Retrospective #305: My Troubled Relationship with Food

This is a hard thing to admit, but easy to see, if you know me. While I am still 150 pounds lighter than I was in 2002, I am 37 pounds heavier than I was at my lowest in 2017, and that’s no accident. I ate myself that way. I am, in fact, still fat. With a Body Mass Index (BMI) of 32, I am still smack in the middle of “obese.” And even at my lowest weight (188 pounds), my BMI (27) was still at the high end of overweight! How did the weight regain happen? Well, I’ll tell you.

Before I do, though, I want you to know that I am, today, much, much healthier than I was in 2002. And I don’t mean just being less fat. I have a much better and more stable blood sugar level, and I have been able to give up and stay off virtually all of the oral anti-diabetic medications I was taking back then. My Type 2 diabetes is now, clinically speaking, “in remission.” My fasting blood sugars are almost always below 100mg/dl (weekly average), and my A1c’s are low 5s.

And my cholesterol profile has dramatically improved, with HDLs more than doubled (usually 80s) and triglycerides cut by 2/3rds (usually 50s). See my Retrospective posts # 281, #282 and #283 for a 35-year history with charts.

And probably most import, my hsCRP’s, the chronic systemic inflammation marker, are now usually <1.0mg/dl, down from +/-6mg/dl). And because of my stellar lipid (cholesterol) profile, my doctor took me off statin drugs years ago.

And why is that? Well, while I have re-gained 20% (37 of 187) of my original 375 bulk, I have fundamentally not changed what I usually eat. I still follow a low-carb, high-fat (LCHF) Way of Eating most of the time. But I “cheat.” I’ll sometimes scarf down a roll or two, with butter, brought to the table in a restaurant. Sure, we could say, “no bread,” and sometimes we do, but most of the time we don’t. I also raid the freezer at home occasionally to steal some of my wife’s ice cream. Do you see how easy it is for me to project blame on someone else for my transgressions?

I could blame “habituation to rewarding neural dopamine signaling [that] develops with the chronic overconsumption of palatable foods, leading to a perceived reward deficit and compensatory increases in consumption.” For this quote and a scientific roundup of why obesity is a vexing problem, see my Retrospective #297: “Obesity in Remission.”

How things now stand: Because most of the time I eat LCHF, my Type 2 Diabetes continues in remission. But while I have lost a great deal of weight, I also have Obesity in Remission. So, I must remember to “eat healthy” (for my definition, see Retrospective #301) and that means mostly foods (fat and protein) that do not raise my blood insulin. “Elections have consequences,” and since I elected, on the recommendation of my government and my doctors, to eat processed carbs and sugary foods way in excess, I am forever predisposed to accumulate excess fat. Why is that? I had a genetic predisposition, and I developed Insulin Resistance. Insulin Resistance = carbohydrate intolerance, forever.

But 1) if I eat only the foods I have espoused and recognized as “good” for me, and 2) if I had eaten only when I am hungry, or even when not, just one or two small meals a day instead of the conventional three, I a) probably would not have gained back any weight, and b) I might have continued to lose weight. Per the BMI tables, I shouldn’t weigh more than 170 pounds, the highest “healthy weight” (BMI = 24), or even 150, the middle “healthy weight” (BMI = 22). But I don’t, and I don’t even aspire to those weights. I mean, there is such a thing as obsessive/compulsive disorder.

As you read this rewrite of my original #305 from 2015, my blog posts have reached 390,000 people in the last 9 years. So, it’s very likely that more than a few people (besides me) has benefitted from them. With the “Retrospective Series,” I plan to continue to offer daily help and support through column #500. My goal is to offer very good advice, especially for Prediabetics and Type 2s, who are self-motivated to manage their condition to avoid “the current treatment protocols (that) trap patients in a lifelong regimen of drug management, obesity and escalating diabetes.”

