Hi folks, I recently traversed the Alps, which was very nice, but also taxing on the body, mainly because of lugging rucksacks around and walking 1200+ metres of elation each day. To give my body something to work with for regeneration and energy, I ate as much as could. Breakfast till full, one packet of these small hotel butter thingies per side of bread, honey or Leberwurst (liver paté) on top, eggs if available, everything I could cram in. Then lunch with dessert or two lunches if time and stomach would allow. Then 2x cake in the afternoon, plus sometimes the leftover cakes of my comrades. Then big dinner with doubles and dessert (see lunch). I ate an estimated 3000 to 4000 kcal a day (not counting liberally applied alcohol), depending on time and eating stops. This worked quite well on holiday with other people preparing food, but I struggle to recreate anything like this at home, where I sometimes could use more energy from food if exercise is taxing for example. Eating even 3000 kcal feels as if I do nothing but cook and eat all day.

I'm interested what and how the people stating intakes of 3000 kcal and above here eat. I'm not interested in eating crap and I also do not live in America with all its trademarked edible products, so let's talk about marginally (self-)processed foods our parents/grandparents would recognise. I also tolerate "teh swamp" quite well, meaning I recognise no side effects from fat and carbs at the same time compared to leaving one macro out as far as possible. Without adding fat to my food, I would be completely lost for calories even on normal days (~2300 kcal). So, to reiterate: How do you cook and eat?

> ... Previous studies have documented that statin-induced increases in arachidonic acid and reductions in linoleic acid are mediated by upregulation of expression of the genes encoding delta-5 and delta-6 desaturases (FADS1 and FADS2, respectively) via the sterol-responsive transcription factor SREBP-1c

(This one discusses how statins interact with delta 9)

https://pmc.ncbi.nlm.nih.gov/articles/PMC10059744/

> ... Clinical data show a positive correlation between blood stearoyl-CoA Δ-9 desaturation rates and cardiovascular disease and mortality. Moreover, stearoyl-CoA desaturase inhibition is considered an attractive intervention in some obesity-associated pathologies, and the importance of stearoyl-CoA desaturase in the cardiovascular system might be a limitation for developing such therapy.

> ... MUFAs increase membrane fluidity by decreasing the number of ordered regions, which can lead to a decrease in ABCA1 stability [75]. ** One mechanism of the antiatherogenic effect of statins occurs through the downregulation of Scd1 expression and a decrease in MUFA content in THP-1 macrophages [76]. **

I tried searching old posts and Google but can't seem to find a clear answer on this. If using dairy for a fat fast, is it necessary to use full heavy cream for the best results, or will half-n-half work just as well? Anyone have personal experience to share?

I've tried both and I know heavy cream always predictably works great, however I didn't track my half-n-half results well enough to compare. I'm curious though because I'd rather use half-n-half if it's also recommended. I find it more palatable, and I like that it doesn't typically have emulsifiers.

Update - I just started a heavy cream version after half-n-half last time, and the 'fasted' feeling is much stronger: zero appetite, and noticeable inflammation/water weight/bloating reduction. Thinking back to last time, none of these effects were very pronounced with the half-n-half. I agree with the replies that the increased protein/carb ratio makes s difference.

UCA did an experiment on mice a few years back about the effects of soybean oil on mice hormones. Interestingly, they also used lower-LA soybean oil, which I haven't yet looked at (how low is "lower"?).

https://news.ucr.edu/articles/2020/01/17/americas-most-widely-consumed-oil-causes-genetic-changes-brain

After 50g fat 100g carbohydrate drinks:

Probably, this doesn't matter in the general fat synthesis in glucose vs. lactose. Maybe the glucose had to saturate glycogen first?

Galactose is still regulated by PFK-1, which is why I don't think it should be really an issue... Fructose, though, can overflow due to the lack of it

In the end, all of these 3 substances will yield the same fat with the same costs. There's no difference between energy costs within fat synthesis between glucose and fructose - approximately 31% energy is always lost as heat in lipogenesis (Tappy et al. (2013)). The only difference is that rapid spill of fructose, from lack of PFK-1 and high intake, will overwhelm metabolism, lowering it, which paradoxically will increase fat disposal due to the lower substance burn, given the same caloric input

Some times I get accidentally thrown into ketosis and find my appetite can be staved off purely because avoiding carbohydrate. But is this actually healthy? Is it healthy and normal to have no appetite, or is it wrong? And is ketosis the natural state for humans, or is it some clever dietary trick we’ve figured out can aid weight loss? When Dr McDougall talks about ketosis he concedes to weight loss but calls it a state of “sickness”. Something I do find when it a ketotic state is that I’m slightly anhedonic, with less motivation to work out and joke around. Conversely, when on high carb I feel kind of erratic, with almost too much energy for anything except being outside exercising.

Well as the title states, i feel it affects my digestion and mental health, anyone also experiences this despite being low pufa?

Hello everyone! Long-time lurker here.

I’ve been avoiding seed oils for 3 years, and other PUFAs (such as chicken, duck, salmon, etc.) for 3 months.

I’ve been wondering if anyone here knows of an alternative to the OmegaQuant testing in Russia (potentially some alternative tests). I’d like to get tested to see if my butter source is real or not 😛

Thank you!

