Sunday, December 31, 2017

Type 2 Nutrition #413: “End Date”

My wife recently left a post-surgical office visit with a written prescription for physical therapy (PT). She told me the doctor’s assistant said to call for another office visit when the PT was completed. So, I asked my wife how long was the course of PT that the doctor prescribed. She looked, and said, “End date: TBD by insurer.”
My first reaction was surprise, then anger at the doctor for abdicating on the decision, then anger at the insurer for taking control of medical decisions, then anger at government for letting them dictate to insurers. Making healthcare decisions that affect a patient’s recovery from surgery should always be a matter between doctor and patient, not insurers, whose principal interest is the bottom line. And not big government, where politicians and their staffs are not qualified…and besides are generally corrupted by conflicts of interest.
So, the doctor is not to blame. He or she is in business too – albeit small business, but this column on changes in Medicare demonstrates that even the giant American Medical Association was helpless to alter the course of the “reforms” to Medicare that were enacted to pay for the Affordable Care Act (“Obamacare”). Healthcare represents about 17% of the U. S.’s Gross National Product. It’s a behemoth that overpowers everything else.
So, let’s review where we are: A doctor can no longer prescribe the duration of PT, and insurers shouldn’t, and politicians who have no business doing it at all but ultimately do by the legislation their staffs write, they pass, and the indecipherable regulations government minions then produce, so, in this mess, what’s a patient to do? Answer: Take your healthcare into your own hands! Seriously, it’s your health!
My doctor offers “Concierge Care.” I suspect he’s looking for a way to get out from under all the restrictions, regulations and reporting (the 3R’s). He needs less overhead to handle the billing, and he gets paid more promptly.  It has to be more rewarding, and not just financially.
I declined his Concierge Care option because under the primary Medicare and secondary supplemental that I have from being a former NYC manager, I have very good insurance coverage. Virtually everything is covered and paid for. I even get the Medicare Part B premiums, deducted from my pension check, refunded! And my Medicare Part D prescription drug coverage is subsidized by the Management Benefits Fund.  I am also in pretty good health for my age – much, much better than I was 15 years ago, when I was morbidly obese. When my current doctor took over my former doctor’s practice, he studied my chart and suggested I see him just once a year. Instead, at my insistence, I see him 3 times a year, primarily for blood work.
So, my pitch to you at New Year’s is: Take responsibility for your own health. Don’t rely on your insurer to tell you what to do or how long to do it. And don’t let the government tell you what to eat. They’ve been wrong with that advice for the last 60 years, much longer than anyone now in government and certainly longer than anyone in medical practice has been working. Remember, too, your doctor is/was not educated in nutrition, and the RDs and CDEs in practice today obtained and keep their licenses by learning all the wrong things.
If you’re overweight or pre-diabetic, ask yourself, how did you get that way? Haven’t you been trying to eat a “healthy diet” the way you’ve been told to do for most of your adult life. And haven’t you been exercising regularly? Then what caused you to gain weight or become Insulin Resistant (pre-diabetic)? If you are Insulin Resistant, you are Carbohydrate Intolerant. Does it make sense to continue to eat a “balanced” diet? To “eat everything in moderation,” the way the government and the medical establishment told you to do. Isn’t that what caused you to become Carbohydrate Intolerant? Then why would you continue to do the same thing over and over again and expect a different result? Isn’t that the definition of insanity? Think about it. Seriously!
End of hectoring. Happy New Year, and make it a truly NEW one, for YOU.

Sunday, December 24, 2017

Type 2 Nutrition #412: “Cover” Story

With idle time in my wife’s doctor’s waiting room, I picked up WebMD Magazine’s June 2017 issue. The cover appeared to feature an article asking, “Trouble reaching your A1c goals?” Next to a photo of a middle-aged man, the caption invited the reader to: “See how Jerry does it.” I’m always interested in seeing how other people lower their A1c’s, so I eagerly and naively turned the page…to a 3-page ad for Trulicity.
Somehow I missed the disclaimer on the “cover.” It said (on a black banner), “Special advertising section. This Trulicity promotional cover has been placed on a limited number of WebMD magazines” – just the ones in doctor’s offices, I’d bet. It continued, “It does not constitute an endorsement by WebMD Magazine and no endorsement is implied.” Okay, WebMD gets big bucks for the fake cover, but how about the doctor’s office? Are they not complicit in this non-endorsement endorsement? I think so, and they don’t even get paid for it!
I also missed the small red-type Lilly at the bottom of the false cover. But it was impossible to miss the 3 full pages of information about “non-insulin Trulicity, a once-weekly injectable pen for type 2 diabetics to help [your body] release its own insulin.” They’re careful to say it’s not the first pharmacotherapy med for type 2s. That would be Metformin, introduced in France in 1957 and the UK in 1958. But Metformin works on the liver to suppress unwanted glucose production and improve to insulin sensitivity (glucose uptake), and it’s safe.
As Lilly implies, Trulicity works on the pancreas, an organ that is already overworked, to counter the insulin resistance that is the cause of type 2 diabetes. Does it make sense to put an added burden on the one (and only) pancreas you have to secrete the insulin on which your life depends? Trulicity makes the pancreas work harder; it “helps the body release its own insulin,” to use their own words. Lilly’s not worried, though. When the pancreas eventually wears out, you will graduate to another injectable drug made by Lilly: daily insulin. Have you seen the price increases for insulin lately?
But Lilly and all the other drug manufacturers do not intend you harm. Their drugs are all approved by the FDA for the uses intended, and the uses all conform to the American Diabetes Association's Standards of Medical Care. What’s wrong with this picture? The treatment plan! The treatment treats the symptom of type 2 diabetes—an elevated blood sugar – by forcing the pancreas to produce more insulin. More insulin is what your pancreas has been producing for years before and since your impaired insulin response was discovered (by an elevated fasting blood glucose, or an A1c test).
Your impaired insulin response, aka Insulin Resistance (IR), is the cause of your type 2 diabetes. What caused your IR? Answer: On the government’s advice, in order to avoid eating saturated fat, for 60 years you ate a diet of 55% to 60% carbohydrate, composed of simple sugars and processed, refined, long-chain glucose molecules, euphemistically called “complex” carbohydrates. Over time, you became Carbohydrate Intolerant.
So what’s the best treatment for IR? That’s simple too: reduce your intake of carbs, especially the refined, processed ones, and the simple sugars of course, particularly the liquid ones. From 60% there’s lots of room for lowering. For the generic woman’s 2000kcal/day diet, 60% is 300 grams of carbs/day. Lowering it to 20% would be 100 grams/day. For a man (2500kcal/day = 375 grams/day), lowering it to 20% would be 125 grams.

Sunday, December 17, 2017

Type 2 Nutrition #411: “You don’t eat!”