And, as I did when I wrote the original #305, I want to again thank my editor, Laurie Weakley. She has been a stalwart friend and helper from the beginning, always there with timely and helpful edits and links to scholarly resources. She is an inveterate professional, a tireless fact checker and my overall guiding support. And, she always knows the subject better than I do. Thank you, thank you, thank you, Laurie Weakley. (Too many “thank yous,” Laurie?)

Retrospective #304: I am not making this stuff up!

“Novel differences in the glucose response to HP [higher-protein] vs. NP [normal-protein] breakfasts were observed and were influenced by the frequency of habitual breakfast consumption in overweight adolescents.” This might have made a good tweet, but – and I am not making this up – that was the CONCLUSION from the Abstract of a recent article in the European Journal of Clinical Nutrition (EJCN). I saw this groundbreaking news in Diabetes in Control: “Breakfast Habits Affect Overweight Teen Girls’ Metabolic Responses to Protein-Packed Morning Meals.”

“The primary aim [of the study] was to examine the daily glycemic response to normal-protein (NP) vs. higher-protein (HP) breakfasts in overweight adolescents who habitually skip breakfast (H-BS). The secondary aim examined whether the glycemic response to these meals differed in H-BS vs. habitual breakfast consumers (H-BC),” according to the EJCN. If this sounds elementary, Watson, I’ll generously assume the research was intended to educate overweight/obese late adolescent girls in an online chat line or similar social media or some teen-oriented supermarket magazine. I just can’t believe it was intended to educate medical professionals. Or wait, could it?

The unsurprising outcome was that “those who typically ate a high-carbohydrate breakfast had improved glucose control after they ate a high-protein breakfast.” Quelle surprise!  But the researchers seemed surprised that “the habitual breakfast skippers experienced poorer glycemic control throughout the day when they consumed a high protein breakfast.” Hmmm. Hold the presses: any ingested food affects your circulating blood glucose! It disrupts a low serum insulin status from an overnight fast. It causes glucose, from any carbs and then some from glucogenic proteins, especially in any dairy consumed with breakfast, to enter your bloodstream, resulting in peaks and crashes!

The Abstract (you have to pay to access the full paper) does not tell us what a “normal protein” breakfast is (as compared to a higher-protein breakfast) but you can bet it contains lots of carbs too: juice, porridge (oatmeal) or other cereal with added sugar, yogurt and/or some bread product (bagel with Nutella?).

“These findings may indicate an increased inability among habitual breakfast skippers to metabolize a large quantity of protein,” the corresponding researcher told Diabetes in Control. “However, our data would suggest that once someone begins to eat breakfast, they should gradually transition to a breakfast with more protein – or about 30 grams – to elicit improvements in glycemic control,” the researcher said. Wow! Thirty grams is a lot of protein for breakfast. They must be growing girls.

I think the education of the researcher is a worthy cause and appears to be proceeding swimmingly. For example, among the paper’s findings: “Current scientific evidence shows that sustained elevations in post-meal glucose is a strong contributor of poor glycemic control and is associated with an increased risk for the development of Type 2 diabetes and cardiovascular complications. Because of the potential risk in the long term, identifying dietary strategies that individuals can begin when they are young to reduce post-meal elevations in glucose might prevent the occurrence of Type 2 diabetes and cardiovascular disease.” That’s a safe bet! And well said!

According to the Diabetes in Control write-up, the researcher suggested that “young women should routinely aim for a 350-calorie breakfast with approximately 30 grams of protein. To meet the recommended 30 grams of protein, [the researcher] suggested foods such as scrambled eggs, breakfast burritos with eggs and lean meats, or Greek Yogurt.” Interesting, my breakfast of 3 eggs, fried or scrambled, 1 strip of bacon, a 12-oz coffee with 1-gram of stevia powder and 1½ oz heavy whipping cream (full cream in the UK), and a 1-gram fish oil capsule is just 375 calories, but only 20 grams of protein, 31 grams of fat and 3 grams of carbs.

I also think the researcher needs to take another look at 1) gluconeogenesis and 2) the “standard lunch” the girls ate. But progress is progress.

