Chowdhury et al, More forests & more trees and more "Eureka!" moments with cheese.

Like Siri-Tarino et al, Forests & Trees and "Eureka!" moments, Chowdhury et al is a meta-analysis of many studies. See Association of dietary, circulating, and supplement fatty acids with coronary risk: a systematic review and meta-analysis. I don't have access to the full study, but Google Image Search found Figure 2.

From https://annals.org/data/Journals/AIM/929862/6ff2_Figure_2_RRs_for_coronary_outcomes_in_prospective_cohort_studies_of_circulating_fatty_acid.jpeg

All saturated fatty acids have a RR for CHD of 1.06 (95% CI 0.86 - 1.30).
∴ There's no association between saturated fat intake and the RR for CHD.

Before LCHF'ers do a dance of joy, consider the Forest plot for individual saturated fatty acids.
Palmitic acid has a RR for CHD of 1.15 (95% CI 0.96 - 1.37).
Stearic acid has a RR for CHD of 1.23 (95% CI 0.93 - 1.61).

Red meat & saturated fats synthesised by DNL aren't looking too good. However...
Pentadecanoic acid has a RR for CHD of 0.94 (95% CI 0.67 - 1.32).
Margaric acid has a RR for CHD of 0.77 (95% CI 0.63 - 0.93).
Pentadecanoic acid and Margaric acid combined have a RR for CHD of 0.81 (95% CI 0.62 - 1.06).

See Differences in the prospective association between individual plasma phospholipid saturated fatty acids and incident type 2 diabetes: the EPIC-InterAct case-cohort study.

The above study is about T2DM not CHD, but Dietary intake of saturated fat by food source and incident cardiovascular disease: the Multi-Ethnic Study of Atherosclerosis shows that small amounts (5-10g/day) of dairy SFAs are protective against CHD, possibly due to the Vitamin K2 content.

Of the omega-3 fatty acids...
Eicosapentaenoic acid has a RR for CHD of 0.78 (95% CI 0.65 - 0.94).
Docosahexaenoic acid has a RR for CHD of 0.79 (95% CI 0.67 - 0.93).
Eicosapentaenoic acid and Docosahexaenoic acid combined have a RR for CHD of 0.75 (95% CI 0.62 - 0.89).

Of the omega-6 fatty acids...
Arachidonic acid has a RR for CHD of 0.83 (95% CI 0.74 - 0.92).

Of the trans-fatty acids...
Trans-oleic acid has a RR for CHD of 1.20 (95% CI 0.39 - 3.73).
Trans-linoleic acid has a RR for CHD of 1.36 (95% CI 0.83 - 2.22).

Siri-Tarino et al, Forests & Trees and "Eureka!" moments.

Here's Fig. 2 from Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease:-

Risk ratios and 95% CIs for fully adjusted random-effects models examining associations between saturated fat intake in relation to coronary heart disease and stroke.

The above "Forest" plot has a subtotal RR of 1.07 (95% CI 0.96 1.19). The overall conclusion is that there's no association between saturated fat intake and the RR for CHD. Hmmm.

I looked at the data in Table 3. Of the 16 studies contributing to the CHD results, only 3 of them specify high sat fat intakes over a wide range. The results from these 3 studies are as follows:-

Pietinen et al: RR=0.93 (95% CI 0.6, 1.44).
Mann et al: RR=2.77 (95% CI 1.25, 6.13).
Boniface et al: Pooled RR = 1.37 (95% CI 1.17, 1.65).

The results from Pietinen et al are statistically-insignificant (95% CI values are way above & below 1) with an overall slight protective effect. The results from Mann et al have a RR >> 1 with both 95% CI's >1 and the results from Boniface et al have a RR >1 with both 95% CI's >1.

Other studies either have sat fat intakes varying from very low to low, or specify mean/median sat fat intakes without values for highest & lowest tertiles/quartiles/quintiles etc. Other studies have results that are statistically-insignificant.

However, there are some studies that show a slight protective effect of small amounts of sat fats. How come?

Thanks to George Henderson, I had a "Eureka!" moment. He posted a link to Dietary intake of saturated fat by food source and incident cardiovascular disease: the Multi-Ethnic Study of Atherosclerosis.

Here's Fig. 1 from that study.

HRs and 95% CI's of CVD risk according to quintiles of energy-adjusted SF from different sources (n = 5209).

The Meat SF plot has a net positive slope (bad news, but the range of intake is very small), the Butter & Plant SF plots are random, but the Dairy SF plot has a net negative slope (good news). Dairy saturated fats in amounts of up to 10g/day are protective against CHD. As the Dairy sat fat intake is too small to have a significant effect on lipids, what's the mechanism? I think that it's Vitamin K2. See Chowdhury et al, More forests & more trees and more "Eureka!" moments with cheese.

When you average out the results from all studies, the result is null. This is data dilution statistics.

EDIT: See also Study: Saturated Fat as Bad as Sugar!

