The Nutrition Debate #214: How I Lost 125 Pounds (Part 2)

The Nutrition Debate #214: How I Lost 125 Pounds (Part 2)

In the last column I told how I determined how much carbohydrate and protein I should eat for weight loss, blood sugar control, vastly improved blood pressure, blood lipids, inflammation markers and overall better health. 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.

I lost 60 pounds on Atkins Induction in just nine months (1½ pounds a week) by just writing down everything I ate every day and estimating carbohydrate 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 to eat Very Low Carb (VLC) in 2002, I had been a type 2 diabetic for 16 years, and up to then in complete denial. I left my health care, and my diabetes care in particular, to my doctor. Now, I rely on self-care for my diabetes health.

After 4 years of trying to stay on Atkins Induction (20g of carbohydrate a day), I started to slip and I gained 12 pounds. I then switched to Dr. Richard K. Bernstein’s program (30g carbs/day) for diabetics. I wanted to lose that 12 pounds again and a lot more. That’s when I decided to count the protein I ate too and to keep a more detailed record of what I ate. After researching the protein question, I devised my own method for determining when and how much protein to eat, which I explained in #213. I started out at 90 grams of protein a day. That only left fat and total calories, to decide, and I chose an online site to do all of the calculations. All I had to do was to remember everything I ate and enter the estimated quantities. The software did all the rest.

I determined how many grams of fat to eat a day by backing into the calculation. I wanted to lose 2 pounds a week. At 3500 calories/pound that is 7000 calories/week, or 1000 calories/day. If a mostly sedentary, older male who doesn’t exercise needs 2200 calories/day to maintain his weight, then I would need to eat just 1200 calories/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 Bernstein. I didn’t care about macronutrient ratios or ketosis. I just ate VLC and what I thought was moderate protein. I lost 100 pounds in 50 weeks (2 pounds a week, as planned) starting with this regimen and lowering my protein amount as I went along. I lowered protein from 90 grams to 75 and then to 65 grams a day. Today, I strive to eat just 60 grams of protein a day, which is still 20% above the Nutrition Facts panel guidelines.

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 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 thereafter on any moderate or moderately high protein diet.

As I lost weight, and discovered low carb foods that I liked for breakfast and lunch, and new good fats, and small low carb/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). At present they are 5% carb (15g), 20% protein (60g) and 75% fat (98g). All of these ratios are for 1200 calories a day.  

To sum up, when I eat according to my plan, my body is happy, and I am burning two pounds of body fat a week. It’s pretty easy to do so long as “my body,” which I have come to think of as a separate entity that I am living in, is “happy.” And it is telling me that it is. I just eat small meals at mealtime. 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 (I no longer call it “dinner”) are, in our culture, mealtimes. My body decides what to do with it, to maintain muscle and burn fat.

So, what do I eat? Breakfast is 3 eggs, 1 strip of bacon and a cup of coffee with stevia powder and a little half and half. Lunch is usually a can of sardines (in olive oil!). I drink the oil. And supper is a small portion of protein, usually a fattymeat or fish, and a low-carb vegetable, either tossed in butter or roasted in olive oil. If I snack before dinner, my favorite is radish slices with salt and a dollop of butter or ghee. Sometimes I have a small (measured) portion of nuts. Macadamia nuts have the fewest Omega 6s, while hazelnuts, almonds or pecans have only moderate amounts. Pistachios and cashews are too high in carbs and walnutsmuch too high in Omega 6s. Of course, this also means I will have to have less fat with my supper.

Everything discussed in these 2 columns is addressed in more detail in the preceding 212 columns. Why not have a look?

The Nutrition Debate #213: How I lost 125 pounds (Part 1)

I started eating Very Low Carb (VLC) on Atkins Induction, at my doctor’s suggestion, to lose weight. I am a long-time (28yr) type 2 diabetic so after 4 years I switched to Dr. Bernstein’s program. I have been very successful at both,getting “normal” fasting blood sugars ( 80s and 90s mg/dl) on only 500mg ofMetformin once a day and losing ,at one point, 170 pounds.

