Wednesday, December 25, 2013

The Nutrition Debate #172: “Everybody knows that…”

Have you seen the Geico insurance commercial that starts off with two people and one reads aloud an ad on a billboard: “Did you know that you can save 15% or more in 15 minutes by calling Geico?” And then the other person says, “Everybody knows that.” This comment implies that the tag line is ubiquitous and that the message is oversold.

(In one of the iterations, the guy who was “put down” with the “everybody knows that” quip replies, “Well, did you know that the pyramids were a mistake?” The camera then cuts to the pharaoh’s architect gazing at the pyramids of Giza and comparing them to plans he is looking at showing cubes, not pyramids. He turns to his hapless helper, who just shrugs his shoulders; then the architect says, “Ohhhhh…”)

Well, “Everybody knows that” is what the waitress told me in a lunch place in New Orleans recently when I told her I was diabetic and wanted to know if there was any breading on the Oysters Bienville I was ordering. It turns out there was, and I changed my order to raw oysters; but it made me wonder, if everybody who is diabetic, or pre-diabetic, or even overweight, knows that they are “carbohydrate intolerant,” why do people ignore this simple precept of healthy eating?

 I know, this is the holiday season, and I don’t want to be a hard ass about this -- but eating what “everybody knows” is unhealthy is not going to make you feel good. In fact, it might even make you feel physically bad and it certainly will come with a guilt trip. You’ll pay the price and you know that.

Of course, it is the season for some indulgences, and even those of us who are totally “carbohydrate intolerant” will allow ourselves some. My wife bakes a double batch of about a dozen types of cookies for gifts and for the Christmas table. I will wait until Christmas Eve to have a few, making sure the plates are outside my reach on the table. And I’ll have enough cheese (no crackers) to “count” as an entire meal. My stepdaughter and her husband bring a very nice cheese board up from NYC. Another stepdaughter and her husband from Atlanta will bring homemade aquavit and pâté, and I’ll drink and eat more than my share. My third stepdaughter and her husband host with a true smorgasbord (their Swedish heritage).

So, how can anybody be a Grinch during the holiday season? It’s just that… everybody knows what “healthy eating” means. To be sure, it means different things to different people. People with healthy metabolisms can indulge without much ado. As David Mendoza, a type 2 blogger, advised in a column last January, he just skips dinner for a day or two when he needs to lose a few pounds. Kids will turn a sugar high into hyperactivity and maybe a growth spurt (hopefully a vertical one). Old folks will take a nap when their blood sugar crashes. And people like me will return to normal blood sugars in a few days.

But I am haunted by the man in Louisiana I met last month whose doctor told him it was okay to eat bread with breakfast and who ate spaghetti for lunch and takes oral diabetes meds and basal and mealtime insulin and walks with a limp from the complications of diabetes. I can’t help but think of what lies ahead for him.

I am haunted by the 52 year old 30-year registered nurse (!) whose obituary I read this week and whose family suggested memorial donations be made to the American Diabetes Association.

And I am haunted by the memory of my pharmacist whom I had known for many years when he sold me my first blood glucose meter. That’s when he told me that he was an insulin-dependent type 2 diabetic. We were the same age, and when he died an early death a few years ago from one of diabetes complications or one of its many co-morbidities, his death shocked and saddened me. It was the impetus for me to write about my type 2 diabetes and my weight loss/health benefits experience.  My low-carb WOE lifestyle change produced, besides the intended effect of weight loss, the added unintended and unanticipated salutary effects of vastly improved lipid health and blood pressure. It “cured” my Metabolic Syndrome.

These people – even the man in Louisiana, and certainly the registered nurse and the pharmacist – knew better, or should have known better. Everybody knows, or should now know, that carbohydrates, when you are insulin resistant, are what make your blood sugar go up and stay up. This damages your body, invariably and inexorably leading to chronic conditions and premature death.

Everybody knows that…so please eat responsibly. Do not be self-destructive. If you have to “indulge,” choose to eat too much fat and protein, or wine even, on special occasions, rather than the starchy and sugary treats. That’s what I plan to do. You should have a plan too. Try to anticipate what temptations will be present, then make a plan in advance and resolve to stick to it. It then becomes a matter of personal integrity; you are accountable to yourself for keeping your resolution. Be reasonable, though. Allow yourself some indulgences, with a plan, in advance to limit them, and then stick to your plan.  

It’s worth a try, anyway. January 1st will come soon enough and you can reset your resolve to “fly straight” thereafter. I will. I will set a goal to “not cheat” (mostly) and to lose the weight I will have put on over the holidays. January represents a fresh start. You might like to try Mendoza's approach of skipping dinner. And the super bowl doesn’t come until February 2nd, almost 5 weeks from New Year’s Day. So, there’s plenty of time to lose it. Good luck and thanks to my readers (and especially my editor). Merry Christmas, Happy New Year, and a Happy Holiday Season to all.

Saturday, December 21, 2013

The Nutrition Debate #171: “Dietary Protein and its Impact on Obesity”

“Dietary Protein and its Impact on Obesity” is the title of this précis in Diabetes in Control, a website for physicians that I monitor. It is another “take” on the study published online in Obesity Reviews I reported on here in The Nutrition Debate #170, “Your instinctive ‘appetite for protein’.” Medicalese notwithstanding, the takeaway was the same: “Analysis of percent protein in diet versus total energy intake showed that when a person’s diet was decreased from 20% protein to 10% protein, there was a significant increase in non-protein energy consumption and vice versa.”

“Age, study duration, and baseline BMI had no impact in dietary percent protein versus non-protein energy intake, but sex, however, did,” this analysis reported. “Men tended to have a higher dietary protein intake as compared to women.” This correlates with an early meta analysis I read years ago that reported that men averaged 16% dietary protein vs. 15% for women. Interestingly and I think very significantly, the Standard American Diet (SAD) recommends only 10% dietary protein (50g RDA of protein = 200kcal or10% of a 2,000kcal daily intake for a woman, as stipulated on the government’s mandated Nutrition Facts panel on processed food packaging. This very low 10% recommendation for protein is very problematic for me and ties in nicely with the hypothesis of this study, as we shall see.

