Sunday, April 21, 2019

Retrospective #65: Introducing the “Low Carb Dietitian” (2012)

The “Low Carb Dietitian” is Franziska Spritzler, RD, CDE. The About Me tab on her website in 2012 describes her beginnings as a dietitian some time earlier: “I've always had a strong belief in the power of good nutrition.  After eight years as a court reporter, I became a dietitian because I wanted to help people improve their health by making dietary changes. Once I began working in the outpatient nutrition setting, I quickly developed a passion for diabetes management.  As a Certified Diabetes Educator (CDE), my goal is to provide accurate, useful information and support people's efforts to optimize their blood glucose control and achieve a healthy weight.”
But that’s garden variety stuff. Every dietitian is similarly motivated. But in July 2011, in her first post on her website, Franziska explains why her advice was going to be different. She had a transformative experience. “My purpose in creating this website is to inform people about healthy low carb living.  This site contains information that is likely very different from that which can be found on the websites of other dietitians. However, if you'd told me a year ago that I'd be touting the benefits of a low carb lifestyle, I would have probably said you were crazy!”
Before Franziska saw the light, she followed standard establishment public health community diet and nutrition advice. “I'd been eating a very healthy, semi-vegetarian or pescatarian diet (I consumed dairy, eggs, and fish but no poultry or meat) for many years.  Because of genetically high cholesterol, I limited my saturated fat intake, always ordering egg white omelets instead of regular, eschewing butter and choosing trans-fat-free margarines instead, and avoiding cheese and cream sauces.  I rarely ate desserts, occasionally having just a bite or two of my husband's cake/ice cream/cheesecake, etc., when we were dining out.”
That’s when Franziska, who had recently attained both RD and CDE credentials, got the bad news.
“So, when I received the results from labs that were done for life insurance purposes back in January of this year [2012], I was speechless. Not only was my LDL ("bad") cholesterol elevated, my hemoglobin A1c (a measure of blood sugar levels over a two-to-three-month period of time), although still within normal range at 5.5%, was still far higher than would be expected for someone my size who ate the way I did. Now, while these numbers were not outrageously high, as one who works with people who have diabetes or prediabetes every day, they certainly suggested to me that something was not right with my blood glucose metabolism [emphasis added].  I purchased a glucometer and began testing after meals, and discovered my blood sugar levels at one hour were significantly higher than they should be. Within the next few weeks, I saw that the more carbohydrates I ate, the higher the number would go.  My fasting blood sugar always remained within normal range, however.”
So, since her education and clinical experience had taught her that “something was not right with (her) blood glucose metabolism,” what did she do? Franziska Spritzler tells us the incredible tale of what happened next.
“I made an appointment with an endocrinologist, who wasn't overly concerned since my fasting levels were so normal. He did want to retest my A1c, and by that point, it had increased slightly to 5.6%.  I cut down on the carbs slightly (not too much, though -- I'd been taught that we need enough carbs to keep our brains and other organs working properly), and then I started doing research online about strategies to control postprandial, or post-meal, blood glucose.  It seemed that many people were using low carbohydrate diets with great success in managing their diabetes and postprandial blood sugars. I was skeptical, but once I started reading the available research on carbohydrate restriction, it all started to make complete and perfect sense [emphasis added]. I discovered that the high carbohydrate, low fat diet I'd been taught to believe was ideal was anything but for many people struggling with diabetes, insulin resistance, obesity, and dyslipidemia.  This was quite difficult for me to accept at first, but now that I have, I'm quite excited about the potential to help people struggling with these conditions.”
Franziska has been very successful. After taking charge of her own health, Franziska now travels the world as invited speaker, has written a book, and is now a featured writer on DietDoctor.com. Congratulations, Franziska!

Type 2 Nutrition #483: “…when used with diet and exercise.”

Have you ever noticed how the TV diabetes medication ads always conclude with “…when used with diet and exercise”? That common refrain riles me a bit, but I’ve never examined why. I think it’s time I do.
First off, by self-examination I admit to being something of a curmudgeon. However, I tend to grouse only about the abysmal state of our collective health, including how we (including I) got into this mess. In other respects, I think I have a positive outlook on life, but you’d have to ask the people who know me best if that’s true. Regardless, my readers could fairly describe me as a crusty, grumpy old man. This column, however, is not about me. It’s about why the diabetes ads conclude with the caveat, “…when used with diet and exercise.”
I think it’s a government requirement. The Food and Drug Administration (FDA) has to approve all claims made by drug manufacturers. The FDA also dictates for what and when a drug may be prescribed. That includes as a first course of treatment, as well as any adjunctive therapy if the first medication fails to achieve the primary target. In the case of a drug to treat type 2 diabetes, that would be lowering the patient’s serum blood glucose, usually as measured today by a blood marker, the hemoglobin A1c (hgA1c), or simply, the A1c test.
Metformin is the first drug prescribed today for the treatment of Insulin Resistance (IR), as measured (too late)  by an Impaired Fasting Glucose (IFG). Metformin is generic, cheap and widely accepted as the standard-of-care, almost universally prescribed first after diet and exercise have failed. After Metformin, a generic drug, the clinician has a wide choice of drugs, depending on other risk factors and co-morbidities. That’s when the phrase, “…when used with diet and exercise,” usually appears. The competing drugs all have this in common.
And that’s what gets me riled. Every doc is supposed to tell their overweight and Pre-diabetic patients to “lose weight and exercise” before ANY meds are prescribed.  “Eat less and move more,” “eat a plant-based” or “Mediterranean” diet and get lots of exercise (to lose weight!). And everyone FAILS. They fail to stop or reverse the slow but inexorable slide to drug dependence, eventually “graduating” to Type 2 diabetes. So why do the diabetes ads still advise people to continue this failed strategy?
Answer: The FDA mandates it. But, what does Big Pharma care? It’s a throwaway line because so long as PATIENTS continue to eat what government and their doctor has “prescribed” as a “healthy diet,” T2D WILL BE a “progressive disease,” and the PATIENT will continue to worsen.” BIG PHARMA IS THE BIG WINNER.
There is no downside for Big Pharma. They’re not telling you how and what and when to eat. Certainly no one would say that exercise is not good for you. Besides, exercise is a well-documented way for Type 2 diabetics to slightly improve their insulin sensitivity, which is good. But for weight loss, exercise is not an effective method.
THE ONLY DOWNSIDE IS FOR THE PATIENT. By following the advice to eat what the government “prescribes” as a “healthy diet,” patients are being herded like lemmings into the hands of Big Pharma. Whether this is a corrupt cabal, I’ll leave it for you to decide. But more to the point, in your own self-interest, you might want to ask, why has the advice, “…when used with diet and exercise,” failed? And why does it continue to fail even as you take more medications. Is it because exercise, while a good thing, is not a good way to lose weight
Is it because the “healthy” diet the government prescribes is NOT REALLY A HEALTHY DIET? If eating lots of carbs (like corn) is a good way to fatten beef cattle in a “feed lot,” is it not also a good way to fatten people? Yet, the government’s Nutrition Facts label on all “processed” foods prescribes that the Percent Daily Value (%DV) for carbs recommended for women (on a 2,000kcal diet) is 300g, or 1,200kcal, or 60%. And for men (on a 2,500kcal diet), is 375g, or 1,500kcal, also 60%. Did you know that? Do you think, maybe, that is too many?
If you want to avoid the inevitable “graduation” to a cocktail of anti-diabetic medications, including the ones advertised on TV, you might want to consider dropping your intake of carbs, to 40, 20, 10 or even 5%, like me. 

