Saturday, November 30, 2019

Retrospective #287: “Can Type 2 Diabetes Be Reversed?”

The Nutrition Debate #88,” Reversal of Type 2 Diabetes,” proved to be a very popular post; it has had over 8,200 page- views. But let me be clear: I do not believe that Type 2 diabetes can be “cured,” and so I can understand if someone reading that post (#88) might have felt misled. That was not my intention. Nor was I consciously intending to glom readers by attracting them with “click bait” to an appealing prospect through a headline. I was simply reporting on a paper in a peer-reviewed British medical journal that had precisely that title; that’s why my blog title was in quotes.
The paper was very interesting. Its AIMS/HYPOTHESIS was that “Type 2 diabetes is regarded as inevitably progressive, with irreversible beta cell failure. The hypothesis was tested that both beta cell failure and insulin resistance can be reversed by dietary restriction of energy intake.” Okay, it’s a hypothesis. Its aim is to challenge an assumed truth – one that virtually all medical practitioners believe – that Type 2 diabetes is “inevitably progressive.” And they tested it by “dietary restriction of energy intake” alone. To be clear, they did it with fewer calories, NOT fewer carbohydrates.
The hypothesis sprang from the observation that “normal glucose metabolism is restored within days after bariatric surgery in the majority of people with Type 2 diabetes.”  “There is now no doubt,” they concluded and report in their COUNTERPOINT STUDY, “that this reversal of diabetes depends upon the sudden and profound decrease in food intake, and does not relate to any direct surgical effect.” Again, that’s food (total energy) intake, NOT carbohydrates.
The CONCLUSION/INTERPRETATION of this study was only a little less assertive than their hypothesis: “Normalization of both beta cell function and hepatic insulin sensitivity in Type 2 diabetes was achieved by dietary energy restriction alone. This was associated with decreased pancreatic and liver triacylglycerol stores. The abnormalities underlying Type 2 diabetes are reversible by reducing dietary energy intake.” Okay, they hedge a bit. They say “the abnormalities underlying Type 2 diabetes are reversible…” But they still use the word “reversible.” That’s pretty strong, but they are scientists and provide the data to support their findings: normalization of pancreatic and liver fat cells (triglycerides).
My inveterate editor discovered a follow-up study done by the same researchers, and I reported on in The Nutrition Debate #89, “’Reversal of Type 2 Diabetes’ Revisited.” Unfortunately, it glommed only 725-page views, but in it the authors reported on “individuals (who) began to feed back their personal experiences of attempting to reverse their diabetes.”  CONCLUSION: “These data demonstrate that intentional weight loss achieved at home by health-motivated individuals can reverse Type 2 diabetes. Diabetes reversal should be a goal in the management of Type 2 diabetes.”
This and other work by these researchers earned them the high privilege of presenting the ADA’s “The 2012 Banting Memorial Lecture: Reversing the twin cycles of Type 2 diabetes.”  So, they are clearly not fringe researchers. They are scientists looking for answers to why and how the “underlying abnormalities” of Type 2 diabetes are “reversed.” From my perspective, they have certainly demonstrated to their medical peers that their work deserves a much closer look.
A paper based on the Banting Lecture was published in Diabetes, the American Diabetes Association’s magazine. The abstract concludes: It is now clear that Type 2 diabetes is a reversible condition of intra-organ fat excess to which some people are more susceptible than others.” But they’re talking about “pancreatic and liver triglycerides.” My readers are not particularly interested in their pancreatic and liver triglycerides. People with Type 2 Diabetes want to know how to “eradicate” the damn disease. Ideally with just a pill, and definitely without bariatric surgery!
My readers are also interested in what they can do, if anything, to avoid being “more susceptible.” Well, there is a course of action you can take, and it is stated in the CONCLUSION of the overlooked post, Retrospective #89:
These data demonstrate that intentional weight loss achieved at home by health-motivated individuals can reverse Type 2 diabetes. Diabetes reversal should be a goal in the management of Type 2 diabetes.”
In my book the best way to lose weight is to eat Low Carb, not 3 cans of Optifast (510kcal), the 46.4% carb liquid diet formula used in this study. Very Low Carb is 5% carb, Low Carb 15% carb and even Moderate Low Carb is 25% carb.

Friday, November 29, 2019

Retrospective #286: Avoid wheat, excess fructose and excess linoleic acid (Omega 6s)

Kurt G. Harris, MD, called wheat, excess fructose and excess linoleic acid the Neolithic Agents of Disease (NAD). He was, easily, the early favorite in my search for a dietary regimen that could be stated as a philosophy of eating rather than depending on counting calories, carbs and other macronutrients. I first wrote about him nine years ago in The Nutrition Debate #19. He then dropped out of “the nutrition debate” and later deleted his Archevore website. Today he is a diagnostic radiologist practicing in Sturgeon Bay, WI. Some of his writing is still online at Psychology Today.
Harris didn’t write for Type 2 diabetics like me. He aimed his program at people who wanted to eat in a healthy way to avoid the chronic diseases of modern civilization. Others followed him in this goal and the field became a tangled mess, leading sadly I suspect to his premature retreat. For awhile I hoped he was writing a book. Alas, it seems not.
Harris was inspired by Gary Taubes. His training in scientific method fed his inquiring mind and led to his epiphany. He liked to write and coin words too. If this sounds like a eulogy, it’s only because I fear he is lost to us, and it is our loss.
The three NADs, which he explained in “A Dietary Manifesto – Paleo 2.0,” are just another way of describing his 12-step program (which I list in The Nutrition Debate #19), for “getting started” and going “as far as you can down the list…” The wheat proscription means gluten, and includes the other gluten grains (barley, rye, etc). That’s big.
The excess fructose NAD is also big, but here Harris leaves a little room if you’re not diabetic or prediabetic. Harris is infamous (in Paleo circles) for calling apples “bags of sugar” and most modern fruit “candy bars on a tree.” He concludes, however, “If you are not trying to lose fat [or are carb intolerant as in type 2 diabetes], a few pieces of fruit a day are fine.” Fructose, however, is not only found in fruit. Take a look at “Retrospective #97” for a list of fruits and vegetables and common sweeteners that contain fructose.
Avoiding excess linoleic acid (Omega 6s) is perhaps the hardest dietary goal of the three NADs because it is so hard to know where they hide. Harris advises, “The way to correct the modern excess of n-6 linoleic acid is to avoid the modern sources of it. Stop eating all temperate vegetable oils and veggie oil fried food – cooking and frying oils like corn, soy, canola, and flax, all of it. And go easy on the nuts and factory chicken. These are big sources of n-6, especially the nuts and nut oils.
All fats are combinations of saturated fatty acids (SFAs), monounsaturated fatty acids and polyunsaturated fatty acids (PUFAs), but the combinations vary enormously. Corn and soybean oil are over 50% PUFA, while butter and coconut oil are just 3% and 1.8%. Corn and soybean oil have more than 20 times as many PUFAs as butter and coconut oil.
The ratio of n-6 to n-3 is also important, and corn oil easily has the worst ratio. But in terms of absolute numbers, the best advice is to avoid excess Omega 6s altogether, and that is best done by eliminating all seed and vegetable oils.
To put some “meat” on the PUFA/n-6 advice, I’ve created this table using the USDA’s National Nutrient Database:
Cooking/salad oils & fats (%)
Corn oil
Soybean oil
Canola oil
Olive oil
Butter (incl.+/-16% water)
Coconut oil
So, avoid using all vegetable and seed oils (corn, soybean, Canola, sunflower, walnut, etc.), and then avoid all prepared, baked goods and foods fried in any of these oils. Then go easy on nuts, nut oils and factory chicken, and maybe supplement with Omega 3 fish oils to improve the n6/n3 ratio, and you should get back into pre-Neolithic proportions. If this sounds like Paleo to you, it really isn’t. It’s just a nod to the “ancestral” roots of my dietary journey.