“The study also analyzed high protein intake, but diets with >20% protein did not show significant correlation to decline in energy consumption,” the Diabetes in Control piece reported. “According to the authors, maintaining proper proportions of macronutrients is…important not only for our muscles and cellular building blocks, but also to keep overall non-protein (carbohydrate and fat) energy intake down. The authors also note that the study did not show any great benefit to high protein diets (>20%) which can come with other problems such as kidney failure and/or high cholesterol depending on the protein source.” I have a problem with that last clause, but will not quarrel with it here.

The “Practice Pearls” for this Diabetes in Control piece are as follows:

  • Persons who maintain diets with 15-20% protein intake tend to intake less energy from carbohydrates and fats.
  • Macronutrient energy intake should be calculated as a percentage of total diet; actual protein amount (i.e. grams) doesn't matter as much if it is diluted by the amount of carbohydrates and fats.
  • Persons who fall in low socioeconomic status and women tend to eat less protein.

The original research, “Protein leverage and energy intake,” is copyrighted by the authors, Gosby, A. et. al., Obesity Reviews, and the International Association for the Study of Obesity (IASO). Unfortunately (from the point of view of the wide dissemination of knowledge), the full text is only available by subscription or purchase. But the Summary, a “lay” excerpt of which I quote below, is very well reasoned and illuminating:

“Increased energy intakes are contributing to overweight and obesity. Growing evidence supports the role of protein appetite in driving excess intake when dietary protein is diluted (the protein leverage hypothesis). Understanding the interactions between dietary macronutrient balance and nutrient-specific appetite systems will be required for designing dietary interventions that work with, rather than against, basic regulatory physiology. (bold added) Data were collected from 38 published experimental trials measuring ad libitum intake in subjects confined to menus differing in macronutrient composition. Collectively, these trials encompassed considerable variation in percent protein, carbohydrate and fat. The data provide an opportunity to describe the individual and interactive effects of dietary protein, carbohydrate and fat on the control of total energy intake. Percent dietary protein was negatively associated with total energy intake irrespective of whether carbohydrate or fat were the diluents of protein. The analysis strongly supports a role for protein leverage in lean, overweight and obese humans. A better appreciation of the targets and regulatory priorities for protein, carbohydrate and fat intake will inform the design of effective and health-promoting weight loss diets, food labeling policies, food production systems and regulatory frameworks.”

So, the “protein leverage hypothesis” proffers that 1) increased energy intakes has contributed to overweight and obesity; 2) that protein as a macronutrient in the human diet has been diluted by either or both carbohydrates or fat by the excess intake of one or both of them; and 3) that the “protein appetite” is driving this excess intake of either or both carbohydrate and fat. And the study concluded that the “right” amount of protein is 20%, and that this “protein leverage” applies to “lean, overweight and obese humans.”
Conclusion: “…when a person’s diet was decreased from 20% protein to 10% protein, there was a significant increase in non-protein energy consumption and vice versa.” Reminder: the SAD prescribes an RDA of 10% protein, 30% fat and 60% carbohydrate. Could it be that our government’s recommendations, the Dietary Guidelines for Americans promulgated in 1977 and repeated every 5 years since 1980, are what is making us fat*? It is comforting for me that my target macronutrient distribution is 20% protein, 75% fat and 5% carbohydrate. What’s yours?   * hat tip to Authority Nutrition for the obesity curve table.

Wednesday, December 18, 2013

The Nutrition Debate #170: Your instinctive “appetite for protein”

A new study from the University of Sydney’s Charles Perkins Centre, published online in Obesity Reviews, “shows the overriding drive for dietary protein could be a key factor in the global obesity epidemic,” the release said. It hypothesizes that, “Human’s instinctive appetite is so powerful that we are driven to continue eating until we get the right amount of protein, even if it means consuming far more energy than we need.”

The study “…collated the results of 38 published experimental trials measuring the unrestricted energy intake of people on different diets, also taking into account a broad spectrum of age ranges, BMIs, and diet durations,” the release said.

We found that regardless of your age or BMI, your appetite for protein is so strong that you will keep eating until you get enough protein, which could mean you are eating much more than you should,” said Dr. Alison Gosby, lead author. “As diets shift toward an increased proportion of foods that are higher in carbohydrates or fat, available protein is reduced and energy intake necessarily increases.” This is reminiscent for me of a theory propounded by the Jaminets in their Perfect Health Diet. It is in Chapter 17, “Nutrient Hunger: A Key to Weight Loss,” starting on page 174 of their very good book.

Two more quotes: “The strength of your nutritional drive for protein is frightening within our nutritional environment, where there are a large number of low-protein foods consumed on a regular basis.” And, “We have shown that when people are trying to lose weight they need to look at macronutrient composition, not just calories. If you cut your calories but don’t consider protein intake, you’re going to be hungry and your diet won’t be successful,” Dr. Gosby said (emphasis mine).

So the hypothesis is, “does your metabolic drive for protein cause you to eat too much “energy”? To explore that question, we first need to define “energy in the context of food. Of the three macronutrients that supply nutrition – carbohydrates, fat and protein – only carbohydrates and fat provide “energy.” Dietary protein is not a source of energy, per se; it breaks down to 21 amino acids, some of which the body can’t make and which are therefore called “essential.” Amino acids are the basic machinery of all cells. We need to eat protein every day because, unfortunately, the body has no way to store it.

 Carbohydrates and fat are the body’s main sources of energy. The body is designed to use carbohydrates first, both in the form of glucose stored primarily in the liver and muscles as glycogen, and from the carbohydrates we eat, both sugars and starches, which digest to glucose and are circulated and burned directly for energy. So long as the body has carbs available, either stored or from food, it will use carbs for energy and store any excess carbs as glycogen or fat and any fat eaten as fat.  

