Category Archives: Fat and Oil

Today’s Study On The Risks Of Consuming Saturated Fat

Butter and knifeComparison Of Predictive Performance Of Various Fatty Acids For The Risk Of Cardiovascular Disease Events And All-cause Deaths In A Community-based Cohort, Atherosclerosis, September, 2013

This was a prospective study from Taiwan, 1833 men and women (average age 60) were followed for about 10 years. The relative risk (RR) of death in the highest quartile compared with the lowest quartile (of fatty acids in their blood) was:

1.33 for saturated fats (95% confidence interval [CI], 1.01–1.75, test for trend, P = 0.015)
1.71 for trans fats (95% CI, 1.27–2.31, test for trend, P = 0.0003)
0.77 for EPA (95% CI, 0.59–1.00, test for trend, P = 0.048)
0.89 for DHA (95% CI, 0.68–1.18, test for trend, P = 0.354)

Note that there was a higher risk of death for only saturated fats and trans fats (the RR was above 1.00). Note also that even though the RR was below 1.00, that is, appeared to show protection for the omega-3 fatty acids EPA and DHA, it did not rise to a level of significance, especially for DHA.

“CONCLUSIONS: Our data provides strong evidence to support that plasma saturated fats and trans fats can predict all-cause death and CVD [cardiovascular disease] more effectively than other fatty acid markers.”

High Fat, Especially High Saturated Fat Diets Linked To Muscle Loss

As people age, they lose muscle mass. That muscle loss is called sarcopenia. Inflammation and oxidative stress are thought to be at the root of sarcopenia. Dr. Holly Van Remmen’s research focuses on how oxidative stress damages mitochondria, and:

“The impaired function of mitochondria also has a detrimental effect on the way motor neurons ‘talk’ to the muscle to achieve muscle contraction,” Dr. Van Remmen said.

This new study now implicates dietary fat in these processes:

Dietary Fat and Fatty Acid Profile Are Associated with Indices of Skeletal Muscle Mass in Women Aged 18–79 Years, The Journal of Nutrition, March 2014

“Age-related loss of skeletal muscle mass results in a reduction in metabolically active tissue and has been related to the onset of obesity and sarcopenia. Although the causes of muscle loss are poorly understood, dietary fat has been postulated to have a role in determining protein turnover through an influence on both inflammation and insulin resistance.”

Dietary fat is linked to inflammation and insulin resistance, evidence for which I’ve given over the years.

“This study was designed to investigate the cross-sectional relation between dietary fat intake, as dietary percentage of fat energy (PFE) and fatty acid profile, with indices of skeletal muscle mass in the population setting. Body composition [fat-free mass (FFM; in kg)] and the fat-free mass index (FFMI; kg FFM/m2) was measured by using dual-energy X-ray absorptiometry in 2689 women aged 18–79 y from the TwinsUK Study and calculated according to quintile of dietary fat (by food-frequency questionnaire) after multivariate adjustment.”

Quintiles. Did you see that? They divided the women into 5 groups based on fat intake. Why didn’t the saturated fat study use quintiles? Or quartiles? When you want to see difference among groups, the more groups the better. (The Sat Fat study used 3 groups.)

“Positive associations were found between the polyunsaturated-to-saturated fatty acid (SFA) ratio and indices of FFM, and inverse associations were found with PFE, SFAs, monounsaturated fatty acids (MUFAs), and trans fatty acids (TFAs) (all as % of energy). Extreme quintile dietary differences for PFE were −0.6 kg for FFM and −0.28 kg/m2 for FFMI; for SFAs, MUFAs, and TFAs, these were −0.5 to −0.8 kg for FFM and −0.26 to −0.38 kg/m2 for FFMI. These associations were of a similar magnitude to the expected decline in muscle mass that occurs over 10 y.”

So, as the polyunsaturated-to-saturated fatty acid ratio went up, muscle mass went up. As total fat, saturated fat, monounsaturated fat, and trans fat intakes went up, muscle mass went down.