Saturday, April 20, 2019

Retrospective #64: Very Low Carb Eating: Ten Years Later (2012)

In August, 2002, I had been a morbidly obese Type 2 Diabetic for 16 years. My physician had tried for years without success to get me to lose weight on a “balanced” diet. Then, one day he said to me, “Have I got a diet for you!”
At 375 pounds I had been taking progressively more and more oral diabetes medications since my diagnosis in 1986. I was maxed out on micronase (a sulfonylurea), and Metformin, and had recently started takin Avandia in futile attempts to control my progressively worsening blood sugar. When Avandia didn’t work, I was then (in 2002) going to be left with only one option: to become an insulin-dependent T2, injecting basal and mealtime insulin.
It turns out, though, that my doc had recently read Gary Taubes’s, July 7, 2002, NYT Magazine cover story “What If It’s All Been a Big Fat Lie?”  Out of curiosity he tried the recommended Very Low Carb diet advocated in the story (20 grams of carbs/day), and it worked for him. So, he thought it might work for me too, and as he walked me down the hall to schedule a follow-up appointment, he said, “It’ll probably be good for your diabetes too.”
The result: Within a day on this strict Very Low Carb diet, as a heavily medicated Type 2 diabetic I was experiencing “hypos” (dangerously low blood sugars). I called my doctor, and he told me to stop taking the Avandia. The next afternoon, when I had another hypo, he told me to cut in half the micronase and Metformin. A few days later he said to cut them by half again. He then saw me monthly for a year to monitor my blood and other health markers. In the course of that year I further reduced the micronase from 5mg to 2.5 to 1.25mg and finally completely phased it out. I still take Metformin to suppress gluconeogenesis if, as I sometimes do, I eat too much protein at supper.
In the first 9 months on the Very Low Carb diet I lost 65 pounds (1½ lbs./wk.). I then retired from work and kept that weight off for several years. Then, over the course of a summer, I added back 12 pounds (mostly from eating ice cream before bedtime, as I recall). But by this time, I had also been lurking and learning from Dr. (Richard K.) Bernstein’s online Diabetes Forum. I had also read Bernstein’s “Diabetes Diet” and his “Diabetes Solution,” so I decided to try his program (30grams of carbs a day). It was more focused on blood sugar control for diabetics.
On Bernstein I lost 100 pounds in 50 weeks (2lbs./wk.). Altogether I lost 170 pounds, settling in at 205 pounds. I have since regained some of that weight, but frankly I have been “off the ranch” for a while. I am still, however, much healthier than before. I eat Very Low Carb most of the time and have retained most of the health benefits.
My average HDL has more than doubled (from +/- 39 to +/- 84mg/dL) and my triglyceride average has been cut by 2/3rds (from +/- 150 to +/- 49mg/dl). I try to limit my carb calories to 5% of my calories and my protein to 20%, leaving 75% for fat. I do not limit salt, dietary cholesterol or saturated fat. I eat eggs and bacon and coffee with full cream and pure stevia for breakfast, and just a can of sardines for lunch. For supper, it’s just meat or fish and a low carb veggie with lots of butter or tossed in olive oil and roasted. In a restaurant I’ll have a cocktail (or 2) or two glasses of wine. The only dessert I’ll ever eat is berries (with heavy cream) on a very special occasion. I love a cheese plate (without bread or fruit), but it’s just too much food. I always regret it if I occasionally order it.
After the first year, I continued to see that doctor 3 times a year until his unfortunate demise. I went just to get blood tests to monitor my A1c, lipid profile (cholesterol panel), and other tests he wanted to do (kidney, thyroid, electrolytes and EKG). They were all always normal. And my hsCRP, a chronic systemic inflammation marker, plummeted from “high” to consistently less than 1.0 (very low risk of cardio vascular disease).
My new doctor, after studying my chart on my first visit, suggested I see him once a year. I was pleased that was his initial impression of my health, but I said I wanted to see him three times a year, just to keep track of my success.

Friday, April 19, 2019

Retrospective #63: Impulse Control and Metacognition

Maybe 15 years ago, in an effort to understand how (not why) I had “fallen off the wagon” with respect to my Very Low Carb Ketogenic Diet (VLCKD), I developed an interest in the subject of impulse control. A friend on Dr. Bernstein’s Diabetes Forum (I’m a Type 2 diabetic), suggested I set up a “Google Alert” on the subject, so I did.
One of the first hits introduced me to the term “metacognition,’ which literally means “knowing about knowing.” For my study of impulse control, I translated this to “thinking about thinking.” So, I started a “thread” on “Impulse Control and Metacognition” on the Forum. It got about 50 replies and 3800 views. It was an interesting discussion.
An early reply on the thread from the Forum Moderator suggested that impulse eating might actually be a physiological rather than a psychological issue. She pointed out that Dr. Bernstein has mentioned that with beta cell burnout there is less amylin production, and low amylin levels mean the brain isn’t getting the message that you are not hungry. But I wasn’t interested in finding a pharmacological approach to the problem.
There is also the leptin/ghrelin hormone interaction, but again hormone signaling to/from the hypothalamus is too high brow and still a developing area of science. I wanted to keep my experiment simple and personal, so I started.
In the discussion, I pointed out that when I have been tempted to snack before dinner, or reach into the bread basket in a restaurant, or hit the freezer for ice cream before bedtime, I was aware that a finite idea had entered my mind: “the temptation.” The idea was usually dismissed quickly, but then frequently returned, sometimes quickly and sometimes more than once. On its return, I have sometimes acted on it, always to my later shame and chagrin. I would beat myself up. That was an emotional response. I wanted to explore a more rational response.
My first thought was to put “the idea” out of mind when the temptation first presented. Just deny the thought a foothold. I cleared the brain the way I do when I put my head on the pillow at night to fall asleep. By not “allowing” the thought to stay on the brain, or by substituting another thought for “the temptation,” it went away. It did not persist. If it returned, I just created another distraction. I changed the subject. It could be another idea, a simple distraction, or it could be an action. Whatever it was, the concept was to catch the “bad” thought “in the bud.”
Examples: If I am eating in a restaurant with others and the bread basket is presented, I take it and pass it on. Or I start a conversation (not related to bread). Recently, when eating alone in a restaurant, I distracted myself by becoming engrossed in a newspaper. Another time I watched and listened (unobtrusively) to people at another table. In other words, I quickly took action to side track “the temptation.” Actions are better than abstract ideas like “will power” and “steely resolve.” You have to be limber, imaginative, and prepared for temptation, and act.
Of course, one of the very best ways to suppress “temptation” is for food to be out of sight. If I can see it, I get the idea to eat it! If I don’t see it, I don’t get the idea, usually – even though I know the ice cream is in the freezer or the nuts are in the pantry. The actual sight of food is the “trigger,” and avoiding the sight is the best solution. The difference between seeing the food and not seeing it, for me, is huge. It has nothing to do with hunger or noshing. I can be mildly ketogenic (with low serum insulin) and a stable blood glucose and still cave at the sight of food.
Others have dealt with impulse control in different ways. Some use “healthy fears,” others use the fear of catastrophic outcomes. For me, fears are both too negative and too extreme. But whatever you do to undo or relearn a behavior, even using an irrational fear, it is, in a way, a rational process. It allows you to exercise the mind and be in control of the outcome.
Quickly supplanting the initial temptation with a diversionary response – either thought or action – is my kind of metacognition. Thinking about thinking is the essential precursor, and a diversionary thought is often sufficient. The best outcome, however, is a diversionary action. Quoting Alfred Korzybski from his preface to “Science and Sanity, “…if they are not applied but merely talked about, no results can be expected.”

