Nina Teicholz and The Nutrition Coalition: going to bat for good science, yet again. Seems comprehensive to me.
https://www.nutritioncoalition.us/saturated-fats-do-they-cause-heart-disease
Saturated fats: do they cause heart disease? — The Nutrition Coalition
CFLBob
(Central Florida Bob )
#4
Something that stands out to me is that they lump all fatty acids as just SFA or PUFA. They claim there’s evidence that PUFAs reduce total CVD risk, but neglect the whole Omega 3 vs Omega 6 discussion; the papers usually don’t make a distinction between populations eating salmon or grass-fed cattle vs. industrial seed oils and the few papers that mention omega 3 vs. 6 don’t see a difference between them.
ctviggen
(Bob M)
#5
I think you are correct.
The other thing they do is make statements like “switching from Sat Fat to PUFAs will DO SOMETHING GOOD”, where that “something” is usually reduce heart disease. The problem is that’s not what they did. In other words, they did not run an RCT where they replaced saturated fats with PUFAs. Instead, this is theoretical, typically based on food frequency questionnaires. That is, people who (supposedly) ate more PUFAs experienced less heart disease, and people who (supposedly) ate more saturated fat experienced more heart disease. So, they THEORIZE that replacing saturated fat with PUFAs is a good thing, but they drop the “theorize”.
CFLBob
(Central Florida Bob )
#6
And not just that, but they don’t control for anything else - that I can tell.
So if the people they’re questioning decided to start reducing their sat fats and “eating better” (by the Pyramid), they may have also decided to start exercising or doing any other “healthy lifestyle” recommendations, too. They don’t account for that. Real RCTs are required for that, and like you say, very few of those are RCTs.
ctviggen
(Bob M)
#7
What really bothers me, too, is that I was analyzing a study put out by the Harvard School of Crapidemiology, and they used food frequency questionnaires (FFQs) every FOUR YEARS. Four freaking years. Not yearly. Not quarterly (so you get food changes with seasons). Four years.
Even if I could accurately tell you what I eat today, there is no way I could remember what I ate over the course of four years. Consider today. Last week, I ate three eggs with every “lunch” (my first meal of two meals). This week, I have not had any eggs. I don’t remember how many eggs I ate two or three weeks ago, let alone over 4 years. Also, just in the last two years, I’ve experimented with higher protein and lower fat, and now very high saturated fat. And this is what I remember I’ve done. I know that at times in the past, I tried to eat Paleo. I also tried Whole 30. I’ve tried eating no dairy; some dairy; a lot of dairy. Some fish; no fish. Some red meat; lots of red meat. Bacon; no bacon. I’ve been moving slowly toward eating all animal foods, but I still eat some plants. How many times I week do I eat a certain vegetable? Some, none. For the ones I do eat, I have no idea.
For anyone to base anything on FFQs spaced 4 years apart (and I’ve seen them start at “zero” and give two FFQs spaced 10 years apart and end data analysis at 30 years), is to me, ludicrous. Yet they do this all the time.
atomicspacebunny
(Bunny)
#8
So true and it seems like refined sugars has a lot to do with it also? And micro nutrients like B-6 and its water solubility and Vitamin K-1 and K-2 and D.
The study below focuses on brain development but I like the RTC explanation also:
Background: Nutrition is one of many factors that affect brain development and functioning, and in recent years the role of certain nutrients has been investigated. B vitamins and n–3 polyunsaturated fatty acids (PUFA) are two of the most promising and widely studied nutritional factors. Methods: In this review, we provide an overview of human studies published before August 2011 on how vitamin B6, folate, vitamin B12and n–3 PUFA may affect the brain, their nutrient status and the existing evidence for an association between these nutrients and brain development, brain functioning and depression during different stages of the life cycle. Results: No recommendation can be given regarding a role of B vitamins, either because the number of studies on B vitamins is too limited (pregnant and lactating women and children) or the studies are not consistent (adults and elderly). For n–3 PUFA, observational evidence may be suggestive of a beneficial effect; however, this has not yet been sufficiently replicated in randomized controlled trials (RCTs). Conclusions: We found that the existing evidence from observational studies as well as RCTs is generally too limited and contradictory to draw firm conclusions. More research is needed, particularly a combination of good-quality long-term prospective studies and well-designed RCTs. …” …More
Footnotes:
[1] “…These data suggest that B-6 deficiencies impair the metabolism of (n-3) PUFA from alpha-linolenic acid to EPA and DHA with the most pronounced reduction in the production of DHA. …” …More
[2] “…The influence of vitamin B6 on fatty acids content in serum and liver of rats receiving low protein diets was studied. Addition of B6 decreased linoleic acid (LA) and increased alpha-linolenic acid (ALA)…” …More
[3] “…Intake of Fish Oil, Oleic Acid, Folic Acid, and Vitamins B-6 and E for 1 Year Decreases Plasma C-Reactive Protein and Reduces Coronary Heart Disease Risk Factors in Male Patients in a Cardiac Rehabilitation Program…” …More
[4] “…The predictive powers of a cholesterol test only go so far. If your LDL is low, your C-reactive protein may be a better sign of impending heart trouble. …” …More
[5] Although humans and other mammals can synthesize saturated fatty acids and some monounsaturated fatty acids from carbon groups in carbohydrates and proteins, they lack the delta (Δ) 12 and Δ15 desaturase enzymes necessary to insert a cis double bond at the n-6 or the n-3 position of a fatty acid (1). Consequently, omega-6 and omega-3 fatty acids are essential nutrients. The parent fatty acid of the omega-6 series is linoleic acid (LA; 18:2n-6), and the parent fatty acid of the omega-3 series is ALA ( Figure 2 and Table 1 ). Humans can synthesize long-chain (20 carbons or more) omega-6 fatty acids, such as dihomo-γ-linolenic acid (DGLA; 20:3n-6) and arachidonic acid (AA; 20:4n-6), from LA and long-chain omega-3 fatty acids, such as eicosapentaenoic acid (EPA; 20:5n-3) and docosahexaenoic acid (DHA; 22:6n-3), from ALA (see Metabolism and Bioavailability). …More
[6] “…The desaturase enzymes show preference for the different series of fatty acids in the following order: omega-3 > omega-6 > omega-9. Consequently, synthesis of the omega-9 fatty acid eicosatrienoic acid (20:3n-9, mead acid, or 5,8,11-eicosatrienoic acid) increases only when dietary intakes of omega-3 and omega-6 fatty acids are very low; therefore, mead acid is one marker of essential fatty acid deficiency (36). A plasma eicosatrienoic acid:arachidonic acid (triene:tetraene) ratio greater than 0.2 is generally considered indicative of essential fatty acid deficiency (35, 37). In patients who were given total parenteral nutrition containing fat-free, glucose-amino acid mixtures, biochemical signs of essential fatty acid deficiency developed in as little as 7 to 10 days (38). In these cases, the continuous glucose infusion resulted in high circulating insulin concentrations, which inhibited the release of essential fatty acids stored in adipose tissue. When glucose-free amino acid solutions were used, parenteral nutrition up to 14 days did not result in biochemical signs of essential fatty acid deficiency. Essential fatty acid deficiency has also been found to occur in patients with chronic fat malabsorption (39) and in patients with cystic fibrosis (40). It has been proposed that essential fatty acid deficiency may play a role in the pathology of protein-energy malnutrition (36). …” …More
