87 replies to this topic

[TheFountain]

misterE, You're assuming that everyone on a low carb diet is diabetic.

I thought what he meant basically was that insulin was not the driver of weight gain in non-diabetic individuals. To my understanding, this is essentially correct. Isn't one of the arguments of a couple low carb gurus that insulin production from carb-centric dieting is predominately responsible for the weight epidemics we see in modern times?

[Chupo]

TheFountain,

He's saying that low insulin is bad and goes on to describe lipotoxicity which is seen in diabetics and those with metabolic syndrome. The cause of lipotoxicity is just the opposite of what misterE says. It's chronic hyperinsulinemia. Insulin stimulates lipoprotein lipase, which cleaves fatty acids from triglycerides and ushers them into the cell. Under those conditions fat ends up in places it shouldn't be. When you REDUCE insulin, lipolysis is no longer inhibited and the body quickly clears the fat from the organs they don't belong in.

In this study on people with NAFLD, a low carb diet cleared 55% of hepatic TG in only two weeks compared to 28% in the calorie restricted group.

http://www.ncbi.nlm....pubmed/21367948

Edited by Chupoman, 12 August 2012 - 01:00 PM.

[misterE]

As for estrogen, it's bodyfat that converts testosterone to estrogen, not dietary fat.

True. But there's a heck of a lot of studies showing high-fat diets increase estrogen. While low-fat/high-fiber diets lower estrogen. This is one of the main mechanisms why many scientists link high-fat diets to breast-cancer and prostate-cancer. Just google the terms: "high fat diet estrogen pubmed".

Edited by misterE, 14 August 2012 - 11:00 PM.

[misterE]

So explain to me again how low insulin causes the accumulation of visceral fat.

Low insulin or insulin-resistance causes the adipose-tissue to release FFA's (to be used as energy). These FFA's accumulate around the vital organs in the midsection.

Edited by misterE, 14 August 2012 - 11:06 PM.

[misterE]

He's saying that low insulin is bad and goes on to describe lipotoxicity which is seen in diabetics and those with metabolic syndrome. The cause of lipotoxicity is just the opposite of what misterE says. It's chronic hyperinsulinemia.

Circulating triglycerides cannot enter the adipose-tissue (AT), thus lipoprotein-lipase (LPL) must cleave the FFA's (from the triglycerides) and transport them inside the AT to be once again repackaged and stored as triglycerides. Fatty-acids belong inside the AT. Insulin stimulates the uptake of FFA's into the AT by upregulating LPL. This is normal, and doesn't promote disease. The problem occurs when insulin can no longer "store-fat" so to speak. This is essentially due to the AT being overstuffed with triglycerides [1].

The adipocytes begin to expand as they store more and more triglycerdies. The more triglycerides that are stored within the adipocytes, changes the type of adipocytokines produced by the adipocytes (less adiponectin and more IL-6 for instance) and the less sensitive they become to the effects of insulin. Eventually the adipocytes become insulin-resistant and FFA's begin leaking out of the AT and end up in "ectopic" sites. Ectopic literally means: "where something doesn't belong". So FFA's accumulate places you don't want them to accumulate, like the muscles, liver, heart, pancreas, endothelium etc. This accumulation of FFA's then causes those tissues to also become insulin-resistant. So then you develop full body insulin-resistance (or type-2-diabetes).

Since insulin can no longer bind to it's receptor, due to intracellular interference caused by FFA's. The insulin has nowhere to go and cannot be metabolized properly, therefore it just stays in circulation. You basically end up with a huge amount of circulating insulin that doesn't work properly. This circulating insulin downregulates the binding proteins of IGF-1 and sex-hormones, which then causes unregulated cell-proliferation, which can contribute to cancer or hyperplasia of various tissues (like the skin).


[1] Int J Clin Pract Suppl. 2004 Oct;(143):9-21. Dysfunctional fat cells, lipotoxicity and type 2 diabetes. DeFronzo RA.

Edited by misterE, 14 August 2012 - 11:41 PM.

[Hebbeh]

As for estrogen, it's bodyfat that converts testosterone to estrogen, not dietary fat.