That is why we have always had such a hard time losing weight when we eat carbs for energy. The body sensibly uses carbs, and craves more by making us feel “hungry.” Carbs, by design, are the body’s first source of energy. The body’s metabolic mechanism wants to save stored energy for when carbs are not available, as while we sleep (if we’re ketogenic), or for days or weeks or months when food sources are (or rather were) scarce or non-existent. Unfortunately, or rather fortunately from a survival perspective, in our world today, scarcity of carbohydrates is a virtually unknown phenomenon.

But, when glycogen energy stores are used up, and we eat very few carbohydrates, the body naturally transitions to using fat for energy. It will do this in combination with a low carb intake, or even without any ingested carbohydrates at all, making the very limited amount of glucose the body needs for cells that don’t have mitochondria. Glucose is so essential, in these small amounts, that the body has devised multiple ways to make glucose in the absence of eating carbs or having stored glycogen. Among the ways are gluconeogenesis, a process whereby the liver makes glucose from excess amino acids from digested protein that have been stored there. Another way is by combining the glycerol molecules freed up when a triglyceride, circulating in the blood or stored as a fat cell, is catabolized (broken down) and oxidized (burned) for energy. The body also makes ketone bodies as a byproduct of fat breakdown, and ketone bodies are ideal food for the brain.

Thus, both protein and fat, either ingested as food, or stored in muscle, liver or fat, can be used to make glucose. That’s how important glucose is to the body. If you don’t eat carbohydrates, which break down to glucose, the body will make glucose. I’m not saying you shouldn’t eat carbs. I’m just saying the body is designed to make glucose if you don’t.

So, if you don’t eat carbs for energy, the body must rely on fat for energy. And fat, both dietary and stored, is what it will burn. That’s good, if you’re trying to lose weight. And your body, when is it burning fat for energy, won’t feel “starved” or “hungry.” You will not get the “craving carbohydrates” message, because your body will have transitioned from being a “sugar burning machine” to a “fat burning machine.”

That’s not only natural, it desirable. Both you, who want to lose weight without hunger, and your body, which needs energy and is happy to be burning fat for energy when carbs are all used up or not available, will be in homeostatic balance so long as you have body fat reserves to use, and you don’t eat too much fat so it needs to go to your fat reserves for energy.
So, what amount of protein (percent, not grams) will satisfy our instinctive appetite for protein? This is essential to know if that percent protein is the driver for overeating either carbohydrates or fat. The answer is revealed in my next post, #171.

Saturday, December 14, 2013

The Nutrition Debate #169: When I told her, “I’m diabetic…”

When I ordered 2 fried eggs and a side of bacon for breakfast in a hotel in New Orleans recently, the waitress said the special came with grits and a muffin. When I declined, she countered (mistakenly) that it would save me money. When I told her, “I’m diabetic,” she just looked back at me with a blank expression.

After she left, my wife said the waitress didn’t understand. “Grits and a muffin are not sugar,” my wife said. People don’t understand that all carbohydrates will break down to simple sugars, mostly glucose. Glucose is “blood sugar,” and a normal amount is only about a teaspoon. If you are diabetic or pre-diabetic, you have insulin resistance. Insulin is your cellular gatekeeper, and the door to your cells is “locked.” (Actually, it’s got a chain on the door that allows you to crack it open only a little.) That means your cells pretty much ignore the insulin and thus won’t “take up” the glucose that is circulating in your blood with it. Result: high levels of glucose continue to circulate, raising your risk of CVD and dementia, damaging your nerves and organs (eyes and kidneys) and also the small blood vessels in your extremities, toes especially. End result: 50% of all newly diagnosed diabetics already have some sort of diabetic complications at the time of diagnosis.  

Ignorance about type 2 diabetes is endemic in the populace. People are abetted in this ignorance in part by self-denial. After all, who wants to “give-up” favorite foods! But it is also aided and abetted by institutionalized obstructions: Government in the pocket of Agribusiness and Big Pharma; the medical associations and societies (the AHA, the ADA medical wing), also largely dependent on Agribusiness and Big Pharma for financial support; and the intransigence, implacability and intractability of the medical associations to accept the “inconvenient truth” that the low-fat, high-carb “prescription” it has been dispensing on a population-wide basis for the last half-century has been a huge, failed experiment in nanny-state government, like the ACA (Obamacare). Sound familiar?

Another aspect of this problem “if I’m to avoid eating carbohydrates” is, “what can I eat?” Implied in this question is that “everybody knows” that we shouldn’t eat saturated fat and cholesterol because “they’re artery clogging.” Well, that’s just not true. Countless studies, from the “very beginning” (Ancel Keys and later George McGovern notwithstanding; Google them if you don’t know what I am referring to) have shown, to no avail, that saturated fat is good for you. In fact it is essential for healthy cells. And the liver makes about 90% of our cholesterol (100% for vegans) to use for the production of cell membranes, bile acids and hormones, including vitamin D. Dietary cholesterol is inconsequential. “The body knows.”

Cholesterol is blamed for clogging the arteries when it’s actually repairing (with plaque) the inflamed artery walls whose erosions are filled with small dense LDL particles. It’s the inflammation and the small dense LDL particles that are the problem – not the cholesterol that came to put out the fire. The way to fix this is to increase the HDL particles in your blood (by eating saturated fat) so they can carry the LDL back to your liver before it gets stuck in your arteries. You can also increase the size/quality of your LDL particles from small-dense to large-fluffy by eating a low-carb diet. Unfortunately, evidence suggests that statins only lower your large-buoyant LDL cholesterol, leaving the small dense ones to get stuck.  

Finally, you can also lower your triglycerides by eating low carb. And lowering your systemic inflammation will result in less damage to the endothelial layer of your artery wall in the first place. The best test for that is the hs C-reactive protein, and the best measure of your risk of CVD is your Trig/HDL ratio. It’s one of the strongest predictors of CVD risk, much better than the total cholesterol to HDL ratio that is commonly reported in the lipid panel on a lab report.

