Sunday, August 27, 2017

Type 2 Diabetes, a Dietary Disease #395: All my friends are dying…

I sometimes think about all my friends who are dying. Well, not all of them, but many. And in my case the usual feeling of loss that one experiences is augmented by the feeling that I could have done something about it. Again, not for all of them, but for many. And many who are still alive too. I know this sounds like I think I am a Svengali-like zealot. I plead guilty, but not to the power to save everyone – just a few.
So, I post this blog every week in the hope that someone, somewhere – personal friend or not – will heed the message: “Let food be thy medicine and medicine be thy food” (Hippocrates: 460BC-370BC). And that the food be that which enabled Hippocrates to live to the ripe old age of 90. Real foods. Whole foods, not refined “foods” designed to make you crave more. Not snack foods with flavor enhancers, deli meats embalmed with dextrose and corn syrup, and bread where the third ingredient, after flour and water, is always sugar.
Why do I think that the food we eat is responsible for the steep increase in so many of the “diseases of civilization? Assuredly, I am not alone. The evidence is now overwhelming. What else is there that can explain the precipitous rise in so many chronic diseases, starting about a century ago and accelerating precipitously about 40 years ago? It’s our diet!!!
Doctors are not trained to view diseases as syndromes. They learn to identify specific disease conditions by symptoms, and treat them by writing prescriptions. Epidemiologists look at disease differently too. They do statistical meta analyses and draw conclusions from associations of conditions and outcomes. However, correlations do not prove causality. And epidemiological findings are often flawed by bias and poorly designed analyses with myriad confounding factors.
A year ago I wrote a two-part series on Gerald Reaven’s Unified Hypothesis of Chronic Disease (see Part 1 and Part 2). Reaven was a professor of medicine at Stanford University and gave the 1988 American Diabetes Association keynote Banting lecture on his unified hypothesis, which he called “Syndrome X.” His hypothesis later came to be known as “Metabolic Syndrome.” I first wrote about in 2011 (column #9, here). If you don’t normally open and read my hyperlinks, I encourage you to find the time to read these three. They’re worth it.
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Now, assuming you ignored the above advice, here are my CliffNotes, from Tim Noakes, in Part 1 of the series:
Noakes says, “Reaven’s great contribution has been to show this persistent hyperinsulinemia in insulin resistance, whether or not associated with T2DM, produces a collection of grave secondary consequences.”
“But Reaven’s greatest (and bravest) intellectual contribution is to suggest that insulin resistance and hyperinsulinemia are the necessary biological precursors definitely for four and perhaps for all six of the most prevalent chronic conditions of our day: 1) Obesity; 2) Arterial disease (local: heart attack or stroke; disseminated: T2DM; 3) High blood pressure; 4) Non-Alcoholic Fatty Live Disease (NAFLD); Cancer; and Dementia (Alzheimer’s Disease, also known as Type 3 Diabetes).”
 “The key finding from Reaven’s work,” Noakes says, “is that these conditions are not separate – they are different expressions of the same underlying condition. Thus a patient should not be labeled as having high blood pressure or heart disease or diabetes or NAFLD (or perhaps even cancer or dementia).”
“Instead,” Noakes continues, “the patient should be diagnosed with the underlying condition – insulin resistance – with the realization that the high blood pressure, the obesity, the diabetes, the NAFLD, or the heart attack or the stroke, are simply markers, symptoms if you will, of the basic condition.”“And that basic condition,” Noakes concludes, “is insulin resistance which, simply put, is the inability of the body to tolerate more than an absolute minimum amount of carbohydrates eaten each day.”
Thus we have it: Reaven’s unifying hypothesis of chronic disease: “One disease, one cause, many symptoms.” And that’s why so many of my friends are dying. Our bodies cannot tolerate so many carbohydrates. Now, if only more of my friends (and everyone else) would follow that advice…and save themselves!

Sunday, August 20, 2017

Type 2 Diabetes, a Dietary Disease #394: “Alternative Preventive Medicine”?