Thursday, November 28, 2019

Retrospective #285: “When diet and exercise aren’t enough…”

This copywriter should get a raise, or at least a bonus. The statin drug’s advertising slogan is the very definition of a red herring: an “idiom…used to refer to something that misleads or distracts from the relevant or important issue. It may be either a logical fallacy or a literary device that leads readers or characters towards a false conclusion.” Wiki goes on to say, “The expression is mainly used to assert that an argument is not relevant to the issue being discussed.”
If you’re reading this blog, you probably have been advised ad nauseum by your doctor to “diet and exercise” to lose weight. And if you’re well read and up to date, you know that exercise is not an effective way to lose weight (in spite of all the TV advertisements). Mind you, I’m not knocking exercise; both aerobic and anaerobic exercise have myriad health benefits, but reducing unwanted body fat is not one of them. Besides, it makes me hungry and sweaty.
So, “when diet and exercise aren’t enough,” what’s a person to do? We starve ourselves, lose a few pounds, are hungry, our body responds to restore energy balance and we gain it all back. Then, rinse and repeat. We’re desperate and depressed. We lack the “will power” to “eat less.”  We are susceptible to almost any suggestion.
The ad now has you hooked. It goes on to suggest you should take a statin. And your doctor will surely suggest it, after noting that you failed to lose weight by his “diet and exercise” prescription. And since the diet most doctors pitch is the one the AHA/ACC/AMA/ADA/USDA/HHS/Archer Daniels Midland/Cargill/Quaker Oats and Kellogg’s recommends, you probably are suffering from co-morbidities and exhibit risk factors for CVD and Metabolic Syndrome.
As with most people eating the Standard American diet, besides being overweight or obese, you probably have or are developing hypertension (high blood pressure), and high cholesterol. And your fasting blood sugar may be “slightly high” (“We’ll have to watch that.”) What often isn’t mentioned is that your triglycerides are also borderline high (≥150mg/dL)and your HDL cholesterol (HDL-C) is borderline low (≤40mg/dL for men; ≤50mg/dL for women). 
To the medical/pharmaceutical community it’s this combination of “risk factors” that justifies the statin prescription. After all, even though you’re taking your blood pressure meds, you’ve failed to follow doctor’s orders to lose weight by eating less (on a balanced LOW-FAT diet); now it’s his (or her) turn to treat you effectively by writing a statin prescription. All you have to do is fill the prescription and take it faithfully. Your Total Cholesterol (TC) and LDL-C will go down, and your TC/HDL ratio will improve, and your doctor will write it all down in your chart. And your doctor will feel good, and by extension, you will too.
And that’s the best that “medical science” can do. “When diet and exercise aren’t enough…,” take a pill. Chart notes: 1) patient non-compliant (failed) with “diet and exercise” advice, 2) patient taking BP and cholesterol medications; 3) patient showed improvement in TC, LDL-C and TC/HDL ratio, and 4) follow-up visit for elevated (pre-diabetic) A1c.
Of course, so long as you eat a low-fat, high carb diet, your broken glucose metabolism will get progressively worse. You will continue to gain weight (because you’re Insulin Resistant and therefore Carbohydrate Intolerant, not because you’re eating too much and exercising too little). And your fasting blood sugars or A1c will continue to rise.
Eventually, you are likely to develop Type 2 diabetes. By then you should already have been started on Metformin (another pill). You may, in time, take a “cocktail” of three pills for diabetes alone. I did. Or maybe you’ll start with a SGLT-2 inhibitor and/or injecting a GLP-1 receptor agonist, or go directly to basal and then bolus (mealtime) insulin.
And don’t forget the complications. Microvascular: peripheral neuropathy (amputations), nephropathy (end-stage kidney disease, with dialysis), and retinopathy (blindness). Or Macrovascular: CVD, MI (heart attack), and stroke.
OR, YOU COULD JUST CHANGE WHAT YOU EAT. Take charge of your health. I think Very Low Carb could work for you, but regardless, try something. A change in diet can give you valuable information. There’s so little your doc can do, and so much YOU can do for yourself.  Very Low Carb is how I did it. If you’d like to see how changing what you eat can affect your health, or how it affected mine, read Retrospectives #281, #282 and #283, just published on this blog.

