Retrospective #105: My Low-Carb Eating – Then and Now

Two people who read my column before it is published (my wife and then my editor), have told me recently that the Very Low Carb diet that I espouse is either “too hard” or “unpalatable” and not likely to be tried, especially by “newbies” who are considering Low Carb as the way to go for a Lifestyle Change and Way of Eating.

My goal is good health outcomes: losing weight, feeling great, and three critical and related health markers: blood glucose, blood lipids and blood pressure. Through diet alone, or with minimum medications, patients can avert or delay the onset, and treat and reverse conditions like Type 2 diabetics and Pre-diabetics, heart disease, stroke, many cancers, and even cognitive impairment. Similar outcomes are seen by many people who follow this Lifestyle.

Improvements in the way you feel will manifest quickly when you switch from being a sugar burner to a fat burner. You will see it in the loss of hunger, in feeling full of energy instead of sleepy, in your elevated mood, and in the lab reports that your doctor will see. Your doctor should also be aware of the reductions in all-cause mortality and the co-morbidities of all these diseases of Western civilization that are now widely reported in the scientific literature. 

Whether they know how you did it or not, your doctor will be very happy for you. They won’t have to cajole or hector you to change your ways. They’ll just look at the results – the office scale, the blood pressure cuff, and your lab blood test reports and smile. Then, they will say to you, “Just keep on doing what you are doing.”

Anyway, this is all preface to “then and now.” What my “constructive critics” mean when they tell me I am being too zealous. My wife says, “Not everyone is like you,” and my editor gags at the idea of eating a can of sardines for lunch every day. Okay, I get it. But I didn’t start off like that. I recall that when I first started eating Very Low Carb more than 17 years ago, I ate on average 50 grams of carbohydrate a day some weeks, and 1,800 or even 2,200 calories a day, and occasionally I binged. But I weighed 375 pounds, and I was transitioning from a lifestyle of indulgence to a more disciplined Way of Eating. But I still lost weight – about 2 pounds a week, in toto 170 pounds.

The amazing thing is that within a day or two of starting on strict Atkins Induction (20 grams of carbs a day), I was getting “hypos” every day, and I just had to eat a candy bar (LOL). I called the doctor, and he first told me to stop taking one of three oral meds. Then, the next day when the hypos continued, he ordered me to cut the other two oral meds in half and then soon thereafter to cut them in half again. A few years later, when I switched to Bernstein (30 grams of carbs a day), I was able to drop one of the other two., continuing with just Metformin. From the beginning of eating Very Low Carb, my blood sugars came into control (which they were not even on all three oral meds), and my A1c dropped into the “non-diabetic” range, where it has remained now for 17 years.

So, the message is: You don’t have to be a fanatic to make this Way of Eating work for you. In my opinion, it’s best if you go “all in” because you get the benefit of not being hungry. That’s because you will transition from getting your energy from food to getting your energy from your body fat stores. But start out wherever you can – say at 100 grams a day until you get used to it, or maybe even 20 grams of carbohydrates a meal.

Remember, the Recommended Daily Allowance (RDA) on the Nutrition Facts panel on processed (boxed and bagged) foods is 300 grams of carbohydrate a day for women. That’s 60% of your daily food intake on a 2,000 calorie a day diet, and most people actually do eat between 55% and 60% of their calories from carbohydrates.

Reducing that by two-thirds to 100g/day is a big step in itself. Then, after your body (and your conscious you) has acclimated, if you still haven’t met your blood glucose or weight loss goals, cut them again to say 20 grams of carbs/meal. Eventually, you may get to where I and my body am/are happily now: +/- 15 grams of carbs a day.

Retrospective #104: It’s Not Feckless to Be Fickle

I have mused a few times about how most doctors and dietitians, especially established practitioners, are in a bind. The younger ones can still have an epiphany without ruining their practices. It must be a rude awakening when they do, but they can do it with integrity if they are truth seekers. The older ones, as I see it, have three problems:

1) The mantra when they were schooled in medicine (doctors) and nutrition (dietitians) – never to be cross-fertilized – was the coda of the day: the diet-heart hypothesis (the saturated fat/cholesterol/heart disease hypothesis) from the now widely discredited work of Ancel Keyes. When he joined the Board of the American Heart Association in 1961,, and made the cover of Time Magazine, the “die was cast.” Everybody read Time in those days. Now, it’s just a pamphlet! But the medium spread the message. To this day, the health establishment trumpets it.

2) The specialties in medicine are governed by medical associations that set “Standards of Practice” that are in turn adopted by Medicare and then by private insurance companies. In some ways it makes medical care simpler, quicker and certainly less risky. The older clinician gives you and the standard exam, the standard reimbursable tests using the standard medical codes, for which he gets paid, and the standard treatment: a script for pill(s) and advice to lose weight (“eat a balanced diet”) and “move more” (exercise). Then, you’re outta there. Next patient!

