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 www.proteinpower.com/drmike. 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 (proteinpower.com) and Jason Fung (intensivedietarymanagement.com) 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, cholesterolcode.com/.
“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.
THE TAKEAWAY: “MULTI-DAY FASTING BEFORE A CHOLESTEROL TEST WILL LIKELY SPIKE YOUR LDL-C.”
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!