Wednesday, November 27, 2019

Retrospective #284: The A to Z Weight Loss Study: a Randomized Trial

A dear reader – and I mean that sincerely because I write this blog for my readers – was disappointed (upset, actually) that I said, “…if you are insulin resistant, as almost all fat people are…” Okay, “fat people” is an inflammatory phrase, and I rarely use it, but that is not what upset Valerie. It was an assumption, and a slight exaggeration that I made, that did it. She concluded: “I wish your ‘nutrition debate’ weren’t so one-sided.”
Valerie’s frustration (and upset) is a result of my writing about two overlapping and related but different phenomena: the co-incident epidemics of diabetes and obesity that have come together in the last 40 years. It all began with the publication of the Dietary Goals for Americans in 1977, produced by staff of a Select Committee of Congress, and the Dietary Guidelines for Americans in 1980, first produced in 1980 and then every 5 years by the USDA and HHS. These government attempts to tell the population what to eat have had an enormous impact of our health and wellbeing.
The combination of Type 2 diabetes and obesity is so prevalent today that the word “diabesity” has been coined. However, as Valerie points out, not all “fat” people have Insulin Resistance (IR), a requisite condition for progression from a normal glucose metabolism to Impaired Glucose Tolerance (IGT), Impaired Fasting Glucose (IGT), and then to a diagnosis of incipient Type 2 Diabetes Mellitus (T2DM). That is the Natural “History” of Type 2 Diabetes. Apparently, Valerie is obese but not Insulin Resistant or therefore by definition not a Type 2 diabetic or Prediabetic. Lucky her.
So, I give Valerie her point: There are plenty of slim people with insulin resistance and plenty of fat people (about 20%) without insulin resistance…” Apparently Valerie is one of the 20%. But I will contest her assertion that “fat people without insulin resistance” did not benefit from the “A to Z diet trial.” She states erroneously that “low-carb diets didn’t help [them], if you remember the A to Z diet trial.”
The A to Z Diet Trial, was a “Twelve-month randomized trial conducted in the United States from February 2003 to October 2005 among 311 free-living, overweight/obese (body mass index, 27-40) nondiabetic, premenopausal women.” By definition that means that the participants did not have Insulin Resistance. It was a “Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors…,” published in JAMA in July 2007.
The following are excerpts from the ABSTRACT:
MAIN OUTCOME MEASURES: Weight loss at 12 months was the primary outcome. Secondary outcomes included lipid profile (low-density lipoprotein, high-density lipoprotein, and non-high-density lipoprotein cholesterol, and triglyceride levels), percentage of body fat, waist-hip ratio, fasting insulin and glucose levels, and blood pressure.”
RESULTS: Weight loss was greater for women in the Atkins diet group compared with the other diet groups at 12 months, and mean 12-month weight loss was significantly different between the Atkins and Zone diets. Weight loss was not statistically different among the Zone, LEARN, and Ornish groups. At 12 months, secondary outcomes for the Atkins group were comparable with or more favorable than the other diet groups.”
CONCLUSIONS: Premenopausal overweight and obese women assigned to follow the Atkins diet, which had the lowest carb intake, lost more weight at 12 months than women assigned to follow the Zone diet and had experienced comparable or more favorable metabolic effects than those assigned to the Zone, Ornish, or LEARN diets…”
So, just to be perfectly clear, non-diabetic, premenopausal overweight and obese women who ate the diet with the lowest carbohydrate intake lost the most weight and had the best improvement in related risk factors.
The low-carb diet DID help “fat people without insulin resistance,” and by a large margin. After 12 months, the Atkins cohort actually lost 3 times as much weight at the Zone cohort and twice as much as the average Ornish and LEARN dieter and had “comparable or more favorable metabolic effects” than those on the Zone, Ornish, or LEARN diets.
I’m sorry to have to come down so hard on this point, but it must be made clear to all my readers that low-carb diets DO WORK (for the vast majority of people, if I have to hedge). If you haven’t given it an honest try, you really should.

Tuesday, November 26, 2019

Retrospective #283: TC/HDL, TG/HDL and Triglycerides

Retrospective #281 dealt with HDL cholesterol (HDL-C) and triglycerides (TG). Retrospective #282 took a look at Total Cholesterol (TC), LDL cholesterol (LDL-C) and statin therapy. Now, I will tie them all together and discuss ratios and some recent thinking about using the triglyceride to HDL ratio, and triglycerides alone, to predict CVD risk.
The “lipid” (cholesterol + triglycerides) panel on a typical lab report includes a Total Cholesterol to HDL (TC/HDL) ratio. The standard reference range is <5.0. So, if your TC is 200mg/dL, the limit under which your doctor wants your TC to be, and your HDL is 40mg/dL, the level above which your doctor wants it to be, then your ratio would be 200/40 = 5.0.
Now, since most people’s TC is about 200 or a little higher, and most people who eat a Standard American or “Western” diet will have an HDL hovering around 40, according to this standard most of the population is at risk of Cardio Vascular Disease (CVD). So, what’s a doctor to do? Prescribe a statin, of course! Because a statin, by lowering LDL cholesterol will thus lower Total Cholesterol. Remember the Friedewald formula: TC = HDL + LDL + TG/5.
However, since LDL is not assayed in the typical inexpensive lipid panel lab test, in reality the formula is “transposed” to calculate LDL from the other values which are assayed. So, LDL is calculated as LDL = TC – HDL – TG/5. However, as the math wizards among you will grasp, in the original form, TC = HDL + LDL +TG/5, your TC could be over 200 if any of the components (LDL, HDL or TG/5) was high since TC is the sum of these factors. So, Total Cholesterol is a worthless number. Nevertheless, when you take a statin, Total Cholesterol will get lower, as statins will lower calculated LDL.
As a consequence, if your TC goes lower and your HDL stays the same, your ratio will go lower. For example, a TC of 120 (vs. 200) with an HDL of 40 produces a ratio of 3.0. (120/40 = 3.0). VoilĂ ! Your doctor will tell you that your risk of CVD is now much lower than if your ratio is 5.0, like most people who continue to eat a Western diet but who do not take a statin. If you believe this, I have a bridge to sell you. (Brooklyn Bridge, for those unfamiliar with the old joke.)
But what’s a person to do if taking a statin is not the panacea it’s all trumped up to be? Evidence suggests that “…the strongest predictor of a heart attack” is a different ratio: triglycerides to HDL, or TG/HDL. I wrote about this ratio in Retrospective #27. In #27 I said, “Using this new gold standard, a TG/HDL ≤ 1.0 is considered ideal, a ratio of ≤2.0 is good, a ratio of 4.0 is considered high.” Figure #6 tracks my personal TC/HDL and TG/HDL ratios from 1980 to 2014.
The CONCLUSION in the reference cited in #27 above was: “Elevation in the ratio of TG to HDL-C was the single most powerful predictor of extensive coronary heart disease among all the lipid variables examined.” The full text of the Clinics paper can be seen at Pub Med Central, the U. S. National Library of Medicine, National Institutes of Health. Note that both my TC/HDL and TG/HDL ratios were “borderline bad” until I started eating Very Low Carb in 2002. After, my TG/HDL dropped sharply to “low risk” (≤1.0) in 11/07, and has remained “ideal” ever since.
Now, the latest thinking – this is cutting edge (2014) science folks – is that triglycerides (TGs) alone may be the most reliable risk factor for CVD. So, I plotted another graph charting just my triglycerides.
A cursory glance tells the reader that my TGs averaged about 150 (once again: “borderline”) until I started Atkins Induction (20g of carbs a day) in September 2002. Then, when I started on Bernstein (30g of carbs a day) in September 2006, they fell again. But when I started to supplement with fish oil, and then to eat a can of sardines for lunch almost every day, they plummeted to 21 and have averaged about 50 ever since.
I used to think it was Very Low Carb (Atkins Induction and Bernstein) that caused my triglycerides to be so low. Now that I’ve charted them and researched the milestone dates, I am inclined to think it is the fish oil supplementation and sardines that are the reason. And the reason for my very high HDLs as well. Or maybe just tight compliance with VLC.

