Unintentional Vegan Peating: Amazing So Far

[Amazoniac]

Actually I do think unchewed food is a big problem in indigestion. Even if the substance is hard to digest, a thorough chewing cuts down the indigestion immensely.

I agree, but not enough to cause that, it must be something else. You can ingest whole pieces of carrots mentioned above and they won't have such effect. Since 4 beans or so cannot be responsible for the vomit, you might even argue that the chewed beans were to blame. That, or the inverted push-ups after the meal.

 

[Travis]

Contrary to what some people claim, ω-6 fatty acids increase glucose flux in the same way as ω-3 fatty acids. The ω-3 fatty acids like DHA just do this a little more because they are longer and have more double bonds.

But more specifically they do it a little differently, because it also appears to depend on the exact location of the double bonds and also the lipid's geometry. The ω−3 double bond of DHA (22∶6ω−3) curls around back again towards the lipid membrane to provide a region of relative desaturation at that specific depth, a property the ω−6 osbond acid (22∶5ω−6) lacks. This bond in particular lends DHA better sterol exclusion properties, and should it's additional double bond be placed at ω−20 (i.e. Δ+2) instead it wouldn't function in quite the same manner.

Stillwell, William. "Docosahexaenoic acid: membrane properties of a unique fatty acid." Chemistry and physics of lipids (2003)​

Since our elongation and desaturation enzymes have a greater affinity for α-linolenic acid (18∶3ω−3) than for either γ-linolenic acid (18∶3ω−6) or linoleic acid (18∶2ω−6), I think it reasonable to say 'they are somewhat specific towards towards ω−3 precursors.' Since the ω−6 fatty acids eventually displace the ω−3 fatty acids under an unfavourable dietary ratio by occupying our elongase and desaturase enzymes by competition, to some extent, I think you can make the case that ω−6 restriction is both more important and safer than ω−3 supplementation. I think attempting to 'normalize' the ω−3/ω−6 ratio by simply by supplementing a like amount of ω−3 fatty acids is folly unless perhaps at the smallest doses, or literally just a few drops per day. Brain DHA is very well recycled so we don't need much of it at all, certainly not any more than the unavoidable amounts found in nearly any unrefined food. Since the sum of membranous ω−3 and ω−6 fatty acids remains more-or-less constant, the practical alternative to ω−3 membrane fatty acids—e.g. DHA (22∶6ω−3) and DPA (22∶5ω−3)—is allowing the ingression of the ω−6 fatty acids which displace them: osbond (22∶5ω−6) and arachidonic acids (20∶4ω−6). Omega−3 displacement by omega−6 fatty acids should tend towards the dangerous 2-series prostaglandins, increased cancer risk, increased chance of stroke, and lower transmembrane glucose permeability.

 

[Travis]

Carotene has the same response as PUFA in the body, it suppresses thyroid hormone.

[Citation needed]

 

[RobertJM]

Hello everyone! I'd like to report an interesting unintentional experiment of mine.
I posted recently how i was craving very little animal food for the past 4 months. I also lost weight as I was mostly eating fruits.
I starting eating potatoes for the past 2 weeks or so and I got to the point of 0 animal food cravings.
I'm basically a vegan now without intentionally wanting it. I just don't want animal food.
I started gaining weight again. I mean muscle as I am resistance training. I think the starch in potatoes stimulated back my appetite.
I am currently eating around 2 kg of potatoes and 2 kg of grapes a day. Some white in sugar in coffee. The mental clarity and positivity is insane. I am so verbally fluent, like I speak with a good flow and charisma in everything.
When I try to force some yogurt, I feel worse and sleep worse. I tested this several time in a controlled manner.
I read some of @Travis posts about vegan eating. I do not have the biology knowledge to understand everything he says, but my evidence is telling me that I have a direct positive relation between wellbeing and vegan eating.
I will report back on how things are going. So far, my protein cravings are probably potatos cravings. Thats my salty solid food. And grapes are throughout the day and after main meals. Its laughable how cheap this is.
Anyway, hope this is useful to share!

When you say cheap, you’re just buying those grapes from a wholesaler are you? A cheap deal? Because 2kg of grapes per day where I live will cost £10, which is a lot for grapes alone. Also, they are a clean source? Not heavily sprayed? I just ate some grapes today and could taste the chemicals. They certainly aren’t clean when purchased through major shopping stores. I was just wondering about your ‘cheap’ comment.