3) The problem is, how can a doctor deviate from this? Will he get paid for that non-standard test? How can a doctor change when he has an open mind and sees something that works after so many years of the exact opposite? Admit that what he has been prescribing for many years, doesn’t work that well? That what he has been telling you all these years is wrong? That it is exactly backwards? That the diet-heart hypothesis was not evidence-based, just bad science? Many doctors and scientists have said so, but what will the patient think if his doctor, his trusted personal health advisor, does a complete about face? How can I still be confident? Is he a quack?

Many doctors and nutrition scientists are saying this now, but to be fair, not for the same indications. My doctor, who was a board-certified internist and cardiologist, suggested that I try Atkins Induction – off label, as it were – to lose weight. He had just read Gary Taubes’s July 2002 New York Times Sunday Magazine cover story, “What If It’s All Been a Big Fat Lie.” He had tried it himself, had lost 17 pounds in a little over a month (with no ill effects on his cholesterol panel), and suggested I try it. Ever cautious, though, he did monitor me monthly for a year.

Anyway, most doctors would have a hard time doing what my doctor did, even if they believed in it. But you, their patient, are not in the bind that they are in. You can be “fickle without being feckless.” You’ve got nothing but your improved health at stake (LOL). Not that that’s inconsequential. You, the patient, can change what you eat.

Okay, you don’t have to do “the full Monty” to start with, or ever, for that matter. You could start with just a low carb, moderate protein and high fat diet. That’s still a very big improvement over the way you are probably eating now. The Recommended Daily Allowance (RDA) of the Standard American Diet (SAD), the one on the Nutrition Fact Panel on packaged (boxed and bagged) foods is 60% carbohydrate, 10% protein and 30% fat. You could do 40% carb, 30% fat and 30% protein. That would be a reduction from 300 grams of carbs to 200. Or, you could work your way down to 20% carbs (100 grams of carbs/day on a 2,000kcal/day diet).

Then, after you adjust (and lose weight and lower your triglycerides and raise your HDL), you could try 20 grams per meal, with no snacks (you won’t have any cravings – in fact, you won’t even be hungry). Or, you could do Bernstein (6-12-12 = 30/day), or Atkins Induction (20g/day) or my current Way of Eating. I do 15g of carbs/day. I now eat 5 grams of carbs at breakfast, zero at lunch, and 10 at supper, unless I have a glass or two of wine, which I often do now. That bumps me up to between 25 and 30 grams of carbohydrate a day. And I’m still ketogenic.

The point is: You are not constrained by your profession. You will not be feckless if you change the way you eat. You can be fickle. You can try eating lower carb, or low carb, or very low carb the way I do. It’s okay to do what works for you. It’s your health. It’s your life. And now, it’s your time to decide.

Retrospective #103: Your Mileage May Vary (YMMV)

Your Mileage May Vary (YMMV) is an expression that I didn’t put much stock in when I first read it years ago on a Low Carb Forum. I was a neophyte in the self-management of my Type 2 diabetes, even though I had been a Type 2 for 16 years. Up until then, like most of us, I had left my health care in the hands of my physician. So, in those early days of self-management – if I thought about it at all, I thought that we Type 2s were all pretty much alike.

What prompted me to write about this [in 2013] was a personal experience I had with my blood sugar (BS) control. My most recent A1c was 5.6%. It’s been better and, of course, worse. I had been eating a restricted-calorie, Very Low Carb (+/-15g) ketogenic diet for several months to lose weight and had lost 25 pounds. Five consecutive daily fasting blood glucose readings averaged 90mg/dl, with a tight range. Then, at a small dinner party in our home, I ‘blinked’ (transgressed): I had about a cup of risotto (with Osso Bucco and broccoli rabe) and some dessert (2 homemade cookies and 2 bouillon-cube sized petit fours). My body hadn’t had this much starch and sugar in a long time, and it was not prepared for it. My fasting blood glucose the next morning was 120mg/dl. The next day my FBS was still 117. The next day 114, the next 123, and so on. I had fallen off the ketogenic cliff and had lost BS control.

That’s where YMMV comes in. It depends on your medical history (both the type and degree of metabolic dysfunction and when and how you and/or your doctor responded to the discovery that you were Pre-diabetic or a diagnosed Type 2. I was diagnosed in 1986. The first thing my doctor did, besides advising me to lose weight (“eat less on a ‘healthy’ balanced diet”), was to prescribe a sulfonylurea (SU), a class of oral anti-diabetes medication that makes the pancreas produce more insulin. At the time, sulfonylureas were the only oral anti-diabetes medication prescribed in the U. S. When I continued to eat carbohydrates, and the SU didn’t get my BS under control, my dose was increased until I was ‘maxed-out’ on this med. Then, when Metformin was approved for use in the U. S., I started on and eventually was maxed out on it too and started on a 3^rd oral med. On a “balanced” diet, however, my blood sugar continued to elude control, and my Type 2 diabetes inexorably progressed.