When the lab report arrived in the mail, I was expecting an increase in my A1c. While eating Very Low Carb December to April, but only following a fasting regimen for the last 2 months, my A1c had dropped from 5.8% to 5.3%. By August I figured my system would get used to my routine and adjust. Instead, my A1c dropped another 0.1% to 5.2%. When I expressed surprise to my wife, she blurted, “I’m not surprised. You don’t eat!”
It’s true. I’m not hungry when I fast because, when I do eat, I eat Very Low Carb (VLC). As I result, my body is fat-adapted and obtains its energy from the fat I eat and the fat my body has stored for the purpose, and I still have plenty of that. So, my energy level, i.e. metabolic rate, remains high because when my body fat breaks down, it is used to maintain energy balance. This fat burning process will continue so long as I eat VLC. While glucose and insulin levels in the bloodstream remain low, the body will feed freely, as needed, on its own fat.
In retrospect, my concern that my A1c would rise was unfounded. I didn’t take into account that I had only been fasting for 2 days a week – and for just 2 months – when blood was drawn in April. The A1c test measures glucose on the surface of red blood cells over 3 months. So, when the A1c blood was drawn, I still had “old” red blood cells in my blood. Plus, after April I increased my fasting from 2 days to 3 days a week.
But my wife, feeling like she was on a roll, continued, “That’s why we don’t go out to eat as often as we used to….and you’ve saved a lot of money by our eating out less often. My rejoinder was that I only fast 3 days a week, and that still leaves 4 days a week for eating out! So, my standing offer, to eat out as often as she would like to, stands…and look at all the money she’s saved by not needing to buy food-for-two for 3 days a week! She agreed, and our “Bickersons” episode ended…strangely, I think, because she usually gets “the last word.”
The point is: if you don’t eat, you’re going to 1) lose weight and 2) save money. The secret is: doing it without hunger and without harm. Ketosis is the answer. It is the normal state of man, according to the NIH’s Richard L. Veech (and a host of other researchers in human metabolism). Ketosis begins when your body has finished digesting and absorbing your last meal and begins a period of fasting. The length of time before entering this state differs only in the amount of glycogen (glucose energy) stored in the liver from previously digested carbs.
In addition, if I don’t eat and continue to take Metformin as prescribed, my blood sugar is going to be better controlled. When I asked my doctor to increse my dose from 500mg once a day to 750mg twice a day – a “therapeutic dose” – and started my 300kcal/day regimen, I sometimes got fasting blood glucoses in the 60s, without hypoglycemia. When I told my doctor, he laughed. “You can’t get hypoglycemia on Metformin,” he said. Now, when I follow VLC strictly, my FBGs are in the 70s and 80s. A recent weekly average was 81mg/dl.
So, eating Very Low Carb and fasting 2 or 3 days a week is a win-win-win: You lose weight, you save money, and you and your doctor are pleased that your blood sugar control has improved. And as promoted by one of the Big Pharma ads on TV, when you have better blood sugar control, you have reduced your risk of cardio vascular disease (CVD). Type 2s have twice the risk of CVD as “normal” people. And if you’re been diagnosed with heart disease, you have an even higher risk. See “How Diabetic Do You Want to Be?” to learn more.

Naturally, the question arises: Would it be possible to get an A1c lower than 5.2%? Maybe even in the high 4s? By diet and Metformin alone?  I think it is possible. I also think I can continue to lose weight. When you read this a week before Christmas, I will have lost 185 pounds, just about “half the man I once was.” My target final weight is 171-175 pounds or “200 pounds lost.” And then the hardest goal of all: Maintaining that weight. I imagine it will involve Very Low Carb, One Meal a Day, and my “300kcal full-day fasts” for 2 or maybe 3 days every week. I’ll call it my VLC/OMAD/4-3 diet. I should be there…in the not-too-distant future.

Sunday, December 10, 2017

Type 2 Nutrition #410: My 300kcal “Fasting” Diet

About 10 months ago (the day after the Super Bowl), I began a regimen of full-day “fasting.” I had tried Intermittent Fasting (IF), where I ate within a small window each day (“16-8 fasting”), or I ate just one meal a day (OMAD). I maintained my weight but I didn’t lose. I still wanted to lose a lot of weight, so I decided to just “jump in.” Full-day fasting was new and unfamiliar to me, so I decided to start with alternate day fasting.
It worked. I lost 62 pounds, going from 248 to 186, and my BMI went from 36 to 27. Altogether, since starting Very Low Carb in 2002 at 375 pounds, I’ve lost 189. I’m “not half the man I once was,” my wife quipped.
When people ask, “How’d you lose weight?” I tell them, “Fasting.” Then they ask, “How’s your energy?” They imagine that they would feel weak because their metabolism would slow down due to the loss of energy “in.” After all, we’ve all been told, “a calorie is a calorie” and “Energy in = Energy out,” meaning if we don’t eat, our body is going to defensively slow down until we eat again. And we believe it because, well…’cause it’s intuitive.
Well, it’s not true. It only applies if your diet is largely composed of and DEPENDENT ON carbohydrates for energy. It’s not true for people who eat a diet of mostly fat and protein, limiting carbs to small amounts, in my case just at supper. We are “fat-adapted.” We are “fat burners, not sugar burners.” For us, the “Energy in” is not measured by what we put in our mouth; it is measured at the cellular level – where all the nutrients that are circulating in the blood are taken up by the cells. Thus, you do not slow down because you’re being fed.
How is it that when you eat mostly fat and protein you get to where you can burn body fat? The mechanism is: when you have glucose (from carbs) in the blood, the hormone insulin drives everything you eat into stored body fat and blocks access to your stored fat for energy. But when the level of your blood glucose (from carbs) drops, the level of your blood insulin also drops. That signals the brain to switch from glucose for energy to fat for energy. And then, once the carbs stored as glycogen in the liver are used up, and for so long as you then continue to limit carb intake by mouth to a very low amount, your body will break down body fat for energy.
On a “fasting” day, I have a 12oz coffee with 1½oz of heavy cream (not Half & Half) and 1 gram of pure stevia powder for breakfast. I stay “fat-adapted” with stable blood sugar all morning.
Then, if I’ve been working in the garden and I’m dehydrated, I’ll take some stevia-sweetened iced tea and maybe a little pickle juice for salt. I don’t take anything else by mouth until “supper.” My “fasting” supper is just one 6oz glass of red wine with 8oz of seltzer (a “spritzer”), which I use to wash down pills/supplements.
300kcal Fasting Diet” Macronutrient Composition: Coffee w/cream: Fat: 16g (144kcal), Protein: 1.2g (5kcal), Carbs: 1.2g (5kcal); Total: 154kcal. Spritzer (6oz red wine): Carbs: 4.5g (18kcal), Ethyl alcohol: 18g (126kcal); Total: 144kcal. Fasting day totals: Calories: 298kcal; Protein: 1.2g; Fat: 16g; Carbs: 5.7g; ethyl alcohol: 18g.

If I sense an impulse to eat or drink something after “supper,” I’ll have an ACV (apple cider vinegar) cocktail: 1 Tbs of Bragg’s unfiltered ACV, a few dashes of bitters, and a few drops of liquid stevia, with ice and club soda. The secret for the success of this “300kcal Fasting Diet” is, since I always eat VLC, I am ALWAYS “fat-adapted.”
So, when I return to a “feasting” state, I continue to eat Very Low Carb: The same “breakfast” of coffee with cream and stevia, a small lunch from a can, either 1) Goya Premium squid in its own ink (240kcal) or 2) Brunswick kippered herring fillets in brine (160kcal). I drink the brine. It’s a small lunch; just enough.
Then, for a “feasting” supper, I have a serving of protein with fat and a portion of low-carb vegetable with fat. With this supper I drink 2 glasses of my evening spritzer with my pills. Since I’m not hungry, because I’m fat-adapted, this is plenty. Some days I skip “lunch” and some days both “lunch” and “supper” and fast another day, or two. If you have lots of energy and you’re not hungry (because you’re burning body fat), why not? ;-)