Retrospective #303: Poor Dr. Walter Willett

“The Nutrition Source,” not to be confused with my, “The Nutrition Debate” (heehee), is the Harvard T. H. Chan School of Public Health’s website. With “My Alternate Healthy Eating Index,” I took a poke at their Alternate Healthy Eating Index in 2015 in The Nutrition Debate #229. To be fair, though, because they deign to criticize the USDA’s Dietary Guidelines, as their HSPH’s “Alternate Healthy Eating Index” amply demonstrates, they deserve some notice.

Much of their gravitas was attributable to Dr. Walter Willett, now retired but then Professor of Epidemiology and Nutrition and chairman of the HSPH. Willett was “the principal investigator of the second “Nurses' Health Study,” a compilation of studies regarding the health of older women and their risk factors for major chronic diseases. According to his Wikipedia bio (which he appears to have written), he has published more than 1,000 scientific articles regarding various aspects of diet and disease and is the second most cited author in clinical medicine.”

Staying “King of the Hill” is a rough game. Ancel Keys, despite numerous attempts to dethrone him, stayed King until long after he was smoldering in the grave. In fact, his ghost still casts a ghoulish pale. And Walter Willett has recently managed to do so too, using the same type of rough play as Keys used. A 2013 piece in Forbes, based on a story in Nature, tells how the “Top Science Journal Rebukes Harvard’s Top Nutritionist.” An editorial accompanying the Nature piece was also scathing. Willett’s offense was to say on NPR that an article in JAMA, showing people who were overweight (but not obese) lived longer than those deemed normal weight, was “a pile of rubbish, and no one should waste their time reading it.” He then organized a conference at Harvard expressly to discredit the JAMA piece.

More recently, Nina Teicholz, author of “The Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy Diet,” wrote a New York Times op-ed, “The Government's Bad Dietary Advice.” In it she says, “…the primary problem is that nutrition policy has long relied on a very weak kind of science: epidemiological, or “observational” studies in which researchers follow large groups of people over many years. But even the most rigorous epidemiological studies suffer from a fundamental limitation. At best, they can only show an association, not causation.” Target: Dr. Walter Willett.

“Epidemiological studies can be used to suggest hypotheses but not to prove them,” Teicholz said. “Instead of accepting that this evidence was inadequate to give sound advice, strong-willed scientists overstated the significance of their studies.” Then, she zeros in: “Much of the epidemiological data underpinning the government’s dietary advice comes from studies run by Harvard’s school of public health.” Teicholz doesn’t pull punches. She also takes a hit at the Guideline’s advice on salt by citing an “authoritative Institute of Medicine study.” I cite it in #153: “Salt: Friend or Foe.”

Then, Dr. Willett used his quarterly, “Ask the Expert” interview to address the cholesterol issue. (Remember that the 2015 Dietary Guidelines Advisory Committee said, “cholesterol is not considered a nutrient for overconsumption.”) Largely responding to the Teicholz guest op-ed (that he inexplicably calls the NYT “story” or “article”), Willett says,

“The important point is to have the best possible evidence, and we shouldn’t be basing dietary guidance on just guesses or beliefs. In the case of both the egg issue and the total fat issue we were basically starting with virtually no direct evidence. When the evidence did start to come in – and there were different lines of evidence from our studies based on large cohorts and also short term studies investigating metabolic changes – it showed that people who consume more eggs did not have a higher risk of heart disease even after adjusting for any other factors, and that total fat in the diet was not related to heart disease risk or cancer risk.”

Got that? Willett, a closet vegetarian (some suspect vegan) admits that DIETARY CHOLESTEROL and TOTAL FAT are no longer risk factors for heart disease and cancer. Read that again, please!

But the Forbes piece offers the best rebuke of Willett. “Science is complex, and Willett’s message to his fellow scientists appears to be that the public can’t be trusted with this complexity (except, as noted, when it might be something that he thinks is worthy of research); the question, which the public might ask in turn, is whether Willett can be trusted with complexity given his apparent intolerance for it in other scientists.”  Wow! That’s heavy.