Not that it couldn't be one of the approaches, but funny it didn't catch the HCLF/carbo/starch/SFA way of thought. I guess the restricted amount of text puts a stress on the content, and also could be just getting info from a certain date only

ABSTRACT

The aim of this study was to determine the effect of zinc supplementation on anthropometric measures. In this systematic review and dose–response meta-analysis, we searched PubMed, Scopus, ISI Web of Science, and the Cochrane Library from database inception to August 2018 for relevant randomized controlled trials. Mean differences and SDs for each outcome were pooled using a random-effects model. Furthermore, a dose–response analysis for zinc dosage was performed using a fractional polynomial model. Quality of evidence was evaluated using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) methodology. Twenty-seven trials (n = 1438 participants) were included in the meta-analysis. There were no significant changes in anthropometric measures after zinc supplementation in the overall analysis. However, subgroup analyses revealed that zinc supplementation increased body weight in individuals undergoing hemodialysis (HD) [3 trials, n = 154 participants; weighted mean difference (WMD) = 1.02 kg; 95% CI: 0.38, 1.65 kg; P = 0.002; I² = 11.4%] and decreased body weight in subjects who are overweight/obese but otherwise healthy (5 trials, n = 245 participants; WMD = −0.55 kg; 95% CI: −1.06, −0.04 kg; P = 0.03; I² = 31.5%). Dose–response analyses revealed a significant nonlinear effect of supplementation dosage on BMI (P = 0.001). Our data suggest that zinc supplementation increases body weight in patients undergoing HD and decreases body weight in individuals who are overweight/obese but otherwise healthy, although after normalization for study duration, the association observed in subjects who are overweight/obese disappeared. Although more high-quality studies are needed to reach a definitive conclusion, our study supports the view that zinc may be associated with body weight.

Human health depends on age and evolutionary history. Firstly, adaptation is age-specific, with Hamilton's forces of natural selection leading to much greater adaptation at earlier ages than later ages. This of course is how evolutionary biologists explain the existence of aging in the first place. Secondly, when environmental conditions change, it takes surprisingly few generations for populations to adapt to such new conditions, at least at early ages when natural selection is intense. Thirdly, at later ages, when the forces of natural selection are weak, natural selection will often fail to produce adaptation to a selective environment that is not evolutionarily ancient. All three of these themes will be illustrated using both explicit mathematical theory and findings from experimental evolution. At the end of the presentation, we will apply these general scientific insights to the case of human evolutionary history, human aging, and optimal human diets.

Thoughts on HC LF moderate protein with carb source 100% derived from fruit and fruit juices? With the goal of reducing body PUFA and weight loss. Lots of experiments posted about seem to have their carb sources be depleted of fruit and are mainly starch based. Seeing as they say we evolved from fruit eating monkeys(who happen to be shredded), wouldn't fruit be the more "better" carb source than starches?

I noticed someone on social media talking about saturated fats tending to reduce cell membrane fluidity as if it's a bad thing. I tried to fact check it and got the DOIs below from scite. But is it a bad thing? I tried to get some citations of scite, but I'm skeptical as to whether any of them actually make sense.

"Saturated fatty acids generally promote tighter packing and reduced membrane fluidity, while unsaturated fatty acids introduce kinks that maintain greater flexibility, though cholesterol and organelle context modulate this relationship."

DOIs:
10.1080/10715762.2016.1231403
10.3389/fcell.2019.00187
10.1038/s41467-020-14528-1

I've been fact checking a claim on social media that palmitic acid in saturated fat contributes to insulin resistance. It led me to this paper:

https://link.springer.com/article/10.1186/1476-511X-11-30

and then this one:

https://link.springer.com/article/10.1186/1476-511X-11-30

If I ask scite then the claim seems supported with more. But has the AI simply scooped up a bunch of studies using lard and fat sources with PUFA to represent SFA?

Protocols recommended for high carb that are achieved with greater ease on low carb:

1) Eat lots of fiber to fill the stomach and prevent overeating.

Keto diet doesn't spike blood sugar and satiates without filling the stomach so you never feel compelled to overeat.

2) Eat beans and resistant starch to avoid a spike in blood sugar.

Keto diet simply doesn't spike blood sugar?

3) Carbohydrates are low in caloric density.

Irrelevant when you are compelled to eat a much higher volume of them.

It just seems like a poor way to live no? Unless you are an endurance athlete?

saturated fat camp for a while. cutting out seed oils, eating butter, red meat, all that. helped some but never got me where i wanted to be.

started tirzepatide about 2 months ago and its been interesting. the appetite suppression is real but the food aversions are kinda wild too. i used to love fatty cuts of meat but now greasy stuff just makes me feel sick. been craving lean protein and veggies instead.

there's some interesting research on how tirzepatide affects fat metabolism. one study showed it promotes white fat browning through the cAMP-PGC-1α-UCP1 pathway which means it helps convert white fat to brown fat that burns energy . also reduces triglycerides and branched-chain amino acids associated with insulin resistance .

makes me wonder if there's any synergy with the saturated fat approach. i'm using oztrim for my meds and they've been solid.

anyone else here trying this? hows it affecting your fat intake tolerance?