Sunday, December 3, 2017

Type 2 Nutrition #409: When I used to eat eggs…

When I used to eat eggs (or eggs and bacon) for breakfast, my usual lunch was a can of King Oscar brand, Brisling sardines in EVOO (420kcal with the EVOO). I drank the EVOO and usually added salt. I supplemented with 2 grams of fish oil a day, and still do. As a result I had and still have very low triglycerides (about 50mg/dl). 
Now, however, I think that a can of sardines, especially if you drink the EVOO, is too many calories for lunch, particularly if you are not hungry. I am not hungry at lunch. Hell, I was never hungry at breakfast!
So these days I don’t eat breakfast any more. I just have a 12oz cup of coffee with 1½ oz of heavy cream and 1g of pure stevia powder. Then, if I eat lunch, I have one can of either of my two new favorites:
1. A can of Brunswick kippered herring fillets in brine (160kcal). I drink the brine. It’s a small lunch but enough.
2. A can of Goya Premium squid in its own ink (240kcal), packed in sunflower oil. I do NOT drink this PUFA oil.
Both the kippered herring and the squid are less expensive and fewer calories, and less fat, than the sardines. I also think that they would be a lot more palatable to the ‘normal’ person’s taste, but I like all three equally.
Why was I never hungry at breakfast? And why am I still not hungry at lunch? Because my body is fat-adapted, meaning it has been in a fasted state since a few hours after supper the night before, some 12 hours earlier. At breakfast, my body is in mild ketosis. In the absence of food, and as a consequence of eating Very Low Carb at supper and having low stores of glycogen in my liver from generally eating Very Low Carb, my body has maintained a high metabolic rate and energy balance by breaking down body fat during the nighttime “fast.”
Then, with only heavy cream (NOT H&H) in my morning coffee, that high metabolic rate and energy balance continue. With my lunch choices being only protein and fat, my ketosis and stable blood glucose continue into the afternoon while, without hunger because I am in energy balance, my body continues to burn its own fat.
It wasn’t always like this. When I began to eat Very Low Carb in 2002, I kept careful records. In the beginning it was just estimated carbs. Later, I decided to count protein too, and then fat and total calories. I ate a lot more then than I do now. After all, I was twice the man (literally) I am today, but I don’t keep those records today.
Keeping records, though, was in my nature, and I learned a lot from it. But I learned much more from other low-carbers. I joined this Forum of like-minded people and started asking questions. It was a supportive and safe space. I left another site I visited because all that people wanted to do there was argue about which way of eating was best. On the Bernstein Forum, I was very active for years, first as a student and later as mentor.
When you’re ready to make the shift, there are lots of ways to address a Lifestyle Change. But first you have to become convinced that the one-size-fits-all dietary advice given by the government’s Dictocrats and the “old school” medical establishment, and Big Pharma, has sadly been bad advice. It led to the Diseases of Civilization to which the world has succumbed. So, you have to be ready to break with that and manage your own dietary future. When you are ready, give Very Low Carb (VLC), or even Low Carb, a try. Here’s what you can expect:
       You will lose weight easily because you will not be hungry all the time. You will eat less and feel better.
       You will not need a snack in mid-morning or feel sleepy after lunch, or snack after supper/before bedtime.
       Your health markers will improve: blood sugar (A1c) and lipids (cholesterol), and blood pressure.
Some people have difficulty making the adjustment. I went cold turkey. I drank lots of water and I added salt. To avoid hypos (I was on 3 classes of oral anti-diabetic meds), I stayed in close contact with my doctor, who (as it happens) suggested VLC for me, to lose weight. Over time (15 years), I lost, literally, more than half my body weight (190 pounds), and I feel great! I’ve never been healthier or happier. You will be too. Give it a try!

Sunday, November 26, 2017

Type 2 Nutrition #408: Keto-adapted vs. Fat-adapted

If you eat Very Low Carb (VLC) – not just low carb – you undoubtedly will know the term keto-adapted. There’s no formal definition of VLC because it varies according to your metabolism – the degree of your dysregulated glucose metabolism due to your degree of Insulin Resistance. However, VLC is generally meant to be a dietary intake of less than 50 carb grams a day. For many is means less than 30 grams; for me it is just 15 grams a day.
When someone eats VLC, they generally eat less food because 1) fat is filling and does not induce the pancreas to secrete insulin,  2) protein digests slowly and make you feel full longer, and 3) carbs are digested quickly and they make your blood sugar rise and fall quickly and thus makes you “hungrier, quicker and oftener.” And, if you eat VLC, when your body has used up the energy from the carbs you ate (and some that you have stored in the liver), your body has to turn to fat for energy – the fat you ate and then fat that is stored on your body.
Protein isn’t used for energy directly. It components, amino acids, have myriad other functions in the body; however, most amino acids can be used to make glucose in a pinch or, in type 2 diabetics, even when not needed. That’s one of the reasons type 2s take Metformin, to suppress this unwanted glucose production.
So, generally then, when a fat cell (a triglyceride) is catabolized (broken down) into its parts, you get 3 fatty acid molecules and 1 glycerol backbone molecule. A ketone body is a byproduct of this fat cell breakdown and oxidation. It’s a normal process. Repeating then: Being keto-adapted means that your body is making ketone bodies as part of this normal process where it is breaking down body fat (or dietary fat) for energy.
When eating a VLC Ketogenic Diet (VLCKD), blood ketone concentrations are generally above the 0.5mmol/L level. When they are from 1.5mmol to 3.0mmmol/L, they are optimal. Eating in such a way as to achieve this level of ketone bodies in your blood is healthy. It is, in fact, the normal metabolic state when fasting…as when we eat just one meal a day or one meal every three or four days, the way our hunter/gatherer forebears did.
My recent personal experience with extended 2 and 3 consecutive day fasting supports this view. Many others report similar outcomes. My metabolism has not slowed down. I am fully energized. When I eat VLC on “feasting” days, I know that my body is fully fueled by stored fat while “fasting.” It can do this because, when consistently eating VLC, the body’s blood insulin levels drop, allowing access to body fat (and ketones) for fuel.
The state of being in ketosis – this normal state – is not the same as having a condition called ketoacidosis. As the name implies, ketoacidosis is a diseased state, a serious form of acidosis. With ketoacidosis, the blood concentration of ketones is generally 20-30mmol/L, a full order of magnitude, i.e. 10x, higher. Ketoacidosis is a life-threatening condition and requires immediate treatment and hospitalization. I point this out because some current pharmaceutical advertising inexplicably uses the term “ketoacidosis” as though it were a condition that you could be walking around with. Acidosis is a serious, acute, unrelated medical condition.
Ketosis, on the other hand, while a normal state, is NOT a necessary state to be in in order to be a fat-burner. I have in past somewhat carelessly used the term “keto-adapted.” I do not own nor have I ever used a meter to test ketones. I test my blood for glucose, not ketones. Neither have I ever used keto strips to test my urine.

I have just assumed that I was in ketosis when I ate as few as 15 or 20 or 30 carbs grams a day, and certainly when I was full-day fasting (300kcal/day including only about 5 carb grams). If you are eating VLC (and fewer total calories), and your metabolism is operating at full energy, you are burning FAT for energy. You are fat-adapted, whatever you level of blood ketones. And that is your object: When fasting – as when between widely separated meals – to burn body fat WHILE YOU CONTINUE TO OPERATE AT FULL ENERGY LEVELS. Nature built us this way, to be in “nutritional ketosis.” Otherwise we would have become extinct long ago.

Sunday, November 19, 2017

Type 2 Nutrition #407: Am I non-diabetic now?

