The Warburg "effect" Is, In Fact, A Direct Cause Of Cancer

[Sourdoughbanana]

skimming through those studies, it seems clear that they're referring to added sugars, which I'll always stay away from. You can't expect anything good from empty calories; the word empty meaning neither sufficient vitamins nor minerals (+ whatever phytonutrition fruits bring in). Plus, beware of the unhealthy user bias: I'm lean, very active as should be, get bloods drawn quarterly. Studies on sedentary obese kids sipping on pop mean little to me.

as per Peat:

Refined granulated sugar is extremely pure, but it lacks all of the essential nutrients, so it should be considered as a temporary therapeutic material, or as an occasional substitute when good fruit isn't available, or when available honey is allergenic.

I'm absolutely against all the table sugar / Mexican Coke craze around here. I used to be a Fruitarian, eating whole fruits. Then I added in some low fat dairy, game, and wild fish + shellfish. Never had better health.

My bad for not making that clear - high fructose from whole fruits of course. Or else, it would be identical to saying dairy is harmful because calcium supplements are dangerous.

 

[Elephanto]

@Sourdoughbanana It literally has to do with the metabolic pathways and functional mechanisms of Fructose, not the lack of nutrients in white sugar. Even in the study on obese kids, replacing excess sugar by starch which had a positive effect on all parameters is unlikely to be explained by greater nutritional value (bread/pasta and white rice with little amount of minerals and vitamins being some of the most popular starches).

 

[Sourdoughbanana]

it has everything to do with the lack of nutrients in the dietary source of fructose.

http://www.sciencedirect.com/science/article/pii/S0098299702000900

Mg depletion induced a severe insulin resistance that was shown to be dependent, at least in part, upon a defective tyrosine kinase activity of the insulin receptors. Furthermore, Bolan et al. reported that a high fructose diet-induced insulin resistance observed in rats was not due, as currently believed, to fructose itself, but rather to the low Mg content of such commercial diets

Effect of magnesium deficiency on lipid metabolism in rats fed a high carbohydrate diet. - PubMed - NCBI

In liver, magnesium-deficient rats fed sucrose showed a significant increase in triglycerides, lactate and alpha-glycerophosphate and a significant decrease in glycogen.

for as long as studies are going to feed sick people with nutrient void foods, science will stall.

 

[Wagner83]

@Sourdoughbanana ...white rice with little amount of minerals and vitamins...

Someone on here made me realize it's not necessarily true according to this website and for that type of rice in particular:
Rice, white, short-grain, raw Nutrition Facts & Calories
If you then cook until complete absorption of water with coconut water and a kale broth made out of it it becomes stellar.

 

[Elephanto]

Someone on here made me realize it's not necessarily true according to this website and for that type of rice in particular:
Rice, white, short-grain, raw Nutrition Facts & Calories
If you then cook until complete absorption of water with coconut water and a kale broth made out of it it becomes stellar.

Interesting but I guess it would depend on the level of refinement and content of the soil, since most white rice I've bought have almost nothing in nutritional value (if accurate) except a few brands I came across previously. I've been making sure to supplement B1 and eat it with sources of Potassium to be safe.

@Sourdoughbanana You ignore the actual mechanisms of Fructose whereby fatty acid synthesis genes are increased much more potently than with Glucose and where gut microbiota is negatively affected to promote intestinal permeability and endotoxemia. Low nutritional value might contribute to some negative effects, but it doesn't remove or counter-balance the effects that I showed with mechanistic studies. If it's only a matter of nutritional value, then why does Glucose show contrasting effects when the other variables are constant ?

 

[Sourdoughbanana]

I know fructose metabolism very well, having a doctorate in science with extensive biochemistry classes.

What I’m saying and that is included in Peat’s references, is that there’s more to the story than fructose biochemistry. Never go reductionist - what happens with real whole Foods isn’t the same as in the double blind randomized controlled trial. Again, references included in Peat’s article.

 

[Elephanto]

Never go reductionist

I agree, which is why we shouldn't deduct that because a substance shows beneficial effects with a low amount, net overall benefits should remain with an high amount. It's almost as if a bell curve is accurate to describe most aspects of life as we know it (too low fat intake/too high fat intake, inactivity/excess physical activity, undereating/overeating, undersleeping/oversleeping etc). That said, experimentation and self-observation shall trump any dogma.

 

[Sourdoughbanana]

Some references:

Natural honey lowers plasma glucose, C-reactive protein, homocysteine, and blood lipids in healthy, diabetic, and hyperlipidemic subjects: comparison... - PubMed - NCBI

Artificial honey slightly decreased cholesterol and LDL-C and elevated TG. Honey reduced cholesterol, LDL-C, and TG and slightly elevated high-density lipoprotein-cholesterol (HDL-C).

Honey consumed for 15 days decreased cholesterol (7%), LDL-C (1%), TG (2%), CRP (7%), homocysteine (6%), and PGL (6%), and increased HDL-C (2%).

