Sunday, May 17, 2015

Saturated Fat Intake: Now and Then

National dietary guidelines have been under attack for being associated with the development of the obesity epidemic.  In defence of national dietary guidelines, many have argued that we are fatter simply because we do not follow them.  I agree with that, I don’t think the dietary guidelines made us fat and the dietary guidelines seem to be healthier than what most people currently eat.  Although I think they can be improved, an idea many people surely have, but for different reasons.  Anyway, there has been at least one instance where we have adhered pretty well to the dietary guidelines, and that is that we have reduced our intake of SFA.  Indeed, one of the arguments that gets used in favour of the diet heart hypothesis is that CHD mortality has declined in over the last ~50-60 years and was due in part to reductions in SFA intake.  I have a few objections to this:

·         While SFA has decreased during this period, it seems to have been mostly replaced by refined carbohydrates, which pretty much everyone agrees won’t reduce the risk of CHD based on the total-C:HDL-C ratio [1] and observational studies [2] [3]
·         The evidence even from favourable meta-analyses of observational studies suggests that reducing SFA will only reduce CHD if it is replaced by PUFA [2] [4].  Even though we have modestly increased in PUFA intake during that period [5]* (in absolute terms), the magnitude of the decrease in CHD mortality (from data used by diet heart advocates), far exceeds what is predicted from favourable meta-analyses of observational studies
·         Simply excluding inadequately randomised trials (Finnish Mental Hospital Study) results in the RR for CHD mortality being 0.99 (CI = 0.83-1.20, P = 0.95).  More importantly, the RR for CHD mortality from ‘adequately controlled’ trials excluding the Sydney Diet Heart is 1.04 (CI = 0.85-1.26, P = 0.72) (blog)
·         It ignores other factors such as a dramatic decline in smoking [6], advancements in medical care and environmental toxins [7]

* In that paper, Ramsden, et al estimated PUFA intake from 1909 to 1999.  In summary linoleic acid increased 2.58-fold from 2.79% to 7.21% and alpha-linolenic acid increased 1.85-fold from 0.39% to 0.72%, whereas changes in long chain PUFA were relatively fairly minor [5]


Regarding the decline in SFA intake I wanted to get a rough idea as to how much we have reduced our intake of SFA in the last ~50-60 years, hence the second half of this post:

NHANES

The following tables come from NHANES, which probably is probably the most accurate measure of trends in SFA intake, but unfortunately the surveys didn’t begin until the 1970’s, by which time the general public had received the advice to reduce SFA and cholesterol for many years [8]

Men
1971-1974
1976-1980
1988-1994
1999-2000
Difference
Calories
2450
2439
2666
2618
+6.9%
Fat (%)
36.9
36.8
33.9
32.8
-11.1%
SFA (%)
13.5
13.2
11.3
10.9
-19.3%
Fat (g)
100.5
99.7
100.4
95.4
-5.0%
SFA (g)
36.8
35.8
33.5
31.7
-13.7%

Women
1971-1974
1976-1980
1988-1994
1999-2000
Difference
Calories
1542
1522
1798
1877
+21.7%
Fat (%)
36.1
36
33.4
32.8
-9.1%
SFA (%)
13.0
12.5
11.2
11.0
-15.4%
Fat (g)
61.9
60.9
66.7
68.4
+10.6%
SFA (g)
22.3
21.1
22.4
22.9
+3.0%

USDA Food Supply Data

The USDA’s document Nutrient Content of the U.S. Food Supply, 1909-2000 suggests that SFA intake between 1950-1959 and 1960-1969 was 16.0% and 15.7% respectively, which decreased to a little over 12% at the end of 20th century.  This method overestimates food intake (on average, Americans do not consume 3500-3900 calories and over 20g of fibre) but would be more accurate at measuring nutrients as a percentage of total calories (although this data suggests protein intake was between 10-12% of total calories, whereas it’s probably closer to 15-18%) [9].  (Graph on the left is SFA intake in %, graph on the right is SFA intake in grams)


The Diet Heart Trials

In the diet heart trials the control diet was designed to be very similar to the standard diet served at the institutions or the one that the participants regularly consumed.  So the SFA intake of the participants at baseline and/or of those in the control group may reflect SFA intakes of the time