Monday, November 25, 2019

Retrospective #282: Total Cholesterol, LDL-C and Statin Therapy

I documented the phenomenal transformation of my triglycerides (TGs) and HDL cholesterol (HDL-C) over the last 35 years in Retrospective #281. Okay, mock me, but this obsessive record keeping does have redeeming value: it gives an objective picture of changes brought about by my diet. The changes started in 2002 when, on my doctor’s advice, I began to eat Very Low Carb to lose weight. He said, as we walked down the hall, “It might even help your diabetes.”
He was “right as rain,” of course. Besides eventually losing 170 pounds, I was able to stop taking almost all of my oral diabetes meds. My daily fasting blood sugars are now consistently under 100, something I hadn’t seen in the previous 16 years of eating a “balanced” diet and leaving my diabetes care to my doctor and prescription meds.  My A1c’s dropped to the mid 5s, my blood pressure improved from 130/90 to 110/70 on fewer meds, and my hsCRP, an inflammation marker, went from “high” to “low” risk of CVD. Finally, my lipid (Cholesterol) panel dramatically improved, specifically HDL-C and TGs, while my Total Cholesterol and LDL-C were stable.
Figure #4, shows a composite history of my HDL-C and TG values over this 35-year odyssey.
About a year after starting to eat Very Low Carb, although already 60 pounds lighter, my doctor started me on a high dose statin. It was warranted, he said, by the guidelines. I was both a long-time Type 2 (since 1986), and I was, he said, at “high” risk for cardiovascular disease. And I was still morbidly obese.
As Figure #5 shows, the statin “worked” in the sense that it lowered both my Total Cholesterol (TC) and LDL Cholesterol (LDL-C) dramatically. Note that before starting on a statin, my TC and LDL-C were “borderline” and “slightly high” respectively. Thirty-two TCs averaged 195 and twenty-eight LDLs averaged 131. These are both “typical” for people who have been eating the Standard American or “Western” Diet for a long time. But for diagnosed Type 2s, who are at higher risk of CVD, an LDL target <100 is recommended. For Type 2s with diagnosed CVD, the goal is <70.
During the five years (12/03 – 10/08) that I took a statin, my TC averaged 125 and my LDL averaged 58 (average of 20 lab tests). You might fairly conclude that the statin worked perhaps too well. Meantime, On Richard K. Bernstein’s 6-12-12 diabetes diet, a Very Low Carb program I began in September 2006, I had lost another 100 pounds in under a year. As a consequence of eating VLC, over the course of 5 years, I had lost 170 pounds, my blood pressure had dropped to below goal, my HDL had more than doubled and my triglycerides had dropped by more than two-thirds.
So, after all my risk factors had improved so dramatically, and all had stabilized, after 10 more months now on low-dose simvastatin, my DOCTOR suggested that I STOP taking statins. Again, see Retrospective #9, “Metabolic Syndrome,” and Retrospective #25, “Understanding You Lipid Panel,” to understand his rationale.
After stopping the statin, my TC increased to 214 and my LDL increased to 125 (average of 19 tests), versus 195 and 131 before.  But while both are still “borderline” by the standard, neither is now of any concern to my doctor. Nor should they be, because of my greatly improved HDL-C and triglycerides. Remember, the old Friedewald formula for calculating LDL: LDL = TC - HDL - TG/5. In 2018, Quest switched to Martin/Hopkins which produces a higher LDL for most people (but not for me, due to my very low triglycerides). PS: If you have a high calculated LDL, it may be due to your high triglycerides. Request a direct measurement to confirm it, OR eat Very Low Carb to lower your triglycerides.
We will also describe some hypotheses and recent scientific studies regarding using triglycerides alone to track and monitor CVD risk…which brings me back to Figure #4 in this post (above) and to Figure #3 in Retrospective #281. If you are persuaded by these data and want to lower your triglycerides (and raise your HDL-C, since they are, as I have shown, inversely related), then I hope you will consider eating Very Low Carb with fish oil supplementation, and of course eating a can of delicious Brisling sardines in extra virgin olive oil (EVOO) for lunch every day, as I did. LOL.

