Do you ever wonder how many of your total calories come from added sugars? Grains? Dairy products? Added fats?
It also shows how many calories are or were available for consumption per capita over time (without accounting for wastage in restaurants). It’s based on U.S. Department of Agriculture data.
A superficial glance suggests that U.S. per capita daily calorie consumption has increased by about 600 from the 1970s until now. But remember, these numbers don’t discount for restaurant wastage. Nor do I see an adjustment for children versus adults. I’ve seen other calculations of and extra daily 150 calories (women) to 300 calories (men). Even the lower numbers could explain our explosion of overweight and obesity.
This is an epic post from my old Advanced Mediterranean Diet blog, originally dated July 6, 2009. That was a watershed year for me because of the ideas in this article. If you or your doctor think low-carb eating is dangerous because it may be higher in saturated fat, this post should convince you otherwise.
I’ve been thinking a lot lately about saturated fats. Weird, huh?The American Heart Association recommends that Americans limit the amount of saturated fats they eat to less than 7 percent of total daily calories. If you eat 2,000 calories a day, no more than 140 of them should come from saturated fats. That’s about 16 grams of saturated fats.
In over two decades of clinical practice, I’ve never run across a patient willing to do that calculation. Not many physicians could tell you the “seven percent rule.”
One of the two major themes of Gary Taubes’ book, Good Calories, Bad Calories, is that dietary saturated fats are not particularly harmful to our health, if at all. From what I’ve been taught, this is sacrilegious. “Saturated fats are a major cause of heart disease and strokes,” I’ve heard and read over and over. In brief, this is the Diet-Heart Hypothesis or the “lipid hypothesis”: Dietary saturated fat, total fat, and cholesterol are directly related to coronary heart disease and other forms of atherosclerosis (aka hardening of the arteries).
In his review of Taubes’ book, Dr. George Bray didn’t even address Taubes’ point about saturated fats, writing instead, “read and decide for yourself.”
That started me thinking either that the Diet-Heart Hypothesis is indefensible or that Dr. Bray is lazy. I don’t think he’s lazy. Dr. Bray is a Grand High Pooh-Bah in the fields of obesity and nutrition.
The American Heart Association in 1957 recommended that polyunsaturated fats replace saturated fats.
U.S. public health recommendations in 1977 were to reduce fat intake to 30% of total calories to lower the risk of coronary heart disease. Slowly, some fats were replaced mostly with carbohydrates, highly refined ones at that. This shift tends to raise triglycerides and lower HDL cholesterol levels, which may themselves contribute to atherosclerosis. Current recommendations are, essentially, to keep saturated fatty acids as low as possible.
One concern about substituting carbohydrates for fats is that blood sugar levels rise, leading to insulin release from the pancreas, in turn promoting growth of fat tissue and potentially leading to weight gain. Some believe that the public health recommendation to reduce total fat (which led to higher carbohydrate intake) is the reason for the dramatic rise in overweight and diabetes we’ve seen over the last 30 years.
Note that if intake of saturated fats is inadequate, our bodies can make the saturated fats it needs from carbohydrates. These are generally the same saturated fats that are present in dietary fats of animal origin. The only exceptions are the two essential fatty acids: alpha-linolenic acid and linoleic acid.
Why would saturated fats be harmful? Apparently because they raise blood levels of cholesterol (including LDL cholesterol – “bad cholesterol”), which is thought to be a cause of atherosclerosis, which increases the risk of coronary heart disease and stroke. I don’t recall seeing any mention of a direct toxic effect of saturated fats (or fatty acids) on arterial walls, where the rubber meets the road. (Saturated fats are broken down in the small intestine to glycerol and fatty acids.)
Dietary saturated fats also raise HDL cholesterol – “good cholesterol” – although not to the degree they raise LDL.Let’s not forget many other factors that cause, contribute to, or predict coronary heart disease and atherosclerosis: smoking, family history, high blood pressure, obesity, diabetes, oxidative stress, homocysteine level, systemic inflammation, high-glycemic index diets, C-reactive protein, lack of exercise, and others. I discussed dietary factorsin my April 14, 2009, blog post.
Often overlooked in discussion of dietary fat effects is the great variability of response to fats among individuals. Response can depend on genetics, sex, fitness level, overweight or not, types of carbohydrates eaten, amount of total dietary fat, etc. And not all saturated fats affect cholesterol levels.