My Type 2 diabetes didn’t stop its progression until I changed my diet. In fact, it reversed to the point of being undetectable as long as I “eat right” (VLC). After starting to eat Very Low Carb (VLC), in the first week I forced to take fewer and fewer oral anti-diabetic meds. Still, it was almost five years before I completely titrated off the SU, so I took an SU at some dosage level for 21 years. So, I wondered, what effect did this have on my pancreas?

Well, I’m not a doctor, so I’ll refer instead to what one of my favorite diabetes specialists, Ralph A. DeFronzo, M.D., has been saying for years. In his Banting-award lecture at the 2008 Annual Meeting of the American Diabetes Association in San Francisco, Dr. DeFronzo said, “By the time that the diagnosis of Diabetes is made, the patient has lost over 80% of his/her β-cell function.” He also said in the first paragraph of the full-text article published by the ADA on the NIH website, “Sulfonylureas are not recommended because, after an initial improvement in glycemic control, they are associated with a progressive rise in A1c and a progressive loss of β-cell function.”

So, where does this leave me? If I had lost over 80% of my β-cells upon being diagnosed, and continued eating a “balanced” diet (with lots of carbs) for another 16 years, my pancreas still needed to make insulin with fewer β-cells. The SU continued to push it to do that because the goal was to control my blood sugar with medications.

So, a disease that starts with insulin resistance progresses to pancreatic β-cell burnout as it responds to that resistance. That is inexorable if you don’t dramatically change your diet. It will likely accelerate if you continue to use a sulfonylurea to get your pancreas to pump insulin. That is the “course of action” of the disease. That course will be inexorable if 1) you don’t change your diet and 2) you don’t stop taking a sulfonylurea. You must do both to protect and preserve what pancreatic β-cell function you have left before it’s too late. If you choose to do both 1) and 2) when you are at an early stage of this disease, YMMV from mine. If you don’t, like me, you may become totally carbohydrate intolerant. And like me, you will not be able to “cheat” from time to time and get away with it.

Retrospective #102: Denial is not a river in Egypt

While floating down a “lazy river” at a resort in Puerta Vallarta, Mexico, I began a conversation with another “floater.” I turned the conversation to my interest in nutrition for Type 2 diabetics and told my new “friend” what I had accomplished a few years before by eating Very Low Carb. I followed Atkins induction (20g of carbs a day) for 9 months and lost 60 pounds. I then described how I had drifted away from VLC for a number of years. It turns out my “friend” was one of those enlightened physicians (a Canadian) who then bluntly exclaimed, “You’re in denial!”

He was right, of course. It’s easy to delude oneself. We do it all the time, every day, in many ways. It’s called rationalization, a process of reasoning, or suspension of reason, that allows us to do something that we know is a “bad” option. It’s a lack of self-awareness. The process is invidious. It sneaks up on us.  It happens in unexpected or unplanned circumstances. That is, unless we are practiced in dealing with it and have made a total commitment.

That passing acquaintance had a lasting impact on my life. After returning home, I returned to my previous VLC Way of Eating and lost another 100 pounds. I was also able to completely eliminate the remaining 5mg of Micronase, a sulfonylurea drug that I was then still taking. And my blood pressure dropped further to 110/70 (on the same meds. I was still taking a minimum dose (500mg once a day) of Metformin. Metformin has since become the first line of defense in the U.S. (after “lifestyle modifications”) for Pre-diabetics and diagnosed Type 2s.

Sulfonylurea drugs accelerate the destruction of pancreatic beta cells. That’s why they have, in some places, fallen into disfavor. They deplete the pancreas’s secretionary power and are one of the reasons why Type 2 diabetes is described in the medical lexicon as a “progressive disease.” It’s the medical treatment that (in part) drives the progressivity. Of course, the other equally egregious reason is that the medical establishment still advocates a “balanced diet,” instead of restricting carbs, to cope with a disease that is defined by carbohydrate intolerance.

The sulfonylurea drugs are harmful because they force an already seriously compromised pancreas to secrete more insulin to deal with elevated blood glucose from the carbs we eat. Dr. Ralph A. DeFronzo, winner of the ADA’s 2008 Banting Medal for Scientific Achievement, stated that “beta cell failure begins earlier and is more severe than previously thought.” Based on this finding, he argues for “the need for early and aggressive treatment to preserve remaining beta cell function and to limit further disease progression.”

Dr. DeFronzo’s very technical paper, later published by the ADA, is available for free with full text and figures on PubMed. Early in it, under the sub-heading “Prediabetes”, Dr. DeFronzo said, “In summary, individuals with IGT [impaired glucose tolerance] are maximally or near- maximally insulin resistant, they have lost 80% of their β-cell function, and they have an approximate 10% incidence of diabetic retinopathy. By both pathophysiological and clinical standpoints, these pre-diabetic individuals with IGT should be considered to have type 2 diabetes.”