Am I non-diabetic now? Seriously. Apparently there’s some disagreement about this. As I said in Type 2 Nutrition #439, a clinician told me that, 31 years after I was diagnosed (later with an 8.9% A1c), and after 15 years of eating Very Low Carb (VLC), with a 5.2% A1c now, I am no longer diabetic. I disagreed. I said that though my Insulin Sensitivity has improved, I am still Insulin Resistant and therefore Carbohydrate Intolerant. I said that I keep my Type 2 Diabetes in remission by restricting carbohydrates (VLC with Intermittent Fasting).
Then, a few weeks ago Megan Ramos, the Director of Jason Fung’s Intensive Dietary Management program, in an emotional rant on Facebook, said that “there are a lot of ‘haters’ out there” who say that, with an A1c of ≈4.5%, she is “not really non-diabetic anymore”; “[She’s] just controlling [her] diabetes with diet.” “Haters”? Huh? Well, isn’t that how she is controlling her diabetes?  Or does she think she is “cured”? In my case, I know that I am NOT cured. If I ate a lot of carbs again, my A1c would skyrocket!!! My guess is that hers would too, regardless of the fact that she doesn’t want to and never will eat that way again (i.e., “pasta 5 nights a week”).
Apparently, people who tell her that she is “just controlling her diabetes with diet” have hit a raw nerve…so I won’t tell her, but I am not a “hater.” I just prefer to look at my condition as one that I need to manage. And it is difficult to manage a condition if I am in denial that I have it. But, I’m willing to take a fresh look at the subject. Am I “non-diabetic” if a doctor who takes my blood (and doesn’t take a history) sees that my A1c is 5.2%? (In my case, besides my Way of Eating, I am also taking 1500mg of Metformin to suppress unwanted glucose production and improve insulin sensitivity, but this does NOT account for my “non-diabetic” A1c.)
So, with respect to my own condition, the matter comes down to whether I take a physiological or a psychological view. I cannot speak to Megan’s approach, nor can I address it from a medical POV; I am not a doctor. Neither am I an insurance underwriter who might take into account my history in setting a life insurance premium. Is it possible, from a life insurance underwriter’s POV, to at one time have been a diagnosed type 2 and then, later in life, to no longer be a diagnosed type 2 diabetic?
Age at onset of diabetes is doubtless a factor too. Incipient type 2 diabetes is undoubtedly more treatable and less intractable at an early age as less beta cell function has been lost. Megan notes that she was diagnosed at age 27 and fortunately found the right treatment immediately. Under Dr. Fung’s direction, she began to eat VLC and incorporated fasting from the get go. In 6 months, she lost 60 pounds and her A1c dropped to 4.5%. Today at 33, Megan takes no diabetic meds that I am aware of, eats LCHF and with fasting is 80 pounds lighter.
I was diagnosed at age 45 but continued to eat a Standard American Diet (neither my doctor nor I knew any better) for the next 16 years. I continued to gain weight and my type 2 diabetes got “worser and worser.” In 2002 I was maxed out on a sulfonylurea (Glyburide) and Metformin and starting on Avandia, a TZD. I weighed 375 pounds. Then, my doctor read Gary Taubes’s “What If It's All Been a Big Fat Lie,” in the New York Times Sunday Magazine (July 7, 2002) and suggested I try the diet described (20g of carbs a day) to lose weight!!!.
Today, 15 years later, thanks largely to eating Very Low Carb, I weigh 190. A little over a year ago, thanks to a suggestion from Megan Ramos, I began full-day fasting. I started with alternate day, then 2-consecutive day and now 3-day 300kcal fasts almost every week. I maintain my 185 pound weight loss by accepting that I have intractable Insulin Resistance and will therefore be Carbohydrate Intolerant for life. As such, while I am now clinically “non-diabetic,” and like Megan intend to stay that way for life, I know that if I ate the way I did before, I would quickly be a “clinical type 2 diabetic” again. Therefore, as a realist I have to say my type 2 diabetes is NOT cured; instead, my type 2 diabetes is IN REMISSION, and that “I control my diabetes with diet.” I will live happily and healthily and hope to remain that way for so long as I accept that reality.

Sunday, November 12, 2017

Type 2 Nutrition #406: Triglycerides and LDL-C while eating Very Low Carb

Michael Eades, MD, somehow has me on an “early notice” email distribution of his blog. He and his wife, Mary Dan (MD), also an MD, are early backers of the LCHF Way of Eating and authors of “Protein Power” (1996), and “Protein Power Lifeplan” (2000), and many other books. He blogs at A recent post was titled, “How to Lower Your Cholesterol, using diet to keep your doctor off your back.”
I had a question about a screen shot of his lab LDL-C so I emailed him, and he explained that it was not “Calculated” by the Friedewald equation but was “Direct.” (The report actually said that; I just missed it.) He then provided me with a link to a post he wrote a few years ago, Low carbohydrate diets increase LDL: debunking the myth. This is another post about the effect of Low Carb diets on TGLs and LDL-C. You’ll need to read to the end of Dr. Mike’s long post to get to it, so I thought it important to give it a column of its own.
Eades writes about a study in the American Journal of Clinical Nutrition. “This study…demonstrates that subjects following the low-carb diet experience a decrease in triglyceride levels and an increase in HDL-cholesterol (HDL) levels; and that these changes are accompanied by a minor increase in LDL-cholesterol (LDL)…” This concerns doctors, he says, since “most people who go on low-carb diets do so to deal with obesity issues, and since obesity is a risk factor for heart disease, it would appear that this small increase in LDL, often seen in those following a low-carb diet, could put these dieters at risk.”
So, noting that the benefits to HDL and triglycerides are offset by “this small increase in LDL-cholesterol seen in those following a low-carb diet,” Eades wondered how the LDL in the study was calculated; the “Methods” link in the study provided the answer: the Friedewald equation: LDL = TC – HDL – TGL/5. IT IS CALCULATED! What’s that you say? It’s not a DIRECT measurement? No, and every standard lab lipid test uses this method.
But, when Friedewald, et al. developed the formula in 1972, they made an exception for people who had a triglyceride number >400mg/dl; however, since most people’s test results were in the 150 – 250mg/dl range, they made no exception for TGL values of <100mg/dl. And as readers here know, people who follow a Very Low Carb or LC/HF diet usually have TGLs in the range of 40 – 90mg/dl. The average of my last 50 is 54mg/dl.
So, Eades searched the archives for scientific papers describing differences between calculated and directly measured LDL-cholesterol in people with low triglycerides. And lo and behold, he found two! One was a case presentation where a 63yo man had a TC of 263, an HDL of 85 and a TGL of 42.  The Friedewald calculated LDL was 170 but it was just 126 when measured directly. Another paper concluded, “Statistical analysis showed that when triglyceride is <100mg/dl, calculated LDL is significantly overestimated (12.17mg/dl average).”
In addition to the over calculation of LDL cholesterol for low-carbers who have TGLs consistently <100mg/dl, Eades reminds us that low-carbers typically have the large fluffy, good type of LDL, not the small, dense type.
Dr. Mike sums this up better than I could: “The moral of this story is that if you have been following a low-carb diet and your triglycerides are low (or if your triglycerides are just low) and your LDL reading comes out a little high – or even a lot high, don’t let anyone mule you into going on a statin or undergoing any therapy for an elevated LDL.  Demand to have a direct measurement of your LDL done.”
And the coup de grace: “Now when you hear people say that low-carb diets may help you lose weight but run your LDL levels up and increase your risk for heart disease, you’ll know this is just so much gibberish.  Sadly, your doctor will probably spout the same thing, and it will be up to you – who after reading this post will know more about this point than 99.9 percent of doctors practicing today – to educate your trained professional.”

