The Nutrition Debate #289: Physician: “First, do no harm” (Primum, non nocere)

This aphorism, commonly and apparently erroneously considered to be a part of the Hippocratic Oath, is nevertheless attributed to Hippocrates (Epidemics, Bk. 1 Sect XI, according to PiedType). And “While there is currently no legal obligation for medical students to swear an oath upon graduating, 98% of American medical students swear some form of oath,” Wikipedia says, and a modified Hippocratic Oath was the most common, according to a 1998 survey of Medical Schools.

“Physician, first do no harm,” is nevertheless, “One of the fundamental principles of medicine according to which the physician should not cause harm to the patient” (Mosby's Medical Dictionary). Regardless of the oath taken (or not taken), it is the moral obligation of the physician to do “the right thing” by his or her patient. Who could disagree with that?

It is therefore all the more interesting that in the original oath (as translated in the Wiki citation above), Hippocrates pledges, “With regard to healing the sick, I will devise and order for them the best diet, according to my judgment and means; and I will take care that they suffer no hurt or damage.” And it was, after all, Hippocrates, the father of Western medicine, who said, “Let food be thy medicine and medicine be thy food.” I first cited this in “The Nutrition Debate #173.”

In #173 I compared what were then two translations in the Wikipedia entry for the Hippocratic Oath. The first had the sentence, “I will apply dietetic measures for the benefit of the sick according to my ability and judgment.” The current translation in the earlier Wiki revised it to, “I will prescribe regimens for the good of my patients according to my ability and my judgment and never do harm to anyone.” Notice the difference? “Apply dietetic measures” was replaced by “prescribe.”

I understand, of course, that pharmacotherapy did not exist in ancient Greece, although herbal medicines, salves, etc. have existed since the beginning of time. But so has the enduring and timeless truth: “Let food be thy medicine and medicine be thy food.” And can any doctor not acknowledge that the best medicine for treating type 2 diabetes is “the best diet?” Then, assuming that every doctor would agree with this prescription, the question arises, why would any doctor not prescribe for every patient a diet much lower in carbs than the 60% carbs that is the USDA’s Nutrition Facts Panel standard? (See #288).

If the physician is truly and sincerely acting in the beneficent spirit of the Hippocratic Oath, why would he or she not literally “…apply dietetic measures for the benefit of the sick according to my ability and judgment?”  The answer to this question is, of course, complicated: There’s the question of 1) laziness, 2) a lack of time, 3) patient “non-compliance,” 4) a dietary plan (restricted calorie, “balanced,” low-fat) that is doomed to fail, 5) guidelines that a doctor must comply with to be paid for services paid for by 3^rd party payers (government agencies like HHS/Medicare and Medicaid and private insurance that must conform with government guidelines and 6) low reimbursement rates by those 3^rd party payers for patient services.

As a consequence, writing a script and updating the patient’s electronic medical record are all that most physicians have time to do. Medicine as practiced today in many large offices is at best just a business; at worst, it’s a sham. I’m lucky. I have a caring physician (I hope he reads this) who is glad to see me and give me the time I need. Now if I can just get nurse to treat me the same way. She has been with him so long that to her I am just another product on the office assembly line. Remember Lucille & Ethel wrapping chocolates on a factory conveyor belt? It was one of the funniest pieces they ever did.

You may have noticed that I failed to mention one more possibility for why a physician would not regard a low-carb diet as the “best medicine” for virtually everyone, but especially for people with Metabolic Syndrome, borderline lipids, chronic systemic inflammation, or who are overweight, obese, pre-diabetic or diagnosed with type 2 diabetes. I didn’t include the possibility that the physician may actually believe that a restricted calorie, balanced, low-fat diet is the best way to lose weight and keep it off and see improvement in all these conditions, plus hypertension (high blood pressure) and reduced risk of coronary heart disease, cardiovascular disease, several types of cancer and even Alzheimer’s disease.