When I began VLC 12 years ago, I was “maxed out” on two classes of oral meds and starting a third. Within a day of starting Atkins Induction, I was getting hypos (BG readings in the 50s and even 40s). I ate some sugar and called my doctor. He told me to cut my oral diabetes meds several times over the next few days. As I lost weight, my blood pressure gradually dropped from 130/90 to110/70 at the same level of meds. Over a period of time my HDL doubled and my triglycerides dropped by two-thirds. My Hb A1cs are now consistently in the mid to high 5s, and both my HDL/TG ratio and my hs C-Reactive Protein are almost always under 1.0. I am never hungry. I have lots of energy, and I feel great. By all these measures I am much healthier today than I was 12 years ago. How did this come about? In gradual steps, except the medication reductions came immediately.

When I first started eating VLC, for a few years I wrote down everything I atebut 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 daily estimated grams of carbohydrates. The math was simple and the method not very accurate, but I was learning about low carb eating. Since I was doing blood glucose measurements before and two hours after each meal (6 pricks/day), I was learning what foods raised my blood sugar and what foods didn’t. Ala Bernstein, I was “eating-to-the-meter.” This is a learning process every diabetic or prediabetic eating low carb for blood sugar control must do.

Then I became interested in how much protein I should eat. I didn’t care for Bernstein’s method of protein measurement. But I did subscribe to his “prescription” to eat a similarly sized, small-to-medium portion of protein with each meal, and to space the meals at regular intervals. He also counseled that, to lose weight you should reduce the portion size of protein for one meal and if that wasn’t enough, a second meal each day. This advice would later guide me to the low side on protein.

Another factor I considered is that about 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 calls for glucose. That is the main mechanism of the drugMetformin: to suppress the up-regulated synthesis of glucose by the liver in the disregulated sugar-based metabolism that many people have developed on the carbohydrate-based Western diet most of us eat today.

How much protein you should eat is dependent on several factors: among them age, gender, and especially 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 such as kayaking or gardening). I don’t like to sweat and besides, aren’t we advised to exercise to “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 proteinthe “experts” said I should eat.

The Nutrition Facts panel required on processed food packaging by the U. S. Government (HHS/FDA) calls for a Minimum Daily Allowance of 50 grams of protein a day. That’s 200 calories of a 2,000 calorie diet or 10%. But which is operative: 50g or 10%? If you eat less than 2,000kcal/day, say just 1,000, that would then be 20% of 1,000, wouldn’t it? More on this later.

An abstract of an authoritative paper I read said that American men eat about 16% protein by calorie and American women 15%. But the measure used by virtually everyone today is expressed in terms of grams of protein per kg of “leanbody weight” (or grams per pound in U.S. measure). This was confounding to me for two reasons: 1) The range of recommendations was so wide, and 2) the definition of “lean body weight” was imprecise, indeterminate and frequently subject to misinterpretation. This latter point is particularly true for the overweight, obese and morbidly obese, like me.  

The “experts” recommend a very wide range of protein amounts. You need to pick one and go with it. I did from the get go. For me (old, male, diabetic, morbidly obese, relatively inactive and without excessive musculature to maintain), I chose 0.6g of protein/lb of ‘lean body weight’ (about 1.3g/kg). The amount is independent of fat weight, since protein builds and maintains muscle and does other things not fat related. The BMI table says that at 5’-11” my “Normal” weight should be 150 pounds. At 0.6g of protein per pound of lean body weight, that’s 90 grams of protein a day. So, that’s where I started.

The Nutrition Debate #212: “Everything I (ch)eat turns to fat.”

The Nutrition Debate #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,numerous 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 the book, or at least my review in #205 here and her deeply troubling observations about the medical “business” that I commented on in #206 here.

Shanahan’s book has hundreds of references, so I lament that this generalization is not sourced. I suppose it should be understood as a summation of the very well sourced material presented in her book. In any case, the quote can be read as the expression of exasperation that we, overweight and obese type 2 diabetics, feel as we continuously try to lose weight. I increasingly suspect that the undiagnosed as well as diagnosed pre-diabetics among us feel the same way. 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 mechanism behind our complex metabolic environment, or milieu intérieur as Claude Bernard, the 19th centuryFrench physiologist, first described homeostasis. And I think 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) and impaired fasting glucose (IFG), the medical terms for incipient type 2 diabetes, gain weight easily and lose weightwith difficulty.

