Saturday, May 18, 2019

Retrospective #92: Why We Eat


Why do we eat?  The simple answer is: We eat because we’re hungry, but this begs the follow-up question, “Why are we hungry?” It also requires a few footnotes for the exceptions. For example, there are many occasions when we eat when we are not hungry, and other occasions when we overeat. We’ll examine the way we have come to eat the way we do: by habit, tradition and culture. Separately, I will answer the question, “Why are we hungry?”
Eating, according to Stephan Guyenet “Ancestral Nutrition and Health,” can be divided into homeostatic and non-homeostatic categories. Homeostatic eating is for hunger only, Guyenet explains, whereas non-homeostatic is all other eating, including eating for pleasure, emotion/stress, social, and ‘mealtime’ eating. I think most of us can readily relate to most of these non-homeostatic categories, if not all of them.
What characterizes these non-homeostatic categories, by definition, is that none of them is driven by hunger. If this sounds like I am repeating myself, I am. I want this point to sink in. Non-homeostatic eating is unnecessary eating.
Eating for pleasure is an indulgence, a pure luxury. Eating to relieve stress is an emotional outlet – a diversion, but it is not driven by hunger. It’s a way to allay anxiety in the way that smoking was and drinking is in such situations.
Social eating, as in hor d’oeuvres at cocktails or before a dinner party, is a custom of hosting and accepting the hospitality of a host. And eating three meals a day – breakfast, lunch and dinner – at prescribed times, regardless of whether or not we are hungry, is a vestigial tradition from a time when most of us lived a life of heavier exertions. Today, eating a “healthy breakfast” is also the result of marketing by cereal and fruit juice manufacturers.
Many cultures today still eat a very light breakfast, have their main meal (dinner) at mid-day, and a light supper at the end of the workday. In any case, even in these cases, eating “regular” meals at fixed times are examples of non-homeostatic eating. If you eat when you’re not hungry. I want you to stop and think about that for a moment.
So, I have now framed the question, and we can return to what we can do to understand, “Why are we hungry?” Unless we’re carb addicted sugar-burners who need a “sugar fix” every few hours when our blood sugar crashes, what impels us to eat? What makes us eat more than is required for leanness. Eating is a choice we make, and as such it is entirely within our control. We should be able to eat or not eat, as we decide. But, sadly, we know that that is frequently not the case today. Are we then unknowingly living on a glucose-fueled metabolism? Not glucose and fat? And are we living on glucose-for-fuel-only because we are eating a LOW-FAT (high-carbohydrate) DIET?
Then, with only homeostatic eating “on the plate” (LOL), we turn to the mechanism that regulates long-term energy balance and body-fat mass? The answer divides the world of eaters into two cohorts: those with normal fat metabolism and those who have developed a disregulated fat metabolism. Suffice it to say that almost everyone who is overweight or obese, or has the symptoms of Metabolic Syndrome, falls into the “disregulated” group.
For both groups the regulator of long-term energy balance is insulin. Those who fall into the disregulated group have become Insulin Resistant. Their cells that are supposed to open receptors to allow them to take up glucose have become resistant to insulin, so the pancreas makes more, and insulin levels rise in the blood. This higher level of insulin in the blood blocks access to our body’s natural fat stores for energy. So instead, they crave the only alternate sources of energy, DIETARY carbohydrates and fat. The result: WE ARE HUNGRY AND WE EAT.
So, what is the solution? How can anyone who is overweight or obese, and especially those who have Metabolic Syndrome or are pre-diabetic or are diagnosed Type 2s, get access to their own body fat stores for use as energy when the body is in need of it for “long-term energy balance”? Answer: Eat a Very Low Carb diet. Eat a diet that is high fat, (mostly saturated and monounsaturated), moderate protein, and VERY low carb. When you eat VERY Low Carb, your blood insulin levels drop and, for needed energy, your body’s fat stores break down and enter the bloodstream. Eating this way long-term guarantees “long-term energy balance” and homeostasis.

Friday, May 17, 2019

Retrospective #91: Very-Low-Carb Breakfasts (and a No-Carb Lunch)