The reason I didn’t mention it is that I can’t believe that there are any doctors left who still believe that. The evidence has been piling up from so many sources, and is now aggregated in huge meta analyses - they cannot not have seen it. Just in case, though, this very comprehensive 12-points-of-evidence elucidation in the January 2015 issue of Nutrition, by Richard Feinman et al., covers just about all the bases. So this can’t be the reason anymore. There must be more to it. Could it be that it’s very hard to switch horses in mid-stream (mid-career)? Will we have to wait until the current generation of doctors all die? Will that be too late for you? The doctor who started me on low-carb (Atkins Induction) was semi-retired. Maybe he figured he had not much to lose. He took a chance and put his patient’s health first. Maybe you, the patient, should too.

The Nutrition Debate #288: Type 2 Diabetics: 10% Protein “May Not Be Enough”

This Medscape Multispecialty piece headline (Anne Harding from Reuters Health Information) was actually, “10% Protein Diet May Not Maintain Muscles in Type 2 Diabetes.” The lede was, “New findings suggest it’s especially important for people with type 2 diabetes to eat enough protein.” This is a message with which I am in complete agreement. Regular readers will recall that I have written about it numerous times including in #130, “How Much Protein Should You Eat?”

What reconnected me to the subject this time was the specific mention of 10% (as not being enough protein). Ten percent protein is the exact amount of protein that the Nutrition Facts Panel on every packaged food product in the United States recommends that everyone eat. Our government’s one-size-fits-all dietary recommendations do not take into account the requirements of different cohorts of the population, excepting those under 2 years of age. In that case, you are allowed to eat more saturated fat (as is found in mother's milk) to help in brain development. After 2 years, I guess your brain stops developing – NOT. (Current research suggests age 25.)  And Type 2 diabetics should eat more fat, more protein, and many fewer carbohydrates than is recommended to the general population. EVERYONE, actually, should eat many fewer.

(Anyway, if you haven’t done the math, the RDA percentages on the side panel of packaged foods are based, as the USDA’s footnote says, on a 2,000 calorie a day diet (for a “woman of a certain age”) to maintain her weight. So, if a “serving” has say 30 carbs, that’s  10% of the RDA for carbs. Here’s how to figure it: 30 grams of carbs x 4 calories/gram of carbs = 120 calories, and 120 calories is 10% of 1,200. From this you can correctly conclude that the 2,000 calorie a day diet that the government recommends everyone eats is 60% carbohydrate. I’m not making this up folks!

Do the math yourself for proteins. If the panel lists the serving as 20 grams of protein, it will say that serving represents 40% of your RDA. Since protein has 4 calories per gram, 20 x 4 = 80 calories which is 40% of 200. And since 200 is only 10% of 2,000 (the total daily calorie allowance), 10% is the amount of protein that the government recommends you eat. Q.E.D.

By reverse math, the balance of your diet is supposed to be fats: 1,200 + 200 = 1,400; 2,000 - 1,400 = 600 calories for fat, and since fat has 9 calories per gram, 600/9 = 66.7 grams of fat. And 600/2000 = 30% fat in a 2,000 calorie diet.)

But I digress. The article cited above was written by Dr. Stephanie Chevalier, et al., of McGill University Health Center – Royal Victoria Hospital in Montreal and was published in Clinical Nutrition. “If it [a 10% protein diet] happens over a long period of time, this could lead to loss of muscle mass. That’s really an issue for our aging population,” Dr. Chevalier said.

The study, in organic biochemistry terms, “involved comparing two groups of obese men and women, all type 2 diabetics, eating isocaloric diets, one of 17% protein and the other 10%. “On a 10% protein diet, diabetic adults showed increased sensitivity to insulin suppression of proteolysis, but inadequate stimulation of protein synthesis, resulting in a low net nitrogen balance than similar patients who ate a 17% protein diet.” Okay, this is above my pay grade too.

The reason, put simply, is that “Insulin is required for the metabolism of all macronutrients, not just glucose, and people with type 2 diabetes have been shown to have insulin resistance to glucose, lipid [fat], and protein metabolism,” Dr. Chevalier told Harding. She added, “Studies have shown that older adults with diabetes have greater losses in muscle mass and strength over time.” The takeway for me is that Insulin Resistance applies to fat and protein metabolism too!