A day or two later, we were having breakfast at a motel in Cajun Country in a place called Thibodaux. I’m told it is home to the 3rd best culinary school in the country. In the breakfast room the “coffee creamer” was “Coffee-Mate,” a sweetened chemical concoction designed to eliminate saturated fat (from milk and cream) and replace it with “sugar” (carbs). I had my usual eggs and bacon but noticed that for the breads they provided “Chef Mark whipped spread,” whose primary ingredient is “partially hydrogenated soybean oil.” “Everybody knows,” don’t they, that that’s trans fat, “Pure” unadulterated poison! 

I had occasion to speak to the motel’s managing partner about these things. He asked, reasonably, as an alternative, what should he be offering his guests? I said “half and half and butter”! When he started to ask about saturated fat, I suggested he talk to the culinary school people about my suggestions. Let’s hope he does and that they give him good advice. They should know better, but who knows, it’s Thibodaux. Sorry, but let this last story illustrate why I am concerned.
The day before we had been on a “Swamp Tour.” With time for lunch before starting out, I asked about a place to eat, mentioning that I was diabetic. Later, our tour guide, who had overheard me, mentioned that he was diabetic too. He told me that he takes orals meds and basal and mealtime insulin. I asked him what he eats. He said his doctor told him he could eat one slice of bread with breakfast. I then asked him what he had just eaten for lunch. He said he had had spaghetti. When I told him what I eat for breakfast and lunch, he just looked back at me with a blank expression. The boat driver told me later his friend had blood sugars in the 300s. And he walked with a limp. This man does not have a good prognosis.

Thursday, December 12, 2013

The Nutrition Debate #168: Does Exercise Work?

This is a hard subject for me to address. As most readers here know, I rarely speak of exercise; but when I do, I say that I don’t do it. Sometimes I joke that I’m allergic to it as it makes me sweat; or, as others have said, including my guru Gary Taubes, exercise makes you hungry, as in “work up an appetite.” I don’t like exercise.

Another reason I don’t mention it is that from the very first day I began this Very Low Carb Way of Eating, (VLC WOE) on Atkins Induction in 2002, I have succeeded in losing weight (my original goal) and vastly – I mean, very, very dramatically – improved my metabolic health (my type 2 diabetes) and my lipid health and my blood pressure, all without a regular exercise program. That is, I don’t go to the gym, or take long walks, or do some other routine on a regular basis. Never have. Never will. And this sets me apart from virtually everyone who uses “diet and exercise” as part of a treatment plan for dealing with Metabolic Syndrome or its components.

Almost everyone who adheres to an exercise program does it 1) with the hope and expectation that they will lose weight and 2) with a low-fat, high-carb weight loss diet that is doomed to fail. And worse, it will further damage their health. They will not lose weight and keep it off, and they will definitely worsen their lipid health, especially their HDL and triglycerides which are a major part of CVD risk.

So, why write about the topic “Does Exercise Work?” Because, apparently it does, and here’s how I have finally come to understand and accept it. At approximately 19:30 in “Fat Chance: Fructose 2.0,” Dr. Robert Lustig’s sequel to his wildly popular YouTube video, “Sugar, the Bitter Truth,” he explains it quite simply.

Lustig: “Exercise does not cause weight loss – does not cause weight loss. What does exercise do? It causes muscle gain. And that’s good, because muscle has mitochondria, and mitochondria burns energy. So, you stay insulin sensitive because you have a place to put your energy instead of in your liver where it causes problems. So, exercise is the single best thing you can do for yourself, but don’t think it’s going to show up on the scale.”

Okay. Simply said, and understood. Type 2 diabetes is characterized by insulin resistance (IR) and, in advanced cases, the depletion of beta cells in the pancreas (80% or more) combined with the inability of the pancreas’s islets of langerhans to make more insulin. So, anything a type 2 diabetic can do to increase his/her insulin sensitivity is really important. And if those little energy factories in my muscle mass work to keep me insulin sensitive, then I need to maintain my muscle mass. But, as part of a regular exercise program? Sorry… Not me.

If I have to switch tactics to rationalize my resistance to a regular exercise program, so be it. My mind is good at this. It reminds me how I have protested to a diabetes educator or medical doctor that “I don’t exercise,” or “I won’t exercise.” Then I tell them that I work from spring to fall in my garden, often 4 to 6 or more hours a day 4 or 5 days a week. Then, in the winter in Florida, I fish from my pedaling kayak in the Indian River lagoon several days a week and sometimes crash the kayak out through the surf to fish in the ocean. They tell me that that’s exercise. Gardening and kayak fishing may not be a formal exercise program, but they are regular.

So, for those of you who do exercise, or know you should, know that it is, in the words of Dr. Lustig, “The single best thing that you can do for yourself.” But don’t look to me to tell you what to do or how to do it. I suppose, like almost everything else (excepting what you eat, I maintain) what kind of exercise is best depends. Age and physical condition are factors, of course, and perhaps your gender should be considered too.

This might be a good place to invoke the novel “workaround” of the new ADA Position Paper on Nutrition Therapy with respect to macronutrients. Paraphrasing, the “evidence is inconclusive as to the ideal type of exercise (replacing the ADA’s “macronutrient distribution”); therefore, goals should be individualized.” That works for me, and apparently for my health care providers too. They “collaborate” as we set my individual goals together. And then they can write on my chart, “patient compliant,” and everything is hunky-dory. 

There’s lot of good advice out there, though. The first advice I remember (back in 2005-2006) was from Dr. Richard K. Bernstein. Chapter 14 of his Diabetes Solution offers his advice on the optimal exercise routine: intense, progressive, anaerobic exercise with no rest in between, alternating days for different muscle groups.

Jeff Volek, PhD, RD, an exercise physiologist who with Stephen Phinney, MD, PhD, wrote The Art and Science of Low Carbohydrate Living, recommends the same: resistance training 2-3 days/week. Volek also co-authored, with Phinney and Eric Westman, MD, the updated Atkins primer, The New Adkins for a New You.  