Chances are you will reject these meal suggestions out-of-hand. Especially lunch. That’s okay. All I can do is “put it out there.” It’s your choice to accept it or not, right? But I gotta tell you: what I did, and what I am suggesting you do, really works. It worked for me, and I think it would work for you too. But you have to try it to find out.
If you eat as described here, as/when you adjust to it, here’s what will work for you: 1) You will not be hungry, either before or between meals – at breakfast, lunch or dinner; 2) you will lose weight, typically 1 to 2 pounds a week, depending on how much you have to lose; 3) you will lose abdominal weight – the central obesity that is so bad for your cardiovascular health; 4) you will “feel healthy,” have lots of energy, and an elevated mood; and 5) as you lose a lot of weight, any weight-related hypertension will improve; and 6) your lipid panel will greatly improve, specifically HDL will increase (mine doubled) and triglycerides will decrease (mine by two-thirds).
Do all these things seem like worthwhile and beneficial outcomes? If you’re not sure, ask your doctor – not about how you intend to achieve them, but about the outcomes 1 through 6 above. Collectively, when these outcomes are “out of whack,” they comprise what is known today as the Metabolic Syndrome (see Retrospective #9, for the parameters). It is a direct outcome of the Westernized diet that we have been eating for the last sixty years, also known as the Standard American Diet (SAD) that is still recommended by government and public health officials. It is also, SADLY, still advocated by most health associations and practicing physicians.
The breakfast I am suggesting you try is designed to provide healthy protein and fat, with minimum carbohydrates. I will provide a few examples. You can vary them, or eat the same one every day as I do, except on Sunday. On Sunday I make a brunch of veal or lamb kidneys with mushrooms and onions, cooked in coconut oil and Marsala. Each of these can be preceded or accompanied by coffee or tea, with heavy cream and stevia powder sweetener.
·         Two eggs (any way – I eat them fried in bacon fat) with two strips of bacon. Nothing else, except coffee/tea.
·         Three eggs, scrambled, with a little full cream and some shredded mozzarella cooked in. Good and gooey!
·         Three eggs, scrambled, with some smoked salmon “tidbits” mixed in. Great protein and Omega 3s!
·         Three eggs, scrambled, with bacalao (shredded dried salt cod), onions and sliced black olives. Yummy!
At present, we are eating the 2-egg breakfast, but occasionally we eat one of the three egg variations. They may appeal to you for several reasons: 1) they omit the bacon, since many people want to avoid “processed meat”; 2) the egg preparations are all delicious and full of flavors; 3) three egg yolks a day, for the choline content, is the recommendation of the Jaminets in “Perfect Health Diet”; 4) salmon and cod are both cold-water fishes with good Omega 3s, and cream and cheese and olives are all healthy fats. You can also add fresh or dried herbs if you like.
Do not be tempted to add bread of any kind, or any whole fruit or any fruit juice, or any “natural” sweetener (i.e., honey), or any cereal, hot or cold, or any milk (just full cream). You don’t need it, and this program WON’T WORK if you don’t follow it. So, don’t be a baby about it. Suck it up and just do it. Just try it for a while.
Then, when you have tried it for a while, and you realize how good you feel while eating this way, and how you are not hungry and you are losing weight, you might want to try “my no-carb lunch.” Okay, hold your nose. Here it is:
·         1 can of Brisling sardines in Extra Virgin Olive Oil (EVOO), or water (avoid any packed in soy bean oil).
When I originally wrote this in 2013, I ate a can of sardines 6 days a week, 5 to 6 hours after breakfast. I was not hungry, but I wanted my body to stay in ketosis from the food I ate and the fat it burned, not from the breakdown of muscle. So, I ate protein (with fat) three times a day at regular 5 to 6-hour intervals, then fasted for 12 to 14 hours to give my body a chance to burn body fat while I fasted and slept 7 hours. That’s what those calories you ate and stored on your body years ago are there for! And so long as you eat this way, you will be rid of them forever.

Thursday, May 16, 2019

Retrospective #90: The “Easy as 1-2-3 Diet”


My wife says, “Most people aren’t like you.” That means she “can’t” do Very Low Carb (VLC) like me because she “can’t” give up… (fill in the blank): a) bread, b) fruit, or c) ice cream – an endless list. That’s okay. I understand that when people say “I can’t,” they mean “I don’t want to.” I understand that is a choice they are free to make.  If they refuse to take charge of their own health – when it becomes clear that their doctors are clueless about how to deal effectively WITH OBESITY and its attendant co-morbidities – then they will inevitably die from the consequences.
If you are one of those who says you “can’t,” then my “Easy as 1-2-3 Diet” is not for you. But if you have an adventurous spirit, you might want to try it for a day or two. I did the “1-2-3 Diet” a while ago, and it worked brilliantly. I lost 7 pounds in 2 days and 9 pounds in 3. I then stopped NOT because I was hungry but because I had achieved my goal, to reverse a trend of weight gain. I stopped the gain and dropped to my target weight for that week. Target weights are good.
My brief diet worked for me in the way I wanted. It would do the same for you if you are already keto adapted, as I was. That means (for the uninitiated) that by eating VLC, I had a low level of glycogen (stored glucose) in my liver. My body was adapted to primarily burning ketones as energy. If you’re not there yet, you probably will get hungry.
Anyway, here’s the “Easy as 1-2-3” diet: You eat a breakfast of 1 cup of coffee with 1 ounce of heavy cream and 1 packet of your choice of artificial sweetener (my choice in 2013 was Splenda). With that you eat 2 strips of bacon and 3 fried eggs. That’s breakfast: 38 fat grams, 26 protein grams, 3 carbohydrate grams, and 465 kcals total.
Then you skip lunch and dinner. Next morning, you repeat the 1-2-3 breakfast; then, no lunch and no dinner.
I did my “Easy as 1-2-3 Diet” for just 2 days, but – here’s the adventure part – I can imagine doing it even longer – maybe for a week. I reached a point many years ago where my body was in balance, where it was in homeostasis while I was eating a VERY low carb, calorie restricted diet: Under 900kcal/day when I eat two meals a day and 1,200kcal when I eat three. My body was telling me that it was getting everything it needs from its energy stores and from the food I eat and the supplements I take. It was the first time I had been there. I listened to my body, and it seemed to be telling me that everything was copasetic. It was satisfied. IT was FED, and I was NOT HUNGRY.
Eating two meals a day, I am still actively losing weight – about 2 pounds a week, exactly according to my plan.
Sidebar: In the Jaminet’s book, “The Perfect Health Diet, -- see Retrospective #38 -- in the section on “How to Raise HDL Levels,” they say “a half bottle of wine per day raises HDL levels by 17 percent.” That’s a good thing. So, if you follow the 2-meal a day basic version, you could eat a small dinner of a fatty meat or fish and a non-starchy vegetable smothered in butter or roasted in olive oil and then add 2 glasses of wine to wash it down. Sound good?
I have been doing Very Low Carb on and off now (in 2019) for 17 years, and I have come to a place where I am very happy with the way I feel and with my health. My mood and my health prospects are much better today than they were 17 years ago (at 78, I’m no “spring chicken”).  And I’m interested in living a lot longer, with “all my marbles.” So, given that I DO NOT GET HUNGRY AT ALL, EVER, ANYMORE, I have two easy choices: 1) Eat according to the “Easy as 1-2-3 Diet” for a day or two, or on alternate days, or some such mix, and 2) eat according to the modified (vinified) two-meal-a-day plan, as we did on our recent vacation. I didn’t lose weight, but I had much more fun.
It’s nice to have choices, especially when they are easy. And they are easy if you don’t feel there are forces beyond your control driving you to eat. Being hungry is a powerful hormonal drive. It makes you seek out food and eat it.  I also know now that I don’t have to convince my wife that “most people aren’t like me.” That’s okay with her, so long as I don’t tell her what to eat. That’s up to her. It’s your choice too.

