Full-fat dairy

Page 451 of the Scientific Report of the 2015 Dietary Guidelines Advisory Committee:

Numerous RCTs have demonstrated that saturated fat (SFA) as compared to mono- (MUFA) or polyunsaturated fats (PUFA) or carbohydrates increases total and LDL cholesterol. Thus, limiting saturated fat consumption has been a longstanding dietary recommendation to reduce risk of CVD.

Teleoanalysis at its best. If I cannot prove A causes C, but I know A causes B and B causes C then I conclude A causes C. The problem here is confusing statistical correlation with Aristotle's logic where the previous conclusion is right. We usually have that A (saturated fat) sometimes causes B (high cholesterol) and B sometimes causes C (CVD). Moreover there are both other causes of B (more below) and other causes of C (people suffer heart attacks with low cholesterol too, doi: 10.1016/j.ahj.2008.08.010). So, we cannot know if A sometimes causes C without checking it directly.

I don't see the point of focusing on CVD instead of overall mortality either. I am not alone. Summary of Chapter 1 from Towards a Paradigm Shift In Cholesterol Treatment (doi: 10.1159/000381654, via Petro, my bolds):

All-cause mortality is the most appropriate outcome to use when investigating risk factors for life- threatening disease. Section 1 discusses all-cause mortality according to cholesterol levels, as determined by large epidemiological studies in Japan. Overall, an inverse trend is found between all-cause mortality and total (or low density lipoprotein [LDL]) cholesterol levels: mortality is highest in the lowest cholesterol group without exception. If limited to elderly people, this trend is universal. As discussed in Section 2, elderly people with the highest cholesterol levels have the highest survival rates irrespective of where they live in the world.

Well, the rest of the summary was unrelated but highly interesting anyway.

There are several factors giving rise to high blood cholesterol. Some of them are tobacco (doi: 10.1016/0002-8703(91)90967-M), hyperinsulinemia (doi: 10.1155/2014/925650, via Ivor) and saturated fat (doi: 10.1136/bmj.314.7074.112). Thinking that an equal amount due to any one of those causes is going to have the same health consequences is naïve at best.

From Cochrane's Reduced or modified dietary fat for preventing cardiovascular disease (doi:  10.1002/14651858.CD002137.pub2, my bolds):

This updated review suggested that reducing saturated fat by reducing and/or modifying dietary fat reduced the risk of cardiovascular events by 14% (RR 0.86, 95% CI 0.77 to 0.96, 24 comparisons, 65,508 participants of whom 7% had a cardiovascular event, I2 50%). Subgrouping suggested that this reduction in cardiovascular events was seen in studies of fat modification (not reduction - which related directly to the degree of effect on serum total and LDL cholesterol and triglycerides), of at least two years duration and in studies of men (not of women). There were no clear effects of dietary fat changes on total mortality (RR 0.98, 95% CI 0.93 to 1.04, 71,790 participants) or cardiovascular mortality (RR 0.94, 95% CI 0.85 to 1.04, 65,978 participants). This did not alter with sub-grouping or sensitivity analysis.

Since my saturated fat intake comes mostly from full-fat dairy (butter and hard cheeses) I am interested in its particular effects.

About its effect on cardiovascular disease must suffice. Two excerpts from Dairy and Cardiovascular Disease: A Review of Recent Observational Research (doi: 10.1007/s13668-014-0076-4, my bolds):

In a prospective study of Swedish adults, total dairy consumption defined as milk, cheese, cream, and butter, collected from a diet history questionnaire, was associated with a 12 % decreased incidence of CVD (HR = 0.88; 95 % CI: 0.77, 1.02, P = 0.05), defined as incidence of fatal or non-fatal heart attack or stroke [20]. When specific dairy foods were examined, this result was attributable to the consumption of fermented milk, in which the highest (~ 200–300 g/day) versus lowest (0 g/day) intake was associated with a 15 % reduced incidence of CVD (HR = 0.85, 95 % CI: 5 – 24 %, P = 0.03) [20]. Neither milk (full-fat or low-fat) nor butter was associated with incidence of CVD in this study [20]. The findings from this study are important for several reasons: they were obtained by utilizing a reliable method of determining food intake, they were reported from fully adjusted models, and they differentiated between dairy foods and their relationship with the incidence of CVD. A prospective study of Swedish adults observing women only demonstrated that the highest (8.4 servings per day) versus lowest (2.2 servings per day) quintile of total dairy food intake, defined as milk (all fat varieties), cultured milk/yogurt, cheese, cream/crème fraiche, and butter (in cooking, on bread, and both) was associated with a 23 % decreased incidence of myocardial infarction (MI), commonly referred to as heart attack (HR = 0.77, 95 % CIL 0.63, 0.95, P < 0.05) [21]. When specific dairy foods were examined, a 26 % decreased incidence of MI (HR = 0.74;–95 % CI: 0.60, 0.91, P = 0.006) was observed in the highest versus lowest quintile of cheese intake, with the highest versus lowest quartile of full-fat cheese associated with a 17 % decreased incidence of MI (HR = 0.83; 95 % CI: 0.68, 1.01, P = 0.035) [21]. Researchers also investigated the relationship of butter in cooking versus used on bread, observing a 34 % increased incidence of MI in women who used butter on bread but not in cooking, a result not attenuated by adjustments for oil and margarine use in cooking [21].

