Sunday, June 17, 2018

Type 2 Nutrition #437: Heading for the cliff

The most memorable scene in the 1991 feminist comedy, “Thelma and Louise,” is at the end.  Let me set the scene: Being chased across the desert by a dozen cop cars, with a cliff in front of them, Thelma says to Louise, “Okay, listen; let’s not get caught.” Louise replies, “What’re you talkin’ about?” Thelma replies: “Let’s keep goin’! Louise: “What d’ya mean?” Thelma: “Go” [nods ahead of them]; Louise: “You sure?” Thelma: “Yeah.”
Now, juxtapose this dialogue, the action that follows, and the consequences, with a current TV commercial for a once-a-week injectable drug to “activate your within.” This drug works, they say, to “help activate your body to release its own insulin.” Why? Because “diabetes can be hard to manage. It’s important to remember that diabetes is a progressive disease, which means it usually changes over time. And when it changes, your doctor might have to change your treatment as well.” In other words, as Thelma said, “Let’s keep goin’!”
But, the pharmaceutical company counsels you, “You are not alone. Millions of people are living with diabetes and going through some of the same things you are.” Now, the image in my mind changes. Imagine you are among millions of lemmings heading for the cliff. “What are you talkin’ about,” you ask? “What d’ya mean?” Well, by the time you’re a candidate for this injectable medicine, you’ve already followed in the footsteps of the lemmings who take oral antidiabetic medicines, like sulfonylureas (see below) and have now “progressed.” Remember, in the ad, you’ve been assured: “Diabetes is a progressive disease,” and “You’re not alone.”
The medical dogma is that progression of type 2 diabetes from Impaired Fasting Glucose (IFG) to Impaired Glucose Tolerance (IGT), to frank type 2 diabetes is a gradual, decades-long continuum. Ralph A. DeFronzo, described it 10 years ago in his Banting Award keynote speaker at the 2008 American Diabetes Association meeting.  I chronicled DeFronzo’s remarks 5 years ago in this column, “Natural History of Type 2 Diabetes.” 
 A hyperlink in my old post will take you to the paper in the ADA’s “Diabetes” in which DeFronzo’s states, “Sulfonylureas are not recommended because, after an initial improvement in glycemic control, they are associated with a progressive rise in A1C and progressive loss of β-cell function  Why is this relevant? Because this new injectable drug “activates your body to release its own insulin.”
Sulfonylureas (SU’s) lower blood glucose “by stimulating insulin release from the Beta cells of the pancreas.” The current generation of SUs, still popularly prescribed, include the glimepiride (Amaryl), glipizide (Glucotrol and Glucotrol XL), and glyburide (Diabeta, Micronase, and Glynase). In the paper cited, DeFronzo says,
“Insulin resistance in muscle and liver and β-cell failure represent the core pathophysiologic defects in type 2 diabetes. It now is recognized that the β-cell failure occurs much earlier and is more severe than previously thought. Subjects in the upper tertile of impaired glucose tolerance (IGT) are maximally/near-maximally insulin resistant and have lost over 80% of their β-cell function” (all emphases added by me).
So, if (repeating myself), as Defronzo says in the first paragraph of his seminal paper in the ADA’s “Diabetes,”
“Sulfonylureas are not recommended because, after an initial improvement in glycemic control, they are associated with a progressive rise in A1c and progressive loss of β-cell function” (emphasis added), then…
Why, pray tell, if you may already have lost 80% of your pancreatic β-cell function on the drugs you have been taking for years, why would you “progress” to a drug that will ACCELERATE the loss of your remaining β-cells?  Wouldn’t that be like Thelma and Louise deciding to drive over the cliff? Quoting Louise, “Are you sure?”
Or could it be that the maker of this new medicine, Lilly, has you covered? It’s also makes and sells insulin, a drug with price increases at 10x the rate of inflation.  Now that’s acceleration!

Sunday, June 10, 2018

Type 2 Nutrition #436: “Science advances one funeral at a time.”