Wednesday, May 15, 2019

Retrospective #89: “Reversal of Type 2 Diabetes” Revisited

Yesterday’s Retrospective #88, “Reversal of Type 2 Diabetes,” when it was originally published in 2013, prompted my brilliant editor to do a search on the Newcastle University authors, including corresponding editor, R. Taylor. And lo and behold, she found a companion piece in Diabetic Medicine, a Journal of the British Diabetic Association dated 2013 January 15, titled, “Population Response to Information on Reversibility of Type 2 Diabetes.”
She also discovered that R. Taylor presented the prestigious, “The Banting Lecture” at the American Diabetes Association 2012 annual meeting. His subject: “Reversing the Twin Cycles of Type 2 Diabetes,” was the very same material he presented in Diabetologia in 2011! The Banting Lecture is given annually by the winner of the Banting Medal for Scientific Achievement Award, the highest scientific award of the American Diabetes Association.
About how she found this current paper, my editor commented, “I mostly wanted to see what areas of expertise these authors had…! I think (they) are on to something important and also wanted to see what they were up to currently. There's an ongoing effort to shorten the time between research and clinical practice. So, their reporting on people trying out their ideas was especially interesting to me. In the med world, this is pretty fast turnaround.
What a consummate professional my editor is!  And how lucky I am to have her!
Below are verbatim extracts of the abstracts from the “Population Response…” and R. Taylor’s Banting Lecture.
Population response to information on reversibility of Type 2 diabetes.
Steven S, Lim EL, Taylor R.
Source
Magnetic Resonance Centre, Institute of Cellular Medicine, Newcastle University, Newcastle upon, Tyne, UK.
Abstract
AIMS:
Following publication of the Counterpoint Study (on the reversibility of Type 2 diabetes using a very low energy diet), the extent of public interest prompted the authors to make available, on a website, general information about reversing diabetes. Shortly thereafter, individuals began to feed back their personal experiences of attempting to reverse their diabetes. We have collated this information on the effects of energy restriction in motivated individuals with Type 2 diabetes that has been achieved outside a research setting.
METHODS:
Emails, letters and telephone communications received between July 2011 and September 2012 were evaluated (n = 77: 66 men, 11 women). Median diabetes duration was 5.5 years (3 months-28 years). Reversal of diabetes was defined as achieving fasting capillary blood glucose < 6.1 mmol/l and/or, if available, HbA(1c) less than 43 mmol/mol (6.1%) off treatment.
RESULTS:
Self-reported weight fell from 96.7 ± 17.5 kg at baseline to 81.9 ± 14.8 kg after weight loss (P < 0.001). Self-reported fasting blood glucose levels fell from 8.3 mmol/l (5.9-33.0) to 5.5 mmol/l (4.0-10.0) after the weight loss period (P < 0.001). Diabetes reversal was considered to have occurred in 61% of the population. Reversal of diabetes was observed in 80, 63 and 53% of those with > 20, 10-20 and < 10 kg weight loss, respectively. There was a significant correlation between degree of weight loss and reported fasting glucose levels (Rs -0.38, P = 0.006). Reversal rates according to diabetes duration were: short (< 4 years) = 73%, medium (4-8 years) = 56% and long (> 8 years) = 43%.
CONCLUSION:
These data demonstrate that intentional weight loss achieved at home by health-motivated individuals can reverse Type 2 diabetes. Diabetes reversal should be a goal in the management of Type 2 diabetes. © 2013 The Authors, Diabetic Medicine, 2013 Diabetes UK.
The 2012 Banting Lecture Reversing the twin cycles of Type 2 diabetes.
Taylor R.
Source
Magnetic Resonance Centre, Newcastle University, Newcastle upon Tyne, UK.
Abstract
It has become widely accepted that type 2 diabetes is inevitably life-long, with irreversible and progressive beta cell damage. However, the restoration of normal glucose metabolism within days after bariatric surgery in the majority of people with type 2 diabetes disproves this concept. There is now no doubt that this reversal of diabetes depends upon the sudden and profound decrease in food intake, and does not relate to any direct surgical effect. The Counterpoint study showed that normal glucose levels and normal beta cell function could be restored by a very low-calorie diet alone. Novel magnetic resonance methods were applied to measure intra-organ fat. The results showed two different time courses: a) resolution of hepatic insulin sensitivity within days along with a rapid fall in liver fat and normalization of fasting glucose levels; and b) return of normal beta cell insulin secretion over weeks in step with a fall in pancreas fat. Now that it [is] possible to observe the pathophysiological events during reversal of type 2 diabetes, the reverse time course of events which determine the onset...can be identified. The twin cycle hypothesis postulates that chronic calorie excess leads to accumulation of liver fat with eventual spill over into the pancreas. These self-reinforcing cycles between liver and pancreas eventually cause metabolic inhibition of insulin secretion after meals and onset of hyperglycaemia. It is now clear that Type 2 diabetes is a reversible condition of intra-organ fat excess to which some people are more susceptible than others. © 2012 The Authors. Diabetic Medicine, 2012 Diabetes. 

Tuesday, May 14, 2019

Retrospective #88: “Reversal of Type 2 Diabetes”