This is would be especially true of the National Diet Heart Study (NDHS), where the researchers also aimed for their control group (group D) to have an intake of SFA of 16-18% that was similar to the national average and cited research that investigated SFA intake.  Unlike the other trials, they created foods to meet this target, but didn’t achieve it, so I’m using the target intake instead.  At baseline the participants reported a SFA intake of 15.6%, but they were likely more health conscious as a lower proportion of the participants were smokers [10]

Trial
Year
Country
SFA in Control Diet
NDHS
1962-1964
United States
16-18%
LAVAT
1959-1968
United States
16.4%
SDHS
1966-1973
Australia
13.5%*
FMHS
1959-1971
Finland
17.2%
MCS
1968-1973
United States
18.3%
DART
1983-1989
United Kingdom
14.9%
STARS
1987-1990?
United Kingdom
17.1%
* The participants in the control group of SDHS were allowed to use high PUFA margarines/oils if they wished, and many did.  As such, the control group reported a high intake of PUFA (8.9%).  Because the control group in SDHS made some dietary changes, it’s probably more appropriate to look at the participants’ baseline intake of SFA which was 16.4% in the experimental group and 15.9% in the control group.

The Seven Countries Study

In 1958-1964, the ‘US railroad’ cohort in the Seven Countries Study reported consuming 125.9g of fat (49.6% TC), 55.3g of SFA (21.8% TC) and 582 mg cholesterol [11], but whether this N of 30 accurately reflects the US average is quite debatable seeing as it’s a much higher figure than the USDA food supply data and the diet heart trials.

Summary 

It appears that the relative intake of SFA was approximately 16-17% of total calories during the mid-20th century and has declined to a little over 10%, a decrease of approximately one third (absolute intake of SFA (grams/day) have decreased to a lesser extent due to an increase in calories).  However, I think these values underestimate the change in consumer choices/purchases over the last ~50-60 years, as animal fats have been replaced by plant fats, due to large reductions in the intake of butter, full fat dairy, lard, lamb and eggs and an massive increase in vegetable oils [5] [9].  This is because food sources of fat contain a mix of SFA, MUFA and PUFA.  So a hypothetical 50% decrease in foods high in SFA would not decrease SFA intake by as much as 50%

5 comments:

  1. Excellent stuff Steve.
    Here's an Australian study showing declining levels of atherogenic pollutants.

    Bua Q, MacLeod M, Fiona Wong F, et al. Historical intake and elimination of polychlorinated biphenyls and organochlorine pesticides by the Australian population reconstructed from biomonitoring data. Environment International
    2015; 74:82–88

    http://tinyurl.com/m5a298m

    It models trends back to 1975, showing a steady decline, but doesn't seem like the last word, seems designed as proof of method for future historical reconstruction.

    There's also this hypothesis by Zeliger, who is all over this issue;

    Zeliger HI. Lipophilic chemical exposure as a cause of cardiovascular disease. Interdiscip Toxicol 2013; 6:55–62.

    And this for BPA - which is the modern, milder version of the old POPs.

    https://www.facebook.com/photo.php?fbid=964833970215420

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    1. Thanks George. It's unfortunately quite an under appreciated topic. I wouldn't be surprised if in 30-50 years time we looked in horror at the some of the practices and standards we have today related to environmental toxins

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  2. Better link to full BPA review here:

    http://onlinelibrary.wiley.com/doi/10.1111/jch.12568/full

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  3. I had to turn back to this post after looking at the subgroup analysis in Hopper 2015.
    Benefit from SFA reduction (in events only) is only seen in studies that increased PUFA, and is not seen in studies published after 2000.
    The big 2000s study is WHI.
    Baseline PUFA in WHI was 7.8%E. Intervention reduced fat, but didn't go below 5%E PUFA.
    Whereas no doubt in a 60s trial baseline PUFA would have been near that 2.79%, and the interventions would have cleared the 5%.
    So we reach a state today where it would require very good compliance with an unusually restrictive diet to get "controls" like the controls in the 60's and 70's with regard to PUFAs; in fact, today it's lowering PUFA that has to be the "intervention".

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    Replies
    1. The SFA>PUFA trials actually had really high PUFA intakes:
      Rose = at least 15.2%
      LA vets = 15.6%
      MRCT = unknown but P:S ratio of 1.8 (so probably ~14-18%)
      Oslo = 20.6%
      Sydney = 15.1%
      Finnish = 12.7%
      Minnesota = 14.7%
      DART = 9.7%
      STARS = 7.3%
      And average PUFA in the control groups was ~5%, which is consistent with average US consumption at the time
      http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3076650/

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