Sunday, November 24, 2019

Retrospective #281: HDL-C and Triglycerides

“A picture is worth a thousand words,” the saying goes. Well, I have three “pictures” that I think will get your attention. They are graphs of my 70+ lab tests for HDL cholesterol and serum triglycerides between 1980 and 2014. By definition, they are n=1 (me only), and therefore could be dismissed as “anecdotal.” Alternatively, you could consider them a “case study.” I tend to think that Fig. #1, the “early years, “are illustrative of the general population for people eating the Standard American or “Western” Diet. Fig. #2, the “middle years and Fig. #3, the “later years” reflect the changes that can – and did occur in my case – with a dramatic change in what you eat.
Figure #1 (below) shows my HDL-C as the almost perfectly flat blue line from 1980 through September 2002, eating as I did the Standard American Diet. The first 11 tests (from 1980 until 12/01) are all in the high 30s and low 40s (range 37 to 42; average 39), which is “low,” i.e. just below “normal” range for 40 for men (50 for women).
Do you know what your HDL cholesterol is? You should. HDL and triglycerides are more important than your Total Cholesterol (TC) and LDL scores. The reason your doctor tracks your Total Cholesterol is that, by prescribing a attain, he or she can lower LDL and TC. My doctor put me on a statin in December 2003.
The upper line, in red, tracks 17 triglycerides (TG) over the same period. They are more variable (TGs usually vary from 20 to 23 percent, and can range as much as 40% (fasting vs. non-fasting). Note that they are not “high” (>200), but they hover around the “borderline” level of >150. The average is 143 (range 107 to 187). Neither of these tests would get your average doctor too exercised. He would say he’s going to “watch” them and to “continue taking the statin.”
Figure #2 shows HDL-C after I started eating Very Low Carb (20g of carbs a day!) I followed it faithfully for 9 months, then a “sort of” maintenance for the next three years. I then went “off plan” in the summer of 2006, and to get back on track, I started Richard K Bernstein’s 6-12-12 plan for diabetics (30g of carbs a day) for a year (9/06 to 9/07). Note that during this 5-year period (9/02 to 9/07) my HDL-C slowly increased from 43 to 60. TGs were lower (average 84, range 36 to 157 with one aberrant (222). Most doctors would be very pleased with these HDL and triglyceride lab tests, but would still tell you, “keep taking the statin
Figure #3 is by far the most interesting because it is totally “aberrant” to the clinician. It is, in fact, paradoxical.
Note that the blue and red lines are inverted. The HDL-C in virtually every case is greater than the triglycerides! The average of 25 HDL-Cs is 75 (range 52 to 98). The average of 25 TGs is 49 (range 21 to 65). Note also that there is definitely an inverse relationship between HDL-C and TG: when HDLs are high, the corresponding TG is low.
The inversion of HDL-C and TGs) began long after I began eating Very Low Carb. It began while I was in the middle of Bernstein and starting to take fish oil supplements (April 2007) and eating a can of sardines for lunch (July 2007).
I started taking 2 fish oil capsules a day (each 1-gram capsule containing 300mg of EPA and 200mg of DHA). I had read on the Mayo Clinic website that, “There is strong scientific evidence from human trials that omega-3 fatty acids from fish and fish oil supplements (EPA + DHA) significantly reduce blood triglyceride levels. Benefits appear to be dose-dependent, with effects at doses as low as 2 grams of omega-3 fatty acids per day. Higher doses have greater effects, and 4 grams per day can lower triglyceride levels by 25-40%. Effects appear to be additive with...statin drugs…”
In 2007 I was still on a statin. I had lost 170 pounds and my Type 2 diabetes was in remission. Then, on day, when my doctor observed how my HDLs had skyrocketed and my triglycerides had plummeted and concluded that I was no longer at “high” risk of Cardiovascular disease. In 2008, without any “coaching,” my doctor took me off statin drugs. 

Saturday, November 23, 2019

Retrospective #280: Putting Fat Loss on Autopilot

The key to losing body fat “on autopilot” is learning to “fly” in a space without turbulence or cross-winds – where you can just sit back and let your body “fly” on autopilot. This requires that you navigate to a place where there is less resistance, fewer disturbances and conflicting “traffic.” Your attention will be required at take-off, but once you are up to speed and “on course” – where you have reached a certain comfort level – you can safely put fat loss on autopilot.
The first thing you need to do is go to school. You need to learn how to get into autopilot. But learning how to “fly right” requires that you first have to unlearn what we, and virtually every doctor who is alive and practicing today, has been taught about nutrition, both in medical school and in “postdoc” medical education. That shouldn’t be too difficult for them because they’ll be the first to tell you they didn’t learn diddly squat about nutrition in medical school.  However, medical doctors are required to get Continuing Education “CEUs”” to maintain their licenses, so the best we can hope for is that they recognize that Big Pharma has corrupted them with incentives and self-serving info.
For your own part, if your own experience acquired from observation or experiments leads you to the conclusion that eating a low-fat, high-carb diet is not a good way to lose weight and keep it off, that it’s a bumpy ride– hands on the stick all the way – then you might be open to a change in direction or flying at a different altitude for a smoother ride.
A Very Low Carb “eating pattern” is one such alternate flight path. It is like having a tail wind all the way. It’ll require your full attention to get started, but once you’re on the path, it’s “smooth sailing.” No hunger. No cravings. Just effortless, cruising at altitude while you burn body fat for energy. Your body wants a smooth ride. It seeks energy balance. Eat Very low carb, and your body will fly itself. You can sit back and relax; YOU WILL BE ON AUTOPILOT.
The conventional wisdom is that take-off, i.e., getting started, is the hardest part. It wasn’t for me. I went Very Low Carb “cold turkey” 17 years ago. In my recollection it takes only a couple days – maybe 2 or 3 – for the stomach rumblings to stop, after which you won’t feel “hungry” any more, if you eat strictly Very Low Carb. I salted my meals to remain hydrated. Some people drink a cup of bouillon in late afternoon to avoid dehydration/headaches. And if you’re taking meds for diabetes, you’ll need to carefully monitor your blood sugars and stay in touch with your doctor as your BS will dramatically lower, especially if you are taking a sulfonylurea like glipizide or glyburide (Micronase).
I stayed strictly on 20 grams of carbs a day for 9 months and Iost 60 pounds. I then moderated my carb intake a little, but didn’t gain any weight back for several years… until I started cheating (bedtime freezer raids for ice cream).
At first, I kept a food log of everything I ate. I just estimated grams of carbs for everything I ate. I tracked nothing else. I just wanted to raise my awareness about carbs, and my knowledge of what foods contained carbs and how many. Later I used a web-based resource to track calories, fat, protein and carbs, and I began to study macronutrient ratios. Eventually, after I felt well enough educated to make good food choices, I stopped keeping a food log. Now, I just take a fasting blood glucose and weigh myself daily (for raised consciousness), and see my doctor 3 times a year for labs.
But you don’t have to keep a log. Today you can “go to school” by joining an online group of dedicated, enthusiastic low carbers. There are plenty of them. My favorites are Andreas Eenfeldt’s “Diet Doctor” and Megan Ramos’s “The Dr. Jason Fung Fan Club.”  Of course, there are also lots of good books out there, and bloggers like me, to help you.  
If you decide to try it, of course I hope you’ll hang out here. It’s not the upper-deck lounge of a 747, but it’s almost as safe. And in writing some 500 columns over the last 10 years, I have covered just about everything relating to “fat loss on autopilot.” Obviously, I think this is the right way to fly for weight loss, regulating glucose metabolism, metabolic syndrome, lipid health (cholesterol and triglycerides) and chronic systemic inflammation. I have also addressed Type 2’s macrovascular complications (CVD, stroke, some cancers, Alzheimer’s) and microvascular complications (peripheral neuropathy, retinopathy, and nephropathy, i.e., end-stage kidney disease with dialysis), all of which I have avoided.
And each week I discover bloggers who knock my socks off. The skies are full of helpful resources, and most of them are knowledgeable pilots who will guide you to fly above the clouds where the sky is clear and the winds favorable.