“To our knowledge, this is the first population-based study to demonstrate an association between a comprehensive range of dietary fat intake and FFM [Fat Free Mass or muscle mass]. These findings indicate that a dietary fat profile already associated with cardiovascular disease protection* may also be beneficial for conservation of skeletal muscle mass.”

That profile which protects against heart disease and now sarcopenia is:

  • Low dietary fat – of all types.
  • High polyunsaturated-to-saturated fatty acid ratio, which is … more plant food, less animal food.

Mark Bittman: “Butter Is Back”

Mark Bittman just published a column hailing that saturated fat study that I’ve been criticizing:

Butter Is Back, New York Times, 25 March 2014

“Butter is back, and when you’re looking for a few chunks of pork for a stew, you can resume searching for the best pieces — the ones with the most fat.

The days of skinless chicken breasts and tubs of I Can’t Believe It’s Not Butter may finally be drawing to a close.

You can go back to eating butter, if you haven’t already.”

For crying out loud.

Does The Type Of Fat You Eat Affect Blood Glucose?

FingerStick4If you give a group of men one of three meals…

1. High in saturated fat (SFA)
2. High in monounsaturated fat (MUFA)
3. High in polyunsaturated fat (PUFA)

Will there be any difference in blood glucose levels after the meal? (All meals contain the same amount of fat (61% of energy), carbohydrate (33%), and protein (6.3%).

If you answered yes, which group had higher or lower blood glucose?

Here’s what this study* found:

  • Ingestion of the PUFA meal resulted in an improved postprandial insulin sensitivity compared with SFA.
  • Insulin and glucose concentrations were higher after the SFA meal than after the PUFA meal, with intermediate values for the MUFA meal.
  • These data suggest that the effects of replacement of SFA by PUFA may contribute to lower uptake of lipids in skeletal muscle and therefore may protect against the development of insulin resistance in humans.

* PUFAs Acutely Affect Triacylglycerol-Derived Skeletal Muscle Fatty Acid Uptake And Increase Postprandial Insulin Sensitivity, American Journal of Clinical Nutrition, February 2012

Saturated fat comes primarily from dairy products (cheese, butter, cream, milk) and animal foods. The fat in plants tends to be more unsaturated, PUFA and MUFA.

Is Sugar Responsible For Obesity?

Sugars2The following graphs are from:

Challenging the Fructose Hypothesis: New Perspectives on Fructose Consumption and Metabolism, American Society for Nutrition, March 2013

The paper is not objective, but I found the data compelling.

Figure 1 shows that consumption of America’s top 2 sweeteners have either remained constant or dropped off as obesity rates continued to climb.

Figure 1
Historical trends in sucrose and high-fructose corn syrup (HFCS) consumption (availability) versus rates of obesity in adults. After significant gain in market share at the expense of sucrose, HFCS consumption has been decreasing since 1999 and there is no correlation with obesity. From USDA Economic Research Service per capita consumption data, adjusted for loss and WHO Global Database on BMI.

ASNConsumptionDataAndObesity2013_2

Figure 1 may be misleading, because if you add refined sugar and HFCS, along with other caloric sweeteners, there is a trend that aligns with obesity,* at least to about the year 2000.

ASNConsumptionDataAndObesity2013_3

So, what happened in 2000 that might have contributed to increasing obesity rates, if it wasn’t sugar? Look at the blue line in the graph below.

Figure 2
Commodity group energy intakes, 1970–2010. Added sugars contribution to the 449 kcal/d increase in per capita energy intake over this period was small in comparison with flour-cereal products and added fats, accounting for less than 8% of the increase. Added sugars intake has been decreasing since 1999. From USDA Economic Research Service average daily per capita energy from the U.S. food availability, adjusted for loss.

ASNConsumptionDataAndObesity2013

I don’t think sugar is “toxic” as Gary Taubes claims, or a “poison” as Robert Lustig claims. Sugar is a carbohydrate; humans have evolved to eat carbohydrates.