She concluded, “For now, it’s probably adequate for people with diabetes to eat diets containing 15% to 20% protein. Ten percent is definitely too low,” she said, definitively. That was comforting to me. My own diet, as my regular readers know, is 20% protein, 5% carbohydrate and 75% fat. My protein plan has been higher in the past (as high as 28%), and usually in fact is higher than 20% since I frequently eat more than the small portion of protein allocated for supper (25g). That’s also why I take a small dose of metformin at supper, to suppress any gluconeogenesis that may result from a larger portion. If you haven’t seen my “ideal” meal plan, this is what it looks like. The breakfast and lunch parts of the plan are always the easiest.

	Fat	Protein	Carbs	Calories	K/G
Breakfast	30	20	4	375	2.07
Lunch	35	15	0	375	3.31
Dinner	33	25	11	450	1.51
Total	98	60	15	1,200	2.02
Percent	75%	20%	5%	100%

The Nutrition Debate #287: Can Type 2 Diabetes Be Reversed?

The Nutrition Debate #88: “Reversal of Type 2 Diabetes,” has proved, to my surprise, to be a very popular post on this blog; it has had over 6,000 page views. Let me be clear: I do not believe that type 2 diabetes can be “reversed,” and so I can understand that someone reading that post (#88) might have felt misled by me. That was not my intention. Nor was I consciously intending to glom readers by attracting them to an appealing prospect through a headline. I was simple reporting on a paper in a peer-reviewed British medical journal that had precisely that title; that’s why my blog title was in quotes.

The paper was interesting. Its “AIMS/HYPOTHESIS” is that “Type 2 diabetes is regarded as inevitably progressive, with irreversible beta cell failure. The hypothesis was tested that both beta cell failure and insulin resistance can be reversed by dietary restriction of energy intake.” Okay, it’s a hypothesis. Its aim is to challenge an assumed truth – one that virtually all medical practitioners espouse – that type 2 diabetes is “inevitably progressive.” And they propose to do it by “dietary restriction of energy intake” alone. To be clear, they mean fewer calories, not fewer carbohydrates. Interesting, huh?

The hypothesis apparently sprang from the observation that “normal glucose metabolism is restored within days after bariatric surgery in the majority of people with type 2 diabetes.”  “There is now no doubt,” they concluded and report in their Counterpoint Study, “that this reversal of diabetes depends upon the sudden and profound decrease in food intake, and does not relate to any direct surgical effect.” To be clear: That’s food (total energy) intake, not carbohydrates.

The CONCLUSION/INTERPRETATION of this study was only a little less assertive than their hypothesis: “Normalization of both beta cell function and hepatic insulin sensitivity in type 2 diabetes was achieved by dietary energy restriction alone. This was associated with decreased pancreatic and liver triacylglycerol stores. The abnormalities underlying type 2 diabetes are reversible by reducing dietary energy intake.” Okay, they hedge a bit. They say “the abnormalities underlying type 2 diabetes are reversible…” But they still use the word “reversible.” That’s pretty strong, but they are scientists and provide the quantitative data to support their findings: pancreatic and liver fat cells (triglycerides).

My inveterate editor discovered a follow-up study that was done by the same researchers, and I reported on in The Nutrition Debate #89, “‘Reversal of Type 2 Diabetes' Revisited.” Unfortunately, it glommed only 367 page views, but in it the authors reported on “individuals (who) began to feed back their personal experiences of attempting to reverse their diabetes.”  CONCLUSION: “These data demonstrate that intentional weight loss achieved at home by health-motivated individuals can reverse Type 2 diabetes. Diabetes reversal should be a goal in the management of Type 2 diabetes.”

This and other work by these intrepid researchers earned them the high privilege of presenting “The 2012 Banting Memorial Lecture: Reversing the twin cycles of Type 2 diabetes” (full text link here). So, they are clearly not crackpots. They are scientists looking for answers to why and how the “underlying abnormalities” of type 2 diabetes are “reversed.” From my perspective, they have demonstrated to their medical peers that their work was at the very least “interesting.”