“Reversal of type 2 diabetes: normalization of beta cell function in association with decreased pancreas and liver triacylglycerol,” appeared in the ADA’s online Diabetologia on 09 June 2011. The authors are all with Newcastle University (UK). The corresponding author is R. Taylor. The Abstract, Introduction and Conclusions follow:
Aims/hypothesis: Type 2 diabetes is regarded as inevitably progressive with irreversible beta cell failure. The hypothesis was tested that both beta cell failure and insulin resistance can be reversed by dietary restriction of energy intake.”
“Introduction: Type 2 diabetes has long been regarded as a chronic progressive condition, capable of amelioration but not cure. A steady rise in plasma glucose occurs irrespective of the degree of control or type of treatment. Beta cell function declines linearly with time, and after 10 years more than 50% of individuals require insulin therapy. The underlying changes in beta cell function have been well described, and beta-cell mass decreases steadily during the course of type 2 diabetes. Overall, there is strong evidence that type 2 diabetes is inexorably progressive, with a high likelihood of insulin therapy being eventually required to maintain glycaemic control.
However, type 2 diabetes is clearly reversible following bariatric surgery. The normalization of plasma glucose concentration follows within days of surgery, long before major weight loss has occurred, and it has become widely assumed that the protective effects of gastrointestinal surgery are mediated by altered secretion of incretin hormones. Improved control of blood glucose in type 2 diabetes by moderate energy restriction has been demonstrated by others. We have hypothesized that the profound effect of a sudden negative energy balance on the metabolism could explain the post-bariatric surgery effect and, specifically, that the decrease in the intracellular fatty acid concentrations in the liver would lead to a lower export of lipoprotein triacylglycerol [i.e., TG or triglycerides] to the pancreas, with the release of beta cells from the chronic inhibitory effects of excess fatty acid exposure. This study was designed to test the hypothesis that acute negative energy balance alone [emphasis added] reverses type 2 diabetes by normalizing both the beta cell function and insulin sensitivity.”
The study design is notable for the use of the word “alone” – especially when you consider the participants’ diet. It was 1 MJ/day (510 kcal/day for non-Brits) of Optifast, which is a “liquid diet formula” by Nestlé Nutrition. This was supplemented with “three portions of non-starchy vegetables.” Total energy intake was 2.5 MJ (600kcal)/day.
This is notable I think because the formulation of Optifast used in this study was 46.4% carbohydrate, 32.5% protein and 20.1% fat. Those macro percents do not include the 3 servings (0.4 MJ or +/-90 calories) of vegetables, essentially all carbs. So, the results are all the more striking since the participants during the 8-week duration of the program ate a high carb, high protein, low fat, mostly liquid diet. And the paradox is about to get even starker.
“Eleven people with type 2 diabetes (aver. age 49.5, BMI 33.6) were studied before and after 1, 4, and 8 weeks. An age-, sex-, and weight-matched group of eight non-diabetic participants was studied also. “After 1 week of restricted energy intake, fasting plasma glucose normalized in the diabetic group from 9.2 to 5.9mmol/l (166 to 106mg/dl US). Insulin suppression of hepatic glucose output improved from 43% to 74% vs. 68% for the control group. Hepatic triacylglycerol (TG) content fell from 12.8% in the diabetic group to 2.9% by week 8; The first-phase insulin response increased during the study period…and approached control values; Maximal insulin response became supernormal at 8 weeks vs. controls; pancreatic triacylglycerol decreased from 8.0% to 6.2%, compared to 6.0% in the control group.”
Conclusions/interpretation: Normalization of both beta cell function and hepatic insulin sensitivity in type 2 diabetes was achieved by dietary energy restriction alone (emphasis mine). This was associated with decreased pancreatic and liver triacylglycerol stores. The abnormalities underlying type 2 diabetes are reversible by reducing dietary energy intake.”
Hmmm. Calorie Restriction alone can reverse Type 2 diabetes. This paper is pretty “brainy” and certainly above my pay grade, but I wonder why others who are qualified to discuss it aren’t.  I am confident that there is no “duality of interest” here. Maybe the answer is our clinicians are too busy learning about the latest pill or injection to treat Type 2 diabetes, or maybe they’re trying to figure out the current reimbursement rules and insurance regulations.

Monday, May 13, 2019

Retrospective #87: Optimal Blood Lipid Levels

Be warned! I was very hot when I wrote this in 2013. I can be intemperate at times, and plain spoken, as for example when I refused the recommendation of an endocrinologist given to me over the phone by his nurse. When she told me that the doctor suggested I “try” a statin, I told her “the doctor really should be ashamed of himself.” The next morning the doctor called me at 7:30 AM, saying I had hung up on his nurse.
That was not true; she hung up on me after I made that comment. Apparently, she hadn’t told him what I’d said, leaving it to me to tell him directly. It added fuel to the fire. He then calmly told me that the LDL value in my Lipid Panel was high and that both the ADA and the AHA guided that my LDL should be below 100mg/dl. I told him that I didn’t care what the ADA and the AHA guidelines said. I then went into a bit of a harangue about Ancel Keys, and suggested the doctor really should “go back to school.” That did it! He declared, “You need to find a new doctor.
I don’t apologize for what I said. I had high hopes that I would find an endo who was enlightened. I haven’t seen an endo in 25 years, seeing only an internist/cardiologist. I failed to find one this time, but it was entirely my fault.
Of course, I could have accepted the prescription he offered and then refused to fill it. Then the doctor could simply have written in my chart that I was “non-compliant,” like all the other “old people” (his PA told me) who “don’t care about their health.”
That’s what she said when I asked her why other patients didn’t follow her recommendation to eat Low Carb. She eats about 60 carbohydrate grams a day. I eat about 15, for glucose control. I am a long-term Type 2 diabetic.
Anyway, in reaching my latest level of self-assurance (arrogance?) about optimal blood lipid levels, I had a fresh recollection of Chapter 41, “Blood Lipids,” in “Perfect Health Diet” (Scribner, 2012), a very good book by Paul and Shou-Ching Jaminet (both PHDs). It is only “background” material for most Type 2s, and they do get “into the weeds” a bit, but I like their approach to healing – finding the root causes rather than treating the symptoms.
Chapter 41 has the following sub-sections: “Optimal HDL Levels,” “How to Raise HDL Levels,” “The Immune Functions of LDL,” “Optimal Blood Lipid Levels,” and “Troubleshooting Blood Lipids.”  
From page 366, here’s what the Jaminets have to say about the optimal blood lipid (cholesterol) levels: “The ideal serum lipid profile that produces the best health and minimizes mortality – looks like this:
·         Total Cholesterol level between 200 and 260 milligrams per deciliter
·         LDL Cholesterol level above 100 milligrams per deciliter
·         HDL Cholesterol level above 60 milligrams per deciliter
·         Triglyceride level around 50 to 60 milligrams per deciliter”
How did my lipid profile compare to the Jaminet’s ideal? Here’s the endo’s lab report for my serum lipid profile:
·         Total Cholesterol level = 245
·         LDL Cholesterol level = 176
·         HDL Cholesterol level = 58
·         Triglyceride level = 54
Okay, my LDL (176) was high – the highest it has ever been (since 1992, when lab reports first starting calculating LDLs). And my Total Cholesterol (245), was the highest ever, going back 40 years to 1974. I am comforted, however, by the knowledge that my TG/HDL ratio was 0.93, which is <1.0 and therefore “ideal.” Altogether, though, as the endo told me, my lipid profile did not fit the ADA and AHA guidelines. I wonder what the Jaminets would have said?
And for the record, my latest (April 2019) lipid panel was: TC = 186; HDL = 80; TC/HDL ratio = 2.3; LDL = 92; non-HDL 106 and triglycerides (TG) = 56. TG/HDL ratio = 0.70. And that was BY DIET ALONE. I DO NOT TAKE STATINS.