Thursday, April 18, 2019

Retrospective #62: Meatless Monday Madness

In summer of 2012 a USDA newsletter to employees produced a minor contretemps within the agency and a major uproar across the USA among beef producers and meat eaters. According to a Fox News alert, the newsletter said, “This international effort encourages people not to eat meat on Mondays.” It asks, “How will going meatless one day a week help the environment? According to the UN, “the production of meat, especially beef [and dairy] has a large environmental impact. Animal agriculture is a major source of greenhouse gases and climate change.”
But USDA spokeswoman Courtney Rowe said the USDA does not endorse the “Meatless Monday” initiative. So, Fox had a little fun in the chicken coop, and the brouhaha passed with little notice due to the 2012 Summer Olympics.
The story, for me however, was how the vegan lobby has embedded itself into the interstitial tissue of the ‘corpus governmentalis,’ or body politic. The pathway of infection of this parasitic movement is the ingestion of vegan messages within the hallways of large centralized government agencies like the USDA, wherein it has colonized and reproduced. The United Nations, of course, is always a target, given that by design it is a receptive host to parasitic attacks of every nature and from all quarters. In the U.S., Washington DC is targeted, especially at times of big top-down government with a compromised immune system such as we had with the Obama administration.
The vegan bug is especially virulent when it is introduced into the alimentary canal. It manifests itself in such forms as the Center for Science in the Public Interest (CSPI). Founded in 1971, the CSPI calls itself a consumer advocacy group focusing on nutrition. They are well known for their longstanding opposition to saturated (i.e. animal-based) fats. It also advocates taxing soft drinks. Critics refer to CSPI as "the Food Police."
Walter Olson of the Cato Institute, a Washington D.C.-based libertarian think tank, wrote that CSPI’s "longtime shtick is to complain that businesses like McDonald’s, rather than [people’s] own choices, are to blame for rising obesity." He called CSPI's suit against McDonald's on behalf of a California mother a "new low in responsible parenting. In the 1980’s CSPI maintained that trans fats were “more healthful” than saturated fats and had persuaded many restaurants, including McDonald's, to switch from lard to trans fats in making French fries. Today CSPI has reversed its position on trans fats, but it still campaigns vigorously against animal (saturated) fats.
Then, in 2009 a more virulent strain of veganism began to infect the body politic in the U.S. and internationally. Robert Goodland, PhD, (now deceased), and Jeff Anhang published their seminal treatise on bovine flatulence, “Livestock and Climate Change: What if the Key Actors in Climate Change were Cows, Pigs and Chickens.” 
Goodland retired as lead environmental officer after 23 years at the World Bank. Previously, in the 1970s, he and I worked together – he as staff ecologist and I staff architect – at the Cary Arboretum in Millbrook, NY. Even at Cary, Goodland was a “mover and shaker.” He proposed (and I built) a solar heated headquarters for the Arboretum.
His bovine flatulence gambit aimed to be no less earth shattering than his solar energy initiative. Cleverly, it is itself parasitic. Its vegan premise attaches itself to one of the Left’s most fundamental and passionate causes, global warming. Their report claims, “Our analysis shows that livestock and their byproducts actually account for at least 32,564 million tons of CO2 per year, or 51 percent of annual worldwide GHG emissions.” Never mind that the UN Food and Agricultural Organization claimed 18 percent. Goodland then posits, “If this argument is right, it implies that replacing livestock products with better alternatives would be the best strategy for reversing climate change. In fact, this approach would have far more rapid effects on GHG emissions and their atmospheric concentrations—and thus on the rate the climate is warming—than actions to replace fossil fuels with renewable [solar] energy.”
So, in the end Goodland forsook solar energy for this Meatless Monday Madness! Never mind that 150 years ago in the U.S. 60 million buffalo emitted more CO2 into the atmosphere via bovine flatulence than 9 million dairy and 31 million beef cattle do today. But don’t tell that to NYC’s mayor Bill DeBlasio. Goodland’s legacy lives on in that city’s school system with the recent introduction of Meatless Mondays. The Madness goes on. Robert would be pleased.

Wednesday, April 17, 2019

Retrospective #61: Stefansson and “The Eskimo Diet”