In patients with hypertriglyceridemia, artificial honey increased TG, while honey decreased TG. In patients with hyperlipidemia, artificial honey increased LDL-C, while honey decreased LDL-C.

Honey decreased cholesterol (8%), LDL-C (11%), and CRP (75%) after 15 days.

Orange juice or fructose intake does not induce oxidative and inflammatory response. - PubMed - NCBI

Caloric intake in the form of orange juice or fructose does not induce either oxidative or inflammatory stress, possibly due to its flavonoids content

There’s also the overall diet which is another variable that can’t be predicted based on fructose biochemistry

https://www.ncbi.nlm.nih.gov/m/pubmed/29695707/

In young healthy adults, a conventional 3-meal structure with orange juice consumed together with meals had a favorable impact on energy balance, whereas juice consumption in-between meals may contribute to a gain in body fat and adverse metabolic effects.

^^^ Was it even freshly squeezed juice? I doubt it.

https://www.ncbi.nlm.nih.gov/m/pubmed/22876038/

Moro juice counteracts liver steatogenesis in mice with diet-induced obesity and thus may represent a promising dietary option for the prevention of fatty liver.

Anyways. Bloodworks and overall health are surrogates of a proper metabolism.

 

[Elephanto]

That study on Moro juice where they drank 4.1 mL of juice per day obviously doesn't qualify as an high intake of sugar. Honey is potently anti-bacterial which would explain its effect on inflammation. Would be good to have access to the full paper as neither the experiment where a CRP-lowering effect or the experiment where a slight TG-lowering effect were found state the amount of Honey.

 

[Tenacity]

I take away from @Sourdoughbanana's points that it's useless to talk about nutrients in isolation. We don't eat 'fructose', we eat whole fruits and juices, and so any research that's conducted should be with whole fruits.

 

[Elephanto]

@Tenacity So it's useless to consider the mechanical effects of Arachidonic Acid since we don't eat "AA", we eat Sunflower Oil or phytonutrient-rich Avocado ? My point is that with nutrients and food-specific components considered, there is possibly a point where overall net benefits on health disappear because of the mechanical effects of excess Fructose; and this hasn't been contradicted yet.

 

[Tenacity]

@Tenacity So it's useless to consider the mechanical effects of Arachidonic Acid since we don't eat "AA", we eat "Sunflower Oil" ? My point is that with nutrients and food-specific components considered, there is possibly a point where overall net benefits on health disappear because of the mechanical effects of excess Fructose; and this hasn't been contradicted yet.

It's not useless, but if a study shows that pure arachidonic acid has one effect and sunflower oil has the opposite, should we fear eating sunflower oil because of its arachidonic acid content? I don't deny your point on the excess of fructose, that seems common sense to me. The question is where that excess lies.

 

[Elephanto]

It's not useless, but if a study shows that pure arachidonic acid has one effect and sunflower oil has the opposite, should we fear eating sunflower oil because of its arachidonic acid content? I don't deny your point on the excess of fructose, that seems common sense to me. The question is where that excess lies.

Omega 3 directly competes with Arachidonic Acid in membranes to impair its conversion into prostaglandins, not exactly the same as Fructose still gets to be metabolized in the presence of phytonutrients. We should fear Fish Oil for other reasons though. About where "excess lies", I would say it's more likely when someone gets all of his carbs from sucrose and sources of free fructose by fear of starch unless this total carbs intake is moderate. It would be hard to argue a number as one could blame it on other parameters of the diet and environment, and this number would vary according to the basal health state. My initial point was more about Sourdough saying he was glad he dropped starch based on a quote that shows Fructose activates an essential enzyme but not considering that this effect doesn't require an high amount of Fructose and that it still happens when starch is also present in the diet.

My intent was mainly 1) to show that these mechanical effects exist and it could be useful to consider if someone has a problem with high sugar intake but doesn't know where it stems from (I've seen at least 3 persons coming on here saying they got a fatty liver since following a Peat diet and I don't spend much time looking at testimonies); though not saying it has to be the cause, just something to consider; and 2) that really the most important thing is experimentation and self-observation so I don't want to bring a dogmatic view that you have to be under x amount of Fructose to be healthy.

 

[Tenacity]

@Elephanto I wasn't using my example to suggest that fish oil was safe, just to illustrate a point.

I don't disagree with anything you've said, I just don't think it's clear where that excess lies. I know a number like 50g has been thrown around before. +1 on self-experimentation.

 

[Sourdoughbanana]

1) to show that these mechanical effects exist and it could be useful to consider if someone has a problem with high sugar intake but doesn't know where it stems from (I've seen at least 3 persons coming on here saying they got a fatty liver since following a Peat diet and I don't spend much time looking at testimonies); though not saying it has to be the cause, just something to consider; and 2) that really the most important thing is experimentation and self-observation so I don't want to bring a dogmatic view that you have to be under x amount of Fructose to be healthy.