In lay terms, both IGT and IFG are the equivalent of “carbohydrate intolerance,” described in The Nutrition Debate #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 The Nutrition Debate #99, “Natural History of Type 2 Diabetes.”

The 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. These changes detailed in laboratory reports and can be summed up by your waist/hip ratio. The most frequently tested are fasting glucose, hemoglobinA1c (HgA1c), the lipid panel (Total Cholesterol, LDL, HDL, and TC/HDL ratio) and triglycerides. Sometimes, when these markers are “out of sync,” a diagnosis of Metabolic Syndrome is made. All too often, the doctor just prescribes a statin and tells the patient to “exercise and eat a low-fat diet to lose weight.”

What’s missing in this “prescription”? Among other things, a test for fasting insulin. I’ll get into the specifics of this test in another column, but for now I want to explain how and why I have come to this conclusion. When I have been very good – that is, when I not only talked the talk but walked the walk, every day in every way – my fasting blood sugars have consistently been in the 80s and 90s. I can point to weeks, even months, of never or very rarely having a FBG over 100. And since it is an elevated blood glucose that causes the pancreas to produce insulin, to transport glucose in the blood to destination cells, a slightlyelevated blood glucose is associated with a slightly elevated serum 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 serum insulin causes fat storage and prevents fat breakdown for energy. My column #5, about GC-BC, presents Taubes’s summation (“10 Certain Conclusions”) from his Epilogue (pg 453-454). It is a very succinct and compelling explanation of the functional role of insulin in homeostasis, and a must read.

Anyway, these days my fasting blood glucose readings have been regularly 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 “cheat” a little almost every day;always just before or at any time after dinner. And I pay the price. It’s just a little “cheat,” so I don’t gain weight, but neither do I lose any weight EVEN THOUGH I AM EATING NO MORE THAN +/- 1500-1800 CALORIES ON MOST CHEAT DAYS.

What’s happening, I hypothesize, 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. My body’s autonomically functioning metabolism, the milieu intérieur, “gets the message” that as long as I have a supply of quick energy every night (the “cheats” that break down to carbs), 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: my slightly elevated serum insulin circulating my slightly elevated glucose. If this is still a little unclear to you, dear reader, read Taubes’s “10 Certain Conclusions” (linked above) through a few times.

The Nutrition Debate #211: Eggs and Satiety

Kris Gunnars at Authority Nutrition recently posted this PubMed link to a 2005 abstract from the Journal of the American College of Nutrition (J Am Coll Nutr). It is titled, “Short-term effect of eggs on satiety in overweight and obese subjects.” Curiously, there were no comments on this article in Pub Med, an official governmental organ of ncbi/nlm/nih. Maybe, in 2005, eating eggs, due to their saturated fat and cholesterol, was still a no-no, and no one in the “scientific/medical” community could figure out how to support the idea that whole eggs (yolks included) could be part of a “healthy eating” pattern. Fortunately, that perception has since changed. Whole eggs are one of the healthiest foods on earth.

The OBJECTIVE of this small prospective, randomized, crossover-design study was clearly stated: “To test the hypotheses that among overweight and obese participants, a breakfast consisting of eggs, in comparison to an isocaloric equal-weight bagel-based breakfast, would induce greater satiety, reduce perceived cravings, and reduce subsequent short-term energy intake.” Thirty women with BMIs of at least 25 between the ages of 25 and 60 years were recruited to participate.

The RESULTS were clear: “During the pre-lunch period, participants had greater feelings of satiety after the egg breakfast, and consumed significantly less energy.” In addition, “Energy intake following the egg breakfast remained lower for the entire day… as well as for the next 36 hours.”

“CONCLUSIONS: Compared to an isocaloric, equal weight bagel-based breakfast, the egg-breakfast induced greater satiety and significantly reduced short-term food intake. The potential role of a routine egg breakfast in producing a sustained caloric deficit and consequent weight loss should be determined.” In other words, they want the NIH to fund more studies like this!!! Government funded research, remember, is a jobs program, but in this case, one that should be supported (LOL).