Many of the journal articles listed as references below support the idea that the link between dietary saturated fats and coronary heart disease is not strong, and may be nonexistent. Read them and you’ll find that:
“Read and decide for yourself,” indeed. I think you’ll begin to question the reigning dogma.
For example, here’s a conclusion from the Hooper article (from 2001):
In this review we have tried to separate out whether changes in individual fatty acid fractions are responsible for any benefits to health (using the technique of meta-regression). The answers are not definitive, the data being too sparse to be convincing. We are left with a suggestion that less total fat or less of any individual fatty acid fraction in the diet is beneficial.
And a conclusion of the J.B. German article:
At this time , research on how specific saturated fatty acids contribute to coronary artery disease and on the role each specific saturated fatty acid play in other health outcomes is not sufficient to make global recommendations for all persons to remove saturated fats from their diet. No randomized clinical trials of low-fat diets or low-saturated fat diets of sufficient duration have been carried out; thus, there is a lack of knowledge of how low saturated fat intake can be without the risk of potentially deleterious health outcomes.
Zarraga and Schwartz (2006) conclude:
Numerous studies have been conducted to help provide dietary recommendations for optimal cardiovascular health. The most compelling data appear to come from trials that tested diets rich in fruits, vegetables, MUFAs [monounsaturated fatty acids], and PUFAs [polyunsaturated fatty acids], particularly the n-3 PUFAs. In addition, some degree of balance among various food groups appears to be a more sustainable behavioral practice than extreme restriction of a particular food group.
Here’s another of my favorite quotes on this topic, from the J.B. German article:
If saturated fatty acids were of no value or were harmful to humans, evolution would probably not have established within the mammary gland the means to produce saturated fatty acids . . . that provide a source of nourishment to ensure the growth , development, and survival of mammalian offspring.
The connection between dietary saturated fat and coronary heart disease is weak.
I may be excommunicated from the medical community for uttering this. You won’t hear it from most physicians or dietitians. They don’t have time to spend 80 hours on this topic, so they stick with the party line. And maybe I’m wrong anyway.
The scientific community is slowly moving away from the original Diet-Heart/Lipid Hypothesis. It is being replaced with stronger anti-atherosclerosis theories that promote:
So, saturated fats and dietary cholesterol are being crowded out of the picture, or ignored. In many cases, saturated fats have literally been replaced by poly- and monounsaturated fats (plant oils). Several clinical studies indicate that’s a healthy change, but it may be related more to the healthfulness of the plant oils than to detrimental effects of saturated fats.
The original Diet-Heart Hypothesis won’t die until the American Heart Association and U.S. public health agencies put a gun to its head and pull the trigger. That will take another 10 years or more.
If you want to hedge your bets, go ahead and limit your saturated fat intake. It probably won’t hurt you. It might help a wee bit. By the same token, I’m not going on an all-meat and cheese, ultra-high-saturated fat diet; I don’t want to miss out on the healthy effects of fruits, vegetables, whole grains, fish, nuts, and low-glycemic index carbohydrates. Some would throw red wine into the mix. This “prudent diet” reflects what I hereby christen The 21st Century Diet-Heart Hypothesis.
If you’re worried about coronary heart disease and atherosclerosis, spend less time counting saturated fat grams, and more time on other risk-reducing factors: diet modification as above, get regular exercise, control your blood pressure, achieve a healthy weight, and don’t smoke. More bang for the buck.
What do you think?
Disclaimer: All matters regarding your health require supervision by a personal physician or other appropriate health professional familiar with your current health status. Always consult your personal physician before making any dietary or exercise changes.
