of 97. This improvement will surely reduce the possibility of the complications of poorly controlled diabetes: retinopathy, neuropathy, and nephropathy (translation: blindness, amputations and end-stage kidney disease). Plus, it reduces the possibility of a much greater chance of a heart attack. Any time your blood sugar is above 140, you are causing damage, and an average of 154 means it is above 140 A LOT. It is, in my opinion, bordering on criminal to counsel patients to only strive to achieve an A1c of 7.0%.

I don’t write about insulin dependent Type 2s because I know very little about it. Years ago, I read Richard K. Bernstein’s Diabetes Solution, the definitive source book on the subject (for both Type 1s and Type 2s), but promptly forgot most of the Type 1 details. His latest edition is very highly regarded among those in the know. It is the “bible” for the growing numbers of T2s as well as T1 diabetics who have discovered THE BEST WAY TO MANAGE AND CONTROL THEIR DISEASE IS TO EAT LOW CARB, with or without an insulin regimen.

But because I rely on my dietary choices (plus a daily, single low-dose Metformin) to directly limit the response of my (broken) blood sugar metabolism, I’ll bet my blood sugar is more stable, with fewer excursions, and therefore better controlled, than my friend’s (except at this particular supper: LOL). I’d even venture to wager that my A1c is lower than his. I didn’t ask him his, though. He, and his doctor apparently, are happy with whatever it is, and he was very happy to be able to say, “I can eat whatever I want.”

This column was originally written in 2014. Sadly, my friend died of “complications” (heart disease) in 2015.

Retrospective #216: Is Low-Carb High-Protein or High-Fat?

The cognoscenti (my regular readers, who are “in-the-know”) know that the answer is “high-fat.” But I squirm in my seat when I hear someone, who appears to be informed on the subject, say, “Low Carb is high-protein.”

That occurred one night in while I was watching one of my favorite TV shows. The subject was a Wall Street Journal “Saturday Essay,” titled, “The Questionable Link Between Saturated Fat and Heart Disease.” This person accurately blamed the obesity epidemic on the American (or Western) diet which is very high in carbs and processed foods; but then he proceeded instead to advocate for a diet high in protein! That is WRONG, WRONG, WRONG!

Diets that are very high in carbohydrates and processed foods ARE the reason we as a civilization for 50 years have been getting fatter and sicker.  The Wall Street Journal got it right. They also correctly noted that the beginning of this very large, population-wide, public health “experiment” in eating “low-fat” can be attributed to Ancel Keys. I first wrote about Keys in Retrospective #3, after Gary Taubes (Retrospective #5) brought him to my attention.

Keys was an American physiologist whose “Six Nation Study” (later revised to “Seven Country Study”) was just bad science. This was just a few years after President Eisenhower had his heart attacks and went on the Pritikin diet. Incredibly, however, low-fat quickly became dietary dogma. Keys made the cover of Time Magazine in 1961 and joined the American Heart Association board. It was later revealed that his studies were “cherry picked.”

Meantime, a low-carb diet, which is the antidote to the fattening low-fat diet (you read that right), is high fat and moderate protein. Let’s talk numbers (percentages). Diets can be classified by what are called Macronutrient Ratios:

The Low Fat Diet: The Standard American Diet (SAD, for short!) is high carb, moderate fat and adequate but low protein. The FDA’s Nutrition Facts Panel on processed foods, based on a 2,000 calorie a day diet, is comprised of 60% carbs, 30% fat and 10% protein. The dietary Dictocrats have recently recognized that simple sugars and processed carbs are too high and have moved slightly away from the 60% carb percentage (but not changed the package labeling). Still, they steadfastly maintained a target of less than 30% fat. That can only mean an increase in protein. To the extent carbs are reduced (from 60%) and fats do not exceed 30% (while advocating a lower percentage), only protein can rise. Remember, there are only three macronutrients: carbs, fat and protein. Something’s gotta go up!

In addition, a plant-based diet is increasingly being advocated by the vegan lobby. All plants are carbohydrates. Most protein (not all – there are some proteins in legumes and nuts) is animal-based. So, the struggle to maintain a high-carb, low-protein macronutrient ratio is an unrelenting battle within the establishment.