There are numerous other exercise physiologists, most of them of the Paleo persuasion, who have also written books. Two that come to mind are Loren Cordain (The Paleo Diet) and Robb Wolf (The Paleo Solution).
For me though, the question is settled. Exercise is good for me because it increases my insulin sensitivity. And I’m going to continue and perhaps increase my regular, intensive gardening and kayak fishing activities.

Saturday, December 7, 2013

The Nutrition Debate #167: An Editorial: “Making the Turn”

A short time ago I wrote a column, “Cowabunga, the ADA makes the turn,” lauding the ADA on their new Position Paper, “Nutrition Therapy Recommendations for the Management of Adults with Diabetes.” The paper was written by and primarily for RDs and CDEs. The groundbreaking aspect of the new guidelines is succinctly summed up thus: “It is the position of the American Diabetes Association (ADA) that there is not a ‘one-size-fits-all’ eating pattern for individuals with diabetes.” In other words, low-carb eating is “healthful,” period.

In the “Cowabunga…” column I noted that this position statement was requested and approved by the ADA Executive Committee, largely comprised of practicing physicians. Nutrition Therapy is pretty much the exclusive domain of RD and CDEs, since doctors are poorly trained and, frankly, generally unqualified to practice in this area. Some clinical practices employ, and others refer their patients to, RDs and CDEs. The RDs and CDEs are now leading the way.

I also noted in my next column that I had some misgivings about the new nutrition guidelines, especially with respect to the ADA’s problematic position on dietary fats. Their reasoning: this aspect of nutrition was beyond the current purview of the ADA’s committee; It would have been “tilting at windmills” for them to take it on. And, in fact, they “ducked.”

The ADA’s new position paper states, “Due to the lack of research [?!] in this area, people with diabetes should follow the guidelines for the general population” (“Dietary Guidelines for Americans, 2010,” 10% of calories from SFAs [saturated fats] to reduce CVD risk.” The paper continues, “Consumers can meet this guideline by replacing foods high in SFA (i.e., full-fat dairy products, butter, marbled meats and bacon, and tropical oils such as coconut and palm) with items that are rich in MUFA and PUFA (i.e., vegetable and nut oils, canola, corn, safflower, soy, and sunflower; vegetable oil spreads; whole nuts and nut butters, and avocado.” Ugh…

While the MUFA (monounsaturated fat) recommendation enjoys universal approbation, the PUFA (polyunsaturated) vegetable and seed oil recommendation is extremely troublesome and problematic. So, the next “windmill” is clearly on the horizon. Dulcinea, be patient. Don Quixote (and Rocinante) are on the way. Which brings me back to the dichotomous nature of the battle. On the one hand, we have the RDs and CDEs who have their domain: nutrition therapy. Then we have the physicians whose bailiwick is medical. Within the ADA, the “ancient wisdom” is the “ADA Standards of Medical Care in Diabetes.” It is all-governing for them.

But, do I see a crack in these standards? A few weeks after the ADA produced their new guidelines, The Lancet, one of the world’s leading medical journals, published weekly, issued this: “Diabetes -- a call for research papers.” What’s so unusual about that? Perhaps I am biased, - okay, I know I am - but I see an opening in the way this call was written. Bear with me for a minute.

In the first paragraph, the “call” notes that oral hypoglycemic agents, and later metformin specifically, became “mainstays of treatment for type 2 diabetes,” but their “precise mode of action…remains poorly defined and controversial,” and that the mode for metformin, “remains to be elucidated.” It then laments, “Although newer treatments with better defined modes of action have been developed, there is still no cure for this disease.” Okay, that’s the traditional thinking about disease in general and diabetes in particular: clinicians diagnose disease and then treat it. They prescribe “diet and exercise” -- the wrong diet, and exercise for weight loss, both of which are fruitless, and then pharmacotherapy, to “delay or prevent” the complications of diabetes, which they define as a progressive disease. So, inevitably, the disease progresses.

Now, The Lancet (el don) to the rescue: it “invites high-quality original research papers to be published to coincide with” the ADA’s Scientific Sessions in San Francisco in June 2014. The scope of research is wide open -- “any aspect of type 1 or type 2 diabetes,” and here’s the point which I see as “making the turn”: “Priority will be given to studies that have the potential to change clinical practice.” Do you see it the way I do? Do you see the potential for a nexus between nutrition therapy and the clinical practice of medicine? Is this a call for research papers that demonstrate that the right diet alone. i.e., low-carb (with perhaps a little help from metformin) can be effective in treating type 2 diabetes (and reduce the risk of overmedication in type 1s)?
Maybe, like the knight-errant, I live in a dream world on the plains of La Mancha. Maybe I should just accept that many people will fail on a low carb diet, but at least now it will not be because they were told that low-carb eating is “unhealthy.” If the ADA’s RDs and CDEs can “make the turn,” why cannot los medicos make it as well? All they need to do is look at the data and instead of saying “due to a lack of research,” accept that the proscription against saturated fat (SFAs) and dietary cholesterol was a humungous mistake. It’s time to get it right and by “publishing your best research…, advance knowledge and add to the clinical approaches needed to limit the global harm of diabetes.” The Lancet appears in earnest. Good on you, I say.

Wednesday, December 4, 2013

The Nutrition Debate #166: What About GMOs?

For the uninitiated, GMOs are genetically modified organisms. “Genetically modified organisms are made by forcing genes from one species, such as bacteria, viruses, animals or humans, into the DNA of a food crop or animal to introduce a new trait,” according to a flyer from the Institute for Responsible Technology I picked it up at a screening of the movie “Genetic Roulette” last summer. The Institute is an educational advocacy group, founded in 2003, whose “Campaign for Healthier Eating in America” goal is the rejection of GM foods in the U.S.

