https://www.weightwatchers.com/au/blog/food/why-fruit-counts...
The only thing that makes me stop feeling hungry is my blood sugar going back up to a normal level.
I'm truly envious if there's actually anybody out there who can eat low-calorie bulky foods and actually feel satisfied by the meal. I just feel bloated but still just as hungry as before eating.
But if we compare a 150 calorie bag of doritos with 5 large tomatoes (each one being 33 calories), that feels about comparable in terms of satiating me in terms of giving me a break from hunger for maybe 45 minutes.
On the other hand, just large tomatoes does absolutely nothing for hunger. Which is the indication for me that volume is entirely irrelevant. (And why would volume matter? Your body can't turn volume into calories.)
Only problem with 5 large tomatoes is that it leaves me feeling kind of gross/bloated with that much volume. My stomach will literally feel like it protrudes, which is uncomfortable.
Like if I'm on a diet of 1,200 cal/day to lose weight, eating bulky foods does nothing to make me any less miserable, compared to if I stick to dense protein/fats/carbs. The sensation (and distraction) of hunger remains identical.
Note that some things must be boiled to become safe; pokeweed greens can be boiled (and the water discarded) to reduce alkalinity. The berries, however, are never safe for human consumption.
Don't eat plants; they're trying to kill you! https://www.youtube.com/watch?v=j1cqNDDG4aA
I usually forward it to friends that rant about meat being bad for your health.
So the wrong meat give you all the same lovely effects of systemic inflammation, paradoxical immune suppression, metabolism suppression, and the pile of strange effects from the metabolites and free radicals. Which normally don’t matter much, but start to do when modern consumption of omega-6’s end up significantly more than historical exposure, all year long.
This is one thing to watch out for in rodent studies involving “fat”. In addition to having a very different relationship to fat than humans, the fat they are given is generally very high in omega-6, often being lard (from western raised pigs) mixed with some amount of vegetable oil. Thus because “animal fat” was used, the generally negative outcome then gets wrongly associated with saturated fats. If the study doesn’t give a breakdown of the fatty acid profile, then it’s basically worthless. Unless someone feels like trying to track down the researchers and find the chow product they used. Which is sometimes viable.
https://www.health.harvard.edu/newsletter_article/no-need-to...
I offer my strong encouragement to reevaluate and look on with suspicion about the standard "health advice" that has ultimately been provided and supported by an industry that has been dependent on products with high omega-6s in order to achieve low costs and strong preservative effects. And when I say industry I don't mean some "the man" boogeyman cackling in the shadows, I mean I work in agriculture and the very boring humans up and down the supply chain have a lot of incentives for certain thoughts and behaviors, and are strongly disincentivized to ever stop and say "hey is this a problem?".
Ask yourself this, if it is true that eating more omega-6 fats than humans have historically been exposed to is healthy, then why has turning away from the high saturated fats found in "traditional" european and american foods (piles of butter and carbs) only resulted in a population level increase in cardiovascular disease, obesity, and diabetes? While you can't make a rigorous conclusion from just that correlation, Chesterton’s Fence definitely seems relevant here. To be clear, I consider there to be multiple causes for all three of those issues and no one single fix, but I do consider the omega-6 called linoleic acid to be a particularly strong one. Unfortunately there seems to be different "metabolic gears" people can be in, so just taking a metabolically compromised person and only feeding them butter and carbs may not help and could even hurt their situation.
The food oil industry is well aware of the problems that omega-6s have, but obviously aren't keen on announcing something they are at fault for. What you will see is a quiet move to new varieties of plants bred/modified to produce higher monounsaturated fats in place of polyunsaturated fats. As a side note, this may actually not be the best move. Linoleic acid can induce a lower metabolism (in fact animals that enter torpor seem to require it) however once that happens it appears that the monounsaturated fats found in body fat stores seem to maintain the cycle. So it's unlikely to help those with compromised metobolisms. Another side note, I've heard that consuming very large amounts of linoleic acid can sometimes do the opposite and raise metabolism though I've not explored that much. Frankly it's a bad idea to try and achieve it that way, but it's another example of a surprising reverse of what you'd normally expect. If you ever wonder why there's so many seemingly contradictory relationships, it's because your metabolic pathways are an impossible clusterfuck of nested feedback loops, like if a hydra fucked an ouroboros. Look at this map and despair of ever trying to make a 100% always correct statement even with well done science: http://biochemical-pathways.com/#/map/1
But shortly put, the only thing (probably) correct in that article is that linolenic acid intake does not seem to correlate with arachidonic acid levels (I'm presuming this is in rats). I can say this because I'm reasonably convinced that linoleic (not to be confused with linolenic) also doesn't seem to correlate with arachidonic acid (in rats). So I find it definitely reasonable to take on it's face. The conclusion that omega-6s are somehow then good, is absolute bullshit though. Arachidonic acid is not the only omega-6 with issues. The most well researched one with a laundry list of negative effects is linoleic acid.