The potatoes I can really dig. I absolutely love them. I make mine into chips and add salt and vinegar. But I live a busy work life. I certainly don’t have the time to live it up on potatoes when I’m busy working. But I’d eat them everyday if I could. I usually eat 700g per day on the days that I’ll do ‘em. But I reckon I could do 2kg no problem!

And supplementing calcium on top isn’t difficult for posters above who mentioned this.

 

[Reaper242xx]

[Citation needed]

Uhhh, Ray Peat.

 

[Reaper242xx]

Here we go again...

What's wrong

 

[Kartoffel]

But more specifically they do it a little differently, because it also appears to depend on the exact location of the double bonds and also the lipid's geometry. The ω−3 double bond of DHA (22∶6ω−3) curls around back again towards the lipid membrane to provide a region of relative desaturation at that specific depth, a property the ω−6 osbond acid (22∶5ω−6) lacks. This bond in particular lends DHA better sterol exclusion properties, and should it's additional double bond be placed at ω−20 (i.e. Δ+2) instead it wouldn't function in quite the same manner.

I don't think the insulin sensitizing effect of PUFA has anything to do with their structural properties in a supposed lipid membrane. The insulin sensitizing effect (as well as SFA ability to decrease sensitivity) is almost immediate, and therefore can't be explained by long-term changes in membrane composition. I think the effect is caused by how they are metabolized. I increasingly like the proton FADH2/NADH hypothesis, but there are also many other mitochondrial explanations that take the immediate effects into account without invoking membrane changes. Every double bond in a fatty acid decreases the ratio of FADH2/NADH produced by β-Oxidation. A high FADH2/NADH ratio seems to be a signal, mediated by free radicals generated in ETC complex I, for decreasing insulin sensitivity, and saturated fatty acids like palmitate produce a 0.5 ratio while PUFA produce a much lower ratio in the range 0f .42 or .43 - I think carbs produce a ratio of about .20-.22.

 

[Kartoffel]

What's wrong

I was hinting at the fact that Travis had this discussion with several people already. He says there is no evidence showing that PUFA suppress thyroid function. He is right that nobody has come up with any study directly demonstrating it, and Ray hasn't cited any study directly proving his claim, either. Thus, there is really no point in repeating this discussion, unless you have found any reference. Here, Travis wins (for now).

 

[lollipop]

I agree, but not enough to cause that, it must be something else. You can ingest whole pieces of carrots mentioned above and they won't have such effect. Since 4 beans or so cannot be responsible for the vomit, you might even argue that the chewed beans were to blame. That, or the inverted push-ups after the meal.

Right. See what you mean.

 

[Travis]

I was hinting at the fact that Travis had this discussion with several people already. He says there is no evidence showing that PUFA suppress thyroid function.

But you of course had meant to say β-carotene, which as a far as I can tell is merely implicated in hypothyroidism because its known association with carotenemia. Yet I maintain that the chain of causality is actually reversed by Ray Peat, and there's good evidence to assume that the hypothyroidism causes the carotenemia. There is direct experimental evidence that triiodothyronine transcribes for β-carotene 15, 15'-monooxygenase—the 'carotene cleavage enzyme'—apparently with intent of increasing serum retinol.

Wang, Zhenguo. "Iron dependency of beta-carotene 15, 15'-monooxygenase in Caco-2 TC7 cells." (2008).

'Some hormones were also suggested to affect BCMO gene expression. Glucocorticoid enhanced the duodenal BCMO mRNA during the perinatal period in chick (Yamaguchi et al., 2007), while triiodothyronine (T₃) elevated BCMO mRNA level in 7 day post-confluent Caco-2 BBe cells in both dose- and time- dependent manners. BCMO activity was also enhanced by T₃ treatment in Caco-2 BBe cells incubated with medium containing fetal bovine serum (Yamaguchi and Suruga, 2008).' ―Wang​

It could be worth noting that the dNA sequence encoding human β-carotene 15, 15'-monooxygenase (BCO) has a response element for both triiodothyronine receptor-α and triiodothyronine receptor-β, an observation that can easily be confirmed by entering its dNA sequence into this program with the prior selecting the relevant transcription factors. Hypervitaminosis A can also induce carotenemia, and I think its fair to assume this occurs because carotenses are not cleaved in this state since they're not needed. In both these cases—hypervitaminosis A and hypothyroidism—the homeostatic mechanism of β-carotene cleavage is manifested on the skin due to carotene's strong absorption of light in the 435 nm region, and its cleavage 'decolorizes' the molecule towards transparency.