True. But there's a heck of a lot of studies showing high-fat diets increase estrogen. While low-fat/high-fiber diets lower estrogen. This is one of the main mechanisms why many scientists link high-fat diets to breast-cancer and prostate-cancer. Just google the terms: "high fat diet estrogen pubmed".

Sure...if the person eating the high fat diet (junk food diet) just happens to be a roly poly fat man couch potato...no surprises there. Lots of ways to tell a story...apples to oranges. A higher fat diet does not always have to mean junk food eaten by a fat couch potato. Why do you always cherry pick studies on fat boys??? Do you think there are any fat couch potatoes on a longevity and health forum?

[Chupo]

misterE,

You keep repeating the same garbage even though you've already been proven wrong. Stop being dogmatic and accept the truth. Your diet isn't the only way.

Edited by Chupoman, 15 August 2012 - 02:45 AM.

[Chupo]

As for estrogen, it's bodyfat that converts testosterone to estrogen, not dietary fat.

True. But there's a heck of a lot of studies showing high-fat diets increase estrogen. While low-fat/high-fiber diets lower estrogen. This is one of the main mechanisms why many scientists link high-fat diets to breast-cancer and prostate-cancer. Just google the terms: "high fat diet estrogen pubmed".

Sure...if the person eating the high fat diet (junk food diet) just happens to be a roly poly fat man couch potato...no surprises there. Lots of ways to tell a story...apples to oranges. A higher fat diet does not always have to mean junk food eaten by a fat couch potato. Why do you always cherry pick studies on fat boys??? Do you think there are any fat couch potatoes on a longevity and health forum?

Usually when a study says "high fat" it's high fat AND high carb.

[Hebbeh]

As for estrogen, it's bodyfat that converts testosterone to estrogen, not dietary fat.

True. But there's a heck of a lot of studies showing high-fat diets increase estrogen. While low-fat/high-fiber diets lower estrogen. This is one of the main mechanisms why many scientists link high-fat diets to breast-cancer and prostate-cancer. Just google the terms: "high fat diet estrogen pubmed".

Sure...if the person eating the high fat diet (junk food diet) just happens to be a roly poly fat man couch potato...no surprises there. Lots of ways to tell a story...apples to oranges. A higher fat diet does not always have to mean junk food eaten by a fat couch potato. Why do you always cherry pick studies on fat boys??? Do you think there are any fat couch potatoes on a longevity and health forum?

Usually when a study says "high fat" it's high fat AND high carb.

Yeah...politically correct for junk food.

[misterE]

Hebbeh--

You can believe what you want. But most studies are clear and consistent that eating high-fat diets promote excessive levels of estrogen. Many of these studies were in fact done in normal weight subjects (like vegetarians or Asian women). Plus I'm sure you know that body-fat contains aromatase. Well animal-fat contains the aromatase-enzyme as well, so when you think about it… people eating animal-fat are literally eating aromatase!

[niner]

Well animal-fat contains the aromatase-enzyme as well, so when you think about it… people eating animal-fat are literally eating aromatase!

Enzymes are proteins. When you eat them, they're digested like any other protein. If they survived cooking, they will quickly be deactivated in the stomach.

[misterE]

misterE,

You keep repeating the same garbage even though you've already been proven wrong. Stop being dogmatic and accept the truth. Your diet isn't the only way.

Really?! Well if insulin causes lipotoxicity by increasing LPL (like you claimed), why are diabetics given insulin or metformin (a drug that increases the effects of insulin)?

Lipotoxicity is caused by a lack of insulin-receptor signaling (activation). The reason why hyperinsulinemia exists is because the insulin cannot bind to its receptor... therefore it cannot be metabolized, and since it can't be metabolized it stays elevated in the bloodstream. In other words, insulin remains high in the blood because it is unable to get into the cells. The reason why it can’t get into the cells is because FFA’s downregulate and interfere with the insulin-receptor.

Edited by misterE, 17 August 2012 - 03:59 AM.