About 100 years ago a Canadian ethnologist, Vilhjallmur Stefansson, spent 11 years living among the Inuit in the frozen North. For 9 of those years he ate substantially a diet composed of meat (including fish), some organ meats, and fat with just a little carbohydrate (glycogen contained in the muscle tissue and liver). In the summer months he ate a few berries. Upon his return to ‘civilization,’ from his observations of the Inuit with whom he had lived and of his own health, he postulated that such a diet was sufficient for good health. It was, he averred, a complete diet.
Stefansson’s lectures on his experience with an all meat diet drew derision and cries of charlatan from the scientific and medical community. So, to ‘prove’ his hypothesis, he proposed a daring experiment. He offered himself and a colleague, Karsen Andersen, with whom he had shared his experience in the Arctic, as an in vivo experiment (n=2). In 1928, under supervision of doctors at New York’s Bellevue Hospital, they volunteered to live for 1 year on meat and fat alone. The results, which I first read in Gary Taubes’s "Good Calories -- Bad Calories," were fascinating.
Stefansson’s own account of his Arctic adventures was published, for popular consumption, in Harper’s Monthly in November and December 1935. The balance of this blog post will be the report of W. S. McClellan and E. F. Du Bois, the lead investigators of the Bellevue study. Their paper was brought to my attention by Ginny L who was, in 2012 when this was written, a frequent poster and valued resource on Dr. Richard K. Bernstein’s Diabetes Forum.
The paper, “Prolonged Meat Diets with a Study of Kidney Function and Ketosis,” was published July 1, 1930, in the Journal of Biological Chemistry. Herewith, in their entirety, are the conclusions of the previously skeptical doctors:
1. Two men lived on an exclusive meat diet for 1 year and a third man for 10 days. The relative amounts of lean and fat meat ingested were left to the instinctive choice of the individuals.
2. The protein content varied from 100 to 140 gm., the fat from 200 to 300 gm., the carbohydrate, derived entirely from the meat, from 7 to 12 gm., and the fuel value from 2000 to 3100 calories.
3. At the end of the year, the subjects were mentally alert, physically active, and showed no specific physical changes in any system of the body.
4. During the 1st week, all three men lost weight, due to a shift in the water content of the body while adjusting itself to the low carbohydrate diet. Thereafter, their weights remained practically constant.
5. In the prolonged test, the blood pressure of one man remained constant; the systolic pressure of the other decreased 20 mm. and the diastolic pressure remained uniform.
6. The control of the bowels was not disturbed while the subjects were on prescribed meat diet. In one instance, when the proportion of protein calories in the diet exceeded 40 per cent, a diarrhea developed.
7. Vitamin deficiencies did not appear.
8. The total acidity of the urine during the meat diet was increased to 2 or 3 times that of the acidity on mixed diets and acetonuria was present throughout the periods of exclusive meat.
9. Urine examinations, determinations of the nitrogenous constituents of the blood, and kidney function tests revealed no evidence of kidney damage.
10. While on the meat diet, the men metabolized foodstuffs with FA: G ratios between 1.9 and 3.0 and excreted from 0.4 to 7.2 gm. of acetone bodies per day.
11. In these trained subjects, the clinical observations and laboratory studies gave no evidence that any ill effects had occurred from the prolonged use of the exclusive meat diet.
Stefansson was a very colorful character. He was twice president of the prestigious Explorers Club. He lectured in anthropology at Harvard and was Director of Polar Studies at Dartmouth College. His Wikipedia entry concludes: “Stefansson is also a figure of considerable interest in dietary circles, especially those with an interest in very low-carbohydrate diets. Stefansson documented the fact that the Inuit diet consisted of about 90% meat and fish; Inuit would often go 6 to 9 months a year eating nothing but meat and fish—essentially, a no-carbohydrate diet. He found that he and his fellow European-descent explorers were also perfectly healthy on such a diet. When medical authorities questioned him on this, he and a fellow explorer agreed to undertake a study under the auspices of the Journal of the American Medical Association to demonstrate that they could eat a 100% meat diet in a closely observed laboratory setting for the first several weeks, with paid observers for the rest of [the] year. The results were published in the Journal, and both men were perfectly healthy on such a diet, without vitamin supplementation...."

Tuesday, April 16, 2019

Retrospective #60: Dietary Composition: Dr. Ludwig’s Study

Back in 2012, David S. Ludwig, MD, PhD, and colleagues at New Balance Foundation Obesity Prevention Center (Harvard), and Children’s Hospital, Boston, and Brigham and Women’s Hospital, Boston, and Baylor College of Medicine, Houston, and Vanderbilt University, Nashville, published the results of a well-designed, four-year study in June 27 issue of the Journal of the American Medical Association (JAMA). The purpose was to study “the effect of dietary composition on energy expenditure during weight-loss maintenance “(my emphasis).
Three days later the New York Times published an opinion piece, "What Really Makes Us Fat," loosely based on the study. In it, award winning science writer Gary Taubes, said, “What was done by Dr. Ludwig’s team has never been done before.” He concluded his piece with, “The public health implications are enormous.” (emphasis added)
The study began after all subjects had achieved a 10% to 15% weight loss by a calorie restricted (60%) “run-in” diet. Then, each for 4 weeks, the participants ate three isocaloric (2,000kcal/d) diets: 1) a low-fat diet (60% carbs, 20% fat, 20% protein, high glycemic load); 2) a low-glycemic index diet (40% carbs, 40% fat and 20% protein, moderate glycemic load); and 3) a very-low carb (Atkins) diet (10% carb, 60% fat and 30% protein, low glycemic load).
The JAMA authors concluded: “Our study demonstrates that commonly consumed diets can affect metabolism and components of the metabolic syndrome in markedly different ways during weight-loss maintenance, independent of energy content. The low-fat diet produced changes in energy expenditure and serum leptin that would predict weight regain. In addition, this conventionally recommended diet had unfavorable effects on most of the metabolic syndrome components studied herein. In contrast, the very low carbohydrate diet had the most beneficial effects on energy expenditure and several metabolic syndrome components…” (HDL & triglycerides), emphasis added by me.
Energy expenditure, the primary outcome measure of the study, was measured by state-of-the art stable isotope analysis at Baylor. This outcome was especially stunning: “The results of our study challenge the notion that a calorie is a calorie from a metabolic perspective,” the authors stated. “TOTAL ENERGY EXPENDITURE DIFFERED BY APPROXIMATELY 300 KCAL/D BETWEEN THESE 2 DIETS” (VERY LOW CARB AND LOW FAT), “AN EFFECT CORRESPONDING WITH THE AMOUNT OF ENERGY…EXPENDED IN 1 HOUR OF MODERATE-INTENSITY EXERCISE.”
In other words, as Taubes explained, “…when the subjects were eating low-fat diets, they’d have to add an hour of moderate-intensity physical activity each day to expend as much energy as they would effortlessly on the very-low-carb diet. And this while consuming the same amount of calories. If the physical activity made them hungrier – a likely assumption – maintaining weight on the low-fat, high-carb diet would be even harder,” Taubes wrote.
Taubes then posited, “If we think of Dr. Ludwig’s subjects as pre-obese, then the study tells us that the nutrient composition of the diet can trigger the predisposition to get fat, independent of the calories consumed. The fewer carbohydrates we eat, the more easily we remain lean. The more carbohydrates, the more difficult. In other words, carbohydrates are fattening, and obesity is a fat-storage defect. What matters, then, is the quantity and quality of carbohydrates we consume and their effect on insulin.” These five sentences say it better than a whole book!
Ludwig’s subjects are, frankly, “pre-obese.” As the study states, “only 1 in 6 overweight and obese adults report ever having maintained weight loss of at least 10% for 1 year.” Taubes reasonably says Ludwig’s subjects are “almost assuredly going to get fatter, so they can be research stand-ins for those of us who are merely predisposed to get fat but haven’t done so yet and might take a few years or decades longer to do it.” Does this sound like you?
Taubes then concludes, “From this perspective, the trial suggests that among the bad decisions we can make to maintain our weight is exactly what the government and medical organizations like the American Heart Association have been telling us to do: eat low-fat, carbohydrate-rich diets, even if those diets include whole grains and fruits and vegetables.” NOTE BENE: “…EVEN IF THOSE DIETS INCLUDE WHOLE GRAINS AND FRUITS AND VEGETABLES.”
Your choice: Eat Very Low Carb, or eat whole grains, fruits and vegetables and exercise 1 hour a day to burn them off.