Josephs, H. "Hypervitaminosis A and carotenemia." American Journal of Diseases of Children (1944)​

Seeing things in this way: β-carotene then becomes a useful visual indicator or triiodothyronine, retinol status, and prior carotene ingestion. A reduced expression of β-carotene 15, 15'-monooxygenase resulting from hypothyroidism is also how all scientists— besides Ray Peat—appear to explain the situation. I have seen no published articles claiming the inverted causality or demonstrated convincing evidence of such. And moreover, β-carotene's provitamin A status could make it actually seem 'prothyroid' should retinol also be assumed as being such.

Christopher, R. "Carotenoderma in metabolic carotenemia." Indian pediatrics (1997)

'The conversion of beta-carotene to two molecules of vitamin A is accelerated by thyroxine and hyperthyroidism. The characteristic yellow tint of the skin in hypothyroidism is due to hyper-betacarotenemia. In a study of 36 patients with thyroid dysfunction, the serum level of beta-carotene in the hypothyroid group was significantly higher in relation to the euthyroid controls, and the hyperthyroid group showed significantly lower values (3). This may be related to the known function of the thyroid hormone in facilitation of carotene conversion.' ―Christopher

'Beta carotene, the most effective provitamin, is cleaved into two molecules of retinol by the NADH dependent enzyme, carotene dioxygenase present in the intestinal mucosal cells and liver.' ―Christopher​

 

[tara]

Adding a good amount of potatoes looks good for fuel and protein and minerals.
Long term, you might want to look at cronometer.
Without animal products, I think it's probably good to seek out calcium-rich plants - green leaves, some fruits more than others, etc.
B12 deficiency seems to be a risk for some vegan diets. May not show up immediately, and if you are lucky maybe you'll sustain helpful microbiota to supply this, but may be worth watching if you keep this up for a long time.
Depending on where your foods are growing, there ca be other deficiencies. Zinc, selenium, iodine, ...
Consider a bit of seaweed?

Eating butter with potatoes is also a good idea because the long-chain saturated fatty acids will prevent hypoglycemia by (1) slowing absorption of starch/glucose from the intestine (2) reducing insulin sensitivity, therby preventing excess energy uptake by adipocytes.

And if OP were wanting to keep to plants for now, and coconut oil is too short-chain to do it, then following meals with a bit of good chocolate or other form of cocoa butter might fit the bill?

 

[Travis]

I don't think the insulin sensitizing effect of PUFA has anything to do with their structural properties in a supposed lipid membrane. The insulin sensitizing effect (as well as SFA ability to decrease sensitivity) is almost immediate, and therefore can't be explained by long-term changes in membrane composition. I think the effect is caused by how they are metabolized. I increasingly like the proton FADH2/NADH hypothesis, but there are also many other mitochondrial explanations that take the immediate effects into account without invoking membrane changes. Every double bond in a fatty acid decreases the ratio of FADH2/NADH produced by β-Oxidation. A high FADH2/NADH ratio seems to be a signal, mediated by free radicals generated in ETC complex I, for decreasing insulin sensitivity, and saturated fatty acids like palmitate produce a 0.5 ratio while PUFA produce a much lower ratio in the range 0f .42 or .43 - I think carbs produce a ratio of about .20-.22.

Is the effect really almost immediate for polyunsaturated fatty acids? or did you mean only long-chained saturated fatty acids and sterols demonstrate near-immediate effects? If you were to say that, then I'd have to agree.

I don't think the insulin sensitizing effect of PUFA has anything to do with their structural properties in a supposed lipid membrane.

Are you now contending that the lipid membranes that surround cells are theoretical? Well, you do remember that study in which radioactive glucose had been trapped inside liposomes? the one in which glucose flux had been a function of fatty acid unsaturation and one of the many that'd found DHA superior to all others? The peculiar ability of this lipid to exclude membrane sterols and long chained saturated fatty acids has been thoroughly proven, and I think most would find it intuitive that membrane-intercalated cholesterol should decrease glucose flux. For these considerations: I don't imagine that long-chained saturated fatty acids and sterols can significantly increase insulin resistance the absence of ω−6 fatty acids. The sterol incorporation into membranes, a cardiovascular disease sign, should not occur very readily with a tropical ω−6/ω−3 fatty acid ratio approaching unity. The Israeli's consume a ω−6/ω−3 ratio of about 30∶1, an observation confusing to the people who assume 'all polyunsaturated fatty acids are protective.'