I do think that “foods” that have been isolated, processed, and added to products in amounts not seen in nature can be detrimental. I feel this way about fats and proteins too. (And about supplements.) It’s not good to eat a salad swimming in oil, or to add protein powder to a smoothie, just as it is not good to consume a beverage with 20 spoonfuls of sugar.

* It’s important to note that this trend occurs against the backdrop of a high-fat diet.  You have to look at the whole diet.  Diets high in both fat and refined carbohydrates, including sugar, contribute not just to weight gain (“Wate-On” and “Ensure” and, of course, Wate-On’s Competition) but to increased risks for chronic diseases, notably diabetes and heart disease. Cubans lost weight and lowered their rates of diabetes, heart disease, and cancer by eating a diet of primarily rice and sugar, with very little fat, just 13%!

That Saturated Fat Study: Harvard Responds

WalterWillett2

Walter Willett, MD, Dr. PH

Harvard posted Dr. Willett and colleagues’ response to the dietary fat study I’ve been posting about (here and here). Dr. Willett is chair of the Department of Nutrition at Harvard School of Public Health.

Dietary Fat And Heart Disease Study Is Seriously Misleading, Harvard School of Public Health, 19 March 2014

The journal Annals of Internal Medicine recently published a paper suggesting there is no evidence supporting the longstanding recommendation to limit saturated fat consumption. Media reporting on the paper included headlines such as “No link found between saturated fat and heart disease” and articles saying “Saturated fat shouldn’t be demonized” springing up on social media.

Dr. Willett emphasized that because this meta-analysis contains multiple serious errors and omissions, the study conclusions are misleading and should be disregarded.

Here’s Harvard’s official response as it appears on the Annals of Internal Medicine website:

The meta-analysis of dietary fatty acids and risk of coronary heart disease by Chowdhury et al. (1) contains multiple errors and omissions, and the conclusions are seriously misleading, particularly the lack of association with N-6 polyunsaturated fat. For example, two of the six studies included in the analysis of N-6 polyunsaturated fat were wrong. The relative risks for Nurses’ Health Study (NHS) (2) and Kuopio Ischemic Heart Disease Study (KIHD) (3) were retrieved incorrectly and said to be above 1.0. However, in the 20-year follow-up of the NHS the relative risk for highest vs lowest quintile was 0.77 (95 percent CI: 0.62, 0.95); ptrend = 0.01 (the authors seem to have used the RR for N-3 alpha-linolenic acid from a paper on sudden cardiac death), and in the KIHD the relative risk was 0.39; 95% confidence interval [CI], 0.21-0.71) (the origin of the number used in the meta-analysis is unclear). Also, relevant data from other studies were not included (4 and 5).

Further, the authors did not mention a pooled analysis (6) of the primary data from prospective studies, in which a significant inverse association between intake of polyunsaturated fat (the large majority being the N-6 linoleic acid) and risk of CHD was found. Also, in this analysis, substitution of polyunsaturated fat for saturated fat was associated with lower risk of CHD. Chowdhury et al. also failed to point out that most of the monounsaturated fat consumed in their studies was from red meat and dairy sources, and the findings do not necessarily apply to consumption in the form of nuts, olive oil, and other plant sources. Thus, the conclusions of Chowdhury et al. regarding the type of fat being unimportant are seriously misleading and should be disregarded.