Monday, April 15, 2019

Retrospective #59: The VLCKD: What I Eat and Why


I eat a Very Low Carbohydrate Ketogenic Diet (VLCKD) because I want to lose weight. And I want to do it in a healthy way, and because I want it to be easy (of course) and not involve hunger. I also want to eat in a way that achieves good blood glucose control (I’ve been a Type 2 diabetic for 33 years), and I want to continue to maintain the huge improvements in blood lipids (cholesterol), and blood pressure, and inflammation that I’ve seen since before I lost 170 pounds.
When I started to eat Very Low Carb, I didn’t know that I had a medical condition called Metabolic Syndrome. I had all five indications: central obesity, T2DM (or pre-diabetes), hypertension, elevated triglycerides and low HDL. After a period of time on the VLCKD, all five of these indications were mediated by this diet.
I know I have sufficiently restricted my carbohydrate intake to be in ketosis by testing my blood glucose in a fasting state (before eating breakfast). My body always has a little glucose available for energy, either in the form of glycogen in the liver or muscle cells, or from amino acids stored in the liver from eating too much protein. The liver will make glucose from these glucogenic amino acids through a process called gluconeogenesis. Since I am a Type 2 diabetic with impaired glucose tolerance and insulin resistance, if I eat too many carbohydrates, my fasting blood sugars will rise above ‘normal’ for me. When I return to dietary ketosis, my fasting blood glucose drops to the mid- 80s, with Metformin. That’s me. Your Mileage May Vary. We’re all different.
My pancreatic function and other aspects of my metabolism are broken and have been for many years. Like many Type 2s and even pre-diabetics (diagnosed and undiagnosed!), to maintain healthy blood sugar levels, I cannot tolerate more than very small amounts of carbs, low GI or otherwise. I must accept that I will never be able to do so without blood glucose “excursions” (dangerously high levels of “sugar” circulating in my system. Inevitably, that will lead either to diabetic complications (eye, nerve or kidney disease), or one of the Macrovascular complications that are strongly associated with Type 2 diabetes, such as cardiovascular disease, hypertension, and various cancers. So, what do I need to eat to remain continuously in a mild state of ketosis?
Breakfast and lunch are easy for me because, as Richard K. Bernstein, MD, recommends in his book, “The Diabetes Solution,” I eat the same thing every day. Breakfast is two fried eggs, two strips of bacon and 12 oz of coffee with 1 ½ oz of heavy whipping cream and 1g of pure stevia powder. K:G ratio = 1.88:1.
For lunch, (when I remember to eat it – I’m really not hungry, so I’m not “reminded”), I eat a can of Mediterranean style Brisling sardines in olive oil. I drink the oil in the can too (about 1 Tbs). Lunch K:G ratio = 2.93:1. I sometimes wash it down with diet iced tea (sweetened with liquid stevia). Of course, water would be a better choice.
For dinner, we eat a medium portion of protein (with skin and/or fat on) and a portion of vegetables with melted butter or olive oil. Sometimes, with salmon for example, we use a sauce made with crème fraiche. We like roasted meats, including chicken, spare ribs, lamb chops, short ribs or a petite filet (with a single 8oz filet shared by the 2 of us). We also like to rub our cuts of meat with herbs and olive oil before roasting. We sometimes roast the vegetables too, after tossing them in olive oil and sea salt. Cauliflower, Brussels sprouts and asparagus are especially good this way. We avoid the sugary vegetables (carrots, peas, beets and corn) and of course all the starchy root vegetables. And we do not eat bread at home. (I sometimes cheat with bread in a restaurant.)
This menu usually adds up to about 1,200 calories a day, which is at least 1,000 less that I probably use. The balance of energy comes from my fat stores, as long as I am in dietary ketosis and my blood insulin level is low. That only occurs because my carbohydrate intake is very low, and protein moderate, allowing my dietary and body fat to break down for fuel. This diet is about 5% carb, 20% protein and 75% fat. The K:G ratio of most meals is >1.5. This is a Very Low Carb Ketogenic Diet (VLCKD).                   

Sunday, April 14, 2019

Type 2 Nutrition #481: “I’ve lost 30 pounds!” (Tim Cook, Apple CEO)


If you Google “Tim Cook ‘I’ve lost 30 pounds,’” you'll find several pages touting Cook’s boast about how he used his iWatch to lose weight. Of course, he was mainly promoting the utility of a prospective Apple iWatch app in conjunction with emerging medical technology to help manage health conditions and make our lives better.
The quote appears at about the 8:15 mark in this May 2017 video interview with CNBC’s Jim Cramer. Cramer was trying to get Cook to reveal the next “new” product from Apple. Cook smiled and at first resisted, saying, “I can’t tell you” [about new products]; and then… [here’s where it sounded a bit scripted]:
Cramer, eggs him on with, “Health?”
Cook replies, “You know, this, the watch, has been an incredible move into health, in the wellness and fitness piece.”
Cramer: “You too?” [more script]
Cook: “Yes, I’ve lost 30 pounds, partly [due] to my watch.”
Cramer: [prompting Cook] “…because it prompts us.”
COOK: [finally getting to his pitch] “BECAUSE IT MOTIVATES YOU. IT CONSTANTLY GIVES YOU FEEDBACK. IT CONSTANTLY GIVES YOU REWARDS, AND THIS MAKES A DIFFERENCE…OVER TIME.”
What Cook and Cramer were talking about is an Apple iWatch app in development that tracks blood sugar continuously from a sensor attached to the upper arm just below the surface of the skin. The sensor captures the rise and fall of blood “sugar” in response to several factors, but predominantly to food that is eaten.
If you eat something that causes a large increase, you know that that it will shut down any fat burning your body is doing to supply energy while the “sugar” (glucose from any type of carb) is burned off first. You learn that if you want your body to stay in fat burning mode, instead of glucose mode, you should avoid those foods.
Cook’s pitch and Cramer’s interest are all about business, specifically the conjunction of health science and technology. It’s a crowded field. Scores of innovators are operating under the radar, clamoring to get on the bandwagon for a piece of the mass-market. The early birds certainly have an advantage, but…over time, as technology advances, the products will become commodified, and competition will bring costs down.
In the 2017 interview, Cook was certainly aware that a “high cost” solution was on the market. By March 2018 the FDA had approved the Dexcom 6 Continuous Glucose Monitor (CGM). It costs about $5,000 a year and includes an integrated mobile app which automatically downloads results to a Bluetooth-enabled device.
Then in August 2018 the FDA approved the new Freestyle Libre CGM (about $1,620 a year). It does not have an integrated mobile app yet, but a startup, Ambrosia, has a workaround called BluCon to download results.
Metronic is in the race too but lags at this writing. Stay tuned, though. By the time you read this, who knows?
Medical insurance, including Medicare and “Supplemental,” will only pay for this durable medical equipment and supplies. at the current time. if you are an insulin-dependent diabetic who injects MEALTIME insulin. The government’s policy is designed to help patients avoid life-threatening hypos (hypoglycemia), which, for some diabetics, is an all-too-common and sometimes life-threatening occurrence, often requiring hospitalization.
But Tim Cook’s market is “the wellness and fitness piece” – i.e., the entire rest of the world – who will benefit from an inexpensive app and an affordable sensor that can be integrated with the latest Apple iWatch… BECAUSE IT MOTIVATES YOU. IT CONSTANTLY GIVES YOU FEEDBACK. IT CONSTANTLY GIVES YOU REWARDS, AND THIS MAKES A DIFFERENCE. And almost everyone could stand to lose 30 pounds. Lots of us, even more!