Retrospective #302: A pill to prevent Type 2 Diabetes?

As everyone who regularly reads this blog knows, I am not a pill pusher. I once was a big-time pill-taker, however, until I tried an alternative “treatment plan” for my Type 2 diabetes. I was a passive victim of “the current treatment protocols (that) trap patients in a lifelong regimen of drug management, obesity and escalating diabetes” (see #292).

That stopped when my doctor “prescribed” a Very Low Carb diet, to lose weight. It had the effect of putting my diabetes in clinical remission. I went from being maxed out on 2 oral meds and starting a 3^rd (with an out-of-control FBG) to where I am today, with good glucose control, taking just 1 low-dose Metformin. My A1c’s are always in the 5s.

But this blog is not about Very Low Carb eating. It is about an interesting new study from some Danish researchers. According to a 2015 story in Diabetes in Control, they conducted research on “a large study population of adults (lean and obese, men and women) with normal and impaired glucose regulation.” They are from the Steno Diabetes Center, a Danish hospital and research organization owned by the drug maker Novo-Nordisk, “working in partnership with the Danish healthcare system.”

The abstract appeared in the February 2015 issue of Diabetes, the official journal of the American Diabetes Association. The interesting FINDING, which could prove to be significant: “Reduction in the glucose-regulating hormone glucogon-like-peptide-1 (GLP-1) appears to occur before the development of type 2 diabetes and obesity.”

The lead investigator told Diabetes in Control, “We found that GLP-1 is reduced by up to 25% among people with pre-diabetes and up to 20% among obese people compared to normal-weight people. This indicates that the reduction in GLP-1 is not a consequence of type 2 diabetes, but appears much earlier in the disease development and may predispose people to type 2 diabetes.” These results were all in response to an oral glucose tolerance test (OGTT).

The Diabetes in Control piece also noted, “And what is surprising is that they have also found pronounced differences in GLP-1 secretion between men and women. They observed a higher GLP-1 response among women than men, but when glucose tolerance worsens, the decline in GLP-1 secretion is more pronounced in women than in men.”

Of course, as might be expected from a hospital research department “owned by Novo Nordisk, working in partnership with the Danish healthcare system,” the researchers casually said, “‘These results could have potential clinical implications as well,’ noting that GLP-1 analogs may help delay onset of type 2 diabetes,” Diabetes in Control noted. A GLP-1 analog would be a new drug designed “to PREVENT diabetes for those with prediabetes.” And…for overweight and obese patients too?

They may be on to something here. Preventing the destruction of GLP-1 would be a worthy area for further investigation. But, alternatively, developing a new drug, a GLP-1 analog, to treat the symptom rather than the cause – something that Big Pharma, working in partnership with the…healthcare system (government funding) does so well – would be a sure-fire hit. This could be a blockbuster new drug for Novo Nordisk. Think statins, or blood pressure medications, or any other of “the current treatment protocols (that) trap patients in a lifelong regimen of drug management, obesity and escalating diabetes.”

Hey, I believe in capitalism, and Novo Nordisk is not an eleemosynary enterprise. Novo Nordisk has a pecuniary interest in this research. So, let’s hope the researchers are sincere when they say, according to their press release, “We should use the findings in prevention strategies for type 2 diabetes.” Sounds good. Let them do more studies, even with government funding.

In the meantime, remember to eat Very Low Carb to preserve your GLP-1!

Note: A search in December 2019 on Google Scholar found no updates on the ADDITION-PRO study reported on above. I guess a GLP-1 analog drug is not likely to be developed, or if it was developed, was either not effective, patentable or not profitable. Second notice: Eat Very Low Carb to preserve your GLP-1, seriously. 