Friday, November 22, 2019

Retrospective #279: My fasting blood glucose is 85mg/dl

My Fasting Blood Glucose (FBG) was 85mg/dl (4.22mmol/l) this morning. That’s not “normal” for me. I have a “broken glucose metabolism.” It has been broken for more than half my life. I am Carbohydrate Intolerant. I was diagnosed a Type 2 diabetic over 33 years ago (1986) and was certainly “pre-diabetic” for years before that with Impaired Glucose Tolerance (IGT) and then Impaired Fasting Glucose (IFG). That’s how my Type 2 diabetes was discovered. On my first office visit, an observant GP saw that I was obese and ordered a fasting plasma (blood) glucose test.
In those days the threshold for a diagnosis of Type 2 diabetes was two consecutive lab tests of 140mg/dl or more. (Today it’s 126mg/dl or an A1c test.) That doctor, whom I only saw once (I moved), did the usual thing in those days: he prescribed a sulfonylurea, micronase (generic: glyburide), and probably told me to lose weight by “eating less and exercising more.” The “medically advised” diet in those days hewed to the newly formulated Dietary Guidelines for Americans, first published in 1980 and updated every 5 years thereafter. The 2020 version is being drafted now.
Of course, as everybody knows, it’s virtually impossible to lose weight and keep it off on a calorie-restricted, balanced diet. Your body “craves” more. It doesn’t want you to “starve.” So, it’s constantly signaling  you that you’re “hungry.” I put all these words in quotes because they have become part of the lexicon of dieting by this failed meme. You know it. I know it. You would think that our clinicians would know it too, but the medical profession today is more a business that is governed by the “Standards of Practice” they must follow in order to be paid for the medical codes they submit, and the “bottom line.” Too bad for us that the government has intervened in the patient-doctor relationship.
So, how did my blood sugar get to be 85mg/dl this morning?  A brief history: on the restricted-calorie, balanced diet I probably followed, my weight continued to rise from 300 in 1986 until I weighed 375 pounds in 2002. And my anti-diabetic medications increased as well until I was maxed out on two drug classes and starting a third. I knew that before long, I would become an insulin-dependent Type 2 (or would be dead), if I didn’t change my Way of Eating.
Then, one day in 2002, on a regular office visit, my doctor said to me, “Have I got a diet for you!” A few months earlier he had read Gary Taubes’ “What If It’s All Been a Big Fat Lie,” the New York Times Sunday Magazine cover story. He tried the diet himself, lost 17 pounds, liked his lab tests, and decided to “prescribe” the diet for me. I was ready. I was motivated and willing to try something different. The diet was Very Low Carb (20g/day). I lost 60 pounds in the next 9 months. That was a major “lifestyle change,” but I was able to stick to strictly eating Very Low Carb because it worked!
But even before I lost that weight – the first day I started to eat Very Low Carb, actually – I had a hypo, a dangerously low blood sugar. I called the doctor, and he told me to stop taking the 3rd oral med. The next day, when I had another hypo, he told me to cut the other two classes of meds in half. A few days later he ordered me to cut them in half again. Eventually, I titrated off the Micronase (an SU) altogether, and today I just take a small dose of Metformin with supper. Over time, my A1c’s drop to the mid 5s, my HDL-Cs double (from 39 to 84), my triglycerides dropped 2/3rds from 137 to 49, and my inflammation marker (hsCRP) dropped from “high risk” to “low risk” of cardiovascular disease.
I kept the 60 pounds off for several years and then, over the summer of 2006, I regained 12 pounds. (It could have been the ice cream.) I recommitted to Very Low Carb and switched to “Bernstein” – Richard K. Bernstein’s Diabetes Solution 6-12-12 program” for diabetics. I lost 100 pounds in 50 weeks. Altogether I lost 170 pounds.
Along the way, until I learned (from my meter) what I could eat and what I couldn’t, my total calories dropped, eventually to 1,200 calories/day. My carbs of course have always been VERY low (about 5% today). My diet is mostly moderate protein (20%) and high (75%) “good” fats: saturated and monounsaturated. I try hard to completely avoid polyunsaturated fats (PUFAs). PUFAs are the so-called “vegetable” oils, like soybean, corn, sunflower and Canola oil.
I eat 1-2 small meals a day, with no snacks. If I were snacking, it would only be before supper, with sliced radishes with salt and ghee and diet tonic (vodka optional). I am not ever hungry. I have great energy levels and (at age 78) no health complaints. And when I eat like this for just a few days, my FBG drops from the low 100s to the 70s and 80s. 