Dubnov, Gal. "Omega-6/omega-3 fatty acid ratio: the Israeli paradox." Omega-6/omega-3 essential fatty acid ratio: the scientific evidence. (2003)

 

[andrei]

where do you get fat to eat with the potatoes , 2kg of potatoes everyday must give one hell of an insulin response

When you say cheap, you’re just buying those grapes from a wholesaler are you? A cheap deal? Because 2kg of grapes per day where I live will cost £10, which is a lot for grapes alone. Also, they are a clean source? Not heavily sprayed? I just ate some grapes today and could taste the chemicals. They certainly aren’t clean when purchased through major shopping stores. I was just wondering about your ‘cheap’ comment.

The potatoes I can really dig. I absolutely love them. I make mine into chips and add salt and vinegar. But I live a busy work life. I certainly don’t have the time to live it up on potatoes when I’m busy working. But I’d eat them everyday if I could. I usually eat 700g per day on the days that I’ll do ‘em. But I reckon I could do 2kg no problem!

And supplementing calcium on top isn’t difficult for posters above who mentioned this.

i buy quality grapes for 1.5 dollars /kg. I live in eastern europe so we produce a lot of good fruits.

 

[andrei]

Adding a good amount of potatoes looks good for fuel and protein and minerals.
Long term, you might want to look at cronometer.
Without animal products, I think it's probably good to seek out calcium-rich plants - green leaves, some fruits more than others, etc.
B12 deficiency seems to be a risk for some vegan diets. May not show up immediately, and if you are lucky maybe you'll sustain helpful microbiota to supply this, but may be worth watching if you keep this up for a long time.
Depending on where your foods are growing, there ca be other deficiencies. Zinc, selenium, iodine, ...
Consider a bit of seaweed?

And if OP were wanting to keep to plants for now, and coconut oil is too short-chain to do it, then following meals with a bit of good chocolate or other form of cocoa butter might fit the bill?

I eat some chocolate. I eat brazilian nut for selenium. Fruits and potatoes bring me decent calcium, so i am hesitating to supplement yet. I will start spinach and mushroomss.

 

[Travis]

B12 deficiency seems to be a risk for some vegan diets. May not show up immediately, and if you are lucky maybe you'll sustain helpful microbiota to supply this...

Albert, M. J. "Vitamin B₁₂ synthesis by human small intestinal bacteria." Nature (1980)

​

LeBlanc, J.G. "Bacteria as vitamin suppliers to their host: a gut microbiota perspective." Current opinion in biotechnology (2013)

'The human gastrointestinal tract (GIT) is colonized by a vast array of microorganisms known as the gut microbiota, with up to 10¹¹ bacteria per gram of intestinal content [2]. Apart from its impact on different human functions [2], the intestinal microbiota plays a pivotal role in food digestion and energy recovery, while it can also act as an important supplier of vitamins. In humans it has been shown that members of the gut microbiota are able to synthesize vitamin K as well as most of the water-soluble B vitamins, such as biotin, cobalamin, folates, nicotinic acid, panthotenic acid, pyridoxine, riboflavin and thiamine [3]. In contrast to dietary vitamins, which are adsorbed in the proximal tract of the small intestine, the predominant uptake of microbially produced vitamins occurs in the colon [4,5].' ―LeBlanc​

'Animals, plants and fungi are incapable of cobalamin production and it is the only vitamin that is exclusively produced by microorganisms, particularly by anaerobes [47–49].' ―LeBlanc​

'...was shown to produce a cobalamin-type compound [57]. Notably, propionibacteria and L. reuteri normally occur in the human intestine and may thus (partially) fulfil the vitamin B₁₂ requirement of the host.' ―LeBlanc​

Oxnard, C. E. "Vitamin B₁₂ deficiency in captive monkeys and its effect on the nervous system and the blood." Laboratory animals (1970)

'When allowed to become deficient, rhesus monkeys do not often show obvious changes; for instance, the macrocytic anaemias that occur in man do not appear, individual animals sometimes have greater amounts of haemoglobin, higher red cell counts and higher serum iron levels than are found in recently captive animals, and obvious macrocytosis has not been noted (Oxnard & Smith, 1966). Anaemias that have been found from time to time in isolated animals are microcytic and hypochromic. Macrocytic anaemias reported in rhesus monkeys have been shown to respond to folic acid (and sometimes ascorbic acid) rather than to treatment with vitamin B 12 (reviewed by Smith, 1965).' ―Oxnard​

Childers, J. "Effects of antibiotic-induced vitamin B12 deficiency with and without oral administration of vitamin B12." Ball State University (2017).