Retrospective #301: Healthy Food Choices

Unfortunately, this catch phrase has been co-opted and misused by our government’s “Dietary Dictocrats” to mean mostly things that I and like thinkers consider unhealthy food choices, like unnatural, processed vegetable oils. It has also been used to denigrate saturated fat and, until the 2015 Dietary Guidelines for Americans, total fat and dietary cholesterol. In case you haven’t heard, in 2015 the Dietary Guidelines Advisory Committee advised that DIETARY CHOLESTEROL was “no longer a nutrient of concern for overconsumption,” and that the DGA no longer recommends limiting TOTAL FAT to 30% of total calories. Most people reading this will not have heard this healthy food news.

Healthy food choices, in the sense that I mean, are whole, unprocessed foods, including lots of animal-based proteins with their natural saturated fats, together with fresh, whole, low-carb vegetables (mostly of the above-ground type), and an occasional berry (with heavy whipping cream) and a few nuts some cheese (added to salads, e.g.). It involves the almost complete avoidance of grains, and highly processed foods like all flours and all sugars (cane, beet, corn, even honey) and all processed vegetable oils (soybean, corn, sunflower, canola, etc). So, among my healthy food choices, what are the “healthy food choices” I (we) can make to be healthier?

Eggs from pastured hens: This was an easy choice. At our local farmers’ market, we have a farmer who raises hens in the manner of Joel Salatin’s Polyface Farm in Virginia, made famous in Michael Pollan’s “Omnivore’s Dilemma.” The hens roam freely and roost in a portable hen house that is moved every week to new pastures in which the farm’s ruminants (and pigs) had grazed and left “deposits” to fertilize the fields and nourish the hens. Chickens (and pigs) are omnivores, so the hens get a balanced diet including bugs and, from ageing patties, larvae.

Butter from pastured cows: It stands to reason that cows that are fed a diet of mostly silage will produce milk, cream and butter that have fewer nutrients.  Is it not better for ruminants to eat natural forage instead of fodder? Lab tests of milk and butter have confirmed this. Cows that can graze year-round (“grass fed”) produce milk and butter that is higher in vitamins, minerals and other essential nutrients like Omega 3 fatty acids. Is it not then a better choice to buy butter made from cows that are grazed on forage all year round? We buy butter made from grass-fed cows.

Wild Caught versus Farm Raised Fish: I eat wild-caught fish almost every day (a can of Brisling sardines for lunch), but choosing wild-caught fresh or flash-frozen fish from the supermarket or fish monger’s case or restaurant menu is an easy choice to adopt. Some fish like North Pacific salmon must be wild-caught, but beware of farm-raised salmon from the North Atlantic or South Pacific (Chile). Other types of fish – cod, for example, one of the less expensive species, is always wild-caught and is a white, flaky, non-fishy tasting fish. I make an easy stove-top recipe with fennel and cauliflower. Halibut with celery, also stovetop, is another tasty dish. Why not try these wild-caught species?

Lamb chops: Lamb chops are a very good fatty meat choice for a couple of reasons. The lamb we buy is raised in New Zealand, where they are grass-fed year-round. They are not feed-lot raised. And they are ruminants, so they are a good choice for their fatty acid profile (better than chickens and pigs). And, since lamb chops are small, they make portion control easy. My wife and I eat just two lamb chops each – a rack of 8 makes 2 meals for 2 – making a perfect protein portion for a supper, along with a fresh vegetable either tossed in butter or roasted in olive oil.

Heritage Pork: Supermarket pork, “the other white meat,” has had all the healthy fats bred out of it. Supermarket pork chops taste like sawdust to me unless they are smothered in gravy thickened with flour. You just can’t get away from how dry they are. The answer is to buy heritage breed pork. Breeds to look for are: Berkshire, Tamworth, and Red Wattle. Again, my local farmers’ market is where I buy these superior tasting products, especially chops and roasts.

Artificial Sweeteners: I have finally weaned myself off artificial sweeteners and packets that are marketed as “Stevia” but are mostly dextrose or maltodextrin (sugars). I now use pure stevia leaf extract, a powder with no “bulking agents” to sweeten a cup of coffee and pure liquid stevia to sweeten the unsweetened Lipton’s cold-brew ice tea I drink in the summer. I am also developing a taste for cold water (!), to avoid the “sweet” insulin spike on days when I’m fasting.