The paper based on the Banting Lecture that was published in Diabetes, the organ of the American Diabetes Association. The abstract concludes: “It is now clear that Type 2 diabetes is a reversible condition of intra-organ fat excess to which some people are more susceptible than others.” But they’re talking about “pancreatic and liver triglycerides.” My readers are not particularly interested in their pancreatic and liver triglycerides. They don’t even care that much about their serum triglycerides (although The Nutrition Debate #197: “Triglycerides and Alcohol Consumption,” logs over 1,500 hits). People with Type 2 Diabetes want to know how to “eradicate” the damn disease. Ideally with just a pill!!!

My readers are also interested in what they can do, if anything, to avoid being “more susceptible.” And if they were “more susceptible,” if there is anything they can then do to “reverse” the “condition” to which they have succumbed. My conclusion is that if you are among those who are susceptible, and have succumbed to the condition in the sense that you are diagnosed diabetic or pre-diabetic, and you are sincere about mitigating the risk of diabetic complications (both micro and macro vascular), there is a course of action you can take, and it is stated in the CONCLUSION of the overlooked post #89, to wit:

 “These data demonstrate that intentional weight loss achieved at home by health-motivated individuals can reverse Type 2 diabetes. Diabetes reversal should be a goal in the management of Type 2 diabetes.” And in my book the best way to lose weight is to eat Low Carb, not cans of Optifast, the 47% carb liquid diet formula used in this study.

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

Kurt G. Harris, MD, called wheat, excess fructose and excess linoleic acid the Neolithic Agents of Disease (NAD). He was one of my early favorites in my search for a dietary regimen that could be stated as a philosophy of eating rather than by a dependency on counting calories, carbs and other micronutrients. I wrote about him and his PaNu program four years ago in The Nutrition Debate #19 here. Then he dropped out of “the nutrition debate” and later deleted his Archevore website. Today he is a diagnostic radiologist practicing in Sturgeon Bay, WI. Some of his writing is still online at Psychology Today.

Harris didn’t write for type 2 diabetics like me. He aimed his program at people who wanted to eat in a healthy way to avoid disease. Many others followed him in this goal and the field became a tangled mess, leading sadly I suspect to his premature retreat. For awhile I hoped he was writing a book. Alas, it seems not. Harris was inspired, he wrote, by Gary Taubes (as was I). His epiphany, and his openness and training in scientific method, fed his inquiring mind. He liked to write and coin words and phrases too. If this sounds like a eulogy it’s only because I fear he is lost to us, and it is our loss.

The three NADs, which he fully explains in “A Dietary Manifesto - Paleo 2.0,” are just another way of describing his 12-step program (which I list in The Nutrition Debate #19), for “getting started,” and going “as far as you can down the list…” The wheat proscription means gluten, and of course includes the other gluten grains (barley, rye, etc). That’s big.

The excess fructose NAD is also a big one, but here Harris leaves a little room if you’re not diabetic or prediabetic. Harris is infamous (in Paleo circles) for calling apples “bags of sugar” and most modern fruit “candy bars on a tree.” He concludes, however, “If you are not trying to lose fat [or are carb intolerant as in type 2 diabetes], a few pieces of fruit a day are fine.” Fructose, however, is not only found in fruit, as horfilmania (“Who Knew?” 12/21/14) recently discovered with red cabbage. Take a look at “The Nutrition Debate #97” for a list of common sweeteners, fruits and vegetables that contain fructose.

Avoiding excess linoleic acid (Omega 6s) is perhaps the hardest dietary goal of the three NADs because it is so hard to know where they hide. Harris advises, “The way to correct the modern excess of n-6 linoleic acid is to avoid the modern sources of it. Stop eating all temperate vegetable oils and veggie oil fried food- cooking and frying oils like corn, soy, canola, and flax, all of it. And go easy on the nuts and factory chicken. These are big sources of n-6, especially the nuts and nut oils.”