Personally, as my readers know, I ate a breakfast of 2 eggs and 2 strips of bacon (plus coffee with H&H and sweetener) for almost 10 years. Then, a couple of years ago, after reading Paul and Shou-Ching Jaminet’s Perfect Health Diet (pg. 321), I switched to 3 eggs and 1 strip of bacon (plus coffee) to get my daily dose of choline all in one meal. And I have been telling people for years that, when you eat this breakfast, and this breakfast alone (with no fruit or juice or bread products), you will not be hungry – not in mid-morning, not at lunch, not even at mid-afternoon. I haven’t been hungry at lunch for years.

You may ask, then, “Why do you eat lunch?” That’s a good question. Increasingly I have been asking myself that question too. I even drafted a column a few years ago, “Two meals or three meals a day?” but never published it. The reason, I suspect, is that, again as my readers know, I eat a can of sardines in olive oil for lunch (when I remember to eat lunch). And my editor thinks that the almost daily dose of sardines and olive oil is one of the reasons I have very high HDLs (~90mg/dL) and very low triglycerides (~34mg/dL). I am reluctant to give up such stellar lipids. For the record, my most recent Total Cholesterol was 207 and my LDL 110. But it wasn’t always this way. To see how my HDL and triglycerides changed after I started eating Very Low Carb, see The Nutrition Debate #67 (HDL) here and The Nutrition Debate #68 (triglycerides) here.

Another bit of self-promotion: Take a look at The Nutrition Debate #91, “Low Carb Breakfasts (and a no-carb lunch)” for more ideas on eggs and breakfast and The Nutrition Debate #176, “Eggs, Cholesterol and Choline,” for more information.

So, in conclusion, there’s no question (in my mind) of the “short-term effect of eggs on satiety in overweight and obese subjects,” like me. It also “reduce(d) perceived [“perceived”?!!] cravings, and reduce(d) subsequent short-term energy intake,” including the viable election not to eat lunch at all! I wouldn’t miss it, seriously. If fact, on many days it’s only the clock, not my stomach, that tells me I missed lunch. I also agree completely that “the potential role of a routine egg breakfast in producing a sustained caloric deficit and consequent weight loss should be determined.” Why don’t you try it?

N.B. The eggs I buy are raised by a local farmer who also raises beef and pigs and sells them all at our local farmers’ market. They use a hen mobile (a chicken coop on wheels) that they move from pasture to pasture week by week after the livestock have been themselves moved on to new grazing. Hens are omnivores (like pigs) and so they (and we) benefit from the insects and larvae that they find in the deposits the animals leave behind. This is all explained in The Omnivore’s Dilemma, a book by Michael Pollan in which he canonizes the practices of JoelSalatin of Polyface Farm in Virginia’s Shenandoah Valley.

Trivia: Did you know that Abraham Lincoln’s usual breakfast was a 1 poached egg and coffee. No wonder he was so skinny.

PS: “Too busy to eat breakfast”? Pack one or two hard boiled eggs to eat at your desk. If that’s not enough, add a slice of smoked salmon wrapped around some full-fat cream cheese. There’s a hardy, healthy, very low carb “breakfast on the run.”

The Nutrition Debate #211: Eggs and Satiety

Kris Gunnars at Authority Nutrition recently posted this PubMed link to a 2005 abstract from the Journal of the American College of Nutrition (J Am Coll Nutr). It is titled, “Short-term effect of eggs on satiety in overweight and obese subjects.” Curiously, there were no comments on this article in Pub Med, an official governmental organ of ncbi/nlm/nih. Maybe, in 2005, eating eggs, due to their saturated fat and cholesterol, was still a no-no, and no one in the “scientific/medical” community could figure out how to support the idea that whole eggs (yolks included) could be part of a “healthy eating” pattern. Fortunately, that perception has since changed. Whole eggs are one of the healthiest foods on earth.

The OBJECTIVE of this small prospective, randomized, crossover-design study was clearly stated: “To test the hypotheses that among overweight and obese participants, a breakfast consisting of eggs, in comparison to an isocaloric equal-weight bagel-based breakfast, would induce greater satiety, reduce perceived cravings, and reduce subsequent short-term energy intake.” Thirty women with BMIs of at least 25 between the ages of 25 and 60 years were recruited to participate.