[Chupo]

Low carb diets do not cause lipotoxicity. I've already posted studies showing that it CURES it! Now stop your non-sense. You are why I don't believe a word that comes out of a vegan's mouth. You're so steeped in dogma you can't see the truth when it hits you in the face.

[misterE]

Low carb diets do not cause lipotoxicity. I've already posted studies showing that it CURES it! Now stop your non-sense. You are why I don't believe a word that comes out of a vegan's mouth. You're so steeped in dogma you can't see the truth when it hits you in the face.

So I guess you aren't going to answer my question? If insulin causes lipotoxiticy (like you claimed) why then are diabetics given insulin?

Insulin increases LPL in adipose-tissue. Which means FFA's will be stored in the adipose-tissue where they belong, instead of places they don't, like the muscles or liver.

Edited by misterE, 17 August 2012 - 04:09 PM.

[Chupo]

Low carb diets do not cause lipotoxicity. I've already posted studies showing that it CURES it! Now stop your non-sense. You are why I don't believe a word that comes out of a vegan's mouth. You're so steeped in dogma you can't see the truth when it hits you in the face.

So I guess you aren't going to answer my question? If insulin causes lipotoxiticy (like you claimed) why then are diabetics given insulin?

Insulin increases LPL in adipose-tissue. Which means FFA's will be stored in the adipose-tissue where they belong, instead of places they don't, like the muscles or liver.

You're the one who said low insulin causes lipotoxicity. You are equating low insulin with insulin resistance which is like equating water with fire. Insulin resistance causes MORE insulin to be produced thus hyperinsulinemia.

Type one diabetics are given insulin to keep them alive. If they don't get it, they waste away... just the opposite of what you're saying will happen in the absence of insulin. Type two's shouldn't be given insulin unless their beta cells are worn out. The insulin resistance should be addressed before throwing more insulin at the problem.

One more time, look back at the studies that shows LESS abdominal and organ fat in the low carbers.

Edited by Chupoman, 17 August 2012 - 04:30 PM.

[misterE]

Insulin resistance causes MORE insulin to be produced thus hyperinsulinemia.

Yes, because the insulin is becoming less and less effective and the body needs more to compensate. FFA's cause the "resistance" in the first place. Inhibiting lipolysis decreases FFA's and improves insulin-sensitivity. Unfortunately this also inhibits weight-loss. Low-carb diets (like an all-vegetable diet) or fasting will increase insulin-sensitivity by promoting oxidation of the FFA's. A high-fat/low carb diet is awful because the fat you are oxidizing is constantly being replaced with the fat you are eating. The safest way to undergo lipolysis and fat-oxidation is by keeping insulin-secretion low and also fat intake low. Fasting accomplishes both at the same time.

There are basically two ways to lower FFA's. You can either oxidize them or shove them back into the adipose-tissue. But if you are on a high-fat diet, the FFA's you oxidize will be replaced with the fat you just ate. That is the largest flaw in Atkins-type diets.

[Hebbeh]

The oldest man in the USA at 111 doesn't look or act a day over 65. Although he is vegan, the corner stone of his diet and what he attributes his longevity and healthy to is Olive Oil. In addition to plenty of Olive Oil, he subsists mainly off green veggies and fruit along with honey (think fructose for all you fruit and honey phobias) and Dark Chocolate eating pretty much the same foods every day.

With a non varied diet of green veggies, fruit, olive oil, dark chocolate and honey, his macronutrient ratio has to be higher fat (all the olive oil and chocolate) and moderate carb (green veggies and fruit) with plenty of fructose (fruit and honey) but low protein. He also enjoys garlic with all that olive oil. He doesn't appear to include starches in his diet...other than the 111 birthday cakes.

Much to learn from this man. I totally agree with his life philosophy of all things in moderation. He looks, acts, and talks fantastic at his 111 birthday party. He proves everybody wrong. Don't be scared of healthy fats and fructose (fruit and honey).

http://www.abc15.com...ts-to-longevity

Much thanks to AgeVivo for sharing this here: http://www.longecity...8184-olive-oil/

[Chupo]

misterE,

You keep on talking about diabetes. There are ways to lower glucose as well but you don't talk about that. You can either oxidize it, store it as glycogen, or convert it to triglyrerides. Diabetics have high concentrations of glucose, triglycerides, and FFA. None are good at high levels. Go back and re-read what's been posted before.