To put some “meat” on those recommendations, I’ve created this table using the USDA’s National Nutrient Database:

Cooking/salad oils & fats (%)	SFA	Mono	PUFA	n-6	n-3	n6/n3
Corn oil	12.9	27.6	54.7	53.2	1.2	45.8
Soybean oil	15.7	22.8	57.4	50.4	6.8	7.4
Canola oil	7.4	63.3	28.1	18.6	9.1	2.0
Olive oil	13.8	73.0	10.5	9.8	0.8	12.8
Butter (incl.+/-16% water)	51.4	21.0	3.0	2.2	0.3	6.9
Coconut oil	85.5	5.8	1.8	1.8	0	∞

All fats are combinations of saturated fatty acids (SFAs), monounsaturated fatty acids (Mono) and polyunsaturated fatty acids (PUFAs), but the composition varies enormously. Corn and soybean oil are over 50% PUFA, while butter and coconut oil are 3% and 1.8% respectively. On average, corn oil and soybean oil have over 25 times as many PUFAs as the saturated fats. Canola oil has 10 times as much; olive oil, 5 times as much. Note: The “saturated fats” still have PUFA content.

As most people know the ratio of n-6 to n-3 is also important, and Canola oil has the best and corn oil the worst ratio. But in terms of absolute numbers, the best advice is to avoid excess Omega 6s (n-6s) altogether, and that is best done by eliminating all seed and vegetable oils. Then, as Harris says in his Manifesto, “Along with n-3, the other type of PUFA, it [n-6] is technically an essential fatty acid, but the actual requirement is so small it might be better considered a micronutrient”(emphasis mine).

So, avoid all vegetable and seed oils altogether (corn, soybean, Canola, sunflower, walnut, flax, etc.), and then avoid all prepared, baked goods and foods fried in any of these oils, then go easy on nuts, nut oils and factory chicken, and maybe supplement with Omega 3 fish oils to help the balance, and you should get your ratio back into pre-Neolithic proportions. If this sounds like Paleo to you, it isn’t really. It’s just a little nostalgic look back at the “ancestral” roots of my dietary journey.

The Nutrition Debate #285: “When diet and exercise aren’t enough…”

The copywriter should get a raise, or at least a bonus. This statin drug’s advertising slogan is the very definition of a red herring: an “idiom…used to refer to something that misleads or distracts from the relevant or important issue. It may be either a logical fallacy or a literary device that leads readers or characters towards a false conclusion.” Wiki goes on to say, “The expression is mainly used to assert that an argument is not relevant to the issue being discussed.”

If you’re reading this blog, you probably have been told by your doctor to “diet and exercise” to lose weight. And if you’re reasonably well read and up to date, you know that exercise is not an effective way to lose weight (in spite of all the TV advertisements). I’m not knocking exercise; both regular aerobic and anaerobic exercise have myriad health benefits, but reducing the unwanted body fat is not one of them. Besides, it makes me hungry and sweaty.

So, the slogan suggests that “when [assuming failure] diet and exercise aren’t enough” (and for most people who diet by following the government’s advice to eat a restricted-calorie, balanced, low-fat diet…and exercise as prescribed…it  is not enough), what’s a person to do? We lose a few pounds, are hungry all the time, and gain it all back. We’re desperate and depressed. We lack the “will power” to “eat less and exercise more.”  We are susceptible to almost any suggestion.

Well, folks, you’ve been set up. The ad goes on to suggest you should take a statin. And your doctor will surely suggest it, after noting in your chart that you have failed to lose weight by the “diet and exercise” prescription. And since the diet most doctors pitch is the one the AHA/ACC/AMA/ADA/USDA/HHS/ADM/Cargill/Quaker Oats and Kellogg’s recommends, you probably are suffering from co-morbidities and exhibit the risk factors collectively called the Metabolic Syndrome. (So much concensus, yet so little weight is lost!)

As with most people eating the Standard American or Western Diet, besides being overweight or obese, you probably have or are developing signs of hypertension (elevated blood pressure), and your Total Cholesterol is probably being described as “somewhat elevated,” and your fasting blood sugar may be “slightly high” (“We’ll have to watch that.”) What often isn’t mentioned is that your HDL cholesterol (HDL-C) is borderline low (≤40mg/dL for men; ≤50mg/dL for women) and that your triglycerides are borderline high (≥150mg/dL). 