Selected References Contradicting or Questioning the Diet-Heart Hypothesis (updated February 19, 2012):
Astrup, A., et al (including Ronald Krause, Frank Hu, and Walter Willett). The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010. American Journal of Clinical Nutrition, 93 (2011): 684-688. (The authors believe that replacing saturated fats with polyunsaturated fats (but not carbohydrates) can reduce the risk of coronary heart disease (CHD). For the last four decades, low-fat diets replaced fat with carbohydates. So they believe saturated fatty acids cause CHD or polyunsaturated fatty acids prevent it. I see no mention of total fat intake in this article written by major names in nutritional epidemiology and lipid metabolism. “In countries following a Western diet, replacing 1% of energy intake from saturated fatty acids with polyunsaturated fatty acids has been associated with a 2–3% reduction in the incidence of CHD.” “Furthermore, the effect of particular foods on CHD cannot be predicted solely by their content of total saturated fatty acids because individual saturated fatty acids may have different cardiovascular effects and major saturated fatty acid food sources contain other constituents that could influence coronary heart disease risk.”) A Feb. 19, 2012, press release from the Harvard School of Public Health covered much of the same ground. It’s titled “Time to Stop Talking About Low-Fat, say HSPH Nutrition Experts.”
Siri-Tarino, Patty, et al. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. American Journal of Clinical Nutrition, January 13, 2010. doi:10.3945/ajcn.2009.27725
Skeaff, C. Murray and Miller, Jody. Dietary fat and coronary heart disease: Summary of evidence from prospective cohort and randomised controlled trials. Annals of Nutrition and Metabolism, 55 (2009): 173-201.
Halton, Thomas, et al. Low-carbohydrate-diet score and the risk of coronary heart disease in women. New England Journal of Medicine, 355 (2006): 1,991-2,002.
German, J. Bruce, and Dillard, Cora J. Saturated fats: What dietary intake? American Journal of Clinical Nutrition, 80 (2004): 550-559.
Ravnskov, U. The questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease. Journal of Clinical Epidemiology, 51 (1998): 443-460.
Ravsnskov, U. Hypothesis out-of-date. The diet-heart idea. Journal of Clinical Epidemiology, 55 (2002): 1,057-1,063.
Ravnskov, U, et al. Studies of dietary fat and heart disease. Science, 295 (2002): 1,464-1,465.
Taubes, G. The soft science of dietary fat. Science, 291 (2001): 2535-2541.
Zarraga, Ignatius, and Schwartz, Ernst. Impact of dietary patterns and interventions on cardiovascular health. Circulation, 114 (2006): 961-973.
Mente, Andrew, et al. A Systematic Review of the Evidence Supporting a Causal Link Between Dietary Factors and Coronary Heart Disease. Archives of Internal Medicine, 169 (2009): 659-669.
Parikh, Parin, et al. Diets and cardiovascular disease: an evidence-based assessment. Journal of the American College of Cardiology, 45 (2005): 1,379-1,387.
Hooper, L., et al. Dietary fat intake and prevention of cardiovascular disease: systematic review. British Medical Journal, 322 (2001): 757-763.
Weinberg, W.C. The Diet-Heart Hypothesis: a critique. Journal of the American College of Cardiology, 43 (2004): 731-733.
Mozaffarian, Darius, et al. Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women. American Journal of Clinical Nutrition, 80 (2004): 1,175-1,184.
Related editorial: Knopp, Robert and Retzlaff, Barbara. Saturated fat prevents coronary artery disease? An American paradox. American Journal of Clinical Nutrition, 80 (2004): 1.102-1.103.
Yusuf, S., et al. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet, 364 (2004): 937-952. (ApoB/ApoA1 ratio was a risk factor for heart attack, so dietary saturated fat may play a role if it affects this ratio.)
Hu, Frank. Diet and cardiovascular disease prevention: The need for a paradigm shift. Journal of the American College of Cardiology, 50 (2007): 22-24. (Dr. Hu de-emphasizes the original diet-heart hypothesis, noting instead that “. . . reducing dietary GL [glycemic load] should be made a top public health priority.:)
Oh, K., et al. Dietary fat intake and risk of coronary heart disease in women: 20 years of follow-up of the Nurses’ Health Study. American Journal of Epidemiology, 161 (2005): 672-679.
Parker, Steve. Time to abandon the diet-heart hypothesis? Advanced Mediterranean Diet Blog, May 1, 2009.
Parker, Steve. New study confirms the heart-healthy Mediterranean diet. Advanced Mediterranean Diet Blog, April 14, 2009. (Examination of the Mente study listed above.)
Selected References Supporting the Diet-Heart Hypothesis (by no means exhaustive)
Ascherio, A. Epidemiologic studies on dietary fats and coronary heart disease. American Journal of Medicine, 113 (supplement) (2002): 9S-12S.