My subject’s photo, below the sub-header “Helped America Eat Better,” stares me in the face every day when I sit at my laptop. My computer shares a table covered with a NYT’s obituary page and a harpsichord keyboard I am fine tuning. It is both prophetic, and motivational; I am inspired to unload a little on “the state of things.”
My parents taught me to “never speak ill of the dead” so, while I’m going to violate that aphorism with this piece, I will not be hurtful to the departed personally. Before you say, “Bless your heart,” know that my feelings – my enmity, really – toward the myopic vision of my subject, heralded by the NYT with an 18-column-inch obit, is that society still viewed him in such an exalted status as late as 2017. This man, like so many of his colleagues, actually failed to lead us to “eat better.” But the NYT piece was an obituary, not an op-ed.
I am reminded of one of my favorite last lines in a movie. It is Joey Brown’s in “Some Like It Hot” (see this YouTube video excerpt). Brown proposes marriage to Jack Lemmon, cross-dressing to avoid a mafia hit squad. Lemmon replies in exasperation that he’s in fact a man, to which Brown replies, “Well, nobody’s perfect.”
From the obit: This doctor, a “surgeon, clinician, researcher, teacher and author, was pre-eminent in the study of obesity and nutrition.” Besides his medical degree, he held a doctorate in nutritional biochemistry from MIT and “largely spent his career at Harvard Medical School and Beth Israel Deaconess Medical Center in Boston.” He was professor of nutrition at Harvard, and at Beth Israel was the chief of Nutrition/Metabolism Laboratory and Director of the Center of Nutrition Medicine. He was at the apex of the “nutrition establishment.”
Yet, “what really put him and his colleagues on the world map were publications highlighting inadequate nutritional management of people in the hospital – so-called ‘hospital malnutrition,’” said a former colleague. How did he do that? “He helped develop nutritious liquid diets (Ensure, and others), supplementing them with protein…” In other words, he and Harvard profited handsomely from this misguided commercial collaboration.
He also correlated poor nutrition with obesity – a no-brainer there, but note again this habitual dependency of Harvard nutrition “experts” on epidemiology, or “correlation,” rather than a scientific interest in “causation.” His solution: “Advocate lower-fat diets and help develop gastric by-pass surgery and nutritional liquid diets.”
I’m not suggesting that this good doctor had a Mephistophelean streak; I’m sure he intended well, but like Ancel Keys before him, and others still in positions of  influence (e.g. Walter Willett at Harvard), he rose to power in the politics of the academy by buying into the “eat-less, exercise-more, a calorie-is-a-calorie” meme that is only now beginning to show wear at the edges because of the weakness of the scientific evidence.
His obituary writer noted that “weight loss benefitted patients with type 2 diabetes.” Now, there’s a scientific breakthrough! His obituary also described five strategies the good doctor “developed during four decades of encouraging patients to shed pounds: 1) Make time to prepare healthy meals, 2) Eat slowly, 3) Consume evenly sized meals, beginning with breakfast, 4) Do not skimp on sleep, and 5) Weigh yourself often.” Not bad advice, but pretty banal accomplishments, if you ask me. Forty years of “encouragement…to shed pounds.”
I also think that evenly sized meals sounds too much like “balanced” to me. And nutritious liquid diets like Ensure, even if supplemented to 15% protein, are still 60% highly processed carbohydrates. “Carbohydrates” are not mentioned even once in the entire 2-columned obituary. The emphasis instead is on calorie intake: “Even a small decrease in caloric intake could result in healthier weight,” he is quoted as saying. He summed it up: “Sustained weight loss requires a three-pronged approach: Cut the calories, eat quality food and exercise.”
As Max Planck, the German Nobel-prize winning physicist said in 1906, “Truth never triumphs; its opponents just die out.” Another paraphrased variant is, “Science advances one funeral at a time.” May he rest in peace.

Sunday, June 3, 2018

Type 2 Nutrition #435: Hungry or Undernourished?

