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

I haven’t written about supplements since…wow! I just did a search of almost 400 posts and discovered I have NEVER written about my supplements. I guess it’s because I consider it personal, not in the sense of private – I am transparent about my health – but in the sense of “individualized.” I think it is also because I have read so much about how none of them are necessary or even helpful, like I’ve just been duped or sold a bill of goods.

So, why do I take supplements when there’s no real way to prove that they have helped me? A well designed experiment is impossible; there are just way too many confounding factors. I guess the best answer is that they are “insurance;” besides, most of them are vestigial, that is, I began them before I was initiated in the ways – or the concept anyway – of eating a low carb diet of whole, real food…and I just continued with them. That’s my construct anyway. Besides, some of them I do believe in. So, which would I eliminate and why?

I am prompted to write about this now by a presentation made at Keto Fest in New London, CT last July by podcast meister Ivor Cummins, the “Fat Emperor.” Near the end – maybe his very last sentence – as though it were a hurried, throwaway line, he said: “Don’t forget to take supplemental magnesium and potassium.” No time for an explanation. It was just a given, like everyone knew! Fortunately, I do take them both.

Here’s a complete list of my current supplements. Bear in mind, I am/have been a Type 2 Diabetic for 31 years and eat a Very Low Carb (VLC) or LCHF (Low-Carb, High-Fat) or Ketogenic Diet, with frequent full-day fasting.

With COFFEE with HEAVY CREAM and POWDERED STEVIA, early in the MORNING

●     1g fish oil, containing 300 EPA and 200 DHA, and 5 IU of vitamin E

●     1 tablet high potency men’s multi-vitamin, with vitamin D3, lutein and lycopene

●     100mg capsule of CoQ10, the active form (Ubiquinol)

●     200mg magnesium glyconate, chelated for absorption

●     200mcg of elemental chromium (chromium picolinate), with 18mg L-leucine + 2mg vitamin B6

●     100mg biologically active R-Lipoic acid (alpha lipoic acid), with 150mcg D-Biotin

In addition, I take 2 prescription meds: 750mg metformin Hcl and 25mg HCTZ, a diuretic (for hypertension)

With 6oz RED WINE & 8oz SELZER, about 12 hours later, if FASTING, or with FOOD (my supper meal).

●     1g fish oil, containing 300 EPA and 200 DHA, and 5 IU of vitamin E

●     200mg magnesium glyconate, chelated for absorption

●     99mg potassium, a multi-source blend

●     1 capsule homocysteine modulators: 50mg B6, 400mg folic acid (B9), and 500mcg B12

In addition, I take 3 prescriptions: 750mg metformin Hcl, and 20mg Enalapril & 240mg Verapamil (BP pills)

Candidates for deletion: 1) chromium picolinate, 2) R-Lipoic acid and 3) homocysteine modulators.

Possible additions: 1) a small (250mg) Vitamin C tablet with supper, to help with protein uptake, and a calcium supplement, to help with magnesium uptake. First I need to learn more about their interactions.

My labs are very good. My last A1c was 5.2%. My Vitamin D and B12 are high and very high respectively. My TC is below 200mg, my HDL-C is averages about 80, my LDL-C averages about 100 and my TGs still average around 50, even though I don’t eat a can of sardines for lunch any more. When I do eat lunch, I prefer a can of kippered herring in brine. It’s fewer calories and much less fat, and I’m trying to burn endogenous fat, not exogenous fat! My fasting intake is about 300kcal/day and my feasting intake paradigm is still about 1,200 (15g carbs, 60g protein and 100g fat, mostly saturated/monounsaturated). Finally, my inflammation markers are very low. Now that I have laid it out for everyone to see, what do you think? I invite comments.

Type 2 Diabetes, a Dietary Disease #397: If an A1c of ≥6.5% is defined as diabetic…

If an A1c of ≥6.5% is defined as diabetic, and the goal of the American Diabetes Association (ADA) is to manage your blood sugar such that it does not exceed 7.0%, then it follows ipso facto that the ADA’s guideline to MDs is to maintain you, if you are a type 2 diabetic, in a perpetual disease state. What do you think about that?

Two explanations are possible. I’m not so cynical that I would buy into the easy one: that your doctor, and the health care world that comprises about 1/6^th of the entire U. S. economy, needs to keep you sick for them to prosper. I understand why it’s easy to go there, but I really don’t think there is such a sinister conspiracy. There has to be another, probably much more complex and difficult, explanation for this conundrum.

The other explanation for the low expectation (≤7.0%) of the healthcare community is that, in their clinical experience, it is difficult under the terms of the ADA’s Standards of Medical Care to achieve the “reasonable goal” of an A1c of ≤7.0%, even with all the pharmaceutical options, both oral and injected, that are and come on the market. Big Pharma has expended vast resources over the last half century to manage type 2s health.

Insulin, discovered in 1921, can achieve that goal, but most patients do not want to inject themselves multiple times a day while monitoring and counting everything they eat to maintain “tight control.” Besides, the ADA and most clinicians do not advocate or practice it because there are serious dangers in some situations (coma and death).They are content to let their diabetic patients remain in a perpetual disease state rather than risk having them pass out and be transported to the hospital with life threatening hypoglycemia or ketoacidosis.

The confounding and mitigating factors for the terms of the ADA’s “Standards of Medical Care” include the  American Heart Association (AHA), starting in the 50s, and the U.S. public health establishment, including foremost, beginning in 1977, Government Dictocrats. In that year the Senate Select Committee on Nutrition and Human Needs, aka “the McGovern Commission” produced the “Dietary Goals for the United States.”

Starting in 1980 it was followed every 5 years by the “Dietary Guidelines for Americans” to “govern” what we eat. We followed it, the food manufacturers followed it, and so did the media and medical associations. We ate low fat, low cholesterol, low salt, lean meats, and low-fat cheese and yogurt. A mostly plant based diet.