Thursday, November 21, 2019

Retrospective #278: Skipping Breakfast

“Skipping breakfast doesn't cause weight gain,” Stephan Guyenet, PhD, obesity researcher and blogger at Whole Health Source, mockingly tweeted. Guyenet attached a link to a randomized controlled trial published online in November 2014 in the Journal of Nutritional Science, a Cambridge University Press, UK, peer-reviewed publication.
This study had a HYPOTHESIS, a STUDY DESIGN and an ABSTRACT. The ABSTRACT began, “Eating breakfast may reduce appetite, body weight and CVD risk factors, but the breakfast type that produces the greatest health benefits remains unclear. We compared the effects of consuming a high-fibre breakfast, a non-fibre breakfast, or no-breakfast control on body weight, CVD risk factors and appetite.” They seriously proposed to “clear up” this “unclear” condition.
The RESULT: “Skipping breakfast leads to weight loss but also elevated cholesterol compared with consuming daily breakfasts of oat porridge or frosted cornflakes in overweight individuals: a randomized controlled trial.”
Interestingly, this paper had no CONCLUSION. But, the end of DISCUSSION began, “In summary, the present study shows that in overweight individuals, skipping breakfast daily for 4 weeks leads to a reduction in body weight, but this is accompanied by an increase in total cholesterol compared with consuming either a frosted cornflakes or oat porridge breakfast.” To be clear: Everybody knows that elevated total cholesterol concentrations are bad, right?           
Then – and this is where I started to get cynical – the “summary” continues: “There were no differences in changes in body weight or total cholesterol concentrations between the groups consuming the frosted cornflakes no-fibre breakfast or the group that consumed the high-fibre oat porridge breakfast. These findings suggest that although skipping breakfast may be the more effective strategy to achieve weight loss than eating breakfast, there are associated detrimental effects on total cholesterol concentrations” (emphases added). This is a UK publication, and the “fibre” spelling is for Brits, who eat a lot of “oat porridge.” We call it oatmeal in the U.S.
Let’s cut to the chase. “The present study was funded by the Quaker Oats Center of Excellence.” The Quaker Oats division of PepsiCo made the high-fibre oat porridge used in the study. Their competitor, Kellogg’s, is the world’s second-largest snack company (after Pepsico) and makes the “no-fibre cornflakes.” And they call this “science.”
There was no attempt by the authors, their peer reviewers or the funders to conceal the purpose of funding this study. “The aim,” the ABSTRACT concludes, “of the present study was to investigate the effects of consuming a high-fibre oat porridge, an isocaloric non-fibre cornflakes breakfast, and a no-breakfast water control daily for 4 weeks on body-weight changes, subjective appetite and CVD risk factors in overweight but otherwise healthy individuals.”
Stepping back for a minute from the obvious “editorial bias,” several queer things struck me about this study when I first read it. For one, why wouldn’t any serious, unbiased scientist, who didn’t have a funder to satisfy, and was genuinely interested in a breakfast type that “reduces appetite, body weight and CVD risk factors,” and “produces the greatest health benefits,” include an isocaloric breakfast of bacon and eggs? Well, I guess that is clear now.
For another, according to the Study Design, the “data were collected in 1998 and 1999.” So, why is this old NYC study being dredged up and republicized in the UK in 2014? Perhaps it didn’t pass peer-review muster the first time, or perhaps Quaker Oats/Pepsico was just trying to get some more mileage out of their previously funded research with some new marketing in the U.K. Let’s be clear: Quaker Oats/Pepsico is a world-wide cereal marketer, and this study was just a hack job designed, in the way drug trials are designed, to show skipping a cereal breakfast is detrimental to your health. Nobody intended the outcome to advocate not eating breakfast. That wouldn’t be good for business.
Frankly, I was unaware of the widespread “conventional wisdom” in Guyenet’s mockery that skipping breakfast causes weight gain. I eat an “isocaloric” breakfast of bacon and eggs (protein and fat, not carbohydrates) with heavy whipping cream in my coffee. If I were going to skip a meal – because I wasn’t hungry or I was trying to lose weight, I’d skip lunch, not breakfast. My wife makes breakfast, and she says she married me for better or worse, but not for lunch.

Wednesday, November 20, 2019

Retrospective #277: What is hunger?

“I’m hungry…all the time,” the overweight person frequently says when trying to lose weight on a restricted- calorie, “balanced,” low-fat diet. But is this really hunger? “Wikipedia says hunger “is a condition in which a person, for a sustained period, is unable to eat sufficient food to meet basic nutritional needs.” That is a really bad definition.
The “hunger” a fat person experiences is different from that which a starving person experiences. Any person, fat or otherwise, who for a few days is unable to eat or any food will for a day or two experience stomach rumblings (hunger “pangs”), but then those pangs will go away. As the body adjusts to a total lack of food by mouth, it transitions to another source of “food” for energy: body fat. Body fat, plus water and salt, meets the body’s basic nutritional needs.
However, after all available fat and has been consumed, the body enters starvation” a period of “wasting” in which muscles are broken down for energy and organs begin to fail. But if you are overweight or obese, you want your body to consume your body fat. And when it does, even though you do not eat, you are not hungry because you are “fed.”
In that sense, fat people have a biological advantage over lean: Their bodies can run for a very long time on “stored” energy. It’s part of a normal fed/fasted cycle: The stomach is empty and the ingested ingredients (food by mouth) have been almost completely absorbed from the small intestine into the blood stream for distribution. It’s time to seek more nourishment (first choice), or transition to using backup energy to meet the body’s nutritional needs.
How does the transition occur? What is the mechanism? The glucose that carbs break down into requires insulin to transport it in the blood, and elevated insulin levels tell the liver that stored fat is not needed. In fact, an elevated blood insulin level blocks fat from breaking down. So, if you eat things that break down into glucose (carbohydrates), your body will tell you it needs more “food” to break down. But your body fat is locked up. Ergo, You WILL feel hunger, and if you eat more carbs, when they are used up, you will feel hunger again. YOU are making your body “hungry.”
On the other hand, if you cut back carbs, especially processed, highly refined carbs, and sugar-sweetened beverages, the “sugar” (glucose) in your blood will not be elevated and neither will your blood insulin. In that case, knowing that “sugar” (carbs → glucose) is unavailable, because your blood INSULIN level is low, the liver will release your stored fat.
Your energy will flow as well, if not better, than if you had eaten carbs. Whereas, if you are Insulin Resistant, as almost all fat people are, eating carbs will cause your blood sugar to spike and then crash, leaving you tired and hungry. But when burning body fat, your ENERGY LEVEL will be high and your BLOOD SUGAR LOW AND STABLE (i.e., balanced).
This steady state of fat burning is called ketosis – a condition your body, especially your brain and heart, really likes – you can go for days, even weeks, with high energy levels and stable blood glucose all day long. When I strictly followed the Bernstein program (designed for diabetics) many years ago, I lost 100 pounds in 50 weeks. Before that, in the first 9 months on Atkins Induction, I lost 60 pounds. Over several years, I lost a total of 170 pounds, all without hunger.
It’s hard to give up your favorite foods – foods you’ve eaten for a lifetime. But it isn’t because you need them to stave off hunger. You liked them. They were available and convenient. They’re often prepared, take-out, packaged, drive-up, processed and sweetened, but they’re mostly carbs, and when you eat them, YOU’RE HUNGRY ALL THE TIME.
Once I figured out how to lose weight without hunger, and get control of my blood sugar and Type 2 diabetes – and I learned that by eating a certain way all my health markers would dramatically improve – it was a “no-brainer.”
All I had to do was develop new habits about what I could eat and what I should (try to) avoid. A good way to do that is to get into the habit of eating the same thing for breakfast every day. For me that’s eggs and bacon and coffee with heavy whipping cream and stevia powder. For lunch (if I eat it), it may be a can of kippered herring in brine, or a can of Brisling sardines in EVOO. Supper is usually a protein portion (beef, veal, lamb, pork, chicken or seafood) and one low-glycemic, whole vegetable either roasted in olive oil or tossed in butter. No potatoes, bread, rice, pasta, corn, beets, peas or carrots. And no snacks between meals or after supper. And that’s all folks. You won’t be hungry, I promise.