Retrospective #300: ‘Sugar’ in Food and Blood: a primer on carbohydrates

I saw an ad on TV a while ago for a diabetes drug. The ad explains that, “It (the drug) removes some sugar from your body.” I talked back to the TV and asked, “But how did the sugar (that the drug removes) get into your body in the first place?!!!” And that suggested the corollary question, “If you didn’t eat so many carbohydrates, wouldn’t you have less “sugar” to “remove from your body”? Which begs the question: What foods become “sugar” (glucose) in your blood in the first place? What foods convert to glucose? The answer is: ALL CARBOHYDRATES.

I put sugar in quotes because I am not referring to table sugar. The copywriter and I are referring to “blood sugar” (glucose), the compound that carbohydrates break down into by digestion or conversion by the liver. Table sugar (sucrose), for example, breaks down into fructose and glucose, and dairy carbohydrates break down into galactose and glucose, but starches, which are also ALL carbohydrates, are long-chain glucose molecules that break down to just simple glucose. This monosaccharide glucose, commonly called “blood sugar” or just “sugar,” is what the ad refers to.

If you have been diagnosed with Prediabetes or Type 2 diabetes, it is because you have a high blood “sugar” level. You first developed a precursor condition, Impaired Glucose Tolerance, which progressed to Impaired Fasting Glucose. These conditions collectively are called Insulin Resistance (IR). Insulin secreted by your pancreas is required to move the glucose in the bloodstream and “open the door” to your cells to “take up” the glucose for energy. Insulin Resistance means the “door” is partially blocked; glucose isn’t being taken up by your cells as quickly as it should, so the pancreas sends more insulin. Meanwhile, as the glucose builds up to high levels, it damages your organs and small blood vessels. And you are at high risk for a multitude of diseases. This unifying condition is called Metabolic Syndrome.

Most people who are newly diagnosed Prediabetics or Type 2 diabetics are surprised to learn the “sugar” (glucose) content of common foods. But how much “sugar” do carbohydrates make? To understand the answer in context you need to know how much “blood sugar” is “normal,” that is, normally circulating in the blood of a person (before a meal) who has a normal glucose metabolism. The answer is surprisingly low; it’s 1 teaspoon (5 grams). See Retrospective #232, “A spoonful of sugar.” For an explanation of the math, search the blog of Michael Eades, MD.

As Dr. Eades points out, a diagnosis of Type 2 diabetes is having a “sugar” (glucose) level in your blood equivalent to just 1¼ tsp. Yet, a McDonald’s “small” Coke (16oz) has 8 tsp of sugar, a Big Mac 9 tsp of “sugar,” a large fries 13 tsp of “sugar,” a large chocolate McCafé shake (22oz) 28 tsp of “sugar,” a bagel 10 tsp of “sugar,” a low-fat chocolate milk 5 tsp of “sugar,” a baked potato 7 tsp and an 8 oz container of low-fat fruit yogurt 9 tsp of “sugar.”  For these and more examples, search sugarstacks.com.

If the door to your cells is partially closed by Insulin Resistance, can you really afford to eat 30, 40, 50 times more “sugar” in one meal than your body can handle? Do you really want to become more and more dependent on drugs to take the “sugar” out of your blood that you put into it? You do have a choice, you know. Self management works.

 You don’t have to go crazy. You just need to be aware of what your body can handle (by testing your blood sugar), and be guided accordingly in your food choices. If you don’t, the disease you have acquired (on the government’s advice!) by eating “low fat” and too many foods too high in processed carbohydrates and added sugars for too long will damage your body, and shorten your life…

That’s the choice you have to make. I’m not trying to scare you. I’m trying to educate and inform you about how you can make better choices. You probably know this. I hope you now feel empowered to take the steps you need to take. 