The Low Carb Diet: The macronutrient ratios for a low-carb diet are not defined. They are all over the place. This is okay with me since 1) people’s metabolic status (degree of carbohydrate intolerance) are different and 2) making the transition from 60% carb to a much lower percentage is a very good thing – but for some (who don’t go “cold turkey” like me), it takes time and a lot of effort. So, let’s say for our purposes that a prototypical Low Carb diet is 20% carb, 20% protein and 60% fat. That’s a very dramatic (2/3rds) reduction in carbs, from 60% to 20% (low), and a doubling of protein from 10% to 20% (moderate) and fat, from 30% to 60% (high). That “high fat” is really scary for some people, especially because there is disagreement (and therefore confusion among the public) about what “good” fats are.

For that discussion, Google “the nutrition debate good fats” for some of my columns on fat. But there is another mitigating factor: All these percentages are in calories, and since fat has more than twice as many calories per gram as both protein and carbohydrates (9 vs. 4), you really are eating less than half as much fat (by weight) than you think.

Very Low Carb: I started “Low Carb” dieting at 20 grams a day, which is Very Low Carb: My first ratios (as it turned out) were 10% carb, 30% protein and 60% fat. I later tweaked that to 7% carb, 25% protein and 68% fat. Today, I aspire to eat 5% carb, 20% protein and 75% fat (by calorie, remember, not weight). Of course, we don’t eat percentages; we eat portions, which are envisioned in the mind’s eye by mass (weight). These quantities and calorie percentages are determined by software that some of the compulsive among us (including me) have used.

Low Carb is really moderate protein and high fat. The lower the carb percentage, the higher the fat. Some call it, Low Carb High Fat (LCHF). What does your Eating Plan look like?

Retrospective #215: Just Google, “The Nutrition Debate” (in quotes)

I’ve been writing this column since 2010. I started posting once a week, then twice, now, as Retrospectives, daily rewrites at thenutritiondebate(dot)com. Some readers follow me by RSS feed, others on Facebook and twitter, yet others by a link from other sites. Most readers, however, are still introduced to “The Nutrition Debate” by Google searches on topics of interest to them.

Blogger provides me with some simple statistics or my readership by day, week, month and all-time. It also tracks my audience by country, traffic source, and post (column), so I have a broad idea of who, how and what my readership is.

Only 40% of my readers are in the U. S. The Ukraine and Israel garner a little less than 10% each. Russia, France and China come next, then Germany, Canada and the UK. Interestingly, Poland rounds out the top ten. Once in a while I get 1,000 pageviews in a 1-hour period from Israel. Obviously, someone who follow me there posts a link on their site.

I also have loyal followings in Sweden, Hong Kong and Singapore. The Singapore readership in on a site where a very popular and avuncular social network leader writes on the subject of “Clean Eating.” He provides occasional links to my columns and has even posted a few as permanent resources for his followers.

It’s interesting to me that I have so many readers in Ukraine-Russia and China. I suppose that people there have “hijacked” my content (with or without attribution, who knows?) and appear to read everything I write. Some sites are commercial (e.g., department stores), others are pornographic sites. All are in a Slavic language. I don’t object, mind you. I write this column for educational purposes. There is no revenue, and I have no interest in commercializing it.

This might also be a good time to mention that I have a wonderful and intrepid volunteer editor, a person who makes my writing clearer, checks my facts, and whose digital resources are almost as vast as Google’s (slight exaggeration there). Her acumen in all things health and nutrition is only exceeded by her generous heart and her interest in spreading the word about good nutrition and healthy eating. I am unabashedly in awe of her.

So, since Google seems to be the main, continuing source of new readers, I encourage this method of using that search engine. Just as Google has a “feeling lucky” search function, you could do the same. Just type “The Nutrition Debate” (in quotes) in the “window,” (or, thenutritiondebate(dot)com), hit “enter,” and let ‘er rip. I guarantee that my blog will come up on the first page, or in the latter case, first.

Of course, if you want to do a more targeted search, you could do something more “advanced.” Enter “The Nutrition Debate” and another word or phrase of interest to you (or a column number, i.e., #xxx. Let Google do the work! To see how well this works, I just entered “the nutrition debate triglycerides” and all ten (10) Google results were columns that I have written on triglycerides. This works very well in the absence of “tags,” “labels,” or “key words.”

On the other hand, if you’d like to see a list of all the columns I’ve written, in some browsers you can see a list.“The Nutrition Debate List of Columns, appears at the top right corner of the post, listed under “Favorite Links and Videos.” This works in Chrome, but, alas, not in IE.