GMOs are thus distinguishable from hybridization. A hybrid is a cross between two related species or cultivars. Hybridization has happened naturally throughout history through cross-pollination, but gardeners, farmers and horticulturists have created the bulk of modern hybrids. GMOs are created by injecting an unrelated species into the DNA of a food crop or animal. For example, a gene from the California bay tree, inserted into a rapeseed plant, produces canola oil with more lauric acid. Most commercially available GMO products use bacteria to transform a plant, such as Bacillus thuringiensis (Bt), a soil bacterium. However, more bizarre combinations are under development such as “PopEye pigs” that have a spinach gene which reduces the saturated fat in favor of linoleic acid. (More PUFA, what a bad idea!)

According to the same brochure, “there are eight GM food crops: corn, soy, canola (oil), cottonseed (oil), sugar from sugar beets, Hawaiian papaya, and a small amount of zucchini and yellow crookneck squash. Derivatives of these GMOs, such as vegetable oil, corn syrup, and soy lecithin, are found in more than 70% of supermarket foods. GMOs are also fed to animals that provide meat, milk, and eggs.”

For me, it’s pretty easy to largely avoid GMOs, which out of a prudent amount of caution, I regard as a good thing to do. I don’t eat corn (except for a few locally-grown ears during our local growing season), soy (except for organic fermented soy sauce), canola oil (no fried foods or mayonnaise made with canola oil), no added sugars, period (either cane or beet), and no papaya. But we do, however, occasionally sauté or grill zucchini and/or yellow squash in season.

Finally, we don’t drink milk and only buy organic, heavy whipping cream for use in our coffee. All our eggs are bought at a farmers’ market where I can see for myself that the hens are pasture-raised. In fact, they mimic Joel Salatin’s Polyface Farm method of rotational pasturing. I like cheese, and there may be a problem there. I also like fatty meats, and I’m afraid GMOs are fed to some of the meats we buy, especially beef and chicken. I’m not worried about veal, though, because I buy it from a local farmer I know, or lamb, since it is produced in New Zealand and is likely grass fed/finished. Pork I’m not sure about, and all our fish is wild caught.

But, the Institute for Responsible Technology warns us that “processed foods often have hidden GM sources (unless they are organic or declared non-GMO).” The brochure contains a list of about 100 such ingredients. Their advice: “To avoid GMOs, you can avoid brands with the at-risk ingredients, purchase organic products, or look for non-GMO labels, especially the third party Non-GMO Product Verified seal. To make it easier,” they say, “go to or download the free iPhone app ShopNoGMO, for a list of thousands of verified non-GMO products.” Here are some “tips” from the Institute for Responsible Technology brochure:

·         If a non-organic product made in North America lists “sugar” as an ingredient (and NOT pure cane sugar), then it is almost certainly a combination of sugar from both cane and GM sugar beets.

·         The sweetener aspartame (also known as NutraSweet and Equal) is derived from genetically engineered organisms. Numerous studies and thousands of consumer complaints link it with disorders ranging from seizures to tumors.

·         GMOs are in infant formulas. Independent laboratory tests found significant amounts of genetically engineered soy in four popular soy-based infant formulas: Similac Soy, Enfamil Prosobee, Walmart Soy, and Gerber Good Start Soy.

·         In addition, these brands almost certainly contain derivatives from GM corn and milk from cows treated with GM bovine growth hormone. The government’s WIC program, which distributes free infant formula to more than 2 million moms in all 50 states, only offers GMO brands.

“Note: The only commercial non-GMO infant formulas that we have identified thus far are the organic brands.”

“The general public has the false impression that genetic engineering is precise. In truth, it’s sub-microscopic shooting from the hip, resulting in unpredictable  and potentially dangerous changes in the organisms’ DNA and the health properties of food,” according to Robin Bernhoft, MD, Surgeon, and former president of the AAEM.
Given that the diet/heart hypothesis was a giant epidemiological experiment on the entire US population, and the evidence today that it was a giant mistake, I think a cautious approach to GMOs is justified. Eat real food!

Saturday, November 30, 2013

The Nutrition Debate #165: Obesity is Not the Problem

Robert Lustig’s UCTV YouTube video sensation, “Sugar, the Bitter Truth,” has been seen almost 4 million times. Recently, the UCSF pediatric endocrinologist made a sequel, “Fat Chance: Fructose 2.0,” that will also go viral. It’s 86 minutes long, so you’ll need to set aside a block of time to watch it, but it’s worth it. Here’s a 45 second excerpt I transcribed (starting at +/-12:00) that fits in with a theme I’ve been beating the drum about since The Nutrition Debate #9, “The Metabolic Syndrome,” published almost 3 years ago.

Lustig: “Obesity is not the problem. It never was. They want you to think it’s the problem, but it ain’t the problem. What is the problem? Metabolic Syndrome is the problem. The cluster of diseases that I’ve described to you. That’s where all the money goes. Obesity costs almost nothing. Metabolic Syndrome is 75% of all health care costs today. And there’s the list right there. [Slide lists: DIABETES, HYPERTENSION, LIPID ABNORMALITIES, CARDIOVASCULAR DISEASE, NON-ALCOHOLIC FATTY LIVER DISEASE, POLYCYSTIC OVARIAN DISEASE, CANCER, DEMENTIA] Everybody with me now? Do I have your attention?”

A brief recap – What is Metabolic Syndrome”? And how is it diagnosed? Definitions vary but most have five “risk factors” in common, with the first always being obesity. It is variously defined as “central obesity,” or what I have coined “omental adiposity”, or a Body Mass Index (BMI) ≥30, or elevated waist circumference (men ≥40 inches, women ≥35 inches). The other four “risk factors” are elevated triglycerides (≥150mg/dl), reduced HDL, the “good” cholesterol (men ≤40mg/dl, women ≤50mg/dl), elevated blood pressure (≥130/85mm Hg, or use of medications for hypertension) and elevated fasting glucose (≥100 mg/dl, or use of medications for hyperglycemia). If you “present” with 4 out of 5, you have Metabolic Syndrome. Do I have your attention?

The corollary to “obesity is not the problem” is equally riveting: “everyone’s at risk,” as Lustig explains: “Everyone’s at risk, because everyone is exposed.” That, of course, begs the question: exposed to what?