The RESULTS were clear: “During the pre-lunch period, participants had greater feelings of satiety after the egg breakfast, and consumed significantly less energy.” In addition, “Energy intake following the egg breakfast remained lower for the entire day… as well as for the next 36 hours.”

“CONCLUSIONS: Compared to an isocaloric, equal weight bagel-based breakfast, the egg-breakfast induced greater satiety and significantly reduced short-term food intake. The potential role of a routine egg breakfast in producing a sustained caloric deficit and consequent weight loss should be determined.” In other words, they want the NIH to fund more studies like this!!! Government funded research, remember, is a jobs program, but in this case, one that should be supported (LOL).

Personally, as my readers know, I ate a breakfast of 2 eggs and 2 strips of bacon (plus coffee with H&H and sweetener) for almost 10 years. Then, a couple of years ago, after reading Paul and Shou-Ching Jaminet’s Perfect Health Diet (pg. 321), I switched to 3 eggs and 1 strip of bacon (plus coffee) to get my daily dose of choline all in one meal. And I have been telling people for years that, when you eat this breakfast, and this breakfast alone (with no fruit or juice or bread products), you will not be hungry – not in mid-morning, not at lunch, not even at mid-afternoon. I haven’t been hungry at lunch for years.

You may ask, then, “Why do you eat lunch?” That’s a good question. Increasingly I have been asking myself that question too. I even drafted a column a few years ago, “Two meals or three meals a day?” but never published it. The reason, I suspect, is that, again as my readers know, I eat a can of sardines in olive oil for lunch (when I remember to eat lunch). And my editor thinks that the almost daily dose of sardines and olive oil is one of the reasons I have very high HDLs (~90mg/dL) and very low triglycerides (~34mg/dL). I am reluctant to give up such stellar lipids. For the record, my most recent Total Cholesterol was 207 and my LDL 110. But it wasn’t always this way. To see how my HDL and triglycerides changed after I started eating Very Low Carb, see The Nutrition Debate #67 (HDL) here and The Nutrition Debate #68 (triglycerides) here.

Another bit of self-promotion: Take a look at The Nutrition Debate #91, “Low Carb Breakfasts (and a no-carb lunch)” for more ideas on eggs and breakfast and The Nutrition Debate #176, “Eggs, Cholesterol and Choline,” for more information.

So, in conclusion, there’s no question (in my mind) of the “short-term effect of eggs on satiety in overweight and obese subjects,” like me. It also “reduce(d) perceived [“perceived”?!!] cravings, and reduce(d) subsequent short-term energy intake,” including the viable election not to eat lunch at all! I wouldn’t miss it, seriously. If fact, on many days it’s only the clock, not my stomach, that tells me I missed lunch. I also agree completely that “the potential role of a routine egg breakfast in producing a sustained caloric deficit and consequent weight loss should be determined.” Why don’t you try it?

N.B. The eggs I buy are raised by a local farmer who also raises beef and pigs and sells them all at our local farmers’ market. They use a hen mobile (a chicken coop on wheels) that they move from pasture to pasture week by week after the livestock have been themselves moved on to new grazing. Hens are omnivores (like pigs) and so they (and we) benefit from the insects and larvae that they find in the deposits the animals leave behind. This is all explained in The Omnivore’s Dilemma, a book by Michael Pollan in which he canonizes the practices of JoelSalatin of Polyface Farm in Virginia’s Shenandoah Valley.

Trivia: Did you know that Abraham Lincoln’s usual breakfast was a 1 poached egg and coffee. No wonder he was so skinny.

PS: “Too busy to eat breakfast”? Pack one or two hard boiled eggs to eat at your desk. If that’s not enough, add a slice of smoked salmon wrapped around some full-fat cream cheese. There’s a hardy, healthy, very low carb “breakfast on the run.”

The Nutrition Debate #210: “Diet and Exercise May Help Prevent Diabetes” – Duh!

I couldn’t believe this headline in my Medscape Alert email, so I opened the link and read the lede: “NEW YORK (Reuters Health) – Lifestyle changes made by people at high risk of diabetes appear to reduce their chance of developing the disease over the next two decades, according to a study from China.” Well, I wasn’t mistaken. This revelation does appear to have been made by a group of doctors, albeit in China. But, that Reuters Health would pick it up and assign a reporter to write it up, and then to issue the story from New York, is utterly amazing to me.