Sunday, November 5, 2017

Type 2 Nutrition #405: LDL-C and TGL while Fasting

One of the speakers at Keto Fest in New London last July was Dave Feldman, a self-described engineer, software developer and entrepreneur. He made a rather geeky presentation about his high LDL-C. My notes from his talk: “LDL-C has many jobs.” “Its primary job is to distribute energy from fat” (triglycerides or TGL). “Multi-day fasting before a cholesterol test will likely spike your LDL-C.” That last sentence got my attention.
Then I saw that both Michael Eades ( and Jason Fung ( had also credited Feldman on this hypothesis. It turns out he’s attracted a lot of attention in the Low Carb/High Fat and fasting worlds. Here’s a related sample from Feldman’s website,
“There’s just a few of us that think the same thing as I do. That cholesterol is the red herring. That mostly, this is due to higher demand for fat-based energy coming from storage in the form of triglycerides being carried by VLDLs. The cholesterol being measured resides in those VLDL-originating LDL particles, which is why its quantity is inverted from the total amount of dietary fat I eat.
More fat in my low carb diet? Less need for fat-based energy from storage, less VLDLs mobilized, less cholesterol riding along with it. Lower cholesterol score.
Less fat in my low carb diet? More need for fat-based energy from storage, more VLDLs mobilized, more cholesterol riding along with it. Higher cholesterol score.
My doctor’s appointment is typically on a Tuesday, and I generally don’t fast on weekends, but I often do on Monday. So, I made a mental note to be sure to eat fat on any fasting Monday before an appointment. Check!
I should also note that Dave Feldman is also what is known in lipidology medicine as a “hyper-responder.” “The term, ‘hyper-responder,’” Feldman says, “has been used within the ketogenic/low carb, high fat (keto/LCHF) community to describe those who have a very dramatic increase in their cholesterol after adopting a low carb diet.” This is not common, but occurred to Feldman and is the reason he began his investigations and developed “The Feldman Protocol,” a hypothesis to explain this “inverse correlation.”
Dave’s Protocol is much too complex for this blog, but if you happen to be one of the few to whom this has occurred, I strongly encourage you to click on the link above and delve into the substance of his experiments.
For my part, eating just Very Low Carb (without fasting), my LDLs and TGLs have all been very good. I wrote about them a few years ago here, here and here. Note in my case, by following a strict VLC diet, TGLs dropped about 2/3rds and HDL more than doubled. I also recently did a 14-year TGL average of 50 tests, beginning 1 year after I started VLC, and the result was 54mg/dl. The average of 15 or so in the early years was 49mg/dl.
Since starting full-day fasting, my TC has gone from 198 to 201 and then 196. My HDL-C has gone from 85 to 74 and 74. My LDL-D has gone from 101 to 114 to 100; my TGLs have gone from 60 to 67 to 108. Hmmm. Also, my blood pressure has gone from 130/80 to 125/70 and 120/80. And my A1c has gone from 5.8 to 5.3 and 5.2. This is the “expected” (default) response to switching from the low-fat, very high carb Standard American Diet to a Low-Carb/High-fat diet. Dave Feldman’s hyper-responder response is not typical, but his work on investigating the mechanism is interesting and may prove useful in explaining these (and my) anomalies.
It explains to my satisfaction, at least, my rise in TGL from my historic low averages (49 and 54) to my most recent 108. Since TGLs are a surrogate for VLDL, this corroborates Feldman’s premise given above: “higher demand for fat-based energy coming from storage in the form of triglycerides being carried by VLDLs…”

Sunday, October 29, 2017

Type 2 Nutrition #404: “If you’re feeling signs of sleepiness…”

In his magazine, “The Good Life,” Dr. Oz’s Rx of the Month (March ‘17), is, “If you’re feeling signs of sleepiness, pull over and take a nap – it’ll help.” D’ya know what would help even more? Don’t eat a carb-loaded lunch!
Dr. Oz’s suggestion is based on the assumption that the driver in his set-up piece is sleep-deprived. We’re a “chronically sleep-deprived nation,” the article says. “Skipping even a few hours of sleep nearly doubles your risk for an accident,” according to an AAA report cited. But you know what produces “signs of sleepiness” as much and much more frequently? Answer: a metabolism that has crashed because of a low blood sugar.
If you have Insulin Resistance, as you likely do if you meet the criteria for Metabolic Syndrome, or have been told you are either pre-diabetic or a type 2 diabetic, you have a chronically elevated level of insulin in your blood. In that case, your chronically elevated blood insulin level will block access to energy from body fat which a healthy metabolism would have between meals. Your blood insulin level remains elevated as your pancreas continues to make insulin in an attempt to overcome the resistance to the uptake of glucose from your blood.
Without that access to energy from your body fat, your metabolism will have to slow down to maintain energy balance, called homeostasis. Among other things, you will feel “signs of sleepiness.” You’ve crashed. And you will soon be hungry again…for more carbs. Yes, it’s a vicious cycle. By continuing to feed your body carbs by mouth, you deny it the body-fat fuel it needs to be “energized” and in balance at a higher metabolic rate.
Of course, you do have an alternative: You can gain access to your body fat reserves to give your body the energy it needs to maintain a stable, high metabolic rate. That is, to remain in energy balance (homeostasis) but at a normal, high metabolic rate. Your body will not need to slow down and “crash.” How? Listen up!
Most people in the U. S. eat their evening meal between 6 and 8pm. Digestion of carbs and fat starts almost immediately and is usually complete within an hour or two. Protein takes longer, up to 4 to 5 hours. Then the body rests (and we sleep), and while we sleep it runs on sugar in the blood and stored in the liver. When the “sugar” stores are nearly exhausted, it enters ketosis, where it naturally breaks down body fat for energy.
This is a normal process. It is called the overnight fast. We all do it. And survive. And we wake up in the morning feeling refreshed from the rest and the fast! And then we eat “breakfast.” Get it? “break-fast.” The problem began when we began to create a cycle of carbohydrate addiction: we started by eating a breakfast loaded with carbs, starting with fruit juice. Pure sugar water! Then we ate toast or a muffin or worse, a bagel. Pure “sugar” glucose! Then we ate cereal or oatmeal. All carbs (glucose)! And in 2 hours we’re hungry again.
Suggestion: Try 2 eggs, any style, even hard boiled if you don’t have time to prepare them in the morning. If you do cook, fry them in bacon grease (enjoy a bacon ‘side’). This “break-fast” is all protein and fat. No carbs!
Or, if you’re not hungry (like me), just have a cup of coffee. I have mine with heavy whipping cream (a ‘fat bomb’) and pure powdered stevia (not in packets of stevia combined with maltodextrin or dextrose – other words for sugar). If you do this, you are in effect extending your fast. You will be surprised at how your energy level, and your blood sugar, will remain stable all morning long. I’ve been skipping breakfast for a few years now, and I often forget to eat lunch. Or don’t think about it until 2 or 3 or even 4 in the afternoon. Really!
I think it’s a red herring to attribute “signs of sleepiness” to sleep deprivation. I know that many families have to get up early and stay up late and that sleep deprivation is a problem for some. But “signs of sleepiness” are much more likely to be attributable to a metabolism that slowed down because access to its own fat stores for energy was blocked by a chronically elevated blood insulin associated with pre-diabetes and type 2. If you are overweight and are developing insulin resistance, that is most likely why you get tired after a carb-laden meal.