Denial is a touchy subject. It is touchy because it is very personal. Addressing it requires the ability to look at oneself in an objective way. That confrontation can be pretty messy if our lives are complicated. We all have family and friends who care about us but who do not know about the advances in understanding the optimal way to treat people whose damaged metabolisms cannot tolerate dietary carbohydrates. To the extent practicable, the optimal way is to not eat carbohydrates. That course of treatment works for everybody who has insulin resistance, is Pre-diabetic, or has been diagnosed with Type 2 diabetes. It is also a great way for anybody to lose weight. Take an honest look at your own life, and ask yourself if you are in denial. Then, ask yourself, are you ready to change, now?

Denial is not a river in Egypt. This blunt pronouncement may be said by a close friend/counselor, or even an enlightened physician, to not so gently make a point about the need to confront a matter. In fact, it could be said to affect a change that may be life altering. It was that way for me once. I remember it well.

Retrospective #101: Why I’m Never Hungry

I have had a raised consciousness about food and feeding since I began writing this blog. And one of the things I have observed is when I feel hungry. Of course, hunger is not an emotion; it is a physiological signal that has been sent and received that motivates us to eat. The signal travels from our stomach, where the hormone ghrelin senses it is empty, via the vegus nerve to the hypothalamus in the center of the brain. That is the central place where hunger signals are interpreted and controlled. It’s from there that the signal is sent. And we act. We eat.

The “empty stomach” message works well whether you have a normal glucose metabolism or a disregulated glucose metabolism like so many of us have developed. It has become disregulated because, as recommended by our government, for most of our lifetime we have eaten the Standard American Diet (SAD, ironically). According to the Nutrition Facts Panel on boxes and bags of food products, that diet is 60% carbohydrate, 10% protein and 30% fat. That’s 300g (1,200kcal) of carbohydrate, 50g (200kcal) of protein, and 66.6g (600kcal) of fat. Total: 2,000kcal.

It’s 60% carbohydrate in part because the government wants us to reduce the fat in our diet. So, what are you supposed to do? Your only choices are to increase carbs or protein. And if you eschew animal products, to avoid saturated fat and cholesterol, as Big Brother would have you do, what can you eat? More carbs, of course.

To feed the disregulated metabolism our contemporary lifestyle offers us lots of packaged, pre-processed, and easily digested “food” to choose from, most of which are carbs. We eat them, we digest them quickly, we get quick energy, and then as they quickly empty from the stomach, we get the “hungry again” signal. That’s why carb eaters and especially carb addicts are always hungry. That’s why many diets recommend between meal snacks, or even 5 or 6 “small meals” a day. If you have done these diets, you know it is because you are hungry. Now you know why.

So, why am I not hungry? I eat a restricted calorie diet that is very low carb. Most of the time I think I am in a mild state of ketosis. That allows my body to burn fat instead of “sugar” (glucose) for energy. Stored energy, my body fat, is my targeted fuel source. That’s why I need to eat a restricted carb and a restricted calorie diet. I need to be in negative calorie balance to lose weight. I am doing this without hunger and – take note – without exercise.

I am not hungry at breakfast because, allowing a few hours for digestion, my body has been in a mild ketogenic state for maybe 10 of the 14 hours since I last had a meal or anything to eat. That means I didn’t eat a bed-time snack. When I am in ketosis, my body is happily burning fat for energy. It doesn’t need ‘sugar’ (glucose) for fuel, so it doesn’t send a hunger signal to the brain. This is a natural state, called ketosis.

But, if I eat a breakfast anyway, I eat a small ketogenic meal: fried eggs, bacon and a cup of coffee with full cream and stevia powder. After that small meal I can easily go ‘till late in the day without hunger because I am still in ketosis. But again, mostly for cultural reasons, for lunch I eat a very small meal of zero carbs: just protein and fat, usually a can of sardines in water (with added salt), or a can of kippered herring, and iced tea –and I stay in ketosis.

Then, an hour or so before supper, I sometimes sit down to watch the news and snack on radishes with salt and a “schmeer” of ghee or butter. At other times, I’ll snack on celery and anchovy paste. The idea is to eat just a little fat to satiate, or bulk to distend the stomach, to short circuit a tendency to eat too much supper.

I always used to eat too much at the evening meal. Again, I think it was a cultural thing. For most Americans, dinner is the big meal of the day, and cultural habits require a conscious effort to break. Dinner has always been a big problem for me. My wife put too much on my plate (Sorry, Honey), and I always ate it all. (I can’t blame her for that!) We learned as kids not to leave food on the plate. (Blame it on our parents instead.) Now, with my wife’s help (Thanks, Honey!) I am eating a small supper, and I am passing up 2nds (even with really “palatable” food, as it always is). We have a vast choice of menu options: fatty meats, poultry, and seafood (fin fish and crustaceans), plus a low-carb vegetable roasted in olive oil or finished with lots of butter. In other words, another small ketogenic meal. This makes losing weight easy. I’m burning body fat for energy balance. And that’s why I’m never hungry. 