Retrospective #299: Why Maintaining Weight Loss is So Hard

The excerpt I posted from the Lancet Diabetes and Endocrinology comment in Retrospective #297, “Obesity in Remission,” brought to mind a segment from “Choices,” the 2^nd of four hour-long videos reviewed in The Nutrition Debate #275, “Weight of the Nation.” You might have missed it. But if you are having trouble losing weight or, having been successful, are now putting weight back on, you should read #297, and this blog post.

Starting at minute 17 in “Choices,” Rudolph Leibel, MD, Co-Director of the New York Obesity Research Center at the Columbia University Medical Center, said, “Individuals losing weight are NOT metabolically the same as they were before they lost weight.” “The weight reduced individual will be requiring about 20% less (sic) calories per day relative to what somebody of that weight who’s never lost weight would eat…in order to keep at that body weight.”

“Consider two individuals – same gender, same age, exactly the same body weight – one of whom is at that body weight as a result of let’s say a 10 or 15% weight reduction, the other who’s been at that weight for their entire adult life. If that reduced weight individual goes out to lunch with her friend, and they both order the same meal, that will represent a 20% overeating for the weight-reduced individual, and be quite normal for the individual who’s not in that state. 20% might seem like a little, but 20% excess calorie intake a year will account for the inexorable weight regain.”

“AS FAR AS WE KNOW, THIS PHENOMENON DOES NOT GO AWAY,” Dr Leibel says. “So, being successful for a year or two doesn’t mean that you’re going to be able to go back to eating what like a person who’s never lost weight.”

“Does that seem unfair?” an off-camera voice asks an overweight woman. “Sure, it does seem unfair,” she replies. It’s unfair that I just can’t lose the weight and go back to the way a normal thin person lives their life, but that’s part of the price you pay for allowing yourself to get overweight in the first place.”  That’s the thinking of this well-meaning and very well-funded, widely-viewed and deeply-flawed HBO series. Blame yourself. You’re hungry, and you want to eat.

You can choose to blame yourself. You failed. It was your fault. You tried to follow the Government’s Dietary Guidelines since 1980, and your doctor’s advice since at least 1961 when the American Heart Association started telling us (him or her and you) to eat less saturated fat and cholesterol. That’s also when Agribusiness took the cue and started making more “low-fat” manufactured foods with added sugars and processed carbohydrates.

Or you can blame them (the government’s dietary advice, Agribusiness, Big Pharma, and your hapless doctor) and choose to eat many fewer carbs and more fat – both saturated and monounsaturated, but not polyunsaturated fats (vegetable and seed oils), which are harmful. The Omega 6 overload clogs your cells with rancid and oxidized LDL-C.

You will feel fuller when you eat fatty meats and fish and a few low-carb veggies, and therefore eat less naturally. Fat satiates. Protein digests slowly. Your blood sugar will stabilize, your cholesterol will improve, especially HDL and triglycerides. Your inflammatory marker (CRP) will too, and AS YOU LOSE LOTS OF WEIGHT, without hunger, your blood pressure will come down. And you will need to take fewer or even no medications for all of these conditions.

All these good things happened to me. And when I regained some (just a little) of the weight I lost, but continued to eat low-carb, high-fat – just too much of it – the only thing that went up was the number on the scale. All the other health makers maintained the improvements so long as I continued to eat low-carb, high-fat.

Like many of my readers, I have developed a “biological predisposition for energy storage.” I gain weight when I eat the Standard American Diet (SAD) that the government and my doctor recommend. And I live in “an environment that promotes high energy intake.”  The RESULT: an obesity–promoting interaction between the two:  I gain weight.

This condition is called Insulin Resistance. It is chronic and “does not go away,” as Dr. Leibel observed. My genes reacted to the overload of sugars and processed carbohydrates that replaced the saturated fat and cholesterol that government and my doctors advised me not to eat. This “heart healthy” diet made me fat and deprived me of the fat-soluble vitamins (A, D, E, and K) necessary for wellbeing…and caused me to develop my Carbohydrate Intolerance.