Sunday, May 12, 2019

Type 2 Nutrition #485: Grocery store bread is processed food.

I found “Grocery store bread is processed food” scribbled on a “Post It” next to my laptop, so since I fancy myself a lay Type 2 nutrition educator, it must be that it was my intention to write about it. So, here goes.
Most people grow up eating a lot of bread at home. I did not. I was lucky. My father grew up during the Great Depression. Later he had a good job and regarded our family as too bourgeois to use bread fillers like “Hamburger Helper.”  My mother didn’t serve bread with supper either. Like most kids, though, we ate sandwiches. They were a lunch-box staple, together with fruit and cookies, for school every day.
Store-bought bread, at least the kind sold in a plastic wrapper, has to have a long shelf life. Silvercup is the brand I remember. It was white and spongy. I didn’t learn until recently that what made it spongy was sugar. Here’s a challenge: Look at the label on any loaf of bread sold with a wrapper in the supermarket. I defy you to find one where sugar, HFCS, or some other form of sugar, is not, after flour and water, the third ingredient.
The glycemic index is a scale from 1 to 100 which measures the rate at which a food will raise blood sugar. A slice of white bread is 100 on the glycemic index! No other food will make a Type 2, or Pre-diabetic or Insulin Resistant’s blood sugar rise faster and farther than white bread. Two slices of Walmart's white bread contain 23g of carbohydrate (including added sugar) and 5g protein (from gluten in the flour).
Why is bread the very definition of a high-glycemic food? Because it is a PROCESSED food, made from highly REFINED white flour (and 3g of ADDED sugar). Flour starts to break down into glucose when enzymes in saliva contact it! And sugar is a simple carb that only needs to divide once (in your mouth!) to become glucose.
Why is a processed food like white bread so much worse for you and your blood sugar control than say an apple? (To be clear, I’m not advocating you eat, as we learned as kids, “an apple a day.” I just want to explain the difference.) The carbs in white flour are 100% glucose molecules. Glucose makes your blood sugar rise. 
The principal nutrients of an apple are simple sugars: sucrose (a disaccharide of glucose and fructose. Glucose and fructose are monosaccharides. The glucose molecule goes into your blood to be circulated and taken up for energy. The fructose molecule does not. It goes directly to your liver, for detoxification. If you need more glucose for energy, your liver converts the fructose to glucose. If you don’t need more, it stores it as glycogen. But if the liver is already full of glycogen, it uses a process called “de novo lipogenesis” to convert the excess fructose to fat. That’s right! The liver makes fat from the excess sugars glucose and fructose.
An apple also has high fructose content. After water (86%) and fiber (3%) the remaining 11% of an apple by weight are simple sugars: 20% the disaccharide sucrose (half glucose/half fructose), 23% “free” glucose and 57% “free” fructose. The “free” molecules are monosaccharides. So, when the sucrose breaks down to monosaccharides, an apple is 33% glucose and 67% fructose. Only the 33% glucose in an apple raises your blood sugar versus 100% in a slice of white bread. You already know what the fructose does to your liver. Ugh!
Years ago, I met a nurse in a swimming pool (in Mexico) who told me her husband had a fatty liver. This was at least a decade before Non-Alcoholic Fatty Liver Disease (NAFLD) was among the conditions associated with Metabolic Syndrome. We now know that you don’t have to be obese to have NAFLD. It’s the visceral fat within and around your internal organs that causes NAFLD. I wish I’d known that in the swimming pool in Mexico.
Today, white bread is the standard bearer for the “bad boy” foods we’ve eaten ever since we carried a sandwich to school eons ago. And government still tells us to eat it. Look at Choose My Plate from the HHS/USDA and Create Your Plate from the American Diabetes Association, respectively. But don’t expect the government to change. Agribusiness and Big Pharma have too much at stake to let that happen any time soon.

