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Wellness Wednesday for April 17, 2024

The Wednesday Wellness threads are meant to encourage users to ask for and provide advice and motivation to improve their lives. It isn't intended as a 'containment thread' and any content which could go here could instead be posted in its own thread. You could post:

  • Requests for advice and / or encouragement. On basically any topic and for any scale of problem.

  • Updates to let us know how you are doing. This provides valuable feedback on past advice / encouragement and will hopefully make people feel a little more motivated to follow through. If you want to be reminded to post your update, see the post titled 'update reminders', below.

  • Advice. This can be in response to a request for advice or just something that you think could be generally useful for many people here.

  • Encouragement. Probably best directed at specific users, but if you feel like just encouraging people in general I don't think anyone is going to object. I don't think I really need to say this, but just to be clear; encouragement should have a generally positive tone and not shame people (if people feel that shame might be an effective tool for motivating people, please discuss this so we can form a group consensus on how to use it rather than just trying it).

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This leads to farces like "Learning and Memory Impairment in Rats Fed a High Saturated Fat Diet" They analyze the fatty acid composition of their lard and it is only 30% saturated. Despite this, the study uses lard as their Saturated fat intervention.

You can hardly hold this random rat study against me.

I encourage you to check the studies in the meta and see that this is not going on.

Specific to Hooper et al. (2020) that your linked article uses for it's argument, I am looking at their studies and am having trouble finding which showed a benefit from substituting polyunsaturated fat with saturated fats.

Review says:

Eleven RCTs (11 comparisons) assessed SFA intake during the study period and showed that SFA intake in the intervention arm was statistically significantly lower than that in the control arm (Black 1994; DART 1989; Ley 2004; Moy 2001; Oxford Retinopathy 1978; Simon 1997; STARS 1992; Sydney Diet‐Heart 1978; Veterans Admin 1969; WHI 2006; WINS 2006).

...

There was a 21% reduction in cardiovascular events in people who had reduced SFA compared with those on higher SFA (RR 0.79, 95% CI 0.66 to 0.93, I² = 65%, 11 RCTs, 53,300 participants, 4476 people with cardiovascular events, Peffect = 0.006, Analysis 1.35). This protective effect was confirmed in sensitivity analyses including only trials at low summary risk of bias (Analysis 1.36), that aimed to reduce saturated fat (Analysis 1.37), that significantly reduced saturated fat intake (Analysis 1.38), that achieved a reduction in total or LDL cholesterol (Analysis 1.39), or excluding the largest trial (WHI 2006, Analysis 1.40).

Table 4 additionally shows that reducing total fat has no impact on cardiovascular events.

However, the figure in question still shows that when dietary saturated fat reaches >12% of calories, markers improve! Risk of Stroke goes way down. CVD goes down.

It would be a big surprise indeed if a moderate amount of saturated fat is bad, but a small or large amount is good. The relationship is most likely to be linear.

Weight isn't studied in the Meta-analysis at all.

It was, of course.

There was evidence that reducing SFA intake resulted in small reductions in body weight (MD ‐1.97 kg, 95% CI ‐3.67 to ‐0.27, I² = 72%, 6 RCTs, 4541 participants, Analysis 4.3), and body mass index (MD ‐0.50, 95% CI ‐0.82 to ‐0.19, I² = 55%, 6 RCTs, 5553 participants, Analysis 4.4).

How much protein do you need?

This appears to be a study on untrained men? I agree that if you're okay with the average untrained physique, 44g is enough (and also not that far from the recommendation of 54g for a 150lb person).

Isoleucine and valine are specifically the Amino Acids that are problematic, but really to avoid them you need to avoid protein.

Most of these are mouse studies, so let's look at the first one.

The restricted protein group in this study was eating protein at the RDA of 0.8 g/kg, which again is fine for people without aspirations to build muscle (which doesn't apply to OP).

The study doesn't seem to report if the change in weight loss between PR and CR is significant or not. However, looking at figure 1, id suspect not, especially when removing the 300 pound guy in the PR group.

As far as metabolism goes, figure 2 shows that the CR had a much lower metabolic rate at baseline vs the PR group, so the randomization seems to have failed. The PR group's variance is way bigger too, perhaps due to the aforementioned outliers.

Here's a more sophisticated metabolic ward study with three isocaloric overfeeding diets with varying protein content. They're using dexa scans, CO2 respiration rate, and doubly labeled water to measure body comp, resting energy expenditure and total energy expenditure, which are gold standard methods.

https://jamanetwork.com/journals/jama/fullarticle/1103993

Overeating led to a significant increase in resting energy expenditure in both the normal and high protein groups. This increase occurred mainly in the first 2 to 4 weeks and the slopes of the regression lines were not significantly different from each other (Figure 4). In contrast, resting energy expenditure in the low protein group did not change significantly with overfeeding, and the slope of the regression line was not different from 0, but was significantly less than the other 2 groups (P < .001; Figure 4).

The metabolic efficiency of weight gain (defined as the excess energy intake divided by weight gain5) was significantly higher in the low protein group (75.1 MJ/kg [95% CI, 54.1-96.0 MJ/kg]) than in the high protein group (38.0 MJ/kg [95% CI, 18.6-60.5 MJ/kg]; P = .04).