Dr. Lustig precedes his “obesity is not the problem” mantra with a nice explanation of the implications of the difference between subcutaneous fat (fat near the surface of the skin) and visceral fat (fat around the abdominal organs).The latter is the “bad” type of obesity. He starts with a diagram showing 30% obese and 70% “normal” weight, “and everybody assumes that the problem is this group over here [the 30% obese] because 80% of the obese population is sick in some fashion: type 2 diabetes problems, lipid problems, hypertension, cardiovascular disease, cancer, dementia, non-alcoholic fatty liver disease, polycystic ovarian disease, etc.”

“But,” he continues, “you do the math on this, 80% of 30% [of the 240 million adult population] is 57 million, and it is those 57 million that are bankrupting the country, so it’s the obese person’s fault only, and that’s the way everyone views this. This is wrong. This is a mistake. This is a disaster, actually, ‘cause it’s not correct. Here’s the real story. In fact, 20% of the obese population is completely metabolically normal. They have normal insulin dynamics. They don’t get sick. They live a completely normal life, die at a completely normal age, cost the taxpayer nothing. They’re just fat.”

“Conversely, up to 40% of the “normal” weight population has the exact same metabolic dysfunction that the obese do. They’re just normal weight, and so they don’t even know they’re sick until it’s too late; because normal weight people get type 2 diabetes, they get hypertension, they get dyslipidemia, they get cardiovascular disease, they get cancer, they get dementia, etc. etc. And so, when you do the math on that, that’s another 67 million, and so that’s actually outclassing the 57 million obese, and so the total is 124 million; that’s more than half [the adult population] of America.”

So, that’s why Dr. Lustig says, “Everyone’s at risk, because everyone is exposed.” Exposed to what, you ask? Metabolic Syndrome! And how do you treat Metabolic Syndrome? Answer: you “treat” the risk factors: 1) central obesity, 2) elevated triglycerides, 3) reduced HDL, 4) elevated blood pressure, and 5) elevated fasting glucose. And what treatment, pray tell, addresses all five risk factors for Metabolic Syndrome? In case you haven’t figured it out yet, the answer is a Low Carbohydrate Way of Eating. No pills, no injections, no surgery. Just a different way of eating.

Okay, you say, I can see how a low-carb Way of Eating can help me lose weight and control my blood glucose. And I can see that as I lose weight (as almost everyone wants to do anyway), how my blood pressure will go down. (Mine did, from 130/90 to 110/70 on the same meds.) And maybe I can believe that by eating low-carb, I can lose weight without hunger and without snacks, and even keep the weight off, so long as I continue to eat low-carb. But how can I expect that eating low-carb will cause my elevated triglycerides to go down and my HDL to go up? Well, mine did, dramatically: My HDL doubled from 39 to 81, and my triglycerides dropped by about two-thirds, from 137 to 49, just by eating very low carb. Scientifically, an n = 1 means nothing, unless that n = 1 is you!

PS: Here’s another interesting n = 1 on Low Carb Lowers Triglycerides from Dr. Art Ayers’s blog.

Wednesday, November 27, 2013

The Nutrition Debate #164: The Best Snack?

As a long time (27 year) type 2 diabetic who has pretty much controlled the disease (and gotten off 3 classes of oral diabetes meds) by diet alone for the last 11 years, I have long argued that snacks are unnecessary. If you haven’t eaten a Very Low Carb (VLC) breakfast and a no-carb lunch every day, as I do, you may doubt this. You may even say it is not credible. But as incredible as it sounds, it is absolutely true. You have to try this VLC Way of Eating (WOE) to discover this for yourself. You will not be hungry between meals.

I admit to snacking sometimes, either before dinner (radishes or celery usually, sometimes with salt and a little butter or a little whipped cream cheese, respectively), and occasionally after dinner (a controlled portion of nuts). Why? Not because of physical hunger or any other known nutritional need. I describe it as nervous eating, and I always ask myself if I am hungry before I do it, and I always answer “no;” then, I do it anyway. Go figure!

So, when I saw a link to David Mendoza’s column in the Low Carb Diet News titled, “The Best Snack for Weight Loss and Diabetes, I was interested. Mendoza is a well-respected and well read blogger (well-read in both senses) who describes himself as a “freelance medical writer, advocate, and consultant specializing in diabetes.” He has been a type 2 diabetic since 1994 and he started writing about it online in 1995. So, David Mendoza has credibility.

But after I read through his piece about the “best snack,” I felt his credibility was somewhat tarnished, as I’ll explain shortly. First, I want to point out some of the good stuff. Early on in his blog piece he emphasizes this:

“Unlike some other tasty nuts like cashews, almonds are much lower in carbohydrates, which are the part of our diet that is almost solely responsible for raising our blood sugar level. Nothing else in our diet is more important for managing our diabetes than keeping that level in check.”

His point about cashews and carbs is good. Cashews and pistachios (drats; I love them.) are both too high in carbs to be considered as part of a healthy diet for type 2 diabetics. I address this in my column about nuts.

“Some other nuts have a somewhat more favorable ratio of those super-healthy monounsaturated to polyunsaturated fats than almonds. But I avoid them as a matter of taste. I can eat macadamia nuts nonstop until the container is empty, but my body gets so full that I can easily put on a few pounds. On the other hand, I don’t particularly appreciate the taste of other healthy nuts like pecans or walnuts.”

I certainly agree with his point about macadamia nuts. They’re also very expensive. (Does anybody know a source for buying macadamia nuts wholesale?) However, as I mention in my column, for me the only basis for selecting which type of nuts to eat (besides carbs) is their Omega 6 content. In that respect, I disagree with Mendoza. Pecans are marginal at best and walnuts are totally verboten. The very best, excluding again cashews and pistachios because of the carbs, are macadamia nuts, hazelnuts (filberts), and then almonds.