Retrospective #86: Beta Cell Function and Insulin Sensitivity


In early 2013 I made an appointment with an endocrinologist to find out what was going on with my glucose metabolism. I was interested in my % Beta cell function and my % Insulin Sensitivity (and its reciprocal, Insulin Resistance). I had read about a HOMA Assessment test that determines those values, and I wanted to be tested.
I hadn’t been to see an endo in 25 years. In that first visit, he had me go to the out-patient department of a local hospital for a 4-hour oral glucose tolerance test (OGTT). That test confirmed the diagnosis that had been made a few years earlier that I was a Type 2 diabetic. After seeing the test results, he increased my dose for a sulfonylurea (SU), the only oral diabetes medication in use in the U.S. at that time.
It would be another 5 years (in 1995) before another doctor added Metformin, which by then was permitted here. But before long I was maxed out on both the SU and Metformin and was starting on a 3rd class, a TZD (Avandia).
Then, in 2002, to lose weight (NOT to treat my diabetes) my doctor suggested I try the Atkins Induction diet. He had just read the Gary Taubes NYT Magazine cover story, “What If is All Been a Big Fat Lie?”  The first day on Atkins Induction (20 grams of carbs a day), I had a hypo. I called my doctor, and he told me to stop the Avandia. The next day when I had another, he cut the SU and Metformin dosages in half, and then soon thereafter, in half again.
I lost 60 pounds on Atkins Induction, but after a few years, I gained back 12. I then decided to try the Bernstein diet for diabetics. In the next year I lost another 100 pounds and eventually another 22 for a total loss of 170 pounds.
Along the way, I weaned myself off the sulfonylurea, but I still took 500mg Metformin once a day. But, all told, I figured I had been on a sulfonylurea, which pushes the pancreas to secrete more insulin in response to a glucose challenge, for almost 20 years. Referencing Dr. Ralph DeFronzo’s Banting Lecture at the 2008 ADA Annual Convention, I feared I had already lost 80% of my Beta cell function by the time I was diagnosed in 1986!
At the end of the introduction to the full paper published in the ADA magazine, “Diabetes,” Dr. DeFronzo also said, “Sulfonylureas are not recommended because, after an initial improvement in glycemic control, they are associated with a progressive rise in A1C and progressive loss of β-cell function” (emphasis added by me).
Given my history on sulfonylureas and Dr. DeFronzo’s prognostications, I was surprised with the HOMA Assessment test results: Beta Cell function = 68.2%; Sensitivity = 94.6%; and IR = 1.1 (1.057). Has anyone else out there had a HOMA assessment? The nurse who placed the test order said she had been working with this doctor for 10 years and he had never ordered the test before.
The endo told me the test was mostly used in research. Okay, but, I wondered, if not commonly used in clinical practice, does the test have clinical value? What can be learned from it? My first read is that I am not as bad off as I thought I was. True, I have been eating Very Low Carb “on and off” for over 10 years, and for the last four months, “totally on.”  My last HbA1C was 5.7, down from recent low 6s. I had been eating a Very Low Carb “ketogenic” diet, recently about 1,200kcal/day, without hunger. That is because my body is ketoadapted and in ketosis virtually all the time. My body is in homeostatic balance and happy with my dietary intake, my supplements, and with the fatty acids, glycerol and ketone bodies it makes from my body fat that it is breaking down every day for energy.
My daily FBG readings are almost always under 100, and my weekly averages about 90mg/dL. I work hard to keep them under 100. I am very careful to eat Very Low Carb (VLC) and to never eat too much protein.
So, what does my HOMA assessment test reveal? Is my Type 2 diabetes in “clinical remission” because of the way I eat? Has my diet “reversed” my Type 2 diabetes, “normalized” my Beta Cell function and improved my insulin sensitivity? Did my Beta Cells regenerate themselves after years of being depleted?
I hope to learn the answers to these questions from my new endo in my follow-up appointments. I can hardly wait.

Saturday, May 11, 2019

Retrospective #85: Goal Weight and the BMI Table

Like many who are overweight, obese or morbidly obese (what a dreadful term!), I have spent a lot of time over the years thinking – dreaming really, about my goal weight. Those dreams have turned to reality for some of us who have finally found a way to lose weight without hunger and have seen the pounds drop off easily. And they are fat pounds, because we have become “fat burners,” through ketosis, enabling us to burn fat for energy by severely restricting our carbohydrate intake. Now, we are wondering, how far can I go? How far do I really want to go? How thin could I be?
The “experts” tell us not to be too ambitious – to set modest goals, because they know how hard it is to lose weight and how common it is to fail. They tell us that even a 10% (or less) weight loss will make a big difference in our health markers and outcomes, especially for Cardiovascular Disease (CVD). Still, those of us who are losing weight easily can imagine ourselves as much thinner. As I was seeing two pounds of fat dissolve a week for a year (about 5 years ago), I imagined that I could be 187 pounds – half my original 375. At one point I had lost 170 pounds (45% of me) and was 205 pounds, when I stopped losing.
In early 2013 when I wrote this, after regaining 70 pounds over the last four years, I was starting to lose again. My goal was to lose just 50 of the 70 regained and to reach a more modest goal of 225. That would represent a loss of 150 pounds (40%) from the start. That weight was my new goal weight – the one I would strive to maintain for the rest of my life.
But what do all these numbers mean? My wife told me I would look like a scarecrow if I had lost 187 pounds. I would be “just half the man I used to be,” my wife joked. But at 225, I would still be clinically classified as obese. A neighbor who saw me on the street when I was near my low of 205 said, “Are you okay? Are you well?” Funny!
Goal weight is purely personal. Ideal weight is somewhat different. It’s a bit more impersonal. What I call my body type (“big boned”) might actually just be my body image from having lived a lifetime looking at it. Why else would there be just one clinical standard in the U.S. (since 1998 when we adopted the WHO standard) for judging weight?
Body Mass Index (BMI) is now the universal “scale” for both men and women. It requires only height and weight and is, in my opinion, totally unrealistic. Using this index, a person (male or female of any “body type”) who is now 5’-11” tall should weigh between 136 and 172 to be considered “normal “weight. The average “normal weight” for a person 5’-11” person would be 150 pounds. That’s ridiculous. It’s skeletal – as my wife said – a mere scarecrow. My father told me he weighed 150 pounds in the Great Depression, and again when he was diagnosed with Tuberculosis (TB) in 1950. A nine-month stay in the hospital put a little flesh on his bones. After, he weighed 175!
So, my “goal weight” of 225 pounds is still much higher than my “ideal weight.” It is in fact 75 pounds higher. It is higher even than the BMI range (179 to 208) allows for me to be considered “overweight.” In fact, 225 pounds is still considered “obese” for a 5’ – 11” person. The “obese” range is 215 to 279. But that’s okay. It’s my goal weight.
Lean Body Weight is another term that is sometimes used by athletes (and thin people). It includes only a small amount of body fat, to cushion the organs and provide a daily energy reserve and long-term illness. To me it is a foreign concept, an “exotic” species.  It is achievable, no doubt, and the most desirable weight to be, if you have the body type, a favorable set of genes, and a history of eating right and exercising regularly. That’s not me.
However, lean body weight is a very useful weight to use when deciding how much protein to eat to avoid unwanted gluconeogenesis. If you are a Type 2 diabetic who is working hard to achieve optimal glucose control and weight loss through diet, it’s useful. That’s me, but that’s another story.