Simultaneously starting in 1980, we got sicker and fatter and started to develop insulin resistance and type 2 diabetes at increasing rates. A little of this reflects an aging population, but this cannot explain the soaring rates of childhood diabetes. And just look around you on the street, or maybe in a mirror.

The “ship of State,” however, has begun to change course. In 2015 the Guidelines dropped the limit (30%) on total fat and the limit on dietary cholesterol (300mg/day). Eggs and butter, even bacon, are healthy again. Margarine, made from partially hydrogenated vegetable oils (trans fats) is taboo.

But these little known changes, while really significant – seminal, really – are in themselves not sufficient for the type 2 diabetic to reverse his or her disease state and achieve an A1c of less than 6.5% much less the 5.7%, threshold for a diagnosis of pre-diabetes. To reach this goal, or lower, the pre-diabetic needs to change the foods they eat. They need to limit carbohydrates, and not eat the same, one-size-fits-all diet that the government still insists everyone should eat. They need to follow a Low-carb, High-fat (LCHF) Way of Eating.

When you start to eat Low Carb, you will feel better. You blood sugar will stabilize. You will feel less tired and less hungry. You will lose weight. And your A1c will come down. I’ve been a diagnosed type 2 for 31 years and have been eating LCHF for 15. On LCHF I’ve lost 180 pounds and my A1c has gone from 8.9% to 5.2%. With no CVD. It’s still a challenge, but if I hadn’t made this lifestyle change, I wouldn’t be here today to write about it.

Type 2 Diabetes, a Dietary Disease #396: “Intransigent Resistance”

An acquaintance called me recently to say she had been talking to a mutual friend who had said that I had helped her lose 30 pounds (and 2 bra sizes!), by eating low carb. LOL. She (the acquaintance) wanted to know how to do it? Well, my friend suggested, she should call me and ask. So, she did, and I was glad to help.

I am always pleased when my low-carb, moderate-protein, high, healthy-fat message is heeded. I offered to lend her my favorite books to learn the physiology of low carb eating, suggested the best websites for a neophyte to visit, and offered to mentor her, answering any question she had, as I had for our mutual friend.

It turns out that the acquaintance – let’s call her Pam – is a very busy woman and doesn’t have time to learn about the science. She just wants to know what to eat, and what not to eat. Apparently Pam had read that I had lost 60 pounds in 9 months 15 years ago, by following “Atkins Induction” (20 grams of carbs/day). Then, a few years later I had lost another 110 pounds following Dr. Richard K. Bernstein’s “6-12-12 Program,” in which you eat just 30 grams of carbohydrate a day. For some reason, Pam decided she wanted to try Bernstein.

So, I loaned her Bernstein’s “The Diabetes Diet” and his encyclopedic “Diabetes Solution.” I also told her I had recently become an acolyte of Dr. Jason Fung, fasting advocate and author of “The Obesity Code,” about Intermittent and full-day fasting. I had unsuccessfully tried 16-8 for about a year, in which I ate basically just one meal a day, or a small lunch and then supper within an 8 hour window, thus fasting 16 hours a day.

More recently, because I eat Very Low Carb and am therefore FAT-ADAPTED, I transitioned to full-day fasting. So far I have lost about 50 pounds since early February. Concerned that I would be hungry or lacking in energy, I started off with alternate day fasts (Tuesday and Thursday). But because I am FAT-ADAPTED, I was neither hungry nor lacking in energy. My body transitioned easily from fed to fasting states, using glucose from the fed state and then fatty acids from body fat and ketone bodies, the by-products of fatty acid breakdown, for brain food during the fasting state. Because of that smooth and natural transition, my metabolism continued to run at full speed. In fact, my sense is that I am actually more “pumped,” more energized, in my fasting state.

I then described what I put in my mouth on my 300 kcal/day Fasting Regimen: Coffee with heavy cream for “breakfast” and a wine spritzer at the supper hour. Pam asked, “Don’t you drink more water during the day?” I said, “Only if I am dehydrated from working outside on a hot day.” “You should, you know,” she admonished. I said, “I also drink some brine from the pickle jar” (to maintain my electrolyte balance). Pam was apoplectic.

In a later email exchange, I told Pam that she would have to cut way back on fruit to eat Low Carb. To eat Very Low Carb, she’d have to virtually eliminate fruit. Fruit is basically just sugar. Fruit juice is worse.  It’s nature’s candy. Pam replied she had a serious problem with constipation and didn’t want to give up fruit on that account. I replied that that was a rationale that I did not understand, but she didn’t explain how they were associated. I suggested it was an irrational justification, a rationalization, if you will. The subject was dropped.

I then suggested taking magnesium as a mild laxative and sleep aid. Most older adults are deficient in magnesium and should probably take a supplement. Pam then said she currently takes 400mg a day and her cardiologist doesn’t want her to take more. Her cardiologist! That’s new information to me. I replied that I take a full gram a day: 400mg morning and night plus 200mg in a multivitamin. And I had never experienced constipation on a Very Low Carb diet, even before I added a magnesium supplement morning and night.

Finally, I suggested increasing her fat consumption to ease her bowels. She said, “Thank you” and signed off. I guess she, and maybe her cardiologist, think the US Dietary Guidelines still limit dietary fat to 30%, or worse, cause CVD. Not true! Change is a slow process, starting with curiosity and intrigue, with a lot of resistance throughout. Sometimes intransigence shuts down the process completely. “Intransigent Resistance” (IR).

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!

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 2/3^rds 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 2/3^rds 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.

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 1^st 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 4^thQ/Final report on the amended goal. I started the 4^th 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 2^nd 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 2^nd 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 1^st 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.

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.