Lean body mass decreased during the overeating period by −0.70 kg (95% CI, −1.50 to 0.10 kg) in the low protein diet group compared with a gain of 2.87 kg (95% CI, 2.11 to 3.62 kg) in the normal protein diet group and 3.18 kg (95% CI, 2.37 to 3.98 kg) in the high protein diet group (P < .001).

Overall, higher protein intake is more favorable for body composition (holding calories equal), and increased metabolism more than lower protein intake.

Are we looking at the same Hooper study? It's funny how we can both look at it and zoom on different things:

We found little or no effect of reducing saturated fat on all‐cause mortality (RR 0.96; 95% CI 0.90 to 1.03; 11 trials, 55,858 participants) or cardiovascular mortality (RR 0.95; 95% CI 0.80 to 1.12, 10 trials, 53,421 participants), both with GRADE moderate‐quality evidence.

...

There was little or no effect of reducing saturated fats on non‐fatal myocardial infarction (RR 0.97, 95% CI 0.87 to 1.07) or CHD mortality (RR 0.97, 95% CI 0.82 to 1.16, both low‐quality evidence), but effects on total (fatal or non‐fatal) myocardial infarction, stroke and CHD events (fatal or non‐fatal) were all unclear as the evidence was of very low quality. There was little or no effect on cancer mortality, cancer diagnoses, diabetes diagnosis, HDL cholesterol, serum triglycerides or blood pressure, and small reductions in weight, serum total cholesterol, LDL cholesterol and BMI. There was no evidence of harmful effects of reducing saturated fat intakes.

I looked through a few of the studies they reviewed but most don't really demonstrate a low PUFA/high Sat Fat diet anywhere.

The Black Study reduced fat entirely (not substituting PUFA for Sat fat) and found that keeping fat under 20% of calories helped reduce skin cancer.

The DART Study advised men to increase ratio of PUFA to SFA, but: "The advice on fat was not associated with any difference in mortality." Men who were advised to eat fatty fish did better, but I'm open to the idea that it's the O3:O6 ratio that matters, meaning increasing O3 might be beneficial to people (especially in the context of a high O6 diet).

Then we get to the Houtsmuller study, which look like it's going to actually address the PUFA thesis. Two groups of people fed a controlled diet, one diet has 4x as much Linoleic acid as the other. Sounds good. He doesn't give a lot of details about what is in each diets how he assessed the Linoleic acid quantity in the study. But let's take him for his word. There are a couple details that stand out to me:

First is, "The linolcic acid content of diet II was 4 times that of diet I, being 20.4 gr/1000 kcal for group II and 5.3 gr/1000 Kcal for group I."

According to the PUFA hypothesis, it's more like a cliff than a gradient. Humans naturally eat around 4-5 gr a day of PUFA without seed-oil or mono-gastric animal sources. This study has the Sat Fat group get twice that.

The other detail is they mention one of the sources of Sat Fat, "except for 4 patients of group I who preferred butter over saturated margarines." The Sat Fat group's intervention included getting fed partially-hydrogenated margarine. Which means lots of transfats. The negative effect this study found can possibly be explained by the amount of transfats in the Sat Fat arm of the study.

I'll admit I didn't check every study, but the ones I checked aren't really applicable to anything I'm concerned about. The only one I saw that clearly substituted Linoleic Acid for actual Sat Fat was the Sydney Study, which showed that substituting Margarine for Butter actually increased risk of Cardiovascular disease.

That said, the Sydney study Margarine probably had transfats. I'm not going to state that the Sydney study proves Sat Fat is the best, but it does support my primary point, which is that nutritional studies on fats are Terrible, do not account for common confounders, and a meta-analysis of a bunch of terrible studies does not make for good data.

which again is fine for people without aspirations to build muscle (which doesn't apply to OP).

I'm talking about OP's wife. OP seems to want his wife to become slimmer, not a body builder. I'm indicating that to lose weight might require cutting protein down to the bare minimum (around 50g), something that is left out of a lot of advice. Losing lean mass when losing weight can actually be quite good, as you don't want a lot of extra skin hanging around.

Yeah, the meta shows no effect on all cause mortality - but that's not the question we're discussing. I only brought it up since you responded to the graph of mortality outcomes rather than weight outcomes.

To stop gaining weight, decrease mono-unsaturated and poly-unsaturated fat.

In fact, the meta shows that substituting unsaturated for saturated fats reduces weight and there's no association If the studies were actually controlled metabolic ward studies, they'd probably show no effect with isocaloric diets.

According to the PUFA hypothesis, it's more like a cliff than a gradient. Humans naturally eat around 4-5 gr a day of PUFA without seed-oil or mono-gastric animal sources. This study has the Sat Fat group get twice that.

This seems like an extremely specific and unusual claim, perhaps a result of undeniable studies chipping away at the upper limits of what people can defend. We definitely shouldn't privilege weird rat studies over human ones to defend this claim. Linear relationships should be the default assumption.

Losing lean mass when losing weight can actually be quite good, as you don't want a lot of extra skin hanging around.

The lean mass lost is not skin, it's internal organs, muscle mass, water weight, etc. The amount of skin remaining after weight loss does not depend on the diet.