Retrospective #58: What is Dietary (Nutritional) Ketosis?


Fasting ketosis occurs “after a few days of fasting…when liver glycogen stores are depleted” and “the body shifts from a glucose-based metabolism to a fat-based one,” Lucas Tafur explained in 2012 on his now defunct website. It is a physiologic state that the ketone expert, Dr. Richard Veech at The National Institutes of Health, calls “the normal state of man.” But Tafur avers, “It can either be triggered by fasting or by diet.” Therein lies the message.
Dietary ketosis is the adaptive response, or “acquired evolutionary mechanism, [that] shifts [the body] from a glucose-based metabolism to a fat-based one,” Tafur explains. This shift occurs when the carbohydrates are unavailable for fuel. The enzymes that break down fat for energy are controlled by insulin which is very responsive to the presence of carbohydrate. Dietary ketosis is achieved by the sustained and sharply curtailed intake of carbohydrates. How sharply? It varies. Your mileage may vary (YMMV), but for me it’s 20 to 30g of carbs a day.
What is the mechanism and how does it work? (Sorry, but I think some of my readers will find the science both useful). A part of everything we eat becomes fuel. Carbohydrates break down to mostly glucose. That’s good because glucose quickly converts to energy, and the body (the brain, especially) needs a little glucose, NOT carbs – about 30-35 grams a day, either directly as glucose or in a form (e.g. ketone bodies) that substitutes for it perfectly.
Fat (both body fat and ingested) are triglycerides, made up of 3 fatty acid molecules and 1 glycerol molecule. Note the stem ‘gly.’ When each triglyceride molecule is broken down into free fatty acids for fuel, it leaves a glycerol molecule to join with another to make glucose. Thus, about 10% of ingested or stored body fat becomes glucose.
When protein is digested into its component amino acids and is taken up by the body, what is left over goes to the liver. There, when the body needs glucose, the liver makes glucose from those stored amino acids by a process called gluconeogenesis (“glucose-new-creation”). About 54% of the protein we eat is glucogenic, i.e. can become glucose, especially if we eat too much at any one meal. It is stored and then reconstructed and utilized as glucose!
Carbohydrates – almost all of them, from simple sugars to complex starches – digest to glucose. Some starches digest slowly, but simple sugars and highly processed carbs (in products sold in boxes and bags) break down fast to the single-cell sugars glucose, fructose or galactose. In the case of fructose, they are shunted directly to the liver to protect your body from them. Your liver will convert fructose to glucose to glycogen to store in the liver, but if the liver is already full of glycogen, it will convert the fructose to fat by a process called de novo lipogenesis.
The way to achieve the condition called dietary ketosis is this: eat a very low carbohydrate, moderate protein and high fat diet. Expressed as a formula – sorry, again – where K = ketogenic molecules and G = glucose molecules.
 K/G ratio = (0.9*FAT+0.46*PRO)/ (0.1*FAT+0.54*PRO+1*CHO.)
The fat, protein and carbohydrates (CHO) are all entered in grams (weight). A ketogenic ratio of numerator (K) to denominator (G) is >1.5. Thus, the ratio should be at least 1.5 to 1, stated >1.5:1, in each meal, every day.
Because this dietary regimen is very high in fat and very low in carbs, you will not be hungry between meals, so long as you don’t eat carbohydrates. You will be satisfied because fat is satiating and protein digests slowly. But all carbs break down to glucose, and circulating glucose will raise you blood insulin levels and take you out of ketosis.
Once you are in dietary (nutritional) ketosis, fatty acids and ketone bodies are used as the major sources of fuel. But, the “balanced diet” establishment says, this could cause a problem for the brain because fatty acids do not cross the blood-brain barrier. Fortunately, the liver uses the fatty acids from the breakdown of triglycerides (both body fat and ingested fat) to make ketone bodies which enter the brain and substitute for glucose. Ketone bodies are actually a more efficient fuel for the brain than glucose. Ketones as brain fuel are also a desired alternate to glucose if the brain has started to develop Insulin Resistance (aka “Type 3” Diabetes). Increasingly, the ketogenic diet is being used as a therapeutic diet for Mild Cognitive Impairment (MCI), aka early-stage Alzheimer’s Disease.

Saturday, April 13, 2019

Retrospective #57: What is Ketogenic Nutrition?

In mid-2012, on her now defunct blog “Weight Maven,” Beth Mazur introduced me to Lucas Tafur whose domain has also since expired. Lucas Tafur is an interesting story. Before he created the Lucas Tafur site, his blog was called, ahead of its time, “Ketogenic Nutrition.”  It provided me with a nostalgic look back at what proved for me to be a very effective way to lose 170 pounds. Tafur quotes one of the world’s leading experts on ketone bodies, Dr. Richard L. Veech of the National Institutes of Health: "Doctors are scared of ketosis. They're always worried about diabetic ketoacidosis. But ketosis is a normal physiologic state. I would argue it is the normal state of man.”
Put into context, in the continuum of our day-to-day existence, we’re either in a fed or a fasting state. The fed state begins with eating and continues until the food has been digested and absorbed. The fasting state then begins and continues until we eat again. When fasting, the body is said to be in ketosis, a normal physiological state.
When we are in a fed state, we derive our energy largely from glucose. This is called a glycogenic state. When we are in a fasting state, the body derives its energy from our fat stores from our adipose (fat) tissue, which breaks down by lipolysis. Who can doubt that it has been that way for thousands of generations? We were hunters and gatherers, not grazers. That is the way we were “designed” and evolved until, with the “invention” of agriculture about 500 generations ago, and domestication of animals, and foods that could be stored, we became Neolithic.
In just the last few few generations, we have gone further astray, with disastrous consequences. Of course, what has happened in these last few generations is not an evolutionary adaption; it is but an aberration. It is also a completely reversible change once we come to see and accept what “we” (complicit with our agricultural/industrial enterprise and the associated medical, “public health” and media establishments) have done to ourselves. We can return to a fed and then fasting Way of Eating in which ketosis is once again “the normal state of man.”
The old scenario: We hunted, we ate and we were satisfied. After our meal was digested and absorbed, we entered a fasting period, a period of ketosis, as Dr. Veech said, “the normal state of man.” The body used its fat stores, broken down to fatty acids, a glycerol molecule, and ketone bodies, for energy. But, as Tafur then points out, ketosis can “either be triggered by fasting or by diet.” Therein lies the point to which Lucas Tafur was leading us.
The rest of this column is excerpted from Lucas Tafur’s defunct “Ketogenic Nutrition website. “Fasting ketosis develops after a few days of fasting, when liver glycogen stores are depleted. The body, as an acquired evolutionary mechanism, shifts from a glucose-based metabolism to a fat-based one.” “Studies have shown that the adaptive response to fasting is regulated not by energy restrictions per se, but by carbohydrate restriction. This is because the rate limiting enzyme of ketogenesis…is controlled by insulin levels.” (Emphases added by me.)
“The body’s main energy store is adipose tissue. Fat is more calorie-dense, meaning that it yields more energy per gram than glucose. Fat is the body’s preferred fuel, ketones being a “super fuel” that can be used by some tissues that haven’t evolved to use free fatty acids (FFA) such as the brain. Ketone bodies help the body spare amino acids by reducing the need for glucose. This way muscle mass is maintained…. Without ketosis, body protein stores would be cannibalized…. “
“The body stores fat primarily as saturated fat because it is metabolically more efficient than glucose and produces less toxic residue when metabolized. Exogenous glucose is the first substrate to be used because it is toxic to the body. It produces metabolic disregulation caused by hyperglycemia, which triggers an inflammatory and autoimmune response. Ketosis represents the opposite scenario; it protects the body during a life-threatening situation like starvation.” (end quote)
Lucas Tafur, and Beth Mazur, and Kurt Harris (see Retrospectives #18 & #19), were all ahead of their time and have all since disappeared from the scene. They all made contributions to my understanding of nutrition and human metabolism, including Tafur’s description of fasting ketosis. But what is dietary ketosis? See the next Retrospective.