So, if you are one of those who rely on Google (or another search engine), as I do, I encourage you to try this “advanced search technique.” I am too much of a Luddite, or troglodyte, and too lazy at this point, to go back over 500 columns and enter tags, labels and key words. Use technology to search instead. It works for me. Just Google “the nutrition debate” and another key word or phrase, and press “enter.”

Then, if you like what you have read, go to the RSS feed and get my blog delivered every morning to your hand-held device, tablet, laptop, or work station. And please, send me your comments and ideas. I’m always looking for your feedback and subjects of interest to you, me and my readers. It’s helps me get educated too.

Retrospective #214: How I Lost 188 Pounds (Part 2)

In Retrospective #213 I told how, by just restricting carbs, and later protein, that I ate for weight loss, my blood sugar control, blood pressure, blood lipids, and inflammation markers all vastly improved. You (and your doctor) would be very happy to have these results (as I and mine are), but the story doesn’t end there. There is more to tell.

Starting at 375 pounds, I lost the first 60 pounds in nine months (1½ pounds a week) by eating just 20g of carbs a day. I wrote down everything I ate every day, estimating carb grams. No measuring – just guessing. It gave me heightened awareness and accountability for what I decided to eat – and I learned a lot about which foods contained carbs and how they affected my blood sugar. When I started Very Low Carb (VLC) in 2002, I had been a progressively worsening Type 2 diabetic for 16 years. I left my diabetes care to my doctor. Now, I rely on self-care for my diabetes health.

After 4 years, however, I began to slip and gained 12 pounds. I wanted to lose those 12 pounds and a lot more. That’s when I decided to count protein. I devised my own method for determining how much protein to eat, which I explain in Retrospective #213. I started at 90 grams of protein a day (1.1g/kg), later dropping in steps to 60 grams (0.9g/kg).

That only left fat and total calories. I chose an online site to do the calculations. All I had to do was to remember, truthfully, everything I ate and enter the estimated amounts. The software did the rest.

I determined how many grams of fat to eat by backing into the calculation. I wanted to lose 2 pounds a week. At 3,500 calories/pound that is 7,000kcal/wk., or 1,000kcal/day. If a mostly sedentary, older male who doesn’t exercise needs 2,200kcal/day to maintain his weight, then I would need to eat just 1,200 kcal/day to lose 2 pounds a week. And 90 grams of protein + 30 grams of carbohydrate = 120 grams, times 4 calories/gram, equals 480 calories. Subtracted from 1200, that leaves 720 calories for fat. At 9 calories/gram for fat, that means my allowance for fat was 80 grams a day.

That’s where I started on Richard K Bernstein’s 6-12-12 program for diabetics. I didn’t care about macronutrient ratios or ketosis. I just ate Very Low Carb and “moderate protein.” Result: I lost 100 pounds in 50 weeks (2 pounds a week, as planned), lowering my protein as I went along. I lowered protein from 90 grams to 75 and then eventually, today, just 60 grams a day, which is 20% of 1,200kcal and still 20% above the USDA’s guidelines (50g/d or 10% of 2,000kcal).

Later, I became interested in Macronutrient ratios. The diet that worked for me (where I lost 100 pounds) was 10% carbs (30g/day), 30% protein (90g/day) and 60% fat (80g/day). Thirty percent protein is the highest percent most experts recommend for protein, and then only if you have no kidney problems. Your blood markers for kidney disease should be tested by your doctor before you start and rechecked annually on any moderately high protein diet.

As I lost weight, and discovered low carb foods that I liked for breakfast and lunch, and ate good fats, and small low carb and protein suppers, I lowered both my protein and carbs, and increased my fat percentages. My macronutrient ratios changed, from 7% carb (20g), 25% (75g) protein and 68% fat (90g) to 5% carb (15g), 25% protein (75g) and 70% fat (90g). Now, they are 5% carb (15g), 20% protein (60g) and 75% fat (98g). All of these ratios are for 1,200kcal/day.

It’s pretty easy to eat this way because “my body” is telling me that it is “happy.” I have come to think of my body as a separate entity that I am living in. I just eat small meals at mealtimes. This is called “non-homeostatic” eating. That is, I am not eating because my body is telling me to; I am not hungry at mealtimes. I am eating because breakfast, lunch and supper are “mealtimes.” My body decides what to do with the food, to add fat or burn fat and maintain muscle.