Now, to the problem: It turns out “the best snack for weight loss and diabetes” is almonds. And although Mendoza expresses a personal preference for raw almonds (which he keeps in the freezer to give them a little “crunch”), the study he cites is with roasted and salted almonds. The study, however, as Mendoza points out, seems to have a fatal flaw: it was funded by the Almond Board of California. Oh dear…

“A few days ago the European Journal of Clinical Nutrition published the study online in advance of printing it. The abstract of “Appetitive, dietary and health effects of almonds consumed with meals or as snacks: a randomized, controlled trial,” is available at the journal’s website.”

In the positive, Mendoza says, “A big strength of this study by Purdue University and Australian researchers is that it was randomized and controlled. This is a good sized study conducted with the standard controls.”

In the negative, Mendoza states that he sees 3 problems with the study: 1) he cites the funding source, “…although they [the authors] also report that they have no conflicts of interest;” 2) “… we still don’t know why the study participants who snacked on almonds didn’t gain weight.” (For an explanation, check this out); and 3) “…this was also a short study that couldn’t measure the long-term impact of snacking on almonds.”

These are all good points. I’m only disappointed that I had to read to the end to learn that the almond study’s authors, and David Mendoza’s recommendation, were flawed by the study’s inherent conflict of interest. Almonds could be my favorite snack too, but bear in mind that the study’s snack size, 1½ ounces (20 almonds) is 250 calories! That’s half a dinner-time meal (for me). How can anyone hope to lose weight eating a 250 calorie snack on a regular basis?

Saturday, November 23, 2013

The Nutrition Debate #163: So You Think You’re Just Pre-Diabetic?

The lede in a recent piece on USAToday sets the stage: “Higher blood sugar levels, even those well short of diabetes, seem to raise the risk of developing dementia, a major new study finds. Researchers say it suggests a novel way to try to prevent Alzheimer’s disease -- by keeping glucose at a healthy level.” The article was based on a study at the University of Washington, Seattle, and was published in the New England Journal of Medicine.

A piece by Megan Brooks in MedScape Medical News quotes the study’s lead author, Dr. Paul Crane, as saying, “We considered blood glucose levels far into the normal (nondiabetic) range, and even there found an association between higher glucose levels and dementia risk.” “He said the results suggest that the ‘clinical determination of diabetes/not diabetes may miss important associations still there for people who are categorized as not having diabetes’.”

The Associated Press story on the USAToday piece was written by Marilynn Marchione. She quotes Dallas Anderson, a scientist at the National Institute on Aging, the federal agency that paid for the study: “It’s a nice clean pattern -- risk rises as blood sugar does.” According to Marchione, Anderson said, “This is part of a larger picture” and adds evidence that exercising and controlling blood pressure, blood sugar and cholesterol are a viable way to delay or prevent dementia.

Marchione then also quotes Dr. Crane, “At least for diabetics, the results suggest that good blood-sugar control is important for cognition.” And, for those without diabetes, he said, “it may be that with the brain, every additional bit of blood sugar that you have is associated with higher risk. It changes how we think about thresholds, how we think about what is normal, what is abnormal.”

Charles Bankhead of The Gupta Guide at MedPageToday commented, “Nondiabetic patients who developed dementia had a mean blood glucose level of 115mg/dl in the preceding 5 years compared with 100mg/dl in similar patients who did not have dementia. According to Dr. Crane, “the higher levels were associated with almost a 20% [18% actually] increase in the hazard for dementia.”

This piece by Paula Span in The New York Times has another quote from Dr. Crane: “We found a steadily increasing risk associated with ever-higher blood glucose levels, even in people who didn’t have diabetes. There’s not threshold, no place where the risk doesn’t go up any further or down any further.” The association with dementia kept climbing with higher blood sugar levels and, at the other end of the spectrum, continued to decrease with lover levels. He said that this held true even at glucose levels considered normal, she said.

Another recent article from MedPageToday ties blood sugar (A1c) levels to cognitive function NOW, not to the far-off future risk of dementia. The group studied was a population of non-diabetics, aged 50 and up, with BMIs between 25 and 30. Their mean A1c was 5.8%, with a range from 4.3% to 6.5%. The researchers found that “each of the three cognition parameters evaluated was significantly associated with A1c levels…”

The article, titled “Blood Sugar Tied to Cognitive Function,” appeared in The Gupta Guide, Sanjay Gupta, MD, Editor, and was reviewed by staff of the Perlman School of Medicine at the University of Pennsylvania. The researchers “added that ‘lifestyle strategies’ to achieve strict glucose control could prevent age-related cognitive decline, even in individuals with A1c levels currently considered normal…”

So, what’s the takeaway?  What does it mean to change “how we think about thresholds, how we think about what is normal, what is abnormal”? Well, well-designed prospective controlled trials are needed to prove causation, but the association of progressively higher and lower blood glucose with cognitive function, and ultimately dementia, even at so-called “normal” and “nondiabetic” blood sugar levels is undeniably true.

What is considered “normal”? And what is “prediabetic”? From 1979 to 1997 the threshold for type 2 was two consecutive visits with a fasting blood glucose of ≥140mg/dl. In 1997, ≥126mg/dl became the threshold for diabetes. In 2010 the ADA added A1c standards, with an A1c of 6.5% for diabetes (with a “treatment goal” of 7.0%!), and an A1Cs of 5.7--6.4% regarded as “pre-diabetic”. Some physicians, notably Richard K. Bernstein, consider 5.8% to be a full-blown type 2 diabetic. Another, Dr. Ralph DeFronzo, in his Banting lecture at the 2008 ADA convention, said that “By both pathophysiological and clinical standpoints, these pre-diabetic individuals with IGT should be considered to have type 2 diabetes.”
IGT, or Impaired Glucose Tolerance, is defined as a fasting Oral Glucose Tolerance Test result of >140 at 2 hours. Statistically, you are 7-10 years away from diabetes and your heart disease risk is already rising. To test your glucose tolerance, follow the directions here: But if there are no thresholds for an increased risk of dementia, shouldn’t we all adopt “‘lifestyle strategies’ to achieve strict glucose control” and thus potentially “prevent age-related cognitive decline, even in those individuals with A1c levels currently considered normal…”?