Sunday, October 22, 2017

Type 2 Nutrition #403: Denial is not a river…

When someone says their A1c is 6.1% and they’re doing nothing about it – not even taking Metformin – I think, what are they thinking about! Are they waiting until they’re told, as Tom Hanks was, “You’ve ‘graduated’ to full-blown, type 2 diabetes.” As though, after observing “high-normal” blood sugars for 20 years, his doctor was congratulating him! And what is their doctor thinking about? I mean, folks, denial is not a river. I know, it’s an old joke, but that behavior is just bizarre, unless, that is, the Standards of Medical Care – which to be paid by insurance for his or her services a doctor must follow – doesn’t offer a better solution.
That’s what it amounts to, though. Metformin is not generally prescribed to pre-diabetics, although in my opinion it should be. Currently, it’s occasionally  prescribed “off-label,” meaning “used in a manner not specified in the FDA’s packaging insert.” But putting pharmacotherapy aside, what else can a pre-diabetic do to “delay” the onset of frank type 2 diabetes, or as demonstrated in so many recent trials, to proactively REVERSE incipient type 2 diabetes and put this modern lifestyle scourge into complete remission?
Well, the first thing you have to do is acknowledge that you are pre-diabetic. What does that mean? It means that 1) you have a genetic predisposition, 2) you’ve eaten, per nutritional guidelines, a diet unnaturally high in carbohydrates in order to avoid eating saturated fat and cholesterol, and 3) your body has “expressed” an intolerance for so many carbohydrates. Being “pre-diabetic” means you are now carbohydrate intolerant. The condition, Insulin Resistance (IR), is a continuum. And the sooner you address it, the easier it is to manage.
Insulin Resistance is part of Metabolic Syndrome, a constellation of symptoms that put you at much higher risk of heart disease (CVD and CHD) as well as several other chronic diseases of Western Civilization, including Alzheimer’s disease (“type 3” diabetes) and many types of cancer. But Insulin Resistance can be managed by lifestyle changes. You modify your diet so the pancreas does not secrete too much insulin. The only way to do that is to restrict your dietary intake of carbohydrates.
The object of self-management of your Insulin Resistance is to keep your blood insulin level low. There is not a common lab test to measure blood insulin, but a good surrogate is your blood sugar level, either fasting (FBG) or A1c. And there is no drug to lower blood insulin although anaerobic exercise can help.  If you’re Insulin Resistant, the consitent way to lower your blood insulin is to restrict carbohydrates. It is not a “therapy” that will enrich Big Pharma, or Agribusiness, so you’re not likely to hear about it from them. And to avoid financial penalties and sanctions, your doctor is not likely to go against what the Standards of Medical Care dictate.
So, self-management of your pre-diabetes is just something you’re gonna have to do yourself. Perhaps that’s why you’re surfing the web and how you came across this site. If so, we hope you’ll come back. We encourage you to try carbohydrate restriction on your own. Test your blood before and after a meal and see how much it improves when you eat fewer carbs. Do it for 3 months and see your A1c improve and your weight plummet!
Or…here’s an idea. Forget about how much carbohydrate restriction will help your pre-diabetes or type 2 diabetes. Don’t even think about asking your doctor for “permission” to go on a carbohydrate restricted diet to help control your pre-diabetes or type 2 diabetes. Ignore the fact that type 2 diabetes is a dietary disease.
Instead, if you would like to lose a few pounds, and you think your doctor would like that as well, ask if he or she thinks a carb-restricted diet would be a good way to lose weight? Safely! I’ll bet you that you’ll get a “yes.”
Better yet, don’t ask. Help your doctor avoid the risk of financial penalties and sanctions from Medicare. And then, when you next have bloodwork done and your weight and cholesterol – especially triglycerides and HDL-C – and blood pressure and inflammation have all improved, it’ll just be our little secret how you did it. 

Sunday, October 15, 2017

Type 2 Nutrition #402: IGNORANCE is the biggest problem…

I was at a gathering recently where I was having a tĂȘte-a-tĂȘte with Dr. Eric C. Westman, co-founder and medical director of the Heal Clinics. I’ve been a diagnosed type 2 diabetic for 31 years, eating Very Low Carb for the last 15 and writing about it here for the last 7, so when Dr. Westman asked me what I thought was the biggest problem in type 2 diabetes today, I responded, simply, “Ignorance.” He nodded his head in agreement.
I told Dr. Westman that I started this WOE after my doctor had read Gary Taubes’ July 7, 2002, New York Times Sunday magazine cover story, “What If It’s All Been a Big Fat Lie?” My doctor wanted me to lose weight, so he tried it himself first to see if it would be safe and effective. When he lost 17 pounds, he suggested that I try it too, to lose weight! As he walked me down the hall to schedule my next appointment, he said, “It might even help your diabetes.” He had no more than a vague notion about that. Turns out, he was spot on!
My doctor told me to start Atkins Induction after he returned from vacation so he could monitor me closely.
He had my blood sugar “under control” (FBG: 155mg/dl!!!) with 3 classes of oral hyperglycemic meds. He knew, however, that by this standard he would soon have to refer me to an endocrinologist to start an insulin regimen, probably a basal injection once a day and maybe mealtime bolus injections, 3 times a day, as well.
Like so many other clinicians, my doctor believed that my morbid obesity (I weighed 375 pounds) was a CAUSE (frequently hedged as a “risk factor”) of type 2 diabetes. But Taubes had not yet written his ground-breaking magnum opus “Good Calories – Bad Calories” (2007), in which he dispels that notion. In fact, in the Epilogue (page 454) he says, “As I emerge from this research,” 10 “certain conclusions seem inescapable to me.” Today, ten years later, every one of his conclusions is still right on point – as true today as the day he wrote them.
In #5 Taubes says, “Obesity is a disorder of excess fat accumulation, not overeating, and not sedentary behavior.” If this first part sounds like a tautology, it is not. It is fully explained in #6 thru #10. You really should read all 10 “certain conclusions” in the above link. I’ve read it a dozen times over the years.
6.      “Consuming excess calories does not cause us to grow fatter, any more than it causes a child to grow taller. Expending more energy than we consume does not lead to long-term weight loss; it leads to hunger.
7.      Fattening and obesity are caused by an imbalance – a disequilibrium – in the hormonal regulation of adipose tissue and fat metabolism. Fat synthesis and storage exceed the mobilization of fat from the adipose tissue and its subsequent oxidation. We become leaner when the hormonal regulation of the fat tissue reverses the balance.
8.      Insulin is the primary regulator of fat storage. When insulin levels are elevated – either chronically or after a meal – we accumulate fat in our fat tissue. When insulin levels fall, we release fat from our fat tissue and use it for fuel.
9.      By stimulating insulin secretion, carbohydrates make us fat and ultimately cause obesity. The fewer carbohydrates we consume, the leaner we will be.
10.  By driving fat accumulation, carbohydrates also increase hunger and decrease the amount of energy we expend in metabolism and physical activity.”
Gary Taubes’ hormonal explanation of the metabolic science of fat synthesis and breakdown totally refutes the “calories-in, calories-out” (CICO) hypothesis. CICO sounds so logical that it is now “accepted wisdom” without evidence. It’s like that other “truism” of establishment dietary thinking: “Eating fat makes you fat.”
Taubes’s “certain conclusion” #1, “Dietary fat, whether saturated or not, is not the cause of obesity, heart disease, or any other chronic disease of civilization,” deals with that. Of course, he backs up this statement, and all his other conclusions, with 460 pages of convincing research and analysis, 45 pages of links to his sources, and a 66 page bibliography. “Good Calories – Bad Calories” is a bit of a slog, but it’s worth it.