Well, at least they didn’t waste newsprint on this groundbreaking news. The study was first reported online (payment or subscription required) in the April 3^rd (not April Fool’s Day) Lancet Diabetes and Endocrinology. And, there was an interesting aspect to the story: The original study began in 1986 and ended in 1992! In it, 568 people with “higher-than-normal blood sugar levels but not high enough to be diagnosed with diabetes,” were placed into one of three intervention groups (diet, exercise, or diet plus exercise), plus a control group. The current study, begun in 2009, compared medical records and death certificates of 430 participants and 138 controls.

The goal of the original researchers (in 1986) was meritorious: “Diabetes is strongly associated with the increased risk of cardiovascular event and mortality,” the lead investigator of the 2009 study told the Reuters reporter. “They wanted to see if lifestyle changes, which included diet modifications and exercise, would help lower death rates.”As it turns out, they did, and especially for women. But “because there are no data on people’s lifestyle habits during the (original) study period,” “it’s impossible to say…how the participants responded to the interventions,” the new study said. Oh, well. Who can say?

But wait, we do have some data on the diet intervention. It “was meant to help people lose weight and normal-weight people reduce the amount of simple carbohydrate [sugars] they ate and the amount of alcohol they drank.” The Chinese understood perfectly how to prevent diabetes and reduce the risk of cardiovascular disease in the 1980s. So, it is all the more bewildering to me that the lead investigator, a Chinese, would say today, “We have to do something active to delay the development of diabetes in high-risk populations.” How could that be any plainer? What is he unable to see?

The results of the 2009 study were impressive though. “By the end of 2009, they determined that 28% of the intervention group had died, compared to 38% of controls.” “Twelve percent of the intervention group had died of heart-related conditions, compared to 20% of controls.” And, “Almost all of the benefit was found in women – there was very little difference in death rates among men based on whether they went through one of the lifestyle programs.”

The Reuters piece also reported, “The researchers also compared diabetes diagnoses and found that 73% of the intervention group had developed diabetes through 2009,” a very high number indeed but still lower than the control group’s 90%. Reuters related that the Lancet piece reported, “Those finding were similar for men and women.”

Perhaps the biggest takeaway from this Reuters story, though, was this: “The group based lifestyle interventions over a six-year period have long-term effects on prevention of diabetes beyond the period of active intervention.” The lead researcher concluded, “It is worth taking active action to prevent diabetes to reduce the risk of cardiovascular disease and mortality.” Now, if only he could figure out what the action should be… Maybe there’s a clue in the paragraph above that begins, “But wait, we do have some data on the diet intervention.”

The first 3 comments on this online piece were “interesting.” The first, by a pharmacist, was “…and they discovered the warm water.” I’m not sure of the allusion, but I’m pretty sure the comment is intended as sarcasm. The second comment is from an advanced practice ob/gyn nurse. It is, “Oh wow, this is groundbreaking!” I’m almost certain (and hopeful) that this comment is pure mockery. The third comment was from a physician. It was, “Useful study.” If my impressions are correct, and I admit to a confirmation bias here, the pharmacist and the nurse are better informed about diabetes nutrition than the doctor. That, of course, is sad and all the more reason to lament the lack of nutrition education in medical school (see #208, “Teach Doctors Nutrition”), and the profusion of misinformation being disseminated by our government, the medical/big pharma cabal and the big food manufacturing industries in the world today.

Perhaps the value of reporting over and over again the self-evident truth about low-carb eating to lose weight and improve health outcomes has some value after all. Eventually, more and more doctors will open their minds to the science they should have learned when they were in school. I can hope, anyway…

The Nutrition Debate #209: “Maureen Dowd is off today,” the NYT said.

Maureen Dowd was off today, the New York Times said on March 25^th at the bottom of a column, “Butter is Back,” by the NYT’s contributing op-ed writer and food writer, Mark Bittman. The piece he contributed that day was long overdue, in my opinion, and was generally very good – until the last two paragraphs.  At that point he “steered” the drift of his op-ed to his own personal theme, as revealed by the title of his recent book, VB6: Eat Vegan before 6:00 to Lose Weight and Restore Health. I guess the title makes it pretty clear what his confirmation bias is.