Retrospective #100: Liquid Calories

What’s wrong with taking nourishment in liquid form? It’s certainly convenient, and if you make your own “smoothie” or some nutrient-dense concoction in a juicer or blender, you are assured of a “healthy” beverage of your own composition and making, right? Well, “yes” up to a point, but “no” for a host of other, very good reasons.

1)  The calories we drink go quickly “down the hatch” No chewing required. Chewing is the first mechanical step in digestion. It takes energy and time to chew. It also takes time for needed enzymes in the mouth, stomach and small intestine to process chewed solid food into chyme to break it down to where it can be absorbed. If food has already been liquefied, these physiological functions are “side-stepped,” and calories are absorbed more quickly and easily. The order of gastric (stomach) emptying is: liquids first, then carbs, then protein, and then fat and fiber.

 2) “The mechanisms controlling hunger and thirst are completely different,” wrote food writer and nutritionist Katherine Tallmadge in a December 2004 Washington Post article. “Physiologically, your thirst is quenched once your blood and cell volume are increased by water. This sends signals to your brain that you are no longer thirsty. In contrast, hunger is regulated in your stomach and intestines. The hormone Ghrelin secreted in the stomach wall helps you feel full.” Ghrelin doesn’t work as well with liquids as it does with solid foods. “Our bodies don’t detect the calories in these liquid foods the same way as when we eat solid foods,” Tallmadge said.

3)  Liquid calories add up in a way that can be surprising. The liquid calories in smoothies, juice drinks, sodas and even specialty coffees are stealthy. “A White Chocolate Mocha totals 410 calories (whole milk, no whip) or 510 calories with whip. In my world, 510 calories is an entire meal,” says Elaine Magee on WebMD. Tallmadge, in her Washington Post article, concurs: “When you consider that an appropriately sized meal is anywhere from 400 to 700 calories, and one 44-ounce Super Big Gulp is 800 calories, you understand the scope of the problem. A 16-ounce Starbucks blended coffee Frappuccino is 470 calories. A single mixed drink can set you back 300 calories. One glass of wine contains at least 100 calories. “Most caloric drinks consumed before or during a meal are not satiating and have little effect on how much you eat in one sitting or over the course of several meals.”

The good news, Tallmadge notes, is that “since liquid calories don’t contribute to feelings of satiety, cutting back on them doesn’t make people feel deprived; most find the change is an easy one to make.” So, what changes should be considered? The Harvard School of Public Health pondered this question and put together a Beverage Guidance Panel. From the March 2006 issue of the American Journal of Clinical Nutrition, here are their recommendations:

1) Water: Quelle surprise! But pure H₂O does provide “everything the body needs – to restore fluids lost through metabolism, breathing, sweating, and the removal of waste. It’s the perfect beverage for quenching thirst and rehydrating your system” according to the group. We could end this list here! We used to, come to think of it.

2) Tea and Coffee: “Drunk plain, they are calorie-free beverages brimming with antioxidants, flavonoids, and other biologically active substances that may be food for health.” They especially like the strong green tea varieties served in Japan. However, adding cream, sugar, whipped cream and flavorings make it “closer to a dessert.”

3) Low-fat and skim milk and soy beverages: Here’s where the Harvard School of Public Health/Beverage Guidance Panel and I part company. I avoid the carbs in milk and only take heavy cream. I do not avoid saturated fat, and I do avoid soy products altogether: e.g., soy bean oil, soy milk. But I do use naturally fermented soy sauce.

4) Noncalorically Sweetened Beverages: This category includes the “so-called diet sodas and other diet drinks that are sweetened with calorie-free artificial sweeteners. They include stevia in this category, and liquid sugar alcohols.

5) Caloric Beverages with Some Nutrients: This group includes “fruit juice, whole milk (!), sports drinks, vitamin-enhanced waters, and alcoholic beverages (?). This category includes 100% fruit juice, aka a “liquid candy bar.”

6) Calorically Sweetened Beverages: These “least recommended” include drinks sweetened with sugar or high-fructose corn syrup (HFCS). It also includes noncarbonated soft drinks, fruit drinks, lemonade, etc. They’re all just sugar water.

Type 2 Nutrition #487: Fat Cat, Skinny Cat

We have two house cats; one is fat and one is skinny. They were both born to feral moms about 4 years ago, one behind a pizza parlor and the other in a backyard. A non-profit trapped the moms as part of their TNR (Trap/Neuter/Return) program. The moms were spayed, treated and released. The offspring were also trapped or rounded up. We fostered the last one from each litter and eventually adopted both.

The backyard cat is a big, lanky, lean male. His pizza-parlor “sister” is smaller boned and very fat. They both eat the same food: supermarket “Fancy Feast” in 3oz (70kcal) cans, twice a day, plus Purina “complete” Cat Chow, ad libitum.  The Fancy Feast is 11% protein, 2.0% fat, and 21.5% carbs (dry matter basis, calculated). The higher nutrition Cat Chow is 32% protein, 13% fat and 42% carbs (dry matter basis, calculated).