Sunday, October 8, 2017

Type 2 Nutrition #401: “Improve your A1c with a non-insulin option”

Have you seen this diabetes drug commercial on TV? It always makes me laugh. I’ve been a diagnosed type 2 for 31 years, and my last A1c was 5.2%. That was a big improvement from 5.8% eight months ago. The only diabetes medication I took eight months ago and I take now is Metformin. I improved my A1c with another “non-insulin option.” I control my diabetes with Metformin, and I improved my A1c by eating Very Low Carb.
Of course, the TV ad had a different “fix” in mind for you. It was playing on the dread people have for the drudgery of daily insulin injections. Most insulin-dependent type 2s inject a slow-acting basal dose of insulin once a day and then many (most?) inject a fast-acting bolus with each meal. Thus, with this 1 to 4 injections-a-day routine, if you are very careful to avoid hypos, you can achieve “good” blood glucose control. It’s an onerous path to follow.
It doesn’t have to be this way. I weighed over 300 pounds in 1986 when an internist diagnosed me as a type 2 with a high fasting blood sugar (FBS). He started me on an oral anti-diabetic drug of the only class then available in the U.S., a sulfonylurea. Seven years later an endo gave me my first A1c test. It was 8.9%. My FBS was 197. Nine years later (2002) I was maxed out on both the sulfonylurea and Metformin and had started on Avandia.  My FBS was 81, so my doctor had my “progressive” diabetes under control with drugs. But we both knew that when the 3rd class of drugs was no longer effective, I would “graduate” to insulin. I weighed 375 lbs.
So, my doctor now turned his attention to my weight again. He had tried before. I had seen his staff dietician who advocated a “restricted-calorie, balanced diet and exercise.” It didn’t work. I lost weight but promptly regained it. Then, in July 2002 my doc read the New York Times Sunday Magazine cover story, “What If It's All Been a Big Fat Lie,” by the science writer Gary Taubes. He tried the diet described himself, and it worked. When he came back from vacation in September, he asked me to try it too. He wanted to monitor me closely.
The diet was Atkins Induction, which is VERY low carb, just 20 grams a day. On the first day I had a hypo. I called him, and he told me to stop taking Avandia. The next day I had another hypo and he told me to cut the other two drugs in half.  Later that week, when I had yet another hypo, he told me to cut them in half again. So, in just one week, by strictly following a VERY LOW CARB diet, before losing more than a few pounds of water weight, I had dramatically reduced my diabetes meds. My type 2 diabetes had gone into remission.
A year later, in August 2003, I had lost 60 pounds and my A1c was 5.4%. A few years after that, I regained 12 pounds over the summer, so I started on Richard K. Bernstein’s 6-12-12 program for diabetics (30 carb grams a day). Over the course of a year or so, I lost that 12 and another 110 pounds, reaching 205 pounds at the end of 2008. That was my weight when I completed Army Basic Training in 1960! And my A1c was still 5.4%.
Now, 15 years after beginning to eat Very Low Carb, and plenty of “misadventures” (“cheats” with ups and downs), I celebrate by dropping below 200 pounds (186 last week) for the first time since I was in my teens. And although 15 years ago, in 2002, my doctor’s motivation was to get me to lose weight, NOT to treat my so-called “progressive” type 2 diabetes, I have “improved my A1c with a non-insulin option.” Furthermore, I have forevermore avoided progressing to becoming an insulin-dependent type 2. AND MY LATEST A1C WAS 5.2%.
To his credit, although he suggested it to help me lose weight back in 2002, my doctor did have an inkling that eating VERY LOW CARB might help my type 2 diabetes. He said, as he walked me down the hall to schedule my next appointment, “Dan, this diet might help your diabetes too.” Boy, was that an understatement!
Would that more doctors had a similar understanding of the basic relationship between dietary carbohydrates and blood sugar regulation. Type 2 diabetes is, after all, a dietary disease, and the best treatment is self-management by carbohydrate restriction. Your doctor can’t write a prescription for that, BUT YOU CAN!

Sunday, October 1, 2017

Type 2 Nutrition #400: “Not half the man I once was,” my wife quipped

As you can tell from the number above, I have been posting a long time. I have also been a diagnosed type 2 diabetic for 31 years and probably pre-diabetic for a decade or more before that. At my doctor’s suggestion (to lose weight), I’ve been eating Very Low Carb since 2002. About 8 months ago, I added Extended Fasting.
In 2002 I started and stayed on Atkins Induction (20g/day) for 9 months and lost 60 pounds. Four years later I regained 12 and started and then stayed on Bernstein (30g/day) for a year and lost 100 pounds. Later I lost another 20+, reaching 205 in 2008. I regained some later but recently returned to 205 using consecutive 2 and 3-day fasting. This was possible because, while fat-adapted on VLC, I can easily go 2 or 3 days without hunger.
My weight has not been below 205 since I was a teen ager, maybe pre-pubescent! I’m 76 now. But, feeling as healthy and energized as I do, I am going for a new goal: To be half the man I once was. I began in September 2002 at 375. My goal is to get to half that weight, to 187, by end of September 2017, 15 years later. Here goes. (N.B.: If you want to skip the messy parts, don’t bother with the Weekly details; just jump down to Results.)
Week 1: I start this challenge at 207, so I need to lose 20 pounds in 8 weeks. The 1st 4 will be easy. I gained them overnight, literally, so this week I expect to lose at least 6, leaving 14 for the remaining 7 weeks, or 2 pounds a week. That’s very doable. Result: lost 5lb, after regaining 3 Sat. FBG aver: 81mg/dl. Wk 2 goal: 5 lbs.
Week 2: Three restaurant meals this week, including a birthday. Fasting only Mon & Wed. Result: took 3 days to lose the 3 pound gain, and the glucose shot up after the b-day; alas, I lost only 1 pound. FBG aver: 97mg/dl.
Week 3: Starting the week 2 lbs behind, but have no excuses. Should be a good week. Goal: lose 4 lbs to reach 197; Plan: fast Mon-Tue-Wed. Result: lost 5, then regained 2 Sat to 198, net lost 3 pounds. FBG aver: 82mg/dl.
Week 4: Starting week just 1 lb behind. Goal: lose 3 lbs to reach 195. Fasting Mon-Tue-Wed. Result: Small cheats every day, but I lost 3 lbs and reached goal of 195, a 180 lb total loss from 2002. FBG aver: 82mg/dl.
Week 5: Eight pounds to go in 4 weeks, 2 lbs per week. Goal 193. However, gained 4lbs both Sun & Mon, so strict fasting this week; I need to lose 10 lbs. Result: Lost 11, fasting 4 days; net lost 3 lbs. FBG aver: 79mg/dl.
Week 6: Now 1 lb. ahead, but goal is still 2 lbs. Eating ‘normally’ Sun & Mon (company); fasting thereafter. Results: Relaxed a bit and just lost 1 lb to 191, on target. 4 pounds to go, 2 each week. FBG aver: 71mg/dl!
Week 7: Doing a modified fast Mon-Tue-Wed, then Fri and/or Sat if required. Thurs: dining with visiting ‘kids.’ Results: Missed the mark; lost just 1. Too much fat, a little cheating, poor choices Thu. nt. FBG aver: 88mg/dl.
Week 8: Final week of challenge with 3 pounds to go. Very doable with a little discipline. Let’s see if I have it.
Results: A feast on Sunday added 4 lbs. to the challenge, but I “fasted” until I lost NET 4. FBG aver: 79mg/dl.
Results: Well, I did it! These words recall for me the line “We did it!”that Elle Woods squeals in her graduation speech at the end of one of my favorite films, the chick-flick “Legally Blonde.” Except in this case, I did it, all by myself! In the last 8 weeks, using a combination of Very Low Carb on days that I ate “normally,” and Very Low Carb on my so-called “fasting” days, I lost 17 pounds. That was my goal: to get to be “half the man I once was,” at 375 pounds, when I first discovered Very Low Carb in 2002. My doctor suggested I try Atkins Induction (20 carb grams a day) to lose weight. It’s been a long journey, with lots of ups and downs, but I finally reached my goal. Along the way, my health improved greatly, and I feel great. It’s wonderful not to always be hungry.
Next week my wife and I are taking a vacation. We’re going up to the Shaw Festival at Niagara on the Lake. Plans include dinner every night in a nice restaurant and one lunch and a tour of one of the many wineries in the area. When we return, I will begin one more weight loss challenge: To lose another 15 pounds (plus what I gain on vacation) to get down to 171. And then, THE FINAL CHALLENGE: to maintain the 200 pound loss. I will keep my weight between 171 and 175 by a combination of OMAD (VLC), plus Extended Fasting as needed. 