Griel, Amy and Kris-Etherton, Penny. Beyond saturated fat: The importance of the dietary fatty acid profile on cardiovascular disease. Nutrition Reviews, 64 (2006): 257-262. (Primarily a response to the Mozaffarian article above.)
Erkkila, Arja, et al. Dietary fatty acids and cardiovascular disease: An epidemiological approach. Progress in Lipid Research, 47 (2008): 172-187.
In preparation, I collected some random thoughts and did a little research.
What’s the paleo diet?
Fresh, minimally processed food. Meat (lean or not? supermarket vs yuppiefied?), poultry, eggs, fish, leafy greens and other vegetables, nuts, berries, fruit, and probably tubers.
Non-paleo: highly processed, grains, refined sugars, industrial plant/seed oils, legumes, milk, cheese, yogurt.
The paleo diet is also called Old Stone Age, caveman, ancestral, hunter-gatherer, and Paleolithic diet.
Is the paleo diet deficient in any nutrients?
A quick scan of Loren Cordain’s website found mention of possible calcium and vitamin D deficits. Paleoistas will get vitamin D via sun exposure and fish (especially cold-water fatty fish). Obtain calcium from broccoli, kale, sardines, almonds, collards. (I wonder if the Recommended Dietary Allowance for calcium is set too high.)
What About Carbohydrates and Diabetes and the Paleo Diet?
Diabetes is a disorder of carbohydrate metabolism. In a way, it’s an intolerance of carbohydrates. In type 1 diabetes, there’s a total or near-total lack of insulin production on an autoimmune basis. In type 2 diabetes, the body’s insulin just isn’t working adequately; insulin production can be high, normal or low. In both cases, ingested carboydrates can’t be processed in a normal healthy way, so they stack up in the bloodstream as high blood sugars. If not addressed adequately, high blood glucose levels sooner or later will poison body tissues . Sooner in type 1, later in type 2. (Yes, this is a gross over-simplification.)If you’re intolerant of lactose or gluten, you avoid those. If you’re intolerant of carbohydrates, you could avoid eating them, or take drugs to help you overcome your intolerance. Type 1 diabetics must take insulin. Insulin’s more optional for type 2’s. We have 11 classes of drugs to treat type 2 diabetes; we don’t know the potential adverse effects of most of these drugs. Already, three diabetes drugs have been taken off the U.S. market or severely restricted due to unacceptable toxicity: phenformin, troglitazone, and rosiglitazone.
Humans need two “essential fatty acids” and nine “essential” amino acids derived from proteins. “Essential” means we can’t be healthy and live long without them. Our bodies can’t synthesize them. On the other hand, there are no essential carbohydrates. Our bodies can make all the carbohydrate (mainly glucose) we need.
Since there are no essential carbohydrates, and we know little about the long-term adverse side effects of many of the diabetes drugs, I favor carbohydrate restriction for people with carboydrate intolerance. (To be clear, insulin is safe, indeed life-saving, for those with type 1 diabetes.)
That being said, let’s think about the Standard American Diet (SAD) eaten by an adult. It provides an average of 2673 calories a day. Added sugars provide 459 of those calories, or 17% o the total. Grains provide 625 calories, or 23% of the total. And most of those sugars and grains are in processed, commercial foods. So added sugars and grains provide 40% of the total calories in the SAD. (Figures are from an April 5, 2011, infographic at Civil Eats.)
Anyone going from the SAD to pure Paleo eating will be drastically reducing intake of added sugars and grains, our current major sources of carbohydrate. Question is, what will they replace those calories with?
That’s why I gave a thumbnail sketch of the paleo diet above. Take a gander and you’ll see lots of low-carb and no-carb options, along with some carb options. For folks with carbohydrate intolerance, I’d favor lower-carb veggies and judicious amounts of fruits, berries, and higher-carb veggies andtubers. “Judicious” depends on the individual, considering factors such as degree of residual insulin production, insulin sensitivity, the need to lose excess weight, and desire to avoid diabetes drugs.
Compared to the standard “diabetic diet” (what’s that?) and the Standard American Diet, switching to paleo should lower the glycemic index and glycemic load of the diet. Theoretically, that should help with blood sugar control.
A well-designed low-carb paleo diet would likely have at least twice as much fiber as the typical American diet, which would also tend to limit high blood sugar excursions.