So, what do I eat? Breakfast is 3 eggs, 1 strip of bacon and a cup of coffee with heavy cream and a little stevia powder. Lunch is usually a can of kippered herring snacks in brine or Brisling sardines (in olive oil!). And supper is a small portion of protein, usually a fatty meat or fish, and a low-carb vegetable, either tossed in butter or roasted in olive oil. If I snack (before supper only), my favorite is celery with anchovy paste. Sometimes I’ll have olives, or radishes with salt and a dollop of butter, or a small portion of nuts. Macadamia nuts have the fewest Omega 6s, while hazelnuts, almonds or pecans have moderate amounts. Cashews are too high in carbs and walnuts much too high in Omega 6s.

Retrospective #213: How I lost 188 pounds (Part 1)

At my doctor’s suggestion, I started eating Very Low Carb (VLC) in 2002 to lose weight. At the time I had been a long-term (16yr) Type 2 diabetic. I have been very successful, at one point losing 188 pounds. I also had to give up most of my diabetes drugs while getting “normal” fasting blood sugars (80s mg/dl) on only 1 low-dose Metformin once a day.

When I began VLC 17 years ago, I was “maxed out” on two classes of oral diabetes meds and starting a third. Within a day of starting to eat just 20g of carbs a day, I got my first hypo (BG reading in the 50s). I ate a candy bar and called my doctor. Over the next few days he told me to cut my diabetes meds three times, twice by half . As I lost weight, my BP gradually dropped from 130/90 to 110/70 at the same meds. Over time my HDL doubled and triglycerides dropped by two-thirds. My Hb A1cs are now consistently in the mid-5 range, and both my HDL/TG ratio and my hsCRP, an inflammation marker, are both usually under 1.0. I am never hungry. I have lots of energy, and I feel great. By all these measures I am today (age 78) much healthier than I was 17 years ago. How did this happen? I’m going to tell you.

When I first started eating VLC, for a few years I wrote everything down that I ate but only counted estimated carbs. I didn’t measure anything. I just listed everything I ate and guessed at the carb content. I did this in an Excel table I created that totaled the estimated carbohydrate grams daily. The math was simple and the method not very accurate, but I was learning about low carb eating, and I was being totally accountable and brutally honest. I was learning what foods raised my blood sugar. This is a learning process everyone eating Very Low Carb for blood sugar control must do.

Four years later I became interested in how much protein I should eat. I decided to eat a similarly sized, small-to-medium portion of protein with each meal, and to space the meals at regular intervals, ala Richard K Bernstein, MD. Bernstein also counseled that, to lose weight you reduce the portion size of protein for one meal, and if that wasn’t enough, a second meal each day, due to its “insulin effect.” This would later guide me to the low side on protein.

The “insulin effect” is about how half of every gram or ounce of protein you eat is going to become glucose in your blood. This occurs after the protein is digested into amino acids and, if not taken up by your muscles, etc., is stored in the liver. There, through a process called gluconeogenesis, it is converted to glucose when the body needs glucose. That is one of the main mechanisms of Metformin: “to suppress the up-regulated synthesis of glucose by the liver in the disregulated sugar-based metabolism that many people have developed on a carbohydrate-based diet.” This glucose requires insulin for transport and uptake. Elevated insulin in the blood stops weight loss: the “Insulin effect.”

How much protein you should eat is dependent on several factors: among them age, gender, and level of activity. If you are very active, i.e. you exercise regularly, you will need more protein to repair and maintain the muscle tissue you have developed and use. I don’t exercise at all (except in my daily activities: gardening in New York and kayaking in Florida). I don’t like to sweat, and besides, doesn’t exercise “work up an appetite”? If you’re trying to lose weight, as I am, who wants to do that! So, I began a search to find out how much protein the “experts” say I should eat.

The “experts” recommend a very wide range of protein amounts, all based on “weight.” You need to pick one and go with it. The one critical measure, though, is the “weight” that you use. It should be your hypothetical “lean body weight.” The definition of “lean body weight” is difficult to ascertain and frequently misinterpreted and misguided. But lean body weight is what you should use because protein is not required to maintain your fat mass, or helpful in reducing it.

This latter point is particularly true for the overweight, obese and morbidly obese, like me. For me (old, male, diabetic, morbidly obese, relatively inactive and without excessive musculature to maintain), I chose to define “lean body weight” as the middle weight of “normal” in the WHO’s BMI chart for my height, now shrunken with age to 5’-10.”  