A friend, whose father perhaps not incidentally was a medical doctor, recently wrote me, “I tend to believe many of the ideas you have uncovered [?] have valid outcomes.” He described these ideas as “alternative preventive medicine,” and lamented that “modern medicine doesn’t have a great deal of concern for them.” He opined, “They love leaning on prescription solutions.” These comments gave me a lot to ponder.
First, with respect to my friend, he has been reading my columns almost since I began writing them in 2010 and he knows that I don’t just talk-the-talk; I walk-the-walk. Even if he acknowledges that my “ideas” have “valid outcomes;” I have failed to persuade him to follow a Very Low Carb or Low-Carb, High-Fat Way of Eating. Like most people under the care of a specialist physician, I suspect he eats the way (s)he tells him. And today he is still “9-months pregnant” with a large projecting belly (and other health issues).
Second, from my friend’s viewpoint, it sounds to me like “my” ideas are still a voice in the wilderness. It’s true, of course, from an establishment perspective, that low-carb, moderate-protein, high, healthy-fat eating is the opposite of the way we have been told to eat by the establishment for our entire lives. In that sense, this Way of Eating is surely “alternative.” Even Taubes, in his ground-breaking book, “Good Calories – Bad Calories,” describes his “Carbohydrate Hypothesis” (as opposed to the Diet-Heart hypothesis) as “alternative.”
And surely the low-carb, moderate-protein, high-fat Way of Eating is “preventive.” And I don’t mean for just the overweight, obese, pre-diabetic and type 2 diabetics amongst us. I mean for the world’s entire population!
Since 1977, when the Dietary Goals for the United States was published, we have been told to eat a diet of 55%-60% carbohydrates, 30% fats and 10% protein. To this day the Nutrition Facts label on all processed food packaging basically still advises us to eat that way. Some years ago they removed the percentage of protein, and the 2015 the Guidelines eliminated the “eat no more than 30% fat, but the 300 grams of carbs on a 2,000kcal diet for women and 375 grams on a 2,500 kcal diet for men remains. Do the math. For women, 300g x 4kcal/g = 1,200 calories = 60% of 2,000 calories. For men, 375g x 4kcal/g = 1,500kcal = 60% of 2,500 calories.
That percentage of carbohydrates (60%) is way too high. It is the reason we are all (i.e. most of us) fat! That’s how they fatten beef on the feed lot. We eat too many processed carbs and baked goods, and refined sugars and beverages sweetened with high fructose corn syrup or cane sugar. I don’t have to tell you. You know.
So, if we are going to go with Hippocrates’ dictum of “let food be thy medicine and medicine be thy food,” what is a sensible “alternative, preventive medicine”? You don’t have to go to “extreme” measures (unless your medical indications warrant it or you want to – it is safe to give up carbs entirely), here is my suggestion:
     For women, reduce your carb intake to 20% (vs.60%) of 2,000 calories. That’s 100 grams a day and a 2/3rds reduction. You will feel better, lose weight easily, and have better blood lipids, especially HDL-C (the good cholesterol) and TGLs. Look for lower inflammation and, as you lose weight, improved BP.
     For men, reduce your carb intake to 20% of 2,500 calories. That’s 125 grams a day and also a 2/3rds reduction. You will have all the same benefits and feel pumped all day long. No need to snack. Your metabolism will run at full-speed because your blood sugar won’t crash. Honestly. You’ll feel great!
Of course, as you eat fewer carbs, you can increase your protein from 10% to 15% or even 20% and your fats from 30% to as much as 60%. That’s not as much as it seems since fat is more than twice as energy dense as both protein and carbs (9kcal/g for fat vs. 4kcal/g for protein and carbs). Eat more butter, cream and olive oil!
As my friend wrote, this is a “real preventive route to reaching better health.” I just wish he’d take to the road.