 It’s this combination of “risk factors” that justifies, to the medical community, the statin prescription. After all, even though you’re taking your blood pressure meds, you’ve failed to follow doctor’s orders to lose weight by eating less (on a balanced low-fat diet) and exercising more; now it’s his turn to treat you effectively by simply writing a script. All you have to do is fill the prescription and take it faithfully. Your Total Cholesterol (TC) and LDL-C will go down, and your TC/HDL ratio (even though HDL-C is unchanged) will improve (because TC went down). And your doctor will chart that too.

And that’s the best that “medical science” can do for you, folks. “When diet and exercise aren’t enough…,” take another pill, in addition to the blood pressure pill(s) you already take. And note in the chart: 1) patient non-compliant with [bad] diet and exercise advice, 2) patient taking BP and cholesterol medications; 3) patient showed improvement in TC & LDL-C and TC/HDL ratio (no mention of  borderline HDL or trigs); and 4) follow-up visit for (pre-diabetic) fasting blood sugar.

Of course, so long as you eat a low-fat, high carb diet, your slightly broken glucose metabolism will get progressively worse. You will slowly continue to gain weight (because you glucose metabolism is broken, not because you are eating too much and exercising too little). Your fasting blood sugars will rise because of carbohydrate intolerance (a manifestation of Insulin Resistance). Your glucose metabolism has progressed through impaired glucose tolerance (IGT), to the impaired fasting glucose (IFG), what your tests are starting to reveal now.

Eventually, there is a strong likelihood that you will develop full blown type 2 diabetes. By then you will already have been started on metformin. Eventually you may work up to a cocktail of three pills for this condition alone. I did. Or maybe you’ll start with a SGLT2 inhibitor and/or a GLP-1 agonist or insulin injections. The last may be better for you, seriously.

And don’t forget the complications: microvascular (peripheral neuropathy, nephropathy, retinopathy), or macrovascular (CVD, MI, stroke). Or, you could just change your diet… Take charge of your health. I think HFLC could work for you, but regardless, try something. A change in diet can give you valuable information. There’s so little your doc can do; so much you can do for yourself.  A low-carb, high- fat diet is how I did it. If you’d like to see how diet can affect your health, or at least how it affected mine, please read The Nutrition Debate #281, #282 and #283 recently published on this blog.

The Nutrition Debate #284: The A TO Z Weight Loss Study: a Randomized Trial

A dear reader – and I mean that sincerely because I wouldn’t write this blog except for my readers – was disappointed (upset, actually) that I said, “…if you are insulin resistant, as almost all fat people are…” Okay, “fat people” is an inflammatory phrase, and I have never used it before, but that is not what upset Valerie. It was an assumption, and a slight exaggeration that I made, that did the trick. She concluded: “I wish your ‘nutrition debate’ weren’t so one-sided.”

Valerie’s frustration (and upset) is a result of my writing about two overlapping and related but different phenomena: the co-incident epidemics of diabetes and obesity that have come together in the last 35 years. It all began with the publication of the Dietary Guidelines for Americans in 1980, the U.S. government’s attempt to tell us as a population what to eat. That followed the 1977 Dietary Goals for Americans produced by a Select Committee of Congress: the McGovern Commission.

This combination of type 2 diabetes and obesity is so prevalent today that the word “diabesity” has been coined. However, as Valerie points out, not all “fat people” have Insulin Resistance (IR), a requisite condition for progression from a normal glucose metabolism to Impaired Glucose Tolerance (IGT), Impaired Fasting Glucose (IGT), and then to a frank diagnosis of Type 2 Diabetes Mellitus (T2DM). That is the Natural History of Type 2 Diabetes. Apparently Valerie is not Insulin Resistant or therefore by definition a type 2 diabetic (FBG at diagnosis ≥126mg/dL) or pre-diabetic (FBG from 100 to 125mg/dL).