Friday, May 10, 2019

Retrospective #84: Carbohydrate Intolerance – the new ‘buzz’ words

Authors Jeff Volek and Stephen Phinney use the phrase “carbohydrate intolerance” seven times in their introduction to one of my favorite books, “The Art and Science of Low Carbohydrate Living.”  They’re telling us something. They’re want to replace the medical term Impaired Glucose Tolerance (IGT) with “carbohydrate intolerance” to make it more “accessible,” and I think that’s a great idea.
IGT involves hormones, enzymes and cell receptors, and unless you’re a molecular biologist, these terms make the eyes glaze over. Besides, the biological actions that occur within the body are autonomic, whereas for the most part, we eat food consciously. And we don’t eat glucose. We eat carbs. Our digestive system breaks down all carbs, including all simple sugars and all complex carbohydrates (starches), into single molecules, most of them glucose.
So, “carbohydrate intolerance” is an excellent way to describe the common disorder that increasing numbers of people have to eating ALL carbs. I am stressing all carbs because of the popular disinformation campaigns 1) to distinguish between simple sugars (mono and disaccharides) and “complex” carbohydrates, or polysaccharides (starches), and 2) consider processed carbs (like white flour) as preferable to “added sugar” and 3) to differentiate “natural sugars” (as in fruit) from “added” sugars. Sure, whole fruits (not fruit juices) contain small amounts of fiber, but they’re all sugar, folks! They’re all glucose in the blood, where they all get to sooner or later, mostly sooner.
It is true that table sugar and fruit sugar is sucrose and breaks down to 50% glucose and 50% fructose. And that fructose is metabolized differently than glucose; It is diverted to the liver where it is detoxified and frequently stored as fat.) And that all “complex” carbohydrates (starches) break down and are absorbed in the blood as glucose. All glucose will raise blood sugar in the same way, but some complex carbohydrates will raise blood sugar more quickly and higher that sucrose. Example: a slice of bread vs. an apple, a banana or a glass of orange juice.
Another extreme example of misinformation about nutrition is this stupid print advertisement, written by a Registered Dietitian, in a NYS apple growers association: “The complex carbohydrates in apples give your body a longer, more even energy boost compared to high-sugar snacks.” That is false. Utter nonsense. There are no complex carbohydrates in an apple. An apple is 86% water, 3% (indigestible) fiber and 11% simple sugars (67% fructose/33%glucose, when digested). An apple is, in fact, just a delicious high-sugar, high-fructose ‘candy bar’.
So, I applaud the initiative of Volek and Phinney to create a user-friendly “buzz word” to describe the condition that affects a large and rapidly growing “cohort” of the population – those who from eating a “Western Diet,” have succumbed to the common condition known as Metabolic Syndrome. We are the Carbohydrate Intolerant.
We are also the obese, or as the case may be, the overweight. Our metabolisms are broken. We make fat and eat for energy when we should be burning body fat for energy. We are also the hypertensive. And we are the ones with “high cholesterol,” diagnosed as high Cholesterol and high LDL (because LDL can be treated with a statin). Whereas, in fact, we have a more difficult-to-treat form of high cholesterol characterized by low HDL and high triglycerides.
The first step is to recognize yourself – to know that you are a member of this “cohort” that has an association with being obese or overweight, has high blood pressure (because you’re overweight), and has high blood sugar, and high “cholesterol.” And that having all these indications puts you at much higher risk of death or another morbid outcome. Are you motivated yet? Will you accept that you and your doctor have failed to reverse these markers?
A reasoned approach, on the other hand, would be to try a different diet. If you are a Type 2 or even prediabetic, or just overweight and have high blood pressure, you and your doctor already know that carbohydrates raise your blood sugar. That means, YOU ARE CARBOHYDRATE INTOLERANT! Accept it, and then do something about it! 
The consequences of carbohydrate restriction vary, but in general individuals who recognize, accept, and deal with carbohydrate intolerance report weight loss and greatly improved health and quality of life. Why not try it?

Thursday, May 9, 2019

Retrospective #83: “The 8-Hour Diet,” based on “brand new science”