“Hungry or Undernourished?” is what I would call a BIG question. It is way out of my league to propose a scientific answer or even describe the parameters of a proper study. I will venture, however, to tackle the matter as an opinion piece: I think it can be parsed into at least two different lines of reasoning, and I will attempt to posit and briefly explore them. I welcome informed comments from my erudite readers.
The first line of reasoning in the “hungry or undernourished?’” debate is that we will eat until our stomach is full. This is the “common sense” hypothesis; we have all experienced it. When we are “full,” hormones signal us to stop eating. Of course, there are exceptions. We sometimes continue to eat for other reasons. I’m a compulsive peanut eater. There’s also taste and palatability. See this link to carbohydrate-induced overeating (in rats). Lay’s potato chips captured this with the memorable meme, “Bet you can’t eat just one!”
There is a large body of new evidence that the “until full” hypothesis is hormonal. Hunger is regulated by the hypothalamus in the brain which gets signals to induce eating from ghrelin, a hormone produced in the lining of the stomach, and shuts down when another hormone, leptin, signals that hunger has been satisfied. Ghrelin was only discovered in 1999 and appears to have other functions as well. And “leptin resistance” as a cause of obesity is still a mystery. So, this is why the hormonal hypothesis of “eating until full” is also just a hypothesis.
The other line suggests that hunger drives eating until the body has met its requirements for essential nutrients. I know this sounds like a tautology and needs more explanation. It is, of course, more nuanced but at this point in the state of nutrition knowledge, the science is unknown. The theory is that what we eat, not how much, determines when the body is satisfied and hunger stops. Ergo, if your diet consists of nutrient-poor components, aka processed carbs, you will need to continue to eat until your body gets everything it needs.
These essential nutrients or components include the macronutrients and micronutrients. The macros are fats (fatty acids, SFAs, MONOs and PUFAs), proteins (and their 22 amino acids, into which protein breaks down), and carbohydrates, (none of which – repeat, none, are essential). The micronutrients are vitamins, minerals and phytochemicals, many as yet unknown.
My recollection is that this second line of reasoning is suggested in such very good books as “The Perfect Health Diet,” by Paul and Shou-Ching Jaminet, and Catherine Shanahan’s “Deep Nutrition.” It is a rational hypothesis, and I am biased in favor of it in part because the known science about the different fats and the amino acids has pretty well established how important they, or their absence, are to human health.
It also appeals to me because it supports the idea that all dietary carbohydrates, while a good source of quick energy, are not essential nutrients in the human diet. When carbs are not available to eat, our bodies are designed to make all the glucose it needs from protein and fat, through gluconeogenesis. The body also produces ketone bodies (brain food) from fat, and it gets glycogen, to make glucose, from storage and from the animal products we eat (intramuscular, subcutaneous, and from organ meats like liver). Admittedly there still isn’t a lot of hard evidence to support this hypothesis. Philosophically, though, it appeals to me.
If I had to guess, I’d hedge my bet by speculating that the answer ultimately will involve or combine these  hypotheses. In the meantime, we can be guided by what we “know” and eat with the knowledge that bodies will determine how much we need to eat and what a healthy diet is. I find my body likes it best when I eat mostly “healthy” fats (saturated and monounsaturated), and moderate amounts of protein from pastured meats and poultry and wild-caught fish. I try my best to avoid polyunsaturated fat (vegetable oil) altogether and since I am Insulin Resistant (32 years a diagnosed type 2 diabetic), I eat as few carbohydrates as possible.

Sunday, May 27, 2018

Type 2 Nutrition #434: Watch out! Your doctor thinks he/she knows about nutrition