'Vitamin B12 plays essential roles in red blood cell formation as well as being a cofactor used by enzymes present in the body. Humans cannot synthesize vitamin B12, so we rely on our gut microbiota to synthesize vitamin B12 in our gastrointestinal tract for human usage (Stanislawska-Sachadyn et al., 2010, LeBlanc et al., 2011, Martens et al., 2002 & Raux et al., 2000).' ―Childers​

​

'Antibiotics kill the bacteria in our gastrointestinal tract, as well as the bacteria we do not want (Blaser, 2011). This project will provide insight to individuals taking long-term antibiotic treatments as to whether oral administration of vitamin B12 will increase vitamin B12 and decrease homocysteine, methylmalonic acid and reticulocyte serum concentrations in individuals taking long-term antibiotics.' ―Childers​

This would of course seem unlikely were enterally-produced vitamin B not actually absorbed as is often stated or implied. Even more improbable, in my opinion, would be that 1.344 kilodalton molecule not much larger than heme would need the help of the 42,698 kDa intrinsic factor for absorption.

Even should a person assume that cobalamin macrocycles—and not heme macrocycles—are normally excluded without intrinsic factor, they would then have to explain transcobalamin II. It had been demonstrated nearly 20 years ago that transcobalamin II, which is expressed in large intestine, is capable of binding and assimilating cobalamins in a manner completely independent of intrinsic factor.

Pons, Laurent. "Transcytosis and coenzymatic conversion of [⁵⁷Co] cobalamin bound to either endogenous transcobalamin II or exogenous intrinsic factor in Caco-2 cells." Cellular Physiology and Biochemistry (2000)

'We have examined the intracellular route, coenzyme conversion and transcytosis rate of [⁵⁷Co]-labeled cobalamin (Cbl) in function of its presentation to the apical side of Caco-2 cells, either free or bound to intrinsic factor (IF). The free-presented Cbl was progressively bound to endogenous transcobalamin II (TCII) which may stem, in part, from a basolateral to apical passage. Its transcytosis was TCII-mediated as it was abolished when antibodies to TCII were added to the apical medium. The apparent permeability coefficient (P(app)) was estimated at 20.8, 103.5, 0.9 × 10⁻⁵ cm/h for TCII-Cbl, IF-Cbl and haptocorrin-Cbl, respectively. Chloroquine inhibited the transcytosis rate of both TCII and IF-bound Cbl in a dose-dependent manner. Approximately 80% of apical Cbl, bound to either exogenous IF or endogenous TCII, was transported to the basolateral side as intact cyano[⁵⁷Co]Cbl whereas the remainder was converted into Ado-Cbl and CH₃-Cbl within the cells, as shown by HPLC analyses of a 1,000-g pellet and a 12,000-g supernatant. Coenzymatic conversion was virtually abolished by chloroquine. In conclusion, we suggest that apically presented free Cbl is internalized via TCII-dependent transport. The apically internalized CN-Cbl, bound to either IF or TCII, is processed via an acidic vesicle and part of it is converted to coenzymes, whereas bulk of CN-Cbl is transcytosed intact.' ―Pons​

 

[Kartoffel]

But you of course had meant to say β-carotene, which as a far as I can tell is merely implicated in hypothyroidism because its known association with carotenemia.

Yes, sorry for that.

Is the effect really almost immediate for polyunsaturated fatty acids? or did you mean only long-chained saturated fatty acids and sterols demonstrate near-immediate effects? If you were to say that, then I'd have to agree.

If you agree with the latter, what's your explanation for this immediate effect of long-chain saturated fatty acids on insulin sensitivity?