Sunday, August 13, 2017

Type 2 Diabetes, a Dietary Disease #393, My 2nd 30-lb Challenge (Amended): Final Report

Followers may recall that a few months back, in my 1st 30-lb Challenge, I lost 31 pounds in 10 weeks. They may also remember that I then embarked on a 2nd 30-pound challenge, this one of 16-weeks duration. After 12 weeks, I reported a less than stellar performance and amended the 16-week goal from 30 to 15 pounds. This is the 4thQ/Final report on the amended goal. I started the 4th quarter at 215 lbs. The goal is to return to 202 in 4 weeks, then 197 two weeks later. That’ll be over 50 pounds lost with full-day “fasting.”
Week 13: Attended Keto Fest, a festival in New London, CT, organized by 2 Keto Dudes. It was educational and fun, and I ate too much: Eggs/bacon breakfasts (in a hotel), ketogenic lunches (at the festival) and half-priced cherrystones and white wine (dinner on my own), but too much food/wine. I gained 5 pounds. FBG aver: 103!
Week 14: Fasting Mon-Wed-Fri. I dropped 10 pounds from 220 to 210. Amazing! Including an amazing buffet lunch at the Otesaga Hotel in Cooperstown before seeing “Porgy and Bess.” And I cheated a little each fasting day, but only with a protein/fat snack (bought at Keto Fest) with my happy hour spritzer. FBG aver: 99mg/dl.
Week 15: Fasting Mon-Wed-Thurs this week. Tuesday we’ll again have lunch at the Otesaga Hotel before seeing “Oklahoma” at Glimmerglass, and then a light “all protein” supper at home. All went well ‘till Saturday, the annual neighborhood association picnic. I had just one plate of protein and fat, plus 3 cups of my keto clam chowder, and 3 cups of white wine. Virtually no carbs (except in the wine) and no dessert! Alas, I gained 2 pounds for a net 4 pound loss for the week. Next morning: FBS up 29 points. FBG weekly average: 86mg/dl.
Week 16: Need to lose 4-6 pounds this week to reach my target. Glimmerglass (“Xerxes”) on Tuesday, so I will try “IF” Mon+Wed-Thu and maybe Fri. I have a gallon of leftover keto clam chowder: ergo, I will do a modified OMAD (one ‘mug’ a day) fast this week: for ‘supper’ I’ll substitute 12oz of chowder, plus iced tea, for my usual spritzer (6oz red wine + 8oz seltzer): fewer carbs, more fat, no wine. By week’s end I had lost 3 pounds, down to 203 (1 shy of my target). 26 week total: 45 pounds. FBG average this week: 90mg/dl.
Conclusion
Multiple, consecutive day “fasting” is easy, if you’re “fat adapted.” No hunger. Never was any at “breakfast.” Just coffee with cream. No hunger at “lunchtime.” I usually forget about it if I’m busy in the yard, etc. Supper has proved to be a little harder. In recent years I “snacked” before supper. (I say “supper” to suggest a smaller meal than “dinner.”) It’s usually been solid food, recently plain celery; before that radishes with salt and sometimes butter). Since beginning full-day “fasting,” I have substituted a red wine spritzer (6oz wine + 8oz seltzer) for solid food, to wash down my evening pills. In week 16, for 3 days I replaced the spritzer with iced tea, to save 150 calories while I used up leftover, calorie-rich keto chowder. It worked out okay. No cooking.
Other Related Thoughts
The brain is so facile at rationalizing. I have quickly come to accept that losing less than half the weight I wanted to lose in my 2nd 30-lb Challenge was still a good outcome. After all, a pound-a-week-loss really is respectable. Many healthcare professionals would even describe it as commendable. But I consider it a big disappointment. Not exactly a failure, but then I have high expectations for myself (and others, my wife says).
Going Forward
I have, however, gained another insight from this less-than-desired outcome. I have reasoned that to maintain each weight loss, the challenge must continue. And the best way to do that is to continue to set goals – albeit incrementally smaller goals – in successive weight loss campaigns. There are just two variables: elapsed time and weight. Time was the variable in the two original plans: 30 pounds in 10 weeks and then 30 pounds in 16 weeks. When I faltered in the 2nd plan, I cut the goal to 15 pounds in 16 weeks. Going forward, beyond this 16-week challenge, with 15 more pounds to lose, I will propose to lose 5 pounds in the 1st 2 weeks. And then, the “final” 10 in the last 6. Or something like that. We’ll see how it goes. And then? Another challenge?  Of course.