Thursday, April 11, 2019

Retrospective #55: Homage to Gary Taubes


I’ve just read Gary Taubes’s “The Soft Science of Dietary Fat,” published in Science (2001). It’s an early look into a subject that’s since come a long way. I believe it was a foundational piece that was the impetus for his later work.
I read it looking for a way to understand why a friend who has been a Type I diabetic for over 70 years “believes absolutely” that saturated fat and dietary cholesterol are bad for our health and should be avoided.  I’m not trying to change her beliefs. She’s a survivor and an expert on how to manage her disease. I just want to understand why.
Taubes doesn’t need me to defend him either. He “studied applied physics at Harvard and aerospace engineering at Stanford (MS, 1978,”) and then “took his master’s degree in journalism at Columbia University in 1981.” “He has won the Science in Society Award of the National Association of Science Writers three times.” After “The Soft Science of Dietary Fat,” he came to the public’s attention with his blockbuster July 7, 2002 New York Times Sunday Magazine cover story, “What If It’s All Been a Big Fat Lie?” It was the “2nd coming” of the low carb era.
After 5 years of research and writing Taubes went on in 2007 to publish his magnum opus, “Good Calories – Bad Calories” (“The Diet Delusion” in the UK). In an “Afterwords” in the paperback edition, Taubes admits that this epic tome had less impact on the medical establishment than he would have liked. A more accessible book, “Why We Get Fat: And What to Do About It,” came out in 2010. In 2011 he was back on the cover of The New York Times Magazine with “Is Sugar Toxic,” and in 2016, he published, “The Case Against Sugar,” another NYT best seller.
Many physicians and researchers have attributed to Taubes the inspiration for their career direction. He certainly has inspired me. He’s responsible, indirectly I suppose, for the name of this blog, “The Nutrition Debate.” As a “nutrition groupie,” I bundle my own experience with ideas I’ve had and those of experts I read daily to put it “out there” for the world to consider. If the light level behind the mirror of conventional thinking is raised, perhaps the world will come to see the “alternate hypothesis” that Taubes describes in “Good Calories – Bad Calories.” Perhaps, the silver lining of the mirror will dissolve and be transparent. The following is excerpted from Taubes’s 2001 essay.
“The original simple story in the 1950s was that high cholesterol levels increase heart disease risk. The seminal Framingham Heart Study, for instance, which revealed the association between cholesterol and heart disease, originally measured only total serum cholesterol. But cholesterol shuttles through the blood in an array of packages. Low-density lipoprotein particles (“bad” cholesterol) deliver fat and cholesterol from the liver to tissues that need it, including arterial cells, where it can lead to atherosclerotic plaques. High-density lipoproteins (“good” cholesterol) return cholesterol to the liver. The higher the HDL, the lower the heart disease risk. Then there are triglycerides, which contain fatty acids, and very low-density lipoproteins (VLDLs), which transport triglycerides.”
“All of these particles have some effect on heart disease risk, while the fats, carbohydrates, and proteins in the diet have varying effects on all these particles. The 1950s story was that saturated fats increase total cholesterol, polyunsaturated fats decrease it, and monounsaturated fats are neutral. By the late 1970s – when researchers accepted the benefits of HDL – they realized that monounsaturated fats are not neutral. Rather, they raise HDL, at least compared to carbohydrates, and lower LDL. This makes them an ideal nutrient. Furthermore, saturated fats cannot be quite so evil because, while they elevate LDL, which is bad, they also elevate HDL, which is good. And some saturated fats – stearic acid, in particular, the fat in chocolate – are at worst neutral. Stearic acid raises HDL levels but does little or nothing to LDL. And there are trans fatty acids, which raise LDL, just like saturated fat, but also lower HDL. Today, none of this is controversial, although it has yet to be reflected in any Food Guide Pyramid.”
Well, the Food Pyramid is gone, only to be replaced by “My Plate,” arguably a worse representation of a healthy eating pattern. But the modern movement that Gary Taubes spawned has gained enormous momentum. Today, it is a legacy to the work begun by Gary Taubes and his seminal piece, “The Soft Science of Dietary Fat?”

Sunday, April 7, 2019

Type 2 Nutrition #480: CGMs for Non-Insulin Dependent Type 2s?