So, I give Valerie her point that, “…there are plenty of slim people with insulin resistance and plenty of fat people without insulin resistance…” I will resist getting into a “pissing contest” over percentages. I will concede that apparently Valerie is one of them. But I will contest the assertion Valerie makes that “fat people without insulin resistance” did not benefit from the “A to Z diet trial.” She states erroneously that “low-carb diets don’t help [them], if you remember the A to Z diet trial.”

The A to Z diet trial, not to be confused with a statin trial by a very similar name, was a “Twelve-month randomized trial conducted in the United States from February 2003 to October 2005 among 311 free-living, overweight/obese (body mass index, 27-40) nondiabetic [emphasis mine], premenopausal women.” Note: this trial EXCLUDED (type 2) diabetics, which by definition means that the participants did not have IR. It was a “Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors…,”published in JAMA in July 2007. The following are excerpts from the ABSTRACT:

“MAIN OUTCOME MEASURES: Weight loss at 12 months was the primary outcome. Secondary outcomes included lipid profile (low-density lipoprotein, high-density lipoprotein, and non-high-density lipoprotein cholesterol, and triglyceride levels), percentage of body fat, waist-hip ratio, fasting insulin and glucose levels, and blood pressure.”

“RESULTS: Weight loss was greater for women in the Atkins diet group compared with the other diet groups at 12 months, and mean 12-month weight loss was significantly different between the Atkins and Zone diets. Weight loss was not statistically different among the Zone, LEARN, and Ornish groups. At 12 months, secondary outcomes for the Atkins group were comparable with or more favorable than the other diet groups.”

“CONCLUSIONS: In this study, premenopausal overweight and obese women assigned to follow the Atkins diet, which had the lowest carbohydrate intake, lost more weight at 12 months than women assigned to follow the Zone diet, and had experienced comparable or more favorable metabolic effects than those assigned to the Zone, Ornish, or LEARN diets…”

So, just to be perfectly clear, non-diabetic, premenopausal overweight and obese women who ate the diet with the lowest carbohydrate intake lost the most weight and had the best improvement in related risk factors (including “lipid profile (low-density lipoprotein, high-density lipoprotein, and non-high-density lipoprotein cholesterol, and triglyceride levels), percentage of body fat, waist-hip ratio, fasting insulin and glucose levels, and blood pressure.”)

In other words, the low-carb diet DID help “fat people without insulin resistance,” and by a large margin. After 12 months, the Atkins cohort actually lost 3 times as much weight at the Zone cohort and twice as much as the average Ornish and LEARN dieter and had “comparable or more favorable metabolic effects” than those on the Zone, Ornish, or LEARN diets.

I’m sorry to have to come down so hard on this point, but it must be made clear to all my dear readers that low-carb diets do work (for the vast majority of people, if I have to hedge). If you haven’t given it an honest try, you really should.

The Nutrition Debate #283: TC/HDL, TG/HDL and Triglycerides

The Nutrition Debate #281 dealt with HDL cholesterol (HDL-C) and triglycerides (TG), and The Nutrition Debate #282 took a look at Total Cholesterol (TC), LDL cholesterol (LDL-C) and statin therapy. Now, I will tie them all together and discuss ratios and some recent thinking about dysfunctional HDL and using triglycerides alone to “predict” CVD risk.

You may have seen the Total Cholesterol to HDL-C ratio (expressed as TC/HDL) on the lipid panel in a typical lab report. The standard reference range (goal or target) is <5.0. There are no units because both components of the ratio have the same units (in U.S. measure, of mg/dL). So, If your TC is 200mg/dL, the limit under which the clinician wants your TC to be, and your HDL is 40mg/dL, the level above which your doctor wants to see your HDL, then your ratio would be 200/40 = 5.0. You’re living on the edge, the doctor will tell you.

Now, since most people’s TC is about 200 or a little higher, and most people who eat a Standard American or “Western” diet will have an HDL hovering around 40, much of the population is at risk of Cardio Vascular Disease (CVD), according to this standard. So, what’s a doctor to do? Prescribe a statin, of course! Because a statin, by lowering your LDL cholesterol will lower your Total Cholesterol. Remember the Friedewald formula: TC = HDL + LDL + TG/5. (Also, see The Nutrition Debate #25, “Understanding Your Lipid Panel” for an example of a “good” and a “bad” cholesterol panel.