Are you now contending that the lipid membranes that surround cells are theoretical? Well, you do remember that study in which radioactive glucose had been trapped inside liposomes? the one in which glucose flux had been a function of fatty acid unsaturation and one of the many that'd found DHA superior to all others? The peculiar ability of this lipid to exclude membrane sterols and long chained saturated fatty acids has been thoroughly proven, and I think most would find it intuitive that membrane-intercalated cholesterol should decrease glucose flux. For these considerations: I don't imagine that long-chained saturated fatty acids and sterols can significantly increase insulin resistance the absence of ω−6 fatty acids

Remind me again, which study is that exactely? Above you said that you would agree with the statement that long-chain sat fatty acids have an immediate effect on insulin sensitivity. Here you say that you don't think they have a significant effect in the absence of ω−6 fatty acids. So, how do you propose saturated fatty acids cause insulin resistance? In rat studies, butter is the best and safest method to induce insulin resistance quickly, and butter doesn't contain a terrible amount of ω−6 fatty acids, if you compare it to ω−6 rich oils that don't cause short-term insulin resistance in these experiments.

 

[Travis]

Yes, sorry for that.

If you agree with the latter, what's your explanation for this immediate effect of long-chain saturated fatty acids on insulin sensitivity?

I had imagined the stearate and palmitate simply had intercalated into the lipid membrane as free fatty acids and/or triglycerides, not phospholipids, blocking glucose flux by their physical presence. There appears to be often a 'sterol layer' within the membrane where saturated fatty acid would be more soluble, yet as Terma noted there is also the Randle Cycle to consider. I like to consider physical properties first as they're the most fundamental, and ones that always hold true no matter what. The long chained ω−3 fatty acids have a tendency to exclude sterols that is greater than expected, and so far I've seen exception to this. Even when a person bakes a fish, the sterols can be seen as coagulating and floating to the top as DHA gains kinetic energy and excludes them. I feel the ability of ω−6 fatty acids to increase membrane sterol solubility can also be observed through its correlations with the 'fatty streaks' observed in cardiovascular disease, the cholesterol ingression consequent of erucic acid poisoning, and the grey matter sterol infiltration seen in Zellweger's disease. The effect appears to be just as reliable in artificial lipid bilayers as in cell models, and also supported by observations both in the clinic and in the kitchen:

Shaikh, S. "Biophysical and biochemical mechanisms by which dietary N-3 polyunsaturated fatty acids from fish oil disrupt membrane lipid rafts." The Journal of nutritional biochemistry (2012)

'Addition of cholesterol can partially redistribute the DHA acyl chain toward the bilayer center, but the ordering effect of cholesterol is still more pronounced when cholesterol interacts with saturated acyl chains [20].' ―Shaikh​

'The flexible and therefore disordered structure of DHA renders it incompatible with surrounding ordered saturated acyl chains and cholesterol. Rosetti and Pastorino very recently reported with MD simulations that DHA acyl chains do not pack efficiently with saturated acyl chains [21].' ―Shaikh​

'Thus, DHA and perhaps EPA may be promoting the displacement of cholesterol from DRMs to DSMs, which is consistent with NMR and X-ray diffraction data that show DHA has a low affinity for cholesterol [14,40]. Once the cholesterol is displaced toward nonrafts, it is likely to associate with saturated acyl chains.' ―Shaikh​

'The poor affinity between n-3 PUFAs and cholesterol forces some of the cholesterol molecules to move out of the raft into nonrafts, which contributes to the declustering.' ―Shaikh​

Insulin could have an effect of desaturating the membrane by inducing stearoyl-CoA desaturase, converting stearic acid into oleic acid for cell membrane phospholipids. Besides decreasing sterol incorporation through increased water solubility, the desaturation of a lipid makes for one with a lower density and higher kinetic energy.

Waters, K. "Insulin and dietary fructose induce stearoyl-CoA desaturase 1 gene expression of diabetic mice." Journal of Biological Chemistry (1994)

'Fructose administration to fasted diabetic mice induced a 2-fold increase in SCDl mRNA within 6 h and a 23-fold increase within 24 h. Similarly, insulin administration to diabetic mice induced SCDl mRNA from 4-fold within 4 h to 22-fold within 24 h. Insulin plus fructose, however, achieved full induction, with a 45-fold increase of SCDl mRNA and a 10-fold increase in SCDl transcription within 24 h.' ―Waters​

Above you said that you would agree with the statement that long-chain sat fatty acids have an immediate effect on insulin sensitivity. Here you say that you don't think they have a significant effect in the absence of ω−6 fatty acids. So, how do you propose saturated fatty acids cause insulin resistance?

By decreasing glucose flux, thereby raising the amount of insulin required to maintain it.

In rat studies, butter is the best and safest method to induce insulin resistance quickly, and butter doesn't contain a terrible amount of ω−6 fatty acids, if you compare it to ω−6 rich oils that don't cause short-term insulin resistance in these experiments.