Sincerely,

Walter Willett
Frank Sacks
Meir Stampfer

Harvard University

1. Chowdhury R, Warnakula S, Kunutsor S, et al. Association of dietary, circulating, and supplement fatty acids with coronary risk. Ann Intern Med 2014; 160(6):398-406.
2. Oh K, Hu FB, Manson JE, Stampfer MJ, Willett WC. Dietary fat intake and risk of coronary heart disease in women: 20 years of follow-up of the Nurses’ Health Study. Am J Epidemiol 2005;161:672-9.
3. Laaksonen DE, Nyyssonen K, Niskanen L, Rissanen TH, Salonen JT. Prediction of cardiovascular mortality in middle aged men by dietary and serum linoleic and polyunsaturated fatty acids. Arch Intern Med 2005;165:193-199.
4. de Goede J, Geleijnse JM, Boer JM, Kromhout D, Verschuren WM. Linoleic acid intake, plasma cholesterol and 10-year incidence of CHD in 20,000 middle-aged men and women in the Netherlands. Br J Nutr 2012;107:1070-6.
5. Dolecek TA. Epidemiological evidence of relationships between dietary polyunsaturated fatty acids and mortality in the multiple risk factor intervention trial. Proc Soc Exp Biol Med 1992;200:177-82.
6. Jakobsen MU, O’Reilly EJ, Heitmann BL, Pereira MA, Bälter K, Fraser GE, Goldbourt U, Hallmans G, Knekt P, Liu S, Pietinen P, Spiegelman D, Stevens J, Virtamo J, Willett WC, Ascherio A. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Am J Clin Nutr 2009:1425-32.

After reading this, I am curious how this study in the Annals withstood peer review.

When people think “carbohydrates,” do they think … carrots and apples? Do they think beans and lentils? Or do they think highly processed, white-flour-white-sugar breads, boxed breakfast cereals, bagels, pretzels, crackers, cookies, cakes, muffins? If you are cutting back on fat, especially saturated fat, you will, by default, be eating more carbohydrates. It is the former (carrots, apples, beans, lentils, corn, peas, oats, yams, squash) where carbs should ideally be coming from, not the latter. The former is the essence of a whole food, plant-based diet.

That Saturated Fat Study

One more comment about the fatty acid study I posted about a few days ago, the one that found no difference in cardiovascular disease (CVD) risk between those who ate the most vs. those who ate the least saturated fat:

Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysis, Annals of Internal Medicine, 18 March 2014

One way you can arrive at all your groups showing similar risk, which this study found, is when there isn’t much difference in consumption among your comparison groups. Or when most of your participants are consuming saturated fat above a threshold where risk for CVD increases.

About this meta-analysis, Jeff Novick writes:

“One major problem with this study is they did not look at any studies where the saturated fat intake was less than 7%, which is the level recommended by the [American Heart Association]. … Most of the diets had saturated fat intakes in the range of 10-15% (or more).”

7% is a lot of saturated fat. If someone was eating 2000 calories a day, 7% is about 16 grams of saturated fat. For relativity’s sake, there are 2 grams of saturated fat in a 3 ounce serving of beef chuck. One chicken thigh, just 2 ounces, has 3 grams of saturated fat.

Does reducing saturated fat below 7%, what you would find in a whole food, plant-based (WFPB) diet, reduce CVD risk? This study couldn’t say.

Here’s a study that found replacing saturated fat with polyunsaturated fat reduced risk for heart attack.  (Saturated fat comes primarily from animals – meat and dairy. Polyunsaturated fat comes primarily from plants.)

Effects On Coronary Heart Disease Of Increasing Polyunsaturated Fat In Place Of Saturated Fat: A Systematic Review And Meta-analysis Of Randomized Controlled Trials, PLOS Medicine, March 2010

“Conclusions: These findings provide evidence that consuming PUFA in place of SFA reduces CHD events in RCTs.”*

Here’s the press release: Replacing Those Saturated Fats, Harvard, March 2010

“But a new study by researchers at Harvard School of Public Health (HSPH) provides the first conclusive evidence from randomized clinical trials that people who replace saturated fat in their diet with polyunsaturated fat reduce their risk of coronary heart disease by 19 percent, compared with control groups of people who do not.”

For every 5 percent increase (measured as total energy) in polyunsaturated fat consumption, coronary heart disease risk was reduced by 10 percent.

Remember this? “Give that chicken fat back to the chicken!”

* PUFA: Polyunsaturated Fatty Acids
SFA: Saturated Fatty Acids
CHD: Coronary Heart Disease
RCT: Randomized Controlled Trials

Eating Saturated Fat Contributes To Heart Disease: No Evidence?

SaturatedFatsADAMI think there is a lot of evidence implicating saturated fat in disease. However, there’s a new study which is raising doubt as to the effect of saturated fat on heart disease:

Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysis, Annals of Internal Medicine, 18 March 2014

The New York Times reported on it yesterday:
Study Questions Fat and Heart Disease Link

Someone had anonymously linked the New York Times article on my blog. They made no comment.