That’s a question, folks, not news of a new Medicare policy on insurance coverage. The fact is: Medicare will still only cover a Continuous Glucose Monitor (CGM) for type 1s and type 2s who inject meal-time insulin.
Current government policy is designed to avoid hypos and is cost-driven. Hypos from accidental overtreatment with insulin by the patient are acute and can be life threatening if not addressed quickly. They frequently result in emergency room visits and hospitalizations. Regrettably, for non-insulin dependent type 2s, Medicare does not foster a long-term approach to blood glucose self-management (BGSM). They do not consider the costly complications from higher levels of glucose in the blood. And as the cost of treating the complications and co-morbidities of T2D soars, Medicare should cover CGMs for non-insulin dependent T2s.
Diabetic complications take many years to develop. Microvascular complications include 1) nerve damage (peripheral neuropathy), the leading cause of amputations; 2) loss of sight (retinopathy), and 3) end-stage kidney disease (nephropathy), requiring dialysis. The co-morbidities of T2D are macrovascular: some cancers, stroke, and heart disease; the ADA "compliant" patients (with an A1c of 7.0%), have TWICE the risk of CVD.
Why does the government set such a low standard for doctors and patients? Because achieving the ADA’s modest ≤7.0% A1c control goal is still difficult with the government’s one-size-fits-all Dietary Guidelines. Type 2 diabetes is a DIETARY disease, but the Dietary Guidelines for all Americans are still based on an eating pattern that is very high (55-60%) carbohydrate. All carbs sooner or later become “sugar” (glucose) in the blood. Eating so many carbs while trying to manage your blood glucose requires increasingly more meds. But the USDA/HHS, abetted by Big Agriculture and Big Pharma, are stuck in the status quo.
So, if the patient understands this and wants to lower their blood sugars on a day-to-day basis, they need to know what foods (and other factors such as hormones) affect their blood sugar (glucose). The best way to do that is to monitor your blood sugar frequently, and “eat to the meter,” i. e., change what you eat.
As I am not an insulin-dependent type 2 who injects meal-time insulin, my options for obtaining a CGM are limited to cash-only, i.e., out-of-pocket. I recently looked into this and learned the following:
For context, I treat my type 2 diabetes primarily with a Very Low Carb “Eating Pattern.” My only diabetes med is Metformin, and I am assured by my physician, “You can’t get hypoglycemia from just Metformin.” My own experience since 2002 confirms this. I am in no danger whatsoever of hypos, even with extended fasting.  Metformin works on the liver (and gut) and improves insulin sensitivity. It has no effect on the pancreas.
So, if you are not able to use insurance to cover the cost of purchasing a CGM system (sensors and readers, or transmitters and receivers), you have 2 choices: Dexcom and Freestyle Libre. If you don’t have or aren’t eligible to use insurance, cost is the main factor. That eliminates one choice for me.
The new Dexcom G6 (3/18), at about $5,000 US a year, is expensive. It is more accurate in hypos, includes alarms and has an integrated mobile app. It automatically downloads results to a Bluetooth-enabled device. The 10-day sensor is a little bulky, but if you’re insurance eligible, and get hypos, it’s definitely the way to go.
The new Freestyle Libre 14-day (8/18) is much less expensive, but still costly at $1,620 a year ($135/mo). The previous Freestyle Libre included sensors good for 10 days, but the new FDA approved 14-day sensor should now be in pharmacies. It may be slightly less accurate than a Dexcom, but it has a shorter “warmup” period (1 hr. vs. 2 hr.) for new sensors. However, it has no alarms for hypos. It has a 90-day memory and an excellent suite of reports (daily reports and 14-day summaries). It does not have its own integrated mobile app and must be “read” every 8 hours. However, a startup, Ambrosia, has a workaround called BluCon. Given my needs, and the cost disparity, it’s a no-brainer. If I decide to do it, I’ll opt for the Freestyle Libre 14-day.

Retrospective #51: Dietary Cholesterol

Pay attention - dietary cholesterol is the cholesterol you eat. Serum cholesterol is the cholesterol in your blood. They are not only different; they are largely independent of each other. The following excerpt from Wikipedia gets “into the weeds” a bit, but if you want to learn about cholesterol in food, it is necessary to provide a framework.
“While the absolute production quantities vary with the individual, group averages for total human body content of cholesterol, with the U.S population, commonly run about 35,000 mg (assuming lean build; varies with body weight and build) and about 1,000 mg/day ongoing production. Dietary intake plays a smaller role, 200-300 mg/day being common values; for pure vegetarians, essentially 0 mg/day, but this typically does not change the situation very much because internal production increases to largely compensate for the reduced intake” (emphases added).
Assuming a “lean...body build” for the U.S. population is a dubious proposition, as must be obvious to the casual observer. My body is certainly not lean. Neither do I eat just 200-300mg/day of cholesterol. I typically eat 600-650 mg/day. But, the USDA/HHS Dietary Guidelines for Americans (age 2 and older) urged us, until 2015, to eat no more than 300mg/day (200mg with CVD risk factors). Then, on December 14, 2014, the Dietary Guidelines Advisory Committee announced that “…cholesterol is NO LONGER a nutrient of concern for overconsumption.” Finally!
To make sense of all this consider 1): Most societies wean at 3 or 4, and breast milk is 55% fat, mostly saturated, and loaded with cholesterol? “Mother's milk is especially rich in cholesterol and contains a special enzyme that helps the baby utilize this nutrient. Dr. Mary Enig (deceased), the doyenne of lipid chemistry and the author of the definitive biochemistry guide, “Dietary Fats,” said, “Babies and children need cholesterol-rich foods throughout their growing years to ensure proper development of the brain and nervous system.”
And 2): the abstract of, “Diabetes and insulin in regulation of brain cholesterol metabolism,” from the Joslin Diabetes Center and Harvard Medical School, published in Cell Metabolism (2010 Dec 1; 12(6):567-79), begins,  “The brain is the most cholesterol-rich organ in the body, most of which comes from in situ synthesis,”
Yet, many people have deprived themselves for decades of cholesterol-rich foods (shrimp, eggs, butter, cream, liver, marbled steaks) in an effort to comply with the government’s public health guidelines. And many still do!
And 3): Perhaps the most compelling evidence is that vegetarians, who eat 0g/day of dietary cholesterol, have serum cholesterol levels similar to omnivores. Why? “…because internal production increases to…compensate for the reduced intake.” Vegetarians avoid eating cholesterol-loaded foods altogether “but this typically does not change the situation very much.” They have completely given up eating animal-based foods – no cholesterol whatsoever – for a different reason, perhaps, but they did not thereby lower their serum cholesterol “very much.”
The reason, as the numbers In the Wiki-quoted paragraph above note, is that most cholesterol, typically 80-90% of what is contained within the body, is created and controlled by internal production by every cell in the body. As described in Retrospective #24,”… cell structure relies on fat membranes to separate and organize intracellular water, proteins and nucleic acids, and cholesterol is one of the components of all animal cell membranes.”
The Wikipedia entry on atherosclerosis continues: “For many, especially those with greater than optimal body mass and increased glucose levels, reducing carbohydrate intake (especially simple forms), not fat and cholesterol, is often more effective for improving lipoprotein expression patterns [cholesterol panel], weight and blood glucose.“
Unfortunately, Ancel Keys, the father of the (infamous) Lipid Hypothesis, is little known for having said very late in his life, “Cholesterol in the diet doesn't matter at all unless you happen to be a chicken or a rabbit.” “There’s no connection whatsoever between cholesterol in food and cholesterol in blood. And we’ve known that all along.
Given that we were born to drink mother’s milk, and our brain is mostly cholesterol, eating cholesterol-rich foods strikes me as both natural and healthy.  Quoting from the 1970s TV ad, “It’s not nice to fool Mother Nature.”