Sunday, September 24, 2017

Type 2 Diabetes, a Dietary Disease #399: WebMD and Walgreens, a new collaboration

While waiting in my wife’s doctor’s office the other day, I picked up a FREE magazine, “WebMD diabetes, at Walgreens.” I’ve been a type 2 for 31 years, and treating it as a dietary disease for 15, so I didn’t expect that the magazine would have much to offer me, but…was I in for a surprise! It was loaded with material for my blog!
The featured article was “Savor Summer,” with a recipe section: The subtitle was “New ways to bring sweet corn to your table” (my emphasis). But to a carboholic, the added emphasis is unnecessary. The brain sees “sweet” and translates it to “SWEET.  And the food photography was great! Really mouth watering stuff!
“You can almost taste sunshine when you bite into a freshly picked ear of corn,” the article begins, adding, “It’s also nutritious” because it’s “chockful of Carotenoids.” (No mention of sugar.) But then, unabashed, it says, “It’s also a starchy vegetable, easily rounding out your plate with more fiber than a refined grain.” Okay, so it’s not a refined grain. That’s good. But corn is starch. It is pure sugar and starch. For a diabetic, that’s just as bad as a refined grain. The sugar alone is 62% glucose (the rest is fructose) and the starch is 100% glucose.
And if that wasn’t enough, 2 of the 3 corn recipes added honey! Added honey, for diabetics! As if corn wasn’t sweet enough! The recipes had all been reviewed by the WebMD medical editor, an MD, and she could do it with a clear conscience because, by the U. S. Dietary Guidelines “MY PLATE, a healthy meal plan for everyone, even diabetics, – includes ¼ starches. Corn certainly fills the bill. But should a magazine for diabetics, intended to help both type 2 diabetics and pre-diabetics make healthy food choices, suggest and feature recipes that will assure that the pre-diabetic progress to diabetic and the diabetic remains in a diseased state? C’mon!
 Why would the medical community and Big Pharma encourage people who have “presented” with evidence of Insulin Resistance, which equates to Carbohydrate Intolerance, suggest, recommend, and even encourage people to eat a diet comprised three-quarters of carbohydrate (¼ starch and ½ non-starchy vegetables)? Why? One size fits all!!! For 37 years the “Dietary Guidelines for Americans” have ordained that one-size-fits-all. The Guidelines have gone through various iterations, from various food pyramids to today’s “My Plate,” but they all have one thing in common: by following them, you, the diabetic, most assuredly will get sicker and sicker.
Who benefits from this whack-a-mole recommendation? I know, I know. It’s easy to conclude it’s the doctor’s and the pharmaceutical industry, including retailers like Walgreens. And they certainly do benefit. We all get sick, and they take care of us. But that’s their business. They’re just doing what they are in business to do. Altogether, the 23 page Diabetes magazine included 4 pages of corn recipes, 8 pages of other content, and 11 pages of ads, 4 for Walgreens products and 4 for diabetes meds from Lilly and Pfizer, available at Walgreens.
But that’s not where the problem lies. It originated forty years ago when the U. S. government got into the nutrition business. In 1977 a U. S Senate select committee convened and held hearings. So-called “experts” testified. Later, the lay staff of the Committee produced the “Dietary Goals for the United States.” In 1980, and every five years after, HHS has produced the “Dietary Guidelines for Americans.” It’s been a disaster.
The Nutrition Coalition has proposed that the Guidelines be reformed. They say, “Americans have followed the Guidelines, but their health has not improved.” “The Guidelines have not always provided the best dietary advice.” “The science is not settled and in some cases has been reversed,” and “(T)he process of drafting the Guidelines needs reform.” I certainly agree. I have signed their petition and ask you to consider adding your name to the growing community of people like us who are in-the-know. We need Guidelines based on sound scientific evidence. And there will still be plenty of ways in which WebMD and Walgreens can collaborate. And then my wife’s doctor won’t have the shame of having this awful magazine in his waiting room.

Sunday, September 17, 2017

Type 2 Diabetes, a Dietary Disease #398: My Supplements

I haven’t written about supplements since…wow! I just did a search of almost 400 posts and discovered I have NEVER written about my supplements. I guess it’s because I consider it personal, not in the sense of private – I am transparent about my health – but in the sense of “individualized.” I think it is also because I have read so much about how none of them are necessary or even helpful, like I’ve just been duped or sold a bill of goods.
So, why do I take supplements when there’s no real way to prove that they have helped me? A well designed experiment is impossible; there are just way too many confounding factors. I guess the best answer is that they are “insurance;” besides, most of them are vestigial, that is, I began them before I was initiated in the ways – or the concept anyway – of eating a low carb diet of whole, real food…and I just continued with them. That’s my construct anyway. Besides, some of them I do believe in. So, which would I eliminate and why?
I am prompted to write about this now by a presentation made at Keto Fest in New London, CT last July by podcast meister Ivor Cummins, the “Fat Emperor.” Near the end – maybe his very last sentence – as though it were a hurried, throwaway line, he said: “Don’t forget to take supplemental magnesium and potassium.” No time for an explanation. It was just a given, like everyone knew! Fortunately, I do take them both.
Here’s a complete list of my current supplements. Bear in mind, I am/have been a Type 2 Diabetic for 31 years and eat a Very Low Carb (VLC) or LCHF (Low-Carb, High-Fat) or Ketogenic Diet, with frequent full-day fasting.
     1g fish oil, containing 300 EPA and 200 DHA, and 5 IU of vitamin E
     1 tablet high potency men’s multi-vitamin, with vitamin D3, lutein and lycopene
     100mg capsule of CoQ10, the active form (Ubiquinol)
     200mg magnesium glyconate, chelated for absorption
     200mcg of elemental chromium (chromium picolinate), with 18mg L-leucine + 2mg vitamin B6
     100mg biologically active R-Lipoic acid (alpha lipoic acid), with 150mcg D-Biotin
In addition, I take 2 prescription meds: 750mg metformin Hcl and 25mg HCTZ, a diuretic (for hypertension)
With 6oz RED WINE & 8oz SELZER, about 12 hours later, if FASTING, or with FOOD (my supper meal).
     1g fish oil, containing 300 EPA and 200 DHA, and 5 IU of vitamin E
     200mg magnesium glyconate, chelated for absorption
     99mg potassium, a multi-source blend
     1 capsule homocysteine modulators: 50mg B6, 400mg folic acid (B9), and 500mcg B12
In addition, I take 3 prescriptions: 750mg metformin Hcl, and 20mg Enalapril & 240mg Verapamil (BP pills)
Candidates for deletion: 1) chromium picolinate, 2) R-Lipoic acid and 3) homocysteine modulators.
Possible additions: 1) a small (250mg) Vitamin C tablet with supper, to help with protein uptake, and a calcium supplement, to help with magnesium uptake. First I need to learn more about their interactions.
My labs are very good. My last A1c was 5.2%. My Vitamin D and B12 are high and very high respectively. My TC is below 200mg, my HDL-C is averages about 80, my LDL-C averages about 100 and my TGs still average around 50, even though I don’t eat a can of sardines for lunch any more. When I do eat lunch, I prefer a can of kippered herring in brine. It’s fewer calories and much less fat, and I’m trying to burn endogenous fat, not exogenous fat! My fasting intake is about 300kcal/day and my feasting intake paradigm is still about 1,200 (15g carbs, 60g protein and 100g fat, mostly saturated/monounsaturated). Finally, my inflammation markers are very low. Now that I have laid it out for everyone to see, what do you think? I invite comments.