The BMI table says that, at 5’-10”, my middle-of-normal weight should be 150 pounds. In the beginning, though, I thought a “lean body weight” of 150 pounds for me was ridiculous, so I substituted a “goal” or “ideal” weight of 180 pounds. At 0.5g/lb. (1.1g/kg), that worked out to 90g of protein a day. Then, after I had lost over 100 pounds, a “lean body weight” of 150 began to sound realistic, so I reduced it to 0.4g/lb. (0.9g/kg), or 60 grams of protein a day.

Retrospective #212: Everything I (ch)eat turns to fat.

“Once you develop diabetes, your metabolism is deeply committed to converting as many calories as it can into fat.”

We’ve all heard this sentiment expressed, or felt this depressing thought, many times, but I was especially affected recently when I read this quote on page 241 of Cate Shanahan’s Deep Nutrition. I urge you to read this book, or at least my review in Retrospective #205 and her deeply troubling observations about the medical “business” in #206.

Shanahan’s book has hundreds of references, so I lament that the above quote is not sourced. I suppose it should be understood as a summation of the totality of the material presented in her book. In any case, the quote can be read as an expression of exasperation that we, overweight and obese Type 2 diabetics, feel in our unremitting efforts to lose weight. It does seem that everything we eat turns to fat, and it is damnably difficult to lose that fat.

As my readers know, I am always interested (from self-interest as well as for educational purposes) in understanding the mechanisms behind our complex metabolic environment, or milieu intérior as the 19^th century French physiologist, Claude Bernard, described it. And I have gained some insights into why it is that “everything I (ch)eat turns to fat” and why people with impaired glucose tolerance (IGT) gain weight easily and lose weight with great difficulty.

In lay terms, IGT is the equivalent of “carbohydrate intolerance,” described in Retrospective #84, “Carbohydrate Intolerance – the new ‘buzz’ words.”” They are the outward manifestation of a metabolic change called Insulin Resistance (IR), described in more detail in Retrospective #99, “Natural History of Type 2 Diabetes.”

Bottom line: as our bodies transition from a normal metabolism to a dysfunctional metabolism, very commonly accompanied by weight gain as an effect of this dysfunction, not a cause, our bodies undergo several physiological changes. Laboratory reports detail these changes. The most frequently tested are fasting glucose, hemoglobin A1c (HgA1c), and the lipid panel (Total Cholesterol, LDL, HDL, and TC/HDL ratio) and triglycerides. Sometimes, when these markers are “out of range,” a diagnosis of Metabolic Syndrome is made. All too often, though, the doctor prescribes a statin and tells the patient to “exercise and eat a low-fat diet” to lose weight. There’s no pill for that prescription.

How have I come to this conclusion? Have you had a similar experience? When I have been very good – that is, when I not only talked-the-talk but walked-the-walk, every day – my fasting blood sugars are consistently in the 80s. I can point to weeks, even months, of never or very rarely having a Fasting Blood Glucose over 100mg/dl. And since it is an elevated blood glucose that causes the pancreas to produce insulin, to transport to and facilitate uptake of that blood glucose in their destination cells, it is an elevated blood glucose level that causes an elevated blood insulin level.

As my readers know, and as anyone who has read Taubes’ Good Calories-Bad Calories (The Diet Delusion in the UK), or his more approachable Why We Get Fat, elevated blood insulin CAUSES FAT STORAGE and PREVENTS FAT BREAKDOWN for energy. Retrospective #5 presents Taubes’s “10 certain conclusions” from the GC-BC (pg. 453-454). It is a very succinct and compelling explanation of the functional role of insulin in homeostasis, and a must read.

Anyway, recently my fasting blood glucose readings were in the 100 to 125 range. Obviously, while I have been talking-the-talk, I have not always been walking-the-walk. I admit it. I “cheated” a little almost every day; always just before or at any time after dinner. And I pay the price. It was just a little “cheat,” so I didn’t gain weight, BUT NEITHER DO I LOSE ANY WEIGHT, EVEN THOUGH I AM EATING NO MORE THAN +/- 1200-1800 CALORIES MOST DAYS.

What’s happening is that my serum insulin levels are slightly elevated – elevated just enough to turn everything I (ch)eat to fat and stop the breakdown of body fat in storage even though I am eating below my homeostatic level. My body “gets the message” that as long as I have a supply of quick energy every night (the “cheats” that break down to glucose), it can conserve my body fat, and lay on more with every calorie that isn’t needed to maintain my basal metabolism while I sleep. The “signal” is: the slightly elevated blood insulin circulating my slightly elevated blood glucose. If this is still unclear to you, I urge you to read Retrospective #5 with Taubes’s “10 Certain Conclusions.”