“Do you discuss nutrition with your patients?” the Tufts Friedman School of Nutrition Science and Policy survey asked physicians. Three-quarters of them replied “always” or “most of the time.” “Do you feel qualified to talk about nutrition with your patients?” Again, 3 out of 4 said, “Yes.” To which I say, “Watch out!”
I have cause to be concerned. The Medscape article which reported the findings links them to two pieces: 1) A “recent study” that “associates…a sub-optimal diet” with “a substantial proportion of deaths in the United States due to heart disease, stroke and diabetes,” and 2) another that nudges physicians to “know what advice to give.” It couches this advice as “evidence-based nutritional advice” to help healthcare professionals deal with “information overload” on diet and nutrition. The whole point – the pretext for the Tufts “survey” – was  to “educate” physicians and other healthcare professionals with that advice, i.e., their agenda-driven POV.
I agree there’s an association of “heart disease, stroke and diabetes” with a sub-optimal diet…a very strong association. Deaths from heart disease and stroke are much higher among type 2 diabetics and “pre-diabetics.” This association has led to the phrase “cardiometabolic disease” (CMD). But, again, on which diet did they become diabetic and develop heart disease? The Tufts answer (“evidence-base”) is just “association.”
The study was presented at the American Heart Association Epidemiology and Prevention-Lifestyle and Cardiometabolic Health (EPI-Lifestyle) 2017 Scientific Session. The findings were also commented on in Medscape by researchers from the Johns Hopkins Bloomberg School of Public Health and the Welch Center for Prevention Epidemiology. More epidemiologists! Epidemiology suggests hypotheses, not cause and effect!
Why is that significant? Because epidemiology can only address “associated with” and “related to” findings. But that does not deter them. This “poor diet” link, using “comparative risk assessment models,” estimates that 45% of cardiometabolic disease (CMD) deaths were “associated with” 10 dietary factors, and that these factors have “‘probable or convincing evidence’ for causality” (my emphasis). Epidemiologists are shameless in their reckless disregard for a basic tenet of the scientific method: Correlation does not imply causation.
The “10 dietary [death] factors” ranged in descending order from a high of 9.5% for 1) salt (“excess sodium”), to 2) low intake of nuts/seeds, 3) high intake of processed meats, 4) low seafood omega-3 fats, 5) low intake of vegetables, 6) low intake of fruits, 7) high sugar-sweetened beverages, 8) low intake of whole grains, 9) low intake of polyunsaturated fats and finally, at 0.4%, to 10) high intake of unprocessed red meats. Hmmm… Zero point four percent does not strike me as statistically significant, but I guess they just had to include red meat.
We can also be grateful that a low intake of polyunsaturated fats (corn oil, soy bean oil, etc), at 2.3%, ranked only 8th on the list. A higher intake, as they advocate, would, IMHO, only have raised the risk of death greatly.
This is what your doctor, if (s)he was not on the golf course, is learning and says (s)he knows about nutrition. To relieve “information overload,” Tufts gives these 6 educational talking points from the “advice to give” link.
       Choose foods with a wide variety of colors and textures, in their most natural forms. [check]
       Avoid or dramatically minimize processed foods. [check]
       Choose realistic, balanced [not low-carb] diets for weight loss and weight maintenance.
       Consume healthy oils for heart health: fish, olive, avocado. [good, all MONOs, no mention of PUFAs]
       Forego red meat [saturated fat] and live longer [a little editorializing? They just couldn’t resist!].
       Consume fermented foods/probiotics and fiber for gastrointestinal and overall health. [check]
This is just the Government’s plant-based, one-size-fits-all, Mediterranean diet. It doesn’t mention carbs or type 2 diabetes, and if you are currently lean and healthy and ate this way, you could stay healthy. For the rest of us, balanced would need to be carefully defined, and avoiding all polyunsaturated vegetable oils stressed. Personally, though, I would rather embrace carnivory than give up red meat for a 0.4% increase in CMD death.

Sunday, May 20, 2018

Type 2 Nutrition #433: “Lifestyle Programs ‘Could Prevent Diabetes’”

My heart skipped a beat when I saw, in Medscape Medical News, the header, “Lifestyle Programs 'Could Prevent Diabetes.” Had the medical establishment finally come to accept type 2 diabetes as a dietary disease? Had they decided to repudiate the awful advice they’ve been dishing out for half a century and finally effectively address the raging epidemic of obesity, type 2 diabetes and related diseases increasingly plaguing our world?
Or, at the very least, had they perhaps figured out a way to finesse the bad advice for treating these diseases by advocating an intervention before the diseases were firmly established. That would be a brilliant strategy that would in effect, to use an American football metaphor, be an “end run” to evade the usual “middle-of-the-line” defenses. While hope springs eternal, my hopes were soon dashed. It was neither of the above.
The story was just about “updated guidance [that] will give clinicians the confidence to make prevention their priority, indentify those at high risk, and refer them to the UK’s Diabetes Prevention Program.” It was a press release. It did, however, shed some interesting information on what the NHS considers “those at high risk.”
The NHS (National Health Service) is the British equivalent of US’s HHS. The Diabetes Prevention Program was started in 2016. Its crown jewel is the National Institute for Health and Care Excellence (NICE) pilot initiative to offer a place on “an intensive lifestyle change program” to “people who could benefit from advice on their diet and physical activity levels.” The program is currently scheduled to roll out across all of England by 2020.
“Nice says it is currently cost-effective to target people with a fasting glucose between 5.5—6.9 mmol/l [99—124mg/dl]. However, it says those with a higher reading (6.5—6.9mmol/l)[equivalent to 118—124mg/dl] should be prioritized for inclusion because of their increased risk of developing type 2 diabetes.” Geez! All of these people are at “high-risk”for type 2 diabetes. They all have Insulin Resistance and thus incipient T2DM!
Many clinicians and researchers concur with this “extreme” prognostication. Consider that in 1997 the ADA Standard for a medical diagnosis of type 2 diabetes changed from 140mg/dl (7.8 mmol/l) to 126mg/dl (7.0 mmol/l). Yet another change is long overdue. There is already a hue and cry to change the definition of “pre-diabetes,” first classified in 2002. (In Europe 6.1—6.9mmol/L or 110—125mg/dl; in the U.S.: 100—125mg/dl.
The Medscape “good news” spin in the header was inaccurate. It was notthe purpose of the NHS press release.” The NICE center’s director was more on point: “We know that helping someone to make simple changes to their diet and exercise levels can significantly reduce their risk of developing type 2 diabetes.” But perhaps because it is OT to the rollout, he doesn’t explain exactly what those “simple changes” would be.
The story also points out that “(w)hile type 1 diabetes cannot be prevented and is not linked to lifestyle, type 2 diabetes is largely preventable through lifestyle changes.” Indeed! Largely preventable – even reversible – at  least in the sense that if you adhere strictly to specific diet changes, type 2 diabetes can be put into complete remission, that is, completely undetectable by a simple laboratory test such as a fasting glucose or an HbA1c.
To your doctor, that’s a cure! And when this disease is in remission, your risk of kidney failure, preventable sight loss, and amputation is de minimis. And your risk of heart attack and stroke reduced by 50% or more!
Diabetes UK’s head-of-care said, “We know that globally, diabetes prevention programs do work, and we know that with the right advice and support, people with increased risk of developing type 2 diabetes can take simple but significant steps to prevent the condition from developing.” The “right advice,” unfortunately was nowhere to be found in this document or in my search of the NICE site. Methinks perhaps it’s too hot a potato. Maybe they don’t want a “cure.” Maybe they just want a “treatable” condition… to keep the NHS in business.