Both house cats seem to like both foods equally. They clean their dishes and put a big dent in the chow bowl daily. They also snack at an outdoor station where we feed our own small feral colony. That’s how we originally got involved with the local TNR non-profit. A litter of 4 adolescent ferals walked into our backyard about 14 years ago. They were way too old to socialize, so we fed and eventually trapped and TNR’d them all.

The food we give the ferals is the same Cat Chow (32% pro; 13% fat; 42% carbs), plus 2-13.5oz cans of Purina’s “Friskies.” The analysis of these 366kcal cans is again 11% protein, but 2.5% fat, and 27% carbs (dry matter basis). The ferals (and our house cats) also like these offerings equally, scarfing both down twice a day. Both the house cats and the ferals “know” each other and frequently eat side by side at the outdoor stations.

(As an aside, one of the ferals occasionally comes into the house, through a door left open in warm weather, and crosses to the kitchen to eat at the house cats’ station. But never, in the 14 years that we have faithfully fed them all, have any of the ferals ever allowed either of us to touch any of them, or even get close.)

All the ferals are lean. So why, given the way they are fed, is one of our house cats lean and the other fat? They both have access to all 3 types of food. Both have good appetites, and both have equal opportunities for exercise. Both run around the house and yard, frequently chasing each other or birds or butterflies. The big, lean male, is less active – more of a couch potato, but the fat female is completely undeterred by her girth.

If this were simply a comparison between two carnivores – our house cats – eating a high carbohydrate diet, one could hypothesize that the “pizza baby’s” genetic makeup was epigenetically “expressed” when she was exposed to the high-carb Fancy Feast and Friskies diet. Or, that the “pizza baby’s” mom already had those “expressed” genes (she survived by living behind the pizza parlor) and passed them on to her offspring who were thus born predisposed and are therefore likely to get fat on a high-carb diet. And our lean house cat – the “backyard baby” – was perhaps the product of a feral mom who hunted mice and voles and had a different set of genes or similar genes that had not been epigenetically expressed by what she ate. She therefore produced a large, well-shaped, lean male kitten. For further reading, see Dr. Cate Shanahan’s book, “Deep Nutrition.”

Restating the question: Why didn’t the young ferals who wandered into our backyard 14 years ago get fat on our nutritionally poor diet? Is it because they were offspring of a carnivorous mom who ate animal protein and fat and had not had her genes “expressed”? Is that why her offspring aren’t fat cats like our “pizza baby”?

We’ll never know. Our cats will never reproduce. But how about you and your offspring? We’re said to be omnivores, but I would say that humans, while not obligate carnivores, are perhaps facultative carnivores, a species that “does best on a carnivorous diet, but can survive-but-not-thrive on a non-carnivorous one.” This has been amply demonstrated, I think, by the effects that the high carbohydrate diet that we’ve been eating since the dawn of the Neolithic Age, made worse recently by the highly processed industrial foods we now eat.

Retrospective #99: “Natural History of Type 2 Diabetes”

“Natural History of Type 2 Diabetes” is a heading in a paper by Ralph A. DeFronzo, MD. Dr. DeFronzo is using the medical phrase “natural history” to describe the progression of a disease from incidence to diagnosis.

The paper was published in the American Diabetes Association’s magazine, Diabetes, after he presented the Banting award lecture at the ADA’s 2008 annual meeting in San Francisco. This paper caught my attention for a statement Dr. DeFronzo made about Pre-diabetes: “In summary, individuals with IGT [impaired glucose tolerance] are maximally or near-maximally insulin resistant, they have lost 80% of their β-cell function, and they have an approximate 10% incidence of diabetic retinopathy. By both pathophysiological and clinical standpoints, these pre-diabetic individuals with IGT should be considered to have Type 2 diabetes” (emphasis mine).

The takeaway from this is Dr. DeFronzo’s main point: We need a “new paradigm” of early intervention: “The clinical implications of these findings for the treatment of Type 2 diabetes are that the physician [my emphasis] must intervene early, at the stage of IGT [impaired glucose tolerance] or IFG [impaired fasting glucose].”

I am writing this blog primarily for patients in the hope that they will see the need to “intervene early” as well. It is so much easier to control your blood sugar if you have maximal insulin sensitivity and remaining beta cell function. 

DeFronzo begins, “Individuals destined to develop Type 2 diabetes inherit a set of genes from their parents that make their tissues resistant to insulin”  “In liver, the insulin resistance is manifested by an overproduction of glucose during the basal state despite the presence of fasting hyperinsulinemia and an impaired suppression of hepatic glucose production in response to insulin, as occurs following a meal.” (Translation: The liver overproduces glucose while we are fasting despite low blood insulin levels. That is why physicians now prescribe Metformin first to both suppress this unwanted glucose production -- called gluconeogenesis – and improve insulin sensitivity.)