In general, I favor a carbohydrate-restricted paleo diet for those with diabetes who have already decided to “go paleo.” I’m not endorsing any paleo diet for anyone with diabetes at this point—I’m still doing my research. But if you’re going to do it, I’d keep it lower-carb. E.g., under 100 g of digestible carb daily. It has a lot of potential.
Are There Any Immediate Dangers for a Person With Diabetes Switching to the Paleo Diet?
It depends on three things: 1) current diet, and 2) current drug therapy, and 3) the particular version of paleo diet followed.
Remember, the Standard American Diet provides 40% of total calories as added sugars and grains (nearly all highly refined). Switching from SAD to a low-carb paleo diet will cut carb intake and glycemic load substantially, raising the risk of hypoglycemia if the person is taking certain drugs.
Who knows about carb content of the standard “diabetic diet”? Contrary to poplular belief, there is no monolithic “diabetic diet.” There is no ADA diet (American Diabetes Association). My impression, however, is that the ADA favors relatively high carbohydrate consumption, perhaps 45-60% of total calories. Switching to low-carb paleo could definitely cause hypoglycemia in those taking the aforementioned drugs.
One way to avoid diet-induced hypoglycemia is to reduce the diabetic drug dose.
A type 2 overweight diabetic eating a Standard American Diet—and I know there are many out there—would tend to see lower glucose levels by switching to probably any of the popular paleo diets. Be ready for hypoglycemia if you take those drugs.
Paleo diets are not necessarily low-carb. Konner and Eaton estimate that ancestral hunter-gatherers obtained 35 to 40% of total calories from carbohydrates. I’ve seen other estimates as low as 22%. Reality likely falls between 22 and 65%. When pressed for a brief answer as to how many carbohydrate calories are in the paleo diet, I say “about a third of the total.” By comparison, the typical U.S. diet provides 50% of calories from carbohydrate.
Someone could end up with a high-carb paleo diet easily, by emphasizing tubers (e.g., potatoes), higher-carb vegetables, fruits, berries, and nuts (especially cashews). Compared with the SAD, this could cause higher or lower blood sugars, or no net change.
A diabetic on a Bernstein-style diet or Ketogenic Mediterranean Diet (both very-low-carb) but switching to paleo or low-carb paleo (50-150 g?) would see elevated blood sugars. Perhaps dangerously high glucoses.
Any person with diabetes making a change in diet should do it in consultation with a personal physician or other qualified healthcare professional familiar with their case.
Fun Facts provided by the U.S. Department of Agriculture.
It’s estimated that the Old Stone Age diet provided much more omega-3 fatty acids and much less omega-6s, compared to modern Western diets. This may have important implications for development of certain chronic diseases like cancer and heart disease.
I haven’t studied this issue in great detail but hope to do so at some point. Evelyn Tribole has strong opinions on it; I may get one of her books.
I saw an online video of William E.M.Lands, Ph.D., discussing the omega-6/omega-3 ratio. He mentioned free software available from the National Insitutes of Health that would help you monitor and adjust your ratio.
You can see the video here. Dr. Lands’ talk starts around minute 12 and lasts about 45 minutes. He says it’s just as important (if not more so) to reduce your omega-6 consumption as to increase your omega-3. And don’t overeat.
Dr. Jay Wortman has been thinking about whether our bodies prefer to run on carbohydrates (as a source of glucose) or, instead, on fats. The standard American diet provides derives about half of its energy from carbs, 35% from fats, and 15% from proteins. So you might guess our bodies prefer carbohydrates as a fuel source. Dr. Wortman writes:
Now, consider the possibility that we weren’t meant to burn glucose at all as a primary fuel. Consider the possibility that fat was meant to be our primary fuel. In my current state of dietary practice, I am burning fat as my main source of energy. My liver is converting some of it to ketones which are needed to fuel the majority of my brain cells. A small fraction of the brain cells, around 15%, need glucose along with a few other tissues like the renal cortex, the lens of the eye, red blood cells and sperm.Their needs are met by glucose that my liver produces from proteins. The rest of my energy needs are met with fatty acids and these come from the fats I eat.
Dr. Wortman, who has type 2 diabetes, in the same long post also writes about oolichan grease (from fish), an ancestral food of Canandian west coast First Nations people.