1) absolutely, 100% agreed! I’ll see how the experiment goes. Besides, I won’t let go bananas, but they have starch... not a huge deal. I’m convinced the fatty liver people were overdoing a) refined sugar b) total calories c) fatty acids. I’ve also seen them share bloods here and when they looked terrible I was left shaking my head. Drinking a lot of coke, eating some secret ice cream brand, lots of saturated fat with artificial honey and table sugar in that industrial OJ, would yield NAFLD? Who knew

2) since X seems to be a contentious topic where science barely brings an answer - some studies on juices show an improvement in liver health, most studies on refined fructose show NAFLD - I’ll track my blood lipids of course.

We could always quote this study that shows a rate of hepatic glycogenolysis 3.5x lower at rest compared to when exercising.

Regulation of Net Hepatic Glycogenolysis and Gluconeogenesis during Exercise: Impact of Type 1 Diabetes | The Journal of Clinical Endocrinology & Metabolism | Oxford Academic

Keep in mind that their "healthy" subjects have double digit fasted insulin levels (gasp! or rather, again!). So that already sounds like a degree of insulin resistance.

Anyways, a common figure is that the 100ish grams of liver glycogen may be depleted within 1.5 hour of hard training. So how much liver glycogen do we actually burn at rest? How about during our sleep? I don't see it being less than 10 grams per hour.

Ergo, a lot of fruits - assuming we stick to a properly designed dietary plan as per above (60% carbs 20% proteins 20% fats, my ideal macro %, and an incredibly odd rarity in modern studies)

When it comes to PUFAs, well this is Ray Peat’s forum and he thinks little of those, whereas he has written at least 2 articles in defense of sugar vs diabetes and fatty liver. My opinion is that I’ve yet to see a high omega 6 meat (arachidonic acid isn’t found in plants) lead to improvements in inflammation. Omega 3s are different. If it’s linoleic acid we’re after, then we know that 1) conversion of LA to AA is very low 2) real plants (not the oil) pack a degree of vitamin E and other anti oxydants 3) nut consumption for example is associated with improvements in inflammation markers

So what’s the Y amount of PUFAs we can tolerate? There again, can’t resort to much data. I like pine nuts... plus sciadonic acid has a couple of nice studies too!

 

[Sourdoughbanana]

I think this paper states it well; ingestion of fructose by itself can't explain the hepatic disease we typically associate with it. Even though we're all aware of the endless possibilities where stuff could go wrong when we're playing with the fire that is sugar. The oil being, ahem, free fatty acids.

https://www.physiology.org/doi/full/10.1152/physrev.00019.2009

check out
D. Metabolic Fate of an Oral Fructose Load in Healthy Subjects

Studies aimed at delineating the dose threshold at which fructose starts to chronically exert such effects remain to be performed. In addition to that, in everyday life, fructose cannot be blamed as the only culprit for all metabolic disorders. Indeed, a high fructose consumption most of the time clusters with additional “risky” behaviors, such as a hypercaloric diet, a diet rich in saturated fat, or low physical activity. Thus which part of metabolic disorders can be attributed to fructose and which results from interactions with other risk factors?

 

[ecstatichamster]

This isn't an argument for starch avoidance or even high fructose intake. The fact that Fructose has beneficial functions (many that can be achieved at low doses) doesn't imply that it is beneficial in unlimited amount. High Fructose intake has been shown to potently increase lipogenesis.

Divergent effects of glucose and fructose on hepatic lipogenesis and insulin signaling. - PubMed - NCBI

Fructose induced lipogenesis: from sugar to fat to insulin resistance. - PubMed - NCBI

Effects of Dietary Fructose Restriction on Liver Fat, De Novo Lipogenesis, and Insulin Kinetics in Children With Obesity. - PubMed - NCBI

INCREASED FRUCTOSE CONSUMPTION IS ASSOCIATED WITH FIBROSIS SEVERITY IN PATIENTS WITH NAFLD

Fructose and sugar: A major mediator of non-alcoholic fatty liver disease. - PubMed - NCBI
High Fructose intake can increase gut permeability which would explain its effect on endotoxemia. Endotoxins also being a cause of liver damage.
Fructose: A Dietary Sugar in Crosstalk with Microbiota Contributing to the Development and Progression of Non-Alcoholic Liver Disease

I don’t trust those studies. Almost all of them are done with high PUFA chow. Or diets.

It is not plain that these studies are valid.

 

[ecstatichamster]

See

Triacylglycerol Secretion in Rats: Effects of Essential Fatty Acids and Influence of Dietary Sucrose, Glucose or Fructose | The Journal of Nutrition | Oxford Academic

Soybean Oil Is More Obesogenic and Diabetogenic than Coconut Oil and Fructose in Mouse: Potential Role for the Liver

 

[Obi-wan]

The cytosolic acetyl-CoA is used for fatty acid synthesis and the production of cholesterol. Cholesterol can, in turn, be used to synthesize the steroid hormones, bile salts, and vitamin D. -Wikipedia

Saturated fats to cholesterol to hormones, bile salts, and vitamin D...

 

[Mito]

As far as I know, they recycle GSSG back to GSH.