“In muscle, the insulin resistance is manifest(ed) by impaired glucose uptake following ingestion of a carbohydrate meal and results in postprandial hyperglycemia.” “Both obesity and decreased physical activity are insulin resistant states and, when added to the genetic burden of insulin resistance, place a major stress on the pancreatic β-cells to augment their secretion of insulin to offset the defect in insulin action.” (Translation: insulin production increases to deal with both elevated levels of circulating glucose and our impaired insulin action due to insulin resistance.)

And here’s the crux of it: “As long as the β-cells are able to augment their secretion of insulin sufficiently to offset the insulin resistance, glucose tolerance remains normal.” (We have two faulty mechanisms at work here yet our blood glucose levels in response to both fed and fasting states are still NORMAL.) “However, with time the β-cells begin to fail and initially the postprandial plasma glucose levels and subsequently the fasting plasma glucose concentration begins to rise, leading to the onset of overt diabetes.” (Note: postprandial blood sugars rise first, then later fasting blood glucose.) That is the reason that the A1c test has replaced the fasting blood glucose test. The A1c test measures the average of all blood glucose values over a 3-month period and thus captures the elevated postprandial values in the average. Ask your doctor to do an A1c test. Medicare pays for 4 tests per year.)

“Collectively, the insulin resistance in muscle and liver and β-cell failure have been referred to as the triumvirate.” “The resultant hyperglycemia [elevated blood glucose] and poor metabolic control may cause further decline in insulin sensitivity, but it is the progressive β-cell failure that determines the rate of disease progression.”

Dr. DeFronzo’s paper then continues to describe his own research into the β-cell failure rate in detail but let this suffice: “Although the plasma insulin response to the development of insulin resistance typically is increased during the natural history of Type 2 diabetes, this does not mean that the β-cell is functioning normally. To the contrary, recent studies from our group have demonstrated that the onset of β-cell failure occurs much earlier and is more severe than previously appreciated.” That frightening statement is in plain English. I don’t think it requires any translation or interpretation on my part. We (doctors and patients) need a “new paradigm” of early intervention.

Retrospective #98: The “Dreaded Complications” of Type 2 Diabetes

With the meteoric rise in the incidence of Type 2 Diabetes and obesity (“diabesity”, a cool conjunction), and their associated public health implications, the “dreaded complications” of the pandemic should now be front-and-center in the news. They do deserve our attention. They are pretty scary, and fear is a good motivator.

Here’s a truthful note from the American Diabetes Association: “Diabetes increases your risk for many serious health problems. The good news? With the correct treatment and recommended lifestyle changes, many people with diabetes are able to prevent or delay the onset of complications.” This would actually be a gross understatement, except for their use of the word “recommended.” Their “recommended” changes won’t work.

I would say that a Type 2 who follows a Very Low Carbohydrate diet can avoid the complications altogether. However, if you do not control your blood sugar by diet or other means, the NIH’s Medline Plus site tells us: “If you have diabetes, your blood sugar levels are too high. Over time, this can cause problems with other body functions, such as your kidneys, nerves, feet, and eyes. Having diabetes can also put you at a higher risk for heart disease [and] skin problems, digestive problems, sexual dysfunction, and problems with your teeth and gums.”

The order of magnitude of the risks of complications of chronic Type 2 diabetes are described in a Wikipedia entry:  “In the developed world, diabetes is the most significant cause of adult blindness in the non-elderly and the leading cause of non-traumatic amputation in adults, and diabetic nephropathy is the main illness requiring renal dialysis in the United States” (emphases all mine). All of these complications are directly associated with Type 2 diabetes, and they are all the result of damage to the small blood vessels. These complications are all described as microvascular.

Today the main complications of chronically elevated blood glucose are macrovascular disease, which leads to cardiovascular disease (CVD). Wiki lists the following examples: Coronary artery disease (CAD), leading to angina or myocardial infarction (“heart attack”); diabetic myonecrosis (“muscle wasting”); peripheral vascular disease, which contributes to intermittent claudication (exertion-related leg and foot pain); and stroke (mainly the ischemic type).

In addition, Diabetic encephalopathy, the increased cognitive decline and risk of dementia – including Alzheimer’s disease – is observed in and associated with chronically elevated blood sugar, i. e. inadequately controlled Type 2 diabetes. These are just some of the risks, but I said I wasn’t going to scare the bejesus out of you. I guess I lied.

An abstract presented at a poster session at a 2012 ADA meeting is apt. It reported a Swedish observational study of 12,359 patients with poorly controlled Type 2 diabetes. None of the patients had any cardiovascular or coronary heart disease at baseline. The patients averaged 62 years of age with mean disease duration of 9 years. The average baseline A1c was 7.8% and their mean body mass index was 30. Their mean blood pressure was 140/78. 62% were taking antihypertensive (blood pressure) meds and 46% were on lipid-lowering (cholesterol) drugs.