Edited by Chupoman, 18 August 2012 - 01:50 AM.

[Telo]

 

Are you seriously proposing that we don't need 15-25% protein (as energy %)? Or that we should have a zero fat diet? Where would the fat soluble vitamins come from?

I would say the optimal macro nutrient ratio would be 5% fat, 85% starch, 10% protein. Fat-soluble vitamins are soaked up in body-fat. Contrary to popular belief, you don't have to put butter on your carrots to absorb the beta-carotene. Or drink olive oil when you sunbathe.

 

 

I agree about the 10% protein (for longevity and long term health) but 5% fat? Plant based no oil I can understand. But some flax seeds and a handful of walnuts and almonds  would take you much higher than 5 % right? I find it would be hard to find any science supporting avoiding nuts.

 

You say 85% starch. You don't eat any fruit?

 

Otherwise I mostly agree with what you say in this thread, for example about starches being better for health than butter.

I also think the enthusiasm for low carb among the longevity crowd and self hackers is much bigger than what the overall science would suggest is reasonable. 

[Telo]

In response to the original post:

It's clear that americans never went low fat in any shape or form.

Posting facts like these becomes a problem for many low-carbers. It's called cognitive dissonance. 

 

These facts pokes a big hole in the special version of history that's always repeated in the low carb bubble. Everything is the fault of the evil Ancel Keys who together with the government told everyone to eat pure sugar and low fat cookies. And since then we have all been in a big low fat experiment. And look were it got us. We're all fat and sick.

 

And the obvious solution: All carbs are evil (high fructose corn sirup or intact grains doesn't matter). Eat lard. Never mind half a century of science saying butter isn't very healthy -it's all a big conspiracy. The sugar industry has bought every single scientist until now. Finally we have been saved by our heroes Gary Taubes and Nina Teicholts who was brave enough to stand up and speak the truth.

[misterE]

 

 

I agree about the 10% protein (for longevity and long term health) but 5% fat? Plant based no oil I can understand. But some flax seeds and a handful of walnuts and almonds  would take you much higher than 5 % right? I find it would be hard to find any science supporting avoiding nuts.

 

You say 85% starch. You don't eat any fruit?

 

Otherwise I mostly agree with what you say in this thread, for example about starches being better for health than butter.

I also think the enthusiasm for low carb among the longevity crowd and self hackers is much bigger than what the overall science would suggest is reasonable. 

 

 

You could eat flaxseeds and nuts while still keeping your total fat to 5%.

 

A few pieces here and there, but not a fruit-based diet.

 

People like to justify eating rich foods. They would find it much more pleasurable to eat bacon and eggs for breakfast instead of barley or oats.  

[mccoy]

Re.: the demonization of fruit.

I wonder if there are any random clinical trials on the alleged deleterious effects of fresh fruit or if it's all the result of the theoretical speculations of Dr. Lustig. He's sure right about some mechanistic aspects of fructose metabolism, but might have neglected other some important issues (the fact that fruit is not pure fructose but other sugars and phytochemicals+fibers has already been cited).

 

Even Valter Longo, who's not by any means a fan of the low carb or paleo diet, does not include fruit in his longevity diet. 

 

The blue zones populations though do eat fruit, when available and in large quantities. Especially so the Costa Ricans.

 

Again, I'd like to read some well-designed random clinical trials which underline a dose-response relationship of fruit consumption, rather than listen to mere speculation. 

[misterE]

 

 

Again, I'd like to read some well-designed random clinical trials which underline a dose-response relationship of fruit consumption, rather than listen to mere speculation. 

 

Fruit consumption is associated with beneficial health outcomes. 

[mccoy]

Dr. Lustig is not the only voice on fructose over there.

 

There are many other voices which claim the opposite of what he claims, that is, that fructose in natural foods, fruit and even honey, is beneficial. For example:

 

 

Oxid Med Cell Longev. 2018; 2018: 4757893.