Of course not, but I would bet that the rats had also been fed far more ω−6 fatty acids than ω−3 fatty acids prior to that—in the 'rat chow'—thereby increasing the cell membrane's solubility for palmitate, stearate, and cholesterol. I would imagine that tallow would be more effective in the high ω−6 rat in reducing glucose flux, and lard perhaps worse than anything. Yet with a tropical ω−6/ω−3 as seen in primitive islanders, I would imagine that long-chained saturated fatty acids wouldn't have effects of this magnitude because they'd be less membrane-soluble.

 

[Travis]

Meza-Herrera, C. A. "Long-term betacarotene supplementation positively affects serum triiodothyronine concentrations around puberty onset in female goats." Small Ruminant Research (2014)

'Long-term BC supplementation positively affected the release pattern of triiodothyronine over time, suggesting a potential role of BC as a thyroid-activating molecule; these results might possess clinical significance.' ―Meza-Herrera

'Allotments of food and beta-carotene were individually fed to each goat. [...] The only difference in the BC consumption between the examined groups was the BC oral supplementation provided to the BC group.' ―Meza-Herrera

'Blood (10 ml) was collected monthly by jugular venipuncture from all the goats; because several environmental factors such as temperature, season and circadian rhythm cause fluctuation in thyroid hormone levels, all the samples were collected prior to feeding at 07:00 throughout the experimental period. The serum T₃ concentrations were determined in duplicate by solid-phase RIA using components of a commercial kit; the kit utilized antibody-coated tube technology, and the assay was performed without prior extraction of T₃ from the serum. Whereas the intra- and inter-assay CV values for T₃ quantification were 0.55% and 6.98%, the sensitivity of the assay was 0.1 ng m⁻¹.'

'In early June, the goats were randomly distributed in two groups: 1) the beta-carotene group, and 2) the control group. The BC group was supplemented with BC (50 mg/goat/day; orally) during the entire experiment (150 days, from early June to early November). The goats were kept under natural photoperiod conditions from June to November and had free access to water, shade, and mineral salts during the entire experiment.' ―Meza-Herrera

​

'This study was conducted at the Southern Goat Research Unit of the Regional University Unit of Arid Lands Chapingo Autonomous University (URUZA-UACH), Bermejillo, Durango, Mexico. The climate of the area is warm and dry, and the mean annual precipitation and temperature are 217.1 mm and 22.3 °C, respectively. The warmest month is June, with temperatures above 40 °C, whereas the coldest month is January, with the lowest temperature below 0 °C.' ―Meza-Herrera

'Supplementation by BC promoted increased mean serum T₃ concentrations at specific points of the ²⁄₃ and ³⁄₃ experimental period, suggesting a potential role of BC as an activating molecule of the hypothalamic-hypophyseal-thyroid axis.' ―Meza-Herrera

'This study reports, for the first time, the positive action of BC supplementation upon serum T₃ concentrations over time. This result suggests a potential role for BC as an activating molecule in the hypothalamic-hypophyseal-thyroid axis in goats. These results might have physiological and clinical significance.' ―Meza-Herrera
​

Garcin, H. "Thyroid hormones in vitamin A-deficient rats: effect of retinoic acid supplementation." Annals of nutrition and metabolism (1983)

'The supplementation of the vitamin A-deficient diet with 10 μg retinoic acid/g dry diet was followed by an important gain in body weight and by a decrease in serum thyroid hormones.' ―Garcin​

​

'After 7 weeks on a vitamin A-deficient diet the growth of rats slowed down. At that time there was an increase in thyroid hormones.' ―Garcin​

 

[andrei]

Update: potato protein is real. I am gaining muscle.
Also mental sharpness and verbal coherence is at an all time high.
I doubt the obession with grams of calcium per day. Plants give me around 5-700 mg per day and I dont see why i should supplement.

 

[JustAGuy]

Update: potato protein is real. I am gaining muscle.
Also mental sharpness and verbal coherence is at an all time high.
I doubt the obession with grams of calcium per day. Plants give me around 5-700 mg per day and I dont see why i should supplement.

How do you know you are gaining muscle? Over a short time period of a few weeks it’s generally very difficult to say if you made any gains.
I find that if I reduce protein intake and increase carbs my muscles look way bigger, but it’s just extra water being taken into the muscles.