The “Butter is Back” column was brought to my attention on Facebook by my step-daughter, a biochemist, who appeared, by posting it, to endorse it. I “liked” it and added my own commentary there about Bittman’s bias. But that does not detract from the substance of his writing and thinking. Nor does it diminish the impact of his saying so in The New York Times, nor my step-daughter’s in helping to disseminate the broader message through the medium of pop-culture. Both are significant events in our evolving understanding and acceptance of what “Healthy Eating” means.

I am enormously encouraged.

Bittman acknowledged that “the worm is turning.” The most recent example that this is “increasingly evident” was the meta-analysis just published in the journal Annals of Internal Medicine that quickly made headlines around the world. The researchers looked at 72 studies and came to this conclusion: “Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.”

Most media writers quickly took note of the “total saturated fat” part of this bifocal conclusion. I think this may be because 1) the saturated fat message has been ringing in our ears for half a century, and 2) many people have missed their favorite saturated fatty foods. Bittman wrote, “…when you’re looking for a few chunks of pork for a stew, you can resume searching for the best pieces — the ones with the most fat.” And, “…the days of skinless chicken breasts and tubs of I Can’t Believe It’s Not Butter may finally be drawing to a close.” And, “You can go back to eating butter, if you haven’t already.” Hallelujah!

Referring to the scientific findings, Bittman, the guy who personally eschews (before 6PM) animal protein and advocates “eat vegan…to restore health,” now says, “there’s just no evidence to support the notion that saturated fat increases the risk of heart disease. (In fact, there’s some evidence that a lack of saturated fat may be damaging.)” Okay, a guy can change his mind. Or keep an open mind.  In #193, I admired the way Gary Taubes did that in this NYT piece.

But Bittman, on the way to his vegan message, took note of the other, less familiar but just as important conclusion of the Annals piece: “Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids…” Polyunsaturated fats are vegetable (seed) oils, folks. Or, in Bittman’s own words, “...many polyunsaturated fats are chemically extracted oils that may also, in the long run, be shown to be problematic.” Okay, he hedges a little by saying “may,” but I do not. See #203, “A Brief History of Edible Vegetable (i.e. Seed) Oils,” for my take.

The Annals piece, naturally, prompted a firestorm of controversy. Vested interests came out of the woodwork. A good companion piece to Bittman’s aired on National Public Radio (NPR) a week or so later. The accompanying text article, by Allison Aubrey, is titled “Rethinking Fat: The Case For Adding Some Into Your Diet.” It’s a good, “balanced” read.

The magazine Science published an article, “Scientists Fix Errors in Controversial Paper About Saturated Fats,” just before the Bittman op-ed. The “errors” reflect a disagreement about whether the evidence is strong enough to advocate eating less saturated fat and substituting instead more polyunsaturated fat, the way the AHA and other guidelines presently state. The lead author states that the paper’s conclusions are valid and that the paper was “wrongly interpreted by the media.” Bottom line, as both Bittman and I see it, the Annals piece exculpates saturated fats and excoriates polyunsaturated fats.

In “Butter is Back,” Bittman also takes aim at fake food and extols the virtues of real food. He lashes out at all manner of “highly processed ‘low-fat’ carbs” like SnackWells. My favorite: “How you could produce fat-free ‘sour cream’ is something to contemplate.”  He was an early supporter of the slow food movement and of authors like Michael Pollan. The Nutrition Debate #17, “Michael Pollan: Pied Piper of Pseudo Paleo Prandial Principles,” is, I think, a fun and enlightening read.

And be sure to go back and read “Butter is Back.” So long as you are informed and armed for the Vegan end-pitch, it’s an entertaining and informative look at the current state of nutritional science in transition. As Bittman says, “The tip of this iceberg has been visible for years, and we’re finally beginning to see the base.” That’s, indeed, very encouraging.

The Nutrition Debate #208: “Teach Doctors Nutrition”

Driving up the New Jersey Turnpike on our return from Florida, I saw a bumper sticker that lifted my heart in joy: “TEACH DOCTORS NUTRITION.” At 75 miles per hour, I raised both hands from the steering wheel and shouted in exultation, “Hallelujah!” I don’t think the attractive middle aged blonde noticed, but my wife did. She grinned and told me to pay attention to the road.