It’s a meta-analysis with, the authors admit, “potential biases from preferential publication and selective reporting.” Here’s some data:

In observational studies, when the top and bottom thirds of baseline dietary fatty acid intake were compared, relative risks (RRs) for coronary disease were:

1.02 (95% CI, 0.97 to 1.07) for saturated
0.99 (CI, 0.89 to 1.09) for monounsaturated
0.93 (CI, 0.84 to 1.02) for long-chain ω-3 polyunsaturated
1.01 (CI, 0.96 to 1.07) for ω-6 polyunsaturated
1.16 (CI, 1.06 to 1.27) for trans fatty acids

For circulating fatty acids, RRs were:

1.06 (CI, 0.86 to 1.30)
1.06 (CI, 0.97 to 1.17)
0.84 (CI, 0.63 to 1.11)
0.94 (CI, 0.84 to 1.06)
1.05 (CI, 0.76 to 1.44)

In randomized, controlled trials (RCTs), RRs were:

0.97 (CI, 0.69 to 1.36) for α-linolenic
0.94 (CI, 0.86 to 1.03) for long-chain ω-3 polyunsaturated
0.89 (CI, 0.71 to 1.12) for ω-6 polyunsaturated fatty acid supplementations

Note that circulating trans fatty acids had almost the same RR as saturated fat, in fact, trans fats trended more protective? Note also that in RCTs, omega-6 was more protective than omega-3. There is a lot of inconclusiveness here.

These are effects relative to cardiovascular disease (CVD). They did not look at diabetes, arthritis, cancer, or other inflammatory-based diseases. Even if it is true that saturated fat has no impact on CVD, it has been shown to increase the risk for other chronic diseases.

It’s conclusion:

“Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.”

“Not clearly.” Does that remind you of anything? Why did this study get published at all? Recall this study:

Long Term Toxicity Of A Roundup Herbicide And A Roundup-Tolerant Genetically Modified Maize, Food and Chemical Toxicology (FTC), 19 September 2012.

It found more breast cancer, liver and kidney damage in rats fed GMOs.

The publisher was hounded by industry groups like Monsanto to retract it. He resisted for a year, defending it!, then gave in saying:

“Unequivocally, the Editor-in-Chief found no evidence of fraud or intentional misrepresentation of the data. … Ultimately, the results presented (while not incorrect) are inconclusive.”

It was retracted, not because it was incorrect, but because it was “inconclusive.” This present study is also inconclusive. The authors admit as much. Shall we expect it to be retracted? Can you think of any industry that would benefit by keeping this study circulating? Industry doesn’t have to combat science, all they have to do is plant seeds of doubt, and they’ve won.

________Here’s yet another reason why I believe saturated fat contributes to the development of chronic diseases. It was buried in the comments on the New York Times article:

“The results of reducing animal fat consumption in Finland led to greatly reduced cardiovascular disease rates.” -wbgrant

Fat and Heart Disease: Yes We Can Make a Change – The Case of North Karelia (Finland), Annals of Nutrition and Metabolism, July 2009

“The combined efforts of all stakeholders have greatly helped people to reduce the intake of saturated fat and to replace this with unsaturated fat. This has been associated with an improved quality of the dietary fat (e.g. in 1972, over 90% of the population used butter on their bread compared to <5% at present) and a remarkable reduction in blood cholesterol levels. It has led to a 80% reduction in annual CVD mortality rates among the working aged population, to a major increase in life expectancy and to major improvements in functional capacity and health.

There is strong medical evidence that CVD (like many other chronic diseases) is preventable or could be delayed to a more advanced age. A population-based prevention programme is the most cost-effective way and in many cases the only affordable option for major public health improvements. To prevent CVD and to promote heart health, dietary changes are crucial, especially the change in the quality of fat. These changes can have a major impact in relatively short time and can lead to dramatic improvements in public health in the long run.”