Ban Butter, Part 4,400?

By the time I've finished typing this, there will probably be over 4,400 blogs containing the phrase "Ban Butter". I'm not going to call Shyam Kolvekar rude names. He's a heart surgeon so he's probably very good at cutting people's chests open, removing clogged coronary arteries and grafting in veins removed from legs or whatever it is they do. I don't really wanna know!

He obviously doesn't read our blogs, or he wouldn't have said what he did. If he didn't get any money from Unilever for saying it, that's rather foolish. If I'm going to risk being called every rude name under the sun, I want it to be worth my while.

Anyway, in case you missed it, here's Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease.

See also Fats and Fatty Acids in Human Nutrition and specifically Dietary Fat and Coronary Heart Disease: Summary of Evidence from Prospective Cohort and Randomised Controlled Trials.

I personally use Anchor Spreadable (kept in the 'fridge) or Anchor/Kerrygold (kept out of the 'fridge) as they're from grass-fed cows.

Finally, for a little light relief, see Butter vs Margarine.

Update: From Hartke Is Online!

I have a hypothesis.

I was keeping quiet about this, as it contradicts Gary Taubes, Michael R Eades & Richard D Feinman and Eugene J Fine.

Please note: This post is not criticising low-carb, high-fat diets. I'm pointing out that if someone on a low-carb, high-fat diet exercises as much gluttony as they want on roast lamb/pork/duck etc, they may not lose as much weight/body fat as they expected & they may even gain.

I don't want to start a shit-storm, but as I am in the "a calorie is a calorie" (when it comes to weight gain/loss) camp and a lot of the people whose blogs I link to aren't, I need to go public. So, here it is, copied and pasted from the comments section of Diet, Carbs, Fat and Weight Loss, corrected for spelling.

"I would like to propose a theory which explains how fat cells can acquire glucose (& thus correct a deficiency in glycerol-3-phosphate) even when serum insulin level is basal.

Consider muscle cells undergoing anaerobic activity:-

Anaerobic activity is very inefficient and uses pyruvate at a very rapid rate. A deficiency in pyruvate up-regulates all of the up-stream processes, including Glu-T4 transporters so as to maximise pyruvate production.

This explains why resistance training with weights greatly increases muscular insulin sensitivity and why resistance training with weights when depleted of muscle glycogen can cause precipitous drops in blood glucose level.

Ditto for glycerol-3-phosphate in fat cells. In this case, blood glucose level is maintained by the liver & kidneys, which convert the glycerol backbone of triacylglycerols (fats) and other substrates such as lactate, pyruvate & glucogenic amino acids into glucose."

In plain terms what this means is that, like muscle cells, fat cells can acquire as much glucose as they need, independently of carbohydrate intake.

Therefore, if an excess (beyond what the body is burning) of dietary fat is eaten, this can be stored in fat cells even if serum insulin level does not increase.

There. I've said it. I expect comments. Moderation is enabled. All comments that are free from ad-hominem, straw men & other logical fallacies will be published.

EDIT: Here's evidence that dietary fat can be stored in the absence of dietary carbohydrate. It involves doing maths on an Oral Fat Tolerance Test:- On burning, storing and recomposing.

EDIT: Here's evidence that a calorie is a calorie (where weight change is concerned):- Bray et al shows that a calorie *is* a calorie (where weight change is concerned).
 
As a lot of people report that they can eat dietary fat without getting fat (& actually getting lighter & slimmer), there appears to be something "magical" going on. It's generally accepted that fat is the least thermogenic of all the macronutrients & protein is the most thermogenic. I wonder if this is the case for all types of fat and all types of people.

See Butyric Acid: an Ancient Controller of Metabolism, Inflammation and Stress Resistance.

From Battle of the Weight Loss Diets: Who's Winning (at losing):-
Insulin Resistant people lose more weight on low-carb, high-fat (LCHF) diets than high-carb, low-fat (HCLF) diets.  
Insulin Sensitive people lose more weight on high-carb, low-fat (HCLF) diets than low-carb, high-fat (LCHF) diets.

According to Gary Taubes's Carbohydrate Insulin Hypothesis, everyone should lose more weight on low-carb, high-fat (LCHF) diets than on high-carb, low-fat (HCLF) diets. Therefore, Gary Taubes's Carbohydrate Insulin Hypothesis is false.

It's possible that in people who do well on LCHF diets, kcals out on the right hand side of the Energy Balance Equation increase significantly. So keep on keeping on.

EDIT: With the benefit of four more years of knowledge, here's why LCHF & ketogenic diets have an advantage for people who have Insulin Resistance. How low-carbohydrate diets result in more weight loss than high-carbohydrate diets for people with Insulin Resistance or Type 2 Diabetes.

See also:-
Metabolic Advantage of Ketogenic Diets Debunked? An Intriguing Study You Will Want to Read
Is the Fable of Unfettered Fat Burning Derailing Your Low Carb Diet?

See also How stuff works & Enzymes.