Published online 2018 Feb 4. doi:  10.1155/2018/4757893

PMCID: PMC5817209

Honey and Diabetes: The Importance of Natural Simple Sugars in Diet for Preventing and Treating Different Type of Diabetes

Otilia Bobiş, 1 Daniel S. Dezmirean, 2 and Adela Ramona Moise 2

Author information ► Article notes ► Copyright and License information ►

 

 

 

 

2. Fructose and the Hypoglycemic Effect of Honey

Fructose content of honey varies from 21 to 43% and the fructose/glucose ratio from 0.4 to 1.6 or even higher [31–34]. Although fructose is the sweetest naturally occurring sweetener, it has a glycemic index of 19, compared to glucose which has 100 or sucrose (refined sugar) with 60 [35]. Different studies reveal the hypoglycemic effect of honey, but the mechanism of this effect remains unclear. It was suggested that fructose, selective mineral ions (selenium, zinc, copper, and vanadium), phenolic acids, and flavonoids might have a role in the process [10, 11, 31, 33, 36, 37].

There is evidence that fructose tends to lower blood glucose in animal models of diabetes [38, 39]. Mechanisms involved in this process may include reduced rate of intestinal absorption [40], prolongation of gastric emptying time [41, 42], and reduced food intake [43, 44]. Fructose stimulates glucokinase in hepatocytes, which plays an important role in the uptake and storage of glucose as glycogen by the liver. Glucose on the other hand, which is present beside fructose in honey, enhances the absorption of fructose and promotes its hepatic actions through its enhanced delivery to the liver [45, 46].

The pancreas is an important organ in diabetes, because it secrets two glucose-regulating hormones—insulin and glucagon—and honey might protect this organ against oxidative stress and damage with its antioxidant molecules, this being another potential mechanism of hypoglycemic effect of honey [32, 47].

Different studies were made on the effect of fructose on glycemic control, glucose-regulating hormones, appetite-regulating hormones, body weight, food intake, and oxidation of carbohydrates or energy expenditure [38, 44, 48–61].

Fructose administrated alone or as part of sucrose molecule in normal rats improved glucose homeostasis and insulin response compared to rats which received glucose [62]. Other studies show that fructose supplementation in normal or type 2 model of diabetic rats produced lower levels of plasma insulin and glucose, more than other administrated sugars [38].

 

[mccoy]

More on the beneficial effects of fructose, this tiem with a randomized controlled trial:

 

 

The effect of two energy-restricted diets, a low-fructose diet versus a moderate natural fructose diet, on weight loss and metabolic syndrome parameters: a randomized controlled trial Magdalena Maderoa, ⁎, Julio C. Arriagaa , Diana Jalalb , Christopher Rivardb , Kim McFannb , Oscar Pérez-Méndeza , Armando Vázqueza , Arturo Ruiza , Miguel A. Lanaspab , Carlos Roncal Jimenezb , Richard J. Johnsonb , Laura-Gabriela Sánchez Lozadaa,b a Division of Nephrology, Department of Medicine, Instituto Nacional de Cardiología Ignacio Chávez, Juan Badiano no 1 Col Seccion XVI Tlalpan, México City, 14080, México b Division of Renal Diseases and Hypertension, University of Colorado, Denver, CO, USA

 

 