Sunday, August 6, 2017

Type 2 Diabetes, a Dietary Disease #392: “Broccoli May Help Fight Diabetes”

When I read this headline in Medscape Medical News, in a write-up by an MD, of a real research project, my hopes soared. I thought, doctors were adopting the precept that Hippocrates, “Father of Western Medicine,” had made famous: “Let food be thy medicine and medicine be thy food.” Finally, we had come full circle!
The full title of the Medscape précis of the study, which was published in Science Translational Medicine, was “Antioxidant in Broccoli May Help Fight Diabetes.” Nevertheless, I still believed that these medical doctors – the study authors and the Medscape writer – were advocating that we eat a diet of healthy, whole foods. And that there was a dietary fix for those among us who had already developed a lesser or greater degree of Carbohydrate Intolerance, i.e., were overweight, obese, or had been diagnosed pre-diabetic or type 2 diabetic.
And the first sentence of the Medscape piece did not disabuse me of this vision on the horizon – a mirage or hallucination it turns out. It described the antioxidant as “a new option for treating type 2 diabetes.” The second sentence went on to describe the mechanism that the antioxident used, that it “reduces exaggerated glucose production by the liver in type 2 diabetes,” in much the same way that Metformin does.
Unfortunately, in the sixth paragraph, the full story – and the sad truth – emerged: “The study used highly concentrated broccoli extract, which would be equivalent to eating about 5kg [11 pounds!] of broccoli per day.” “Because it’s almost impossible to eat such large amounts of broccoli [diya think?], [the antioxidant] needs to be taken as an extract or concentrate.” Okay. Now, where does this revelation take us?
“We think broccoli extract could be a very exciting addition to treatments that we already have,” the lead researcher said. “When we gave it to patients and measured their glucose control before and 12 weeks after treatment, we saw significant improvement in fasting blood glucose and HbA1c in obese patients with dysregulated type 2 diabetes,” he averred. The results were ‘very encouraging,’ he added.
So, where does this well designed research in basic science lead? Medscape explained: “Currently, they [the researchers] are working with a farmer-owned organization in Sweden…to make the extract available as a functional food preparation.” Aha! A collaboration: Basic Science → Applied Science + Farmer → $$$$ for all.
Diya think I am being cynical? Just read the accompanying Conflict of Interest Disclosure:
“The study was sponsored by Lund University. Lantmännen [the local farmer-owned organization] provided the broccoli extract and placebo for the study, and Lantmännen Research Fund financed part of the study. Lantmännen reports no influence on the study procedures, data analysis, or data interpretation. Rosengren [the lead researcher] had no relevant financial relationships. Two coauthors are inventors on patent applications submitted by Lund University that cover the use of sulforaphane [the antioxidant] to treat exaggerated hepatic glucose production. The rights to use this patent have been licensed to Lantmännen.”
Okay. I wasted my time reading this piece of garbage from the usually reliable Medscape Medical News. But it is medical business news in the sense that universities, even the best of them like Lund, are not above pecuniary interests. They need “research funds” to survive and prosper, just as “local farmer-owned organizations” need money. But this story is not about eating in a healthy way to avoid developing Insulin Resistance (Carbohydrate Intolerance) or even to treat “obese patients with dysregulated type 2 diabetes.”
But, I got to write another curmudgeonly piece to offset my usual lecture about eating Very Low Carb (VLC), losing weight without hunger, and lowering your blood glucose AND blood insulin levels. That’s a saving grace.
So, have doctors come full circle with respect to eating real food? Not in my lifetime, a friend quipped.