Sunday, May 13, 2018

Type 2 Nutrition #432: “I’ve never had a hot flash”

Not me! My editor said this in a comment to a link she sent me. The full quote: “So thanks to Bernstein, I’ve never had a hot flash. I just thought it was luck!” She concluded, “…interesting, how it is always insulin and glucose control.” My editor was referring to the linked article, “Vasomotor Symptoms and Insulin Resistance in the Study of Women’s Health Across the Nation.” It appeared in the Endocrine Society’s Journal of Clinical Endocrinology & Metabolism. She routinely reads this kind of stuff. That’s why I want her as my editor (lol)!
“Vasomotor symptoms (VMS) are classic symptoms of the menopausal transition, experience by up to 70% of women living in the United States,” the abstract says. “VMS have important…implications because women reporting VMS consistently show poorer sleep quality, more negative mood, and impaired quality of life.”
The report drew on annual blood draws and questionnaires over 8 years from 3,075 women aged 42-52 at entry who participated in the Women’s Health study. Hot flashes/sweats were examined in relation to two metabolic factors used to define type 2 diabetes: glucose and the homeostasis model assessment (HOMA).
The study made adjustments for BMI (associated with IR), CVD risk factors, medications and hormonal status. It found that, “compared to no flashes, hot flashes were associated with a higher HOMA” and “were similar for night sweats.” “Findings were statistically significant, yet modest in magnitude, for glucose.”
Beyond the scope of this study, but of interest to the researchers, was the association of the link between menopausal hot flashes/night sweats (VMS) and cardiovascular disease (CVD). “The mechanisms underlying these associations are unclear, due to the incomplete understanding of the physiology of hot flashes,” the report says. The investigators then explored the relation between VMS and CVD from the two well-known studies: Women’s Health Initiative hormone therapy trial and the Heart and Estrogen Replacement Study.
These studies “showed an elevated risk for clinical CVD with hormone use among older women with moderate to severe VMS at baseline relative to women with no/mild VMS.” In addition, “In the Study of Women’s Health Across the Nations, VMS was associated with higher subclinical CVD.” But the findings were mixed. Other work has “examined the associations between VMS and CVD risk factors such as blood pressure.” But until now…
No work has examined the relation between VMS and fasting blood sugar and insulin resistance….” This study was well designed, testing the hypothesis with controls for race/ethnicity, CVD risk factors, body mass index (BMI), the reproductive hormones E2 and FSH, and menopausal stage. The take away for me was the association with BMI, which as mentioned correlates with IR. The researches here noted that the association “did not persist” after adjustment for BMI. In other words: “you lose the weight, you lose the risk.” Take note!
The report concludes, “Considering BMI in relation between insulin resistance and VMS is particularly important given that higher BMI is a potent risk factor for insulin resistance and is associated with greater VMS reporting in perimenopausal and early postmenopausal women.” So, eat Low Carb and get svelte, like my editor, while there’s still time.
Or, if it’s too late for you, ponder another statement from the study with respect to cognitive impairment. This citation “postulates alterations in glucose transport across the blood-brain barrier as a trigger for VMS.” Since glucose is the main brain fuel, and ketones are brain fuel only while eating VLC or during fasting when blood insulin levels are low and fat breaks down for energy, a decline in “glucose transport across the blood-brain barrier” leading to VMS could be problematic. Could ketones substitute for glucose in this way? As my editor observed, “…it’s always insulin and glucose control.” Would following Bernstein’s 6-12-12 or another Very Low Carb regimen enable you to say, “I’ve never had a hot flash”? Or even help a guy get slim and stay healthy?