One of the proposed causes of obesity and metabolic syndrome is the excessive intake of products containing added sugars, in particular, fructose. Although the ability of excessive intake of fructose to induce metabolic syndrome is mounting, to date, no study has addressed whether a diet specifically lowering fructose but not total carbohydrates can reduce features of metabolic syndrome. A total of 131 patients were randomized to compare the short-term effects of 2 energy-restricted diets—a low-fructose diet vs a moderate natural fructose diet— on weight loss and metabolic syndrome parameters. Patients were randomized to receive 1500, 1800, or 2000 cal diets according to sex, age, and height. Because natural fructose might be differently absorbed compared with fructose from added sugars, we randomized obese subjects to either a low-fructose diet (<20 g/d) or a moderate-fructose diet with natural fruit supplements (50-70 g/d) and compared the effects of both diets on the primary outcome of weight loss in a 6-week follow-up period. Blood pressure, lipid profile, serum glucose, insulin resistance, uric acid, soluble intercellular adhesionmolecule–1, and quality of life scores were included as secondary outcomes. One hundred two (78%) of the 131 participants were women, mean age was 38.8 ± 8.8 years, and the mean body mass index was 32.4 ± 4.5 kg/m2 . Each intervention diet was associated with significant weight loss compared with baseline. Weight loss was higher in the moderate natural fructose group (4.19 ± 0.30 kg) than the lowfructose group (2.83 ± 0.29 kg) (P = .0016). Compared with baseline, each intervention diet was associated with significant improvement in secondary outcomes. Reduction of energy and added fructose intake may represent an important therapeutic target to reduce the frequency of obesity and diabetes. For weight loss achievement, an energy-restricted moderate natural fructose diet was superior to a low-fructose diet. © 2011 Elsevier Inc. All rights reserved.

 

[misterE]

From what I understand about fructose metabolism is that when fructose is consumed it is taken up by the liver and converted into liver glycogen, once glycogen capacity is full, fructose can then be converted into fatty-acids like palmitic-acid and others. Lustig says that the conversion of fructose into fatty-acids contributes to insulin-resistance... and it can if you become lipotoxic. Also remember that 30% of the fructose calories being converted into fatty-acids are lost in the process and that most lipotoxicity, ectopic-fat accumulation and fatty-liver often seen in diabetes and insulin-resistance is caused by chronic lipolysis due to insulin-resistant adipose-tissue, not the bit of fat we made from extra fructose.  

[mccoy]

MisterE, it's probably and basically as you say. in the following discussion From Navdeep Chadel, 'navigating metabolism', 2015, page 100, when he says 'if teh liver has met its energetic needs' he means if the liver has already satisfied its storage capacity of glycogen. So the fructose leaves the fructose 6-phosphate path and turns into the glyceraldehyde/Dihydroxyacetone phosphate/glyceraldehyde 3-phosphate path, producing fatty acids and ultimately triglycerides.

 

 

• Most cells do not have GLUT5, the major transporter of fructose. The liver has abundant GLUT5 transporters, making fructose readily accessible for metabolism.
• ... A major regulatory step in glycolisis is phospofructase kinase1. This step is bypassed by fructose entry into glycolisis.IThus, i fthe liver has met its energetic needs, it converst excess fructose into glyceraldeihyde, which is converted into glycerol 3-phosphate, a precusor for triglycerides.
• (my synthesis here) another path which generates fatty acids is fructose→dihydroxyacetone phosphate.

 

So the key seems to be the 'excess' word.  which is underlined in teh following article. Isocaloric comparisons with other sugars do not suggest deleterious effects of fructose, whereas hypocaloric comparison yield detrimental effects.

 

In a few words, fructose is only bad if we already assume sugars in excess. Our body fat percentage can probably suggestg to us if we are at risk to exceed in fructose.

 

Cf. "Effect of Fructose on Established Lipid Targets: A Systematic Review and Meta‐Analysis of Controlled Feeding Trials"

 

Journal of the American Heart Association. 2015

 

http://jaha.ahajourn...ent/4/9/e001700

 

Conclusions    Overall, the updated evidence for the effect of fructose on established lipid targets for cardiovascular disease risk reduction does not support earlier identified thresholds on which current clinical practice guidelines are based. There was no significant effect of fructose on LDL‐C, non‐HDL‐C, apo B, triglycerides, or HDL‐C in isocaloric comparisons with other carbohydrates across individuals with different metabolic phenotypes. There was, however, evidence of a significant triglyceride and apo B–raising effect in hypercaloric comparisons in which fructose supplemented diets with excess calories. In the absence of an effect in isocaloric comparisons, the effect of fructose seen in hypercaloric comparisons appears more attributable to the calories rather than fructose per se.  [...]   [emphasis added]

 

 

 

 

Edited by mccoy, 21 March 2018 - 01:19 PM.

[misterE]

And also remember that replacing starch for sugar lowers hepatic fatty-acid synthesis.