>American Heart Association (AHA)
AHA is a highly biased organization that puts out bad science. They are the Autism Speaks of the health world. If their stamp is on it, be extremely wary.
>"Omega-6 fats are not only safe but they are also beneficial for the heart and circulation," says advisory coauthor Dr. Dariush Mozaffarian, an assistant professor of medicine at Harvard-affiliated Brigham and Women's Hospital.
Jesus titty fucking christ, she couldn't be more irresponsibly and dangerously wrong. Now, there a load of resources one can explore that counter this idea of "heart healthy" omega-6s, but instead of a gish gallop that not even I'm interested in, here's my personal favorites, because it so perfectly illustrates how easily one can walk away with the exact wrong conclusion if the trial isn't thorough enough.
https://journals.physiology.org/doi/pdf/10.1152/ajpheart.004...
See Figure 2. Basically Both Normal and diabetic rats were fed a "normal" diet vs one with very high omega-6. Apoptosis is controlled cell death, in this case measured by caspase-3 activity. The Diabetic rats had their heart cell caspase-3 activity reduced by about half.
So this means, omega6 resulted in less heard cells dying, right? Heart healthy and great for diabetics!
But they also measured something else. Necrosis is uncontrolled cell death (resulting in inflammation and other negative side effects), in this case measured by serum LDH. In Figure 3, they show that serum LDH more than triples.
Basically feeding diabetic rats omega-6 enriched food traded heart cells dying in a controlled manner, with dying in an uncontrolled manner.
P.S. Epidemiology in health research (which the pro-omega-6 crowd is heavily reliant on) is a giant pile of dogshit that can be made to say whatever the author wants, and severely suffers from the replicability crisis that plagues other areas of science where it's hard to actually control and measure everything involved. Beware both the conclusions, as well as the time spent digging through shit to find out that yes, it really was shit.
Also curing processed meats creates NOCs, NAAs, and PAHs: https://www.hsph.harvard.edu/nutritionsource/2015/11/03/repo...
Does "going easy on oxalates" just mean you have fewer than six spinach smoothies per day?
I'm used to these dietary memes cashing out into either trivial claims or nothing burgers.
and
> Frozen commercially available spinach in New Zealand contains 736.6 ± 20.4 mg/100g wet matter (WM) soluble oxalate
while the USDA says about 900 mg per 100 g for American spinach on average.
So roughly 1% of the wet spinach by weight. 1 kilo of high-oxalate spinach probably has 10 - 20 grams of oxalic acid. That's a lot of spinach, but probably chuggable in one day in smoothie format. Far too close to the LD50 estimate for my comfort!
For one large salad, it's unlikely to exceed a couple grams. I'm unsure about the effects of chronic lower dose exposure.
Looking it up, people generally eat 50-200mg of oxalates per day with 1000mg being the outlier high end.
Eat your spinach. If you're worried, then cook it.
Despite your statement I don’t think this knowledge is automatically distributed amongst vegans.
I've gotten two and don't recommend. Things that help, short of the sort of restrictions I'm stuck with: drink lots of water with high-oxalate foods, and eat foods high in calcium with them. The calcium binds with the oxalate in your guts instead of your kidneys and passes right out. Some people dissolve a calcium pill in the water they boil spinach in.
They can see tiny stones in your kidneys with a scan so it's possible to check before you get a real problem, though I don't know if they would without any symptoms.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7600777/
A lot of the "common sense" about oxalates just sound like social media memes.
Avoiding high-oxalate foods if you're prone to oxalate stones isn't a meme, it was the advice of my urologist and the printed pamphlets he gave me. Along with drinking plenty of water, especially with meals as I mentioned above. As for calcium, it's mentioned as protective in your quote.