I did, but I was reminded of my last visit, in both senses of that word, with my latest Florida doctor (see #207). During the “consultation” he was mentoring a medical student. Except to ask if I needed any prescriptions filled, I reckon he had more to say to her than to me. I listened as he pointed out my most recent HDL cholesterol, saying that he was among those clinicians who counted a high HDL to be a “good” thing.

Apparently, there are some practitioners who are skeptical of the value of a high HDL. The lab report actually cited my HDL as (H), meaning outside the Reference Range, which was “40-60” (no units!). All that matters to such doctors, with respect to the lipid panel, is that the patient take statin(s) sufficient to get the patient’s “high cholesterol” (>200mg/dL) under “control.” Statins do that, if nothing else, by lowering LDL cholesterol. My total cholesterol of 207 was flagged (H).

I jumped into the conversation he was having with his medical student to crow about my low triglycerides (34mg/dL on the last test), and to beam that that low count (and all the other lows I have had for over 10 years: 49mg/dL average; see # 68 here) were due to Very Low Carb. The student looked at me blankly for a few seconds, and then said, “Nutrition.” I said, “Yes, I did it by eating a Very Low Carb Ketogenic Diet and 2 grams of fish oil a day and a can of sardines for lunch.”

The doctor grabbed her attention back by pointing out my very good total cholesterol to HDL ratio, which at 2.3 was less than his 3.5 benchmark. I commented that I thought the benchmark was 5.0, and he replied to the effect that, being less than 3.5 meant plaque formation was in regression; a ratio of >5.0 would indicate that plaque was in formation. I hadn’t heard that before, and I admit I was pleased. He turned back to the student and said, “a ratio of 2.3 is really remarkable.”

When I tried to suggest that the explanation for these “remarkable” lab scores was nutrition, asking my doctor if he had looked at my website on nutrition (“The Nutrition Debate”), he replied dismissively “no” and went back to tutoring his student on my lab results. I felt like a cadaver in an anatomy class, except that cadavers don’t have feelings, do they?

Anyway, I applaud that doctors are interested in results (if you consider a low LDL and low total cholesterol a good result); too bad the only way they know how to get them is through pharmacotherapy. Perhaps the medical student’s grasp of the role of “good” nutrition in my own lipid panel will register. The challenge now for her will be to see that she gets educated in what “good” nutrition is. I hope that I planted a grain of doubt in her mind that the way to get “good” results in a lipid panel is not by pharmacotherapy, but by “Healthy Eating.” See column #200 for a discussion of that controversial subject.

For those to whom this is still not clear, I refer you to one of my most popular columns, #25, “Understanding Your Lipid Panel,” from August 2011. Column #27, “...the strongest predictor of a heart attack” is another online favorite. These are both “accessible” explanations of an alternative view of the lipid panel and various other health markers. Another good column, which addresses chronic systemic inflammation (possibly the only benefit of taking a statin) is discussed in column #187, “Chronic Systemic Inflammation and hsCRP.”

Finally, the extremely troubling view of the modern medical profession as practiced as a business today, described in column #206 by Dr. Cate Shanahan in the Epilogue of her very good book, Deep Nutrition (reviewed in #205), came into vivid clarity at the beginning of this consult. My doctor was viewing my medical records on his computer screen and confirming that I was taking my medicines. The first one he asked me about was a drug I had never even heard of. It was a statin. I asked, “Daniel F. Brown, 5/10/41?” and he said “yes.” How could it be, I wondered, that he had me taking a statin?

The answer I suspect, and as Dr. Shanahan relates, is that in large medical practices/businesses today they have “quality improvement programs that track physician prescribing patterns.” “We call it ‘quality,’ but it’s really about money,” an MD told Dr. Shanahan. “The doctors who prescribe the most get big bonuses. Those who prescribe the least get fired.” I suspect my doctor entered in my chart after my previous office visit that he had prescribed a statin for my “high” cholesterol (207mg/dL). With the medical student looking over his shoulder, he “corrected” my medical record to reflect that I was not taking a statin. He probably entered in his doctor’s notes,” “Patient is non-compliant.”