Sunday, May 6, 2018

Type 2 Nutrition #431: May 9th, from a Russian Perspective

Fifteen years ago this week, I had an eye-opening experience…about perspective. As was my daily habit, on the way to work I stopped at a food cart to order breakfast: coffee with heavy cream and artificial sweetener, 2 fried eggs, plain, and 2 strips of bacon.
The cart was owned by a father and son who were post-1989 immigrants from Russia who were both excited to be taking a citizenship course. They quizzed me daily on American History and were always amazed that I correctly answered every question they put to me, except one day…
They asked me, “Do you know what day today is?” I said, “No.” They were both delighted. They’d stumped me! They said triumphantly, “It’s May 9th, the day that World War II ended!” I smiled and replied, “You mean it’s the date WWII ended in Europe.”  They both looked puzzled. I continued, “War continued in the Pacific.” There was a long pause while they thought about that, and then the son said, “Oh, you mean Vietnam!”
I had to explain that for the United States: WWII was fought on two fronts; that the Japanese had attacked the U. S. at Pearl Harbor, Hawaii, on December 7, 1941; and that the Pacific theater of the war didn’t end until August ‘45 when the U. S. dropped atomic bombs on Hiroshima and Nagasaki. Japan then surrendered, September 3, 1945, on what we call V-J Day. Americans refer to the end of WWII in Europe as V-E Day.
To a degree it’s understandable that Russians have a different perspective of WWII. U.S. military losses in 4 years of war on two fronts were only 5% of Soviet military losses in 4 years of war on one front. Every country has a chauvinist view of history, but there’s no denying that U. S. deaths, none on its own territory, were just over 400 thousand, whereas Russian military and civilian deaths, most on their own territory, were 27 million.
A similar disparity exists today in the battle over a healthy diet. The leaders of the public health and medical establishments, and the civilian population that follows their advice, are dying in droves from a multitude of metabolic diseases brought on by the diet they eat. This diet has produced an epidemic of obesity, type 2 diabetes, cardiovascular diseases, including stroke, Alzheimer’s disease, and increased prevalence of many types of cancer, particularly pancreatic cancer
The vast majority of these victims – both the leaders and the unwitting populace who follow them – are engaged in a losing battle. And the agri-industrial complex that abets them, by producing prodigious amounts of processed foods in accordance with the advice to eat less saturated fat, more Omega 6-loaded, processed vegetable oils, and a diet largely comprised of refined carbohydrates and simple sugars, is killing them.
I don’t blame the two Russian men for not knowing about the war the U. S. fought in the Pacific before and after V-E Day. Their government was justly proud of the enormous sacrifice the Soviet Union made to win WWII. Their government should be faulted, however, for educating them poorly. I doubt that they knew, for example, that U. S. industrial production provided huge amounts of war material in Soviet flag ships sent from the U. S. west coast to Vladivostok, free from Jap attack due to a Soviet -Japanese non-aggression pact!
Unavoidably, however, one must conclude that the outcome of the “healthy diet” battle will be determined by the leaders on the field of battle. If you continue to follow the government’s advice, and go into battle led by General Mills and General Foods, and make unhealthy choices, you will end up…well, up the (Battle) Creek.
 The U. S. had a definite advantage in WWII. We had two oceans to protect us, enormous natural resources, the industrial capacity to produce the means to fight, and the individual, human potential to meet the challenge.  Today, as individuals, we are faced with another challenge: to make the right choices about what to eat, free from influence from an inherently conflicted agri-industrial complex. You can still make a decision to improve your chance for survival in this battle. A new perspective can help you make that choice.