However, since LDL is not assayed in the typical inexpensive lipid panel lab test, in reality the formula is “transposed” to calculate LDL from the other values which are inexpensively assayed. So, LDL is now calculated as LDL = TC – HDL – TG/5. However, as the math wizards among you will readily grasp, in the original form, TC = HDL + LDL +TG/5, your TC could be over 200 if any of the components (LDL, HDL or TG/5) was high since TC is the sum of these factors. So, TC is really a pretty worthless number. Nevertheless, when you take a statin, TC will get lower – much lower – as statins will lower your LDL.

And as a consequence, if your TC goes lower and your HDL stays the same, your ratio will go lower. For example, a TC of 120 with an HDL of 40 produces a ratio of 3.0. (120/40 = 3.0). Voilà! Your risk of CVD is now much lower than if your ratio is 5.0, like most people eating a Western diet. If you believe this, I have a bridge to sell you. (The Brooklyn Bridge, for those unfamiliar with the old joke.) But what’s a person to do if taking a pill is not the panacea it’s all trumped up to be?

Epidemiological evidence suggests that “…the strongest predictor of a heart attack” is another ratio: the ratio of your serum triglycerides to your HDL cholesterol, expressed as TG/HDL. I wrote about this several years ago in The Nutrition Debate #27 here. In #27 I said, “Using this new gold standard, a TG/HDL ≤ 1.0 is considered ideal, a ratio of ≤2.0 is good, a ratio of 4.0 is considered high.” Figure #6 tracks my personal TC/HDL and TG/HDL ratios from 1980 to the present.

The CONCLUSION in the reference cited in #27 above was: “Elevation in the ratio of TG to HDL-c was the single most powerful predictor of extensive coronary heart disease among all the lipid variables examined.” The full text of the Clinics paper can be seen here at Pub Med Central, the U. S. National Library of Medicine, National Institutes of Health. Note that both my TC/HDL and TG/HDL ratios were “borderline bad” until I started eating Very Low Carb in 2002. They trended down (except when I went “off diet” in the summers of 2003 and 2006), and dropped sharply to “low risk” when I started Bernstein. Note also that my TG/HDL ratios have been “ideal” (≤1.0) since 11/07, over 7 years and 23 lab reports ago.

Now, the latest thinking – this is cutting edge “science” folks – is that triglycerides alone may be the most reliable risk factor for CVD. The thinking here is that TG, although much more variable than HDL (and TC and LDL), rules out the possibility that high HDL, viewed as generally a very good thing, can also be elevated but “dysfunctional” due to infection, inflammation, diabetes, etc. My editor cited this recent piece in the Public Library of Science (PLOS) to support the new notion. And this piece from PubMed delves into the subject of dysfunctional HDL-C. So, I plotted another graph charting just triglycerides.

 A cursory glance tells the reader that my TGs averaged about 150 (once again: “borderline”) until I started Atkins Induction in September 2002. Then in the summer of 2003 I went “off diet” and my TGs skyrocketed. I returned to “the program” until the summer of 2006 when I started raiding the freezer at bedtime and gained back 12 pounds from the sugar/fat (ice cream). And when I started on Bernstein in September 2006, they fell again. But when I started to supplement with fish oil, and then to eat a can of sardines for lunch almost every day, they plummeted to 21 and have averaged about 50 ever since.

I used to think it was Very Low Carb (Atkins Induction and Bernstein 6-12-12) that caused my triglycerides to be so very low. Now that I’ve charted them and researched the milestone dates, I am convinced it is the fish oil supplementation and the sardines that are the reason. And quite possibly the reason for my high HDLs as well. As I show in Figure #3 in The Nutrition Debate #281 here, there is a very strong inverse correlation between low triglycerides and high HDL cholesterol.

Have you checked your ratios?   Do you know your trig level?