On the Today Show in early January 2013, author David Zinczenco told host Matt Lauer that his new book, “The 8-Hour Diet,” described a way to lose weight based on “brand new science.”  My wife told me about it but was a little vague about how it worked. So, I found the segment on NBCnews.com, and here’s what I saw: lots of goodies: yoghurt, berries, orange juice and bran muffin for breakfast, a big salad, two slices of pizza, cup of soup plus potato chips or French fries for lunch, and a big rib eye steak, potatoes, veggies and a piece of chocolate cake for dinner.
Zinczenco described the diet as “lean protein, good fats, and complex carbs” – the government’s good ole message. The only limiting factor was that all the food for any particular day had to be consumed within an 8-hour window: 9 to 5, 10 to 6, or even 11 to 7. The example given was 10:30 for breakfast, 12:30 for lunch, and 6:30 for dinner. The author said you could do this 8-hour diet for just 3 days a week and lose as much as 5 pounds a week and 20 pounds in 6 weeks.  He tried it himself, he said, and lost 7 pounds in 10 days. He called it “intermittent fasting.”
So, I have to say this diet has obvious appeal for a “healthy” person with “normal” metabolism, Unfortunately, this EXCLUDES anyone with any of the indications of Metabolic Syndrome (see Retrospective #9). It is, however, clever merchandizing to sell a book on the Today Show to an audience of women who aren’t the least bit interested in the mechanism or counting  – only in the eye-appeal of all their favorite foods and the comfort of not having to deny themselves anything except eating for 16 hours a day for three days a week.
Zinczenco points out that that’s not so tough either, since most people already fast between dinner and breakfast. To stress this point, he noted the word breakfast is composed of “break” and “fast.” He also spoke disparagingly of the practice many have today of “grazing all day long,” including sometimes after dinner. For three days a week, at least, that is a “no-no.” He also suggests a morning exercise routine (instead of breakfast) to burn up stored carbs.
But what’s the real physiological mechanism of the 8-Hour Diet?  It works on the principle of the fed state and the fasting state, hardly a brand-new science. It is the basis of the hard scrabble existence of mankind on this earth from the beginning of time. You hunt, you eat, you rest while you digest, and then, when your body tells you that you need to eat again, you burn stored fat while you hunt again.
Quoting “certain conclusion” #2 from Gary Taubes’s “Good Calories-Bad Calories” (see Retrospective #5), your body regulates this “harmonic ensemble” to maintain homeostasis, This cycle continued throughout life and for 500 generations, until the advent of the Neolithic Era 10,000 years ago. The Neolithic introduced cultivated grains, grain storage, domesticated animals, and human settlements. It was a momentous development.
In the Paleo era, after eating, food is digested and absorbed. All carbohydrates and about half the protein we eat eventually becomes glucose, the latter through a process called gluconeogenesis. This is a glucogenic or fed state.
The fasting state begins when the glucose energy from the last meal has left the small intestine (where it was absorbed into the blood stream), and hormones switch the body to ketosis. In a ketogenic state our bodies break down body fat (triglycerides) for energy. This state is called ketosis because when the triglycerides break down to fatty acids and glycerol, they produce ketone bodies.
Dr. Richard Veech of the National Institutes of Health says, “…ketosis is a normal physiologic state. I would argue it is the normal state of man.” The 8-Hour Diet just extends the nightly fast from 12 to 18 hours, 3 days a week.
David Mendoza, an early and frequent low-carb Type 2 diabetic blogger, offered a similar “weight-loss tip.” He said that whenever his weight drifted above “target” (he describes his current weight as “low-normal,” which sounds skeletal to me), he skips dinner that day. He said he has only had to do that 9 times in the last 6 months.
Of course, anyone who follows Intermittent Fasting (IF) knows it has come a long way since “The 8-hour Diet” book in January 2013. If you’re not familiar with my favorite book, Google Dr. Jason Fung’s, “The Obesity Code.

Wednesday, May 8, 2019

Retrospective #82: Obesity Caused by Gut Bacterium!

A few days ago (in late 2012; remember this is a Retrospective series), the Health page of the Financial Times (FT) led with the banner headline, “Scientists Link Obesity to Gut Bacteria.”Call me a skeptic, or even a “conventional thinker” (pulleesse, don’t call me that!), but I’ll just have to “wait and see.”  A lot of serious scientists have been writing about this in the blogosphere lately, but this is the first that I have seen it in the “mainstream” media.
So far, I have been dismissing this talk as too “edgy” and too esoteric for my non-scientific brain to wrap around. Besides, I have just gotten comfortable with – in fact, I’ve fully embraced Gary Taubes’s alternative Carbohydrate Hypothesis. This theorem places the action – or rather the “broken” action, of the hormone insulin at the center of the obesity epidemic. And now some cutting-edge thinkers are moving on to another frontier – the human gut.
It’s a good thing, of course, that science is “advancing” quickly, but scientists would be the first to say that caution is and should be the “order of the day.” And I have no doubt it will. Everything will be “peer reviewed” (for what that’s worth!), and replicated with double-blind, prospective, trials, etc, etc. But journalism is not so constrained, and journalists often get it wrong. And, as a result, so does the public. And then the processed and packaged food industries pick-up on it, and all of a sudden, a box of Cheerios cereal is a cholesterol-lowering drug!
But this rant is not about the gut bacterium reported in the FT.  It is about the response of a lecturer in biological sciences at Durham University (England). I gave a hearty guffaw when I read his reaction to the news. According to the FT, he said, , “If obesity is caused by bacteria, it could be infectious and picked up from some unknown environmental factor, or a parent. IT MIGHT NOT BE BEHAVIORAL AT ALL” (emphasis mine).
I apologize for “shouting” but I just couldn’t believe that he said this. I accept that the vast majority of the lay public believes that nearly 50% of all the adults in the U.S. and the UK are obese because they eat too much and exercise too little. But, for a lecturer in biological science at a leading UK center of research to say it?!! Give me a break!
In an email exchange I had with Gary Taubes on the day before I wrote this post, he told me that he was preparing a rebuttal to the British Medical Journal (BMJ) on a piece they had just published about how low-fat diets were associated with weight loss. I read the piece and decided that it was beyond my ken. I replied to him that I would leave the BMJ to him, and I would continue to fight “the good fight” on a different level. But when I am reminded how far all of us with an open-minded view have to “climb” to overcome ignorance, it is indeed a daunting task.
Anyway, the lead scientist and spokesman for the study, said, “This is a very important phenomenon. It is the last missing piece of evidence [that] bacteria causes (sic) obesity.” I laughed again, and again when the Durham researcher said, “Dr. Zhao’s research paved the way to intervene in obesity and could allow new drugs to be developed for treatment.”
His pharmacological bent reminded me of the drug developers who first came up with statin compounds to lower LDL, and thus Total Cholesterol (TC,) because LDL was the only sub-component of TC that could easily and effectively be lowered with a drug. This led to world-wide sales soon to reach 1 trillion dollars, and to dubious health benefits and myriad risks.
So, while I am skeptical by nature, and that is a good thing both in science and in general, I am still open-minded. I can also hope that this is “a very important phenomenon” and that it is “the last missing piece of evidence” of what causes obesity. And just as cholesterol drugs to lower LDL developed in the 1980s, let’s hope that gut bacteria research, whether relevant to obesity of not, evolves as well. After all, as we frequently hear, “there are 10 times more microbes than human cells in our bodies, and they can be beneficial.” So, as science advances, particularly with recent progress in the knowledge of the human genome, a “breakthrough” of this magnitude would be welcome. Semi-starvation on a “balanced” diet, and boring and tedious daily exercises, don’t work for me. And my Very Low Carb Ketogenic Diet is certainly restrictive and requires a lot of discipline.