Some studies have used 15:0 and 17:0 fatty acids, which are exogenous fatty acids that serve as biomarkers of dairy fat intake, to examine the effect of full-fat dairy consumption on risk of MI. There was no association between full-fat dairy intake and MI among Costa Rican adults from a prospective case–control study that utilized adipose 15:0 and 17:0 fatty acids alongside FFQ to determine consumption of full-fat dairy (defined as butter, buttermilk, cheese, cream, ice cream, butter/margarine mix, milk [whole and semi-slimmed], and yogurt) among participants [27]. Similarly, no significant association between full-fat dairy intake and MI was detected in a prospective study of Swedish adults in which full-fat dairy consumption, (including cream, cheese, butter, fermented products, milk, and ice cream) was assessed by serum 15:0 and 17:0 fatty acids in combination with FFQ [27]. In this study, however, data from the serum fatty acid biomarkers indicated a 26 % reduced risk for first MI associated with full-fat dairy consumption in women [28]. When specific dairy foods were examined, the highest (> 219 g/day) versus lowest quartile (> 33 g/day) of fermented milk intake was associated with a reduced risk of first MI [28]. Furthermore, there was an interaction observed for cheese, with the highest (~20–24 g/day) versus lowest (~ < 7 g/day) quartile of reported intake associated with a reduced risk of first MI in men only [28]. The significance of these findings was attenuated in fully adjusted models, indicating a neutral association between full-fat dairy food intake and first MI in men and women.

Yes, there are those epidemiological studies (based on food-frequency questionnaires) arriving to the opposite conclusion but certainly the evidence is not consistent at all on the deleterious effect of full-fat dairy as expected by its detractors. Still thinking that any cause of high cholesterol is going to have the same cardiovascular consequences under contradictory evidence is wishful thinking. Meddling in people way of eating with this low level of evidence is pure hubris.

Abide to any unsupported longstanding dietary recommendation at your own peril

Addendum: full-fat dairy and weight

From The relationship between high-fat dairy consumption and obesity, cardiovascular, and metabolic disease (doi: 10.1007/s00394-012-0418-1, my bolds):

Results In 11 of 16 studies, high-fat dairy intake was inversely associated with measures of adiposity. Studies examining the relationship between high-fat dairy consumption and metabolic health reported either an inverse or no association. Studies investigating the connection between high-fat dairy intake and diabetes or cardiovascular disease incidence were inconsistent. We discuss factors that may have contributed to the variability between studies, including differences in (1) the potential for residual confounding; (2) the types of high-fat dairy foods.
Conclusions The observational evidence does not support the hypothesis that dairy fat or high-fat dairy foods contribute to obesity or cardiometabolic risk, and suggests that high-fat dairy consumption within typical dietary patterns is inversely associated with obesity risk. Although not conclusive, these findings may provide a rationale for future research into the bioactive properties of dairy fat and the impact of bovine feeding practices on the health effects of dairy fat.

Low Carb Diets and Weight Loss: Long Term

First a personal disclosure. I am on the low carb high fat diet at lower than 150g of carbohydrates most days. I eat more often seafood than red meat. I try to eat as little white meat (with cream) as possible because it approaches tastelessness and it is inferior due to its lower fat content (perhaps I should try duck).

After one year Low Carb advantage vanishes

Well, results of low carb not being clearly superior is likely due to muddying the waters with quite high levels of carbohydrates. In low carb circles the clear limit used for carbohydrates is 150g. That is not an arbitrary number but the estimated amount of glucose that spares protein in full parenteral feeding different than fat, that is, the daily glucose need of our body (ingested or generated de novo from proteins and glycerol) when we are out of ketosis. Beyond this point both fat and glucose have the same sparing effect. Between 150 and 200g is considered moderate in carbohydrates and it is defended by Paul Jaminet for example. Vicente has some blog posts in English commenting upon this misunderstanding in several research papers such as talking about low carb interventions that are not low carb (other and another) or even not so honest reviews and meta-analysis.

[Added on 4/10/2016]
As a matter of fact we can already see the positive effect of a low carb diet at 142g-CHO/day on diabetics even without weight loss in the trial by Gannon & Nuttall.

Of course human beings can thrive at different carbohydrate intake levels. We have Kitavans for example.

Once ill such as with hypertension or diabetes I think low carb high fat should be an approach to check. Feinman et alter^* think it should be the first approach in diabetes management. Not that it is the only one and we have for instance the high carb very low fat rice diet promoted by Kempner back in the day (via Denise Minger) that seems to have reversed diabetes and hypertension too. I am not sure about a too low fat intake effect on our gallbladders though. As a matter of fact the low-carb diet is the one that has been shown to be a good solution to gallbladders stones (via Dr. Eades).

Of course it would be interesting to see the options evaluated on long term studies. Nevertheless its absence doesn't preclude anyone of trying whatever approaches they are attracted to and checking their physiological surrogate markers to them. Dr. Eenfeldt keeps track of those favoring low-carb high-fat.

With respect to body fat loss there are even more strange approaches like the Shangri-La Diet of late Seth Roberts promoting ingestion of flavorless calories (even water with sugar) in order to hack the weight set point. Not that ingesting them as seed oils is safe.

Potential dangers of too low carb

There are those who think (opinion of Paul Jaminet) that too low carbohydrate consumption may have detrimental effects to our health on the long run.

One of these would be a deficit of substrate (the carbohydrate part) for mucin production. Mucin seems to be used by our gut commensal bacteria.

Either way, it will be a good idea to have them in mind if we go too low carb, just in case.

*[Added on 11/7/2023] I am not fond at all of abbreviations and acronyms. I have been trying to use the complete form of et al. but I was using a complete incorrect one as Athaic has pointed out to me recently. Since it is not clear to me if the neutral one (et alia) is correct in every case or not (there are the masculine et alii and femenine et aliae too) I will surrender and will use the abbreviation until I am certain. One inconvenience still persisting will be that it should not be read aloud without using the complete form or translating it simultaneously to English.