After 5 years, the study’s investigators separated the patients into 2 groups: those whose A1c decreased by at least 1% over the 5 years (6,841) and those whose A1c remained stable or increased (5,518). At the study’s conclusion the mean A1c was 7% in the improved-control group (-0.8%) and 8.4% in the poorly controlled group (+0.7%). By then, 12% of the well-controlled group and 20% of the poorly controlled group had developed coronary heart disease (CHD). Cardiovascular disease (CVD) was present in 17% of those in the well-controlled group and 30% of the poorly controlled group. And all-cause mortality was 15% among the group with no improvement in A1c and 10% in the group with improved A1c. Thus, after adjusting for baseline risk factors during the study period, they concluded that “patients who had suboptimal glycemic control and reduced their A1c value by slightly less that 1% were 50% less likely to die within 5 years than were patients whose A1c did not improve.” Wow! A1c down <1%.

So, with an improvement in A1c of less than 1% (7.8 to 7.0%), there is still a 50% benefit. I wonder what the benefit would be for a 2% improvement in A1c? Would the increased risk of cardiovascular disease, coronary heart disease, and all-cause mortality be eliminated completely? That’s something you might want to think about.

Retrospective #97: Fructose in Food

Fructose is commonly thought to be “fruit sugar.” And fruit is generally thought of as a “healthy” food, since it is “natural” (although hybridized to be made sweeter). It has fiber, pectin, micronutrients and phytochemicals, all of whose mysteries we have yet to unwrap. Still, we consider them all beneficial. As a result, there is a widely held perception that since all fruit contains “natural sugars,” it is therefore okay to eat whole fruit in moderation. Besides, who can eat a dozen apples? True enough, except: watch out for apple sauce and apple juice. These two highly processed apple food products are very high in liquefied sugars and especially high in fructose. Pears too.

But fructose, the “natural fruit sugar,” is not just found in fruit. It is present naturally in many other whole foods. Fructose is 40% to 67% of the sugar in fruits, from 38% to 55% of the sugars in some vegetables, and 49% to 82% of the sugar in sweeteners, both natural and manufactured.  Fructose is 50% of the content of granulated sugar, made either from sugar cane or sugar beets. And fructose is 55% of the liquid form of high fructose corn syrup (HFCS) used to sweeten soft drinks in the U.S. HFCS is also used for a variety of other reasons in solid foods, including “mouth feel.” In a loaf of bread, it is brushed on the surface to brown it when baked and to get those whole grains to stick. The HFCS used in baked goods and many more products is a special type that is only 42% fructose.

The table below, created from USDA and Wiki sources, lists common “foods,” including fruits, vegetables and sweeteners (natural, refined and manufactured). It is sorted by total percent fructose.

Sugars in Foods	Sucrose	Free	Free	Other	Total	Total	Fructose/
as % of total sugars	50%F/50%G	Fructose	Glucose	Sugars	Fructose	Glucose	glucose ratio
agave nectar	0%	82%	18%	0	82%	18%	4.47
pear	8%	63%	29%	0	67%	33%	2.06
apple	20%	57%	23%	0	67%	33%	2.01
water melon	20%	55%	26%	0.06	64%	36%	1.81
HFCS55 (beverages)	0%	55%	41%	4%	57%	43%	1.34
sweet red pepper	0%	55%	45%	0	55%	45%	1.21
honey	1%	53%	46%	4.54	53%	47%	1.14
grapes	1%	52%	46%	0	53%	47%	1.12
pineapple	61%	21%	17%	0	52%	48%	1.09
molasses	54%	24%	22%	0	51%	49%	1.03
Granulated sugar	100%	0%	0%	0%	50%	50%	1.00
beet sugar	100%	0%	0%	0%	50%	50%	1.00
brown sugar	97%	1%	1%	1%	50%	50%	1.00
red beet	97%	1%	1%	0	50%	50%	1.00
carrot	75%	13%	13%	0	50%	50%	1.00
popcorn	69%	16%	16%	0	50%	50%	1.00
banana	20%	40%	41%	0	50%	50%	0.98
maple syrup	96%	1%	3%	0	49%	51%	0.96
dried fig	0%	48%	52%	0	48%	52%	0.92
sweet onion	14%	40%	46%	0	47%	53%	0.89
peach	58%	18%	24%	0	47%	53%	0.89
sweet potato	60%	17%	24%	0	46%	54%	0.87
HFCS42 (solid foods)	0%	42%	53%	5%	44%	56%	0.79
apricot	64%	10%	26%	0	42%	58%	0.72
plum	16%	32%	52%	0	40%	60%	0.66
sweet corn	15%	31%	55%	0	38%	62%	0.61

After agave nectar (82% fructose), pears and apples are the worst (2/3rds fructose). And natural sweeteners like honey and maple syrup are about half fructose, and they aren’t even fruit! Only corn is low, but higher in glucose.