Tuesday, November 19, 2019

Retrospective #276: “Why do I eat…even when I’m not hungry?”

“Why do I eat, even when I’m not hungry?” I’ve been asking myself this recently. It is also a question that arises in the HBO Documentary series, “The Weight of the Nation,” that I reviewed in Retrospective #275. It is in Part 4, “Challenges,” that dips briefly into science. The answer is hinted at by Rudolph Leibel, MD, Co-Director of the New York Obesity Research Center, Columbia University Medical Center. “Evolution happens slowly. DNA changes slowly.”
I have asked myself, “Why do I eat…,” many times. I think all of us who are prone to overeat have asked it. At the beginning of Part 1, “Consequences” in “Weight of the Nation,” an obese man says, “You try [to eat less] …and you lose hope.” Another says, “I know I should eat the right things. I’m gonna try.” Then in Part 2, despair returns: Another obese man says, “What can I do? I love good food. I love cheeseburgers. Sure, I know what to do; I just can’t do it.”
Commenting on Retrospective #268, “Help with Cravings,” – a serious student of the science of overeating – said to me, “So, you do not experience cravings? If you do not have them, you are lucky. I have had periods without cravings, and periods with cravings. They are a non-rational desire for something, or an insatiable appetite, even on NO carb. This suggests that there is some unknown biological cause, but nobody knows the cause of cravings.”
I posited the idea, suggested by among others the Jaminets in “The Perfect Health Diet,” that we may eat UNTIL our body is satisfied that it has all the essential nutrients it needs (including for example the fatty acids n3 and n6 and certain essential amino acids from protein. Lacking them, we eat more nutritionally poor and non-essential foods (carbs) to the point of obesity.” This specialized craving hypothesis has a certain appeal to me, but it’s only part of a complex answer. As Francis Collins, Director, National Institutes of Health, says in Part 2, “It’s a challenge for sure!”
For me, the bottom line is to acknowledge that MY BODY is in charge of my well being. That’s hard for me to admit; I do not lack for hubris. But in my own “conscious” self-interest, that is what I must conclude if I am to figure out how “I” can help “it” (my body) maintain homeostasis. Think about all the “insults” I throw at my body every day (eating choices and other behaviors that I do or do not do, like physical activity) that challenge my whole-body condition. If “evolution happens slowly,” and “DNA changes slowly,” my body must suffer from such unremitting “insults”.
But without knowing this “unknown biological cause” of craving – what I will call our “biological imperative,” I attempted almost 10 years ago (2010) to address the subject of why I eat, even when I’m not hungry, in a long thread (200 posts, 4000 hits) I started at Dr. Bernstein’s Diabetes Forum  (registration required), called, “Impulse Control and Metacognition.” My idea was to be “conscious of the “cue,” the impulse to eat when I’m not hungry, and then deal with that impulse by another means, e.g. by distraction (reading, writing a column, yard work, etc.).
Right at the start, the Forum’s Global Moderator commented, “Isn’t it likely the problem is actually physiological rather than psychological?” (Georgette was always so gentle with me; Bernstein was a “safe” place to be if you were interested in getting answers from very knowledgeable people about Type 2 diabetes. Anyway, I replied (this WAS 10 years ago): “I am not pursuing this aspect of it, however, because I know of nothing I can do to manage or control the hormone(s) in question. It is, after all, an autonomic function of homeostasis, the body's self-regulatory system.”
In the matter of hormonal regulation, I am today a lot wiser than I was 10 years ago. I still hold, however, that 99% of our body’s activity is autonomic and totally out of my “conscious control. I have a broken glucose metabolism – I have Insulin Resistance and fewer operative beta cells in my pancreas – ergo, I am Carbohydrate Intolerant. All I can do is “listen” to my body very carefully and do what I think is the right thing to minimize the “insults.” That means I need I watch my carbohydrate intake very carefully to keep my serum insulin level low. I use the scale and my glucose meter daily (for a fasting reading), and I use my triennial doctor’s visits for blood tests (HbA1c, CBC, lipid panel, electrolytes, hs-CRP (for chronic systemic inflammation), and other lab tests.). I figure that if I take care of my body, my body will take care of me. After all, except for my “conscious” self, it’s 99% of me. It’s simple self-interest.