28 replies to this topic

[misterE]

Quick summary:

The size of the fat cell; formally called the adipocyte, determines how sensitive you are to insulin. When fat-cells (adipocytes) are small, the body is obligated to increase insulin-sensitivity to fill up those fat-cells.

The size of the adipocyte determines the type of hormones the adipocyte secretes; some hormones like adiponectin are beneficial while some, like resistin, are not.

The storage of dietary-fat inside fat-cells is healthy fat metabolism. When you eat fatty foods, the best place for that fat to end up is inside the fat-cells. However, the more fat that gets stored within the adipocytes causes them to enlarge. And like said before, when fat-cells enlarge they began to malfunction; they begin to secrete inflammatory hormones, they begin to suck up steroids and most importantly they begin to lose their sensitivity to insulin.

Now insulin has some very important roles in fat-cell metabolism. In healthy people, insulin is supposed to store dietary-fat in the adipocytes and inhibit the adipocytes from undergoing a process called: lipolysis.

This is crucial to understand, because when the fat-cells enlarge they are less able to store dietary-fat and become less sensitive to the inhibitory effects of insulin on the lipolysis process.

When the fat-cells become too large, the body purposely induces insulin-resistance within the fat-cells in order to shrink them and eventually restore insulin-sensitivity. When the fat-cells become insulin-resistant, they do begin to shrink but they release a huge flux of free-fatty-acids (FFA’s) —or commonly called non-esterfied-fatty-acids (NEFA’s)—into the circulation as a consequence, these FFA’s eventually end up accumulating inside the mitochondria of cells in very important organs (like the muscles, pancreas, heart, kidneys, brain, liver, veins, etc) and causes malfunction, inflammation and oxidative-stress within the cells of these organs, causing them to undergo a process called lipoapoptosis. The accumulation of FFA’s in cells also reduces the storage of glucose and amino-acids.

Eating in a way (and practicing techniques) that keep fat-cells small will ensure that you will keep optimal insulin-sensitivity as you age.

Exercise causes acute lipolysis and exports FFA’s to the muscle for oxidation. This in turn will actually increase insulin-sensitivity since the fatty-acids being exported from the adipoctye will actually be oxidize during exercise.

Fasting is another good way of shrinking you fat cells, as it once again it causes the body the shift into a fat-burning mode. Fasting for a day can burn about half a pound of fatty-acids.

Lipolysis is fine as long as you burn more fat than you ingest. Certain foods are notorious for causing fat-cell hypertrophy.

The first foods that need mentioning are saturated-fats found in butter, milk, cheese, meats, eggs, etc. Saturated-fat is very easily stored within the adipocytes, causing them to enlarge.

Vegetable-oils are the most fattening food on the planet. Vegetable-oil (of any kind) is pure fat and all of it gets deposited right into the fat-cells, causing them to enlarge.

Next are nuts, seeds and avocadoes. Many health conscious people eat nuts and avocadoes shamelessly, however this fat is going to be stored… besides, most of the fat in nuts and avocadoes is omega-6, which modern humans have way too much within our bodies already.

Last is fructose. Fructose converts into fat, which in turn can enlarge fat-cells… but by removing the major sources of premade-fat (animal-fats, oils, and nuts) fructose by itself is not as likely to induce fat-cell hypertrophy (when combined with a low-fat/high-fiber, starch based diet).


In order to shrink your fat cells, a protocol of temporarily fasting (24 hours per week) ,combined with daily exercise, combined with a diet of grains, beans, vegetables, stews and soups will do the trick. Once your fat-cells shrink, you will begin to regain your metabolic-health and be able to better store nutrients within the body.

[blood]

Why is almost every post by MisterE is downloaded?

I understand that what constitutes an optimum diet is controversial, but come on.

This is a very interesting topic. Several drugs used for diabetes & metabolic syndrome have an effect of causing a proliferation of small, subcutaneous fat cells, which leads to a reduction of insulin resistance. Some of these drugs also cause a redistribution of body fat (reduction of visceral fat, more subcutaneous fat) which also seems to be beneficial. Of course, it would be good if these changes could be induced solely through dietary choices or calorie restriction. Not sure if they can.

Edited by blood, 04 November 2013 - 08:48 AM.

[misterE]

Why is almost every post by MisterE is downloaded?

What do you mean by this exactly?

This is a very interesting topic. Several drugs used for diabetes & metabolic syndrome have an effect of causing a proliferation of small, subcutaneous fat cells, which leads to a reduction of insulin resistance.

Right, it seems contradictory, but the proliferation of subcutaneous fat-cells (adipocytes) means there is more room for fat to accumulate in a healthy way.

Some of these drugs also cause a redistribution of body fat (reduction of visceral fat, more subcutaneous fat) which also seems to be beneficial.

Storing fatty-acids subcutaneously is the healthy way to store fat, it doesn’t pose harm (and in women, some subcutaneous-fat is considered healthy because it gives women curves, breasts and buttocks, which are considered attractive and means she is fertile).



It is when subcutaneous-fat begins to malfunction (because of enlarged and inflamed fat-cells) that the subcutaneous-fat becomes resistant to the effects of insulin and you get an outpour of FFA’s into the circulation and peripheral-tissues. This cascade now causes insulin-resistance within the entire body.

Of course, it would be good if these changes could be induced solely through dietary choices or calorie restriction. Not sure if they can.

Sure. Insulin does that naturally. Most of these drugs for insulin-resistance or metabolic-syndrome work by enhancing the effects of insulin… for instance:

Insulin promotes the growth of fat-cells (which by itself doesn’t cause obesity unless you fill those fat-cells with fatty, greasy or oily foods). The more fat-cells you have, the more you are protected from lipid-overspill into the peripheral tissues.

Insulin naturally redistributes visceral-fat into subcutaneous areas, by promoting triglyceride accumulation in fat-cells and by inhibiting the release of FFA’s into peripheral tissue, such as the muscle or liver.



Insulin is needed for beta-cell proliferation. And beta-cells are needed for insulin production. Thus if the cycle is broken, you are in danger and your survival goes down quick; FFA’s released from excessive lipolysis accumulate in and on the pancreas and starve it of insulin, thus you get apoptosis within the beta-cells and when the beta-cells begin to die off, you can’t make as much insulin to suppress lipolysis anymore, which means more and more FFA’s will accumulate inside your veins and vital organs around the mid-section (visceral-fat).



That is why I suggest eating a highly insulinogenic diet. Because insulin is quite literally THE CURE to metabolic-syndrome and people with insulin-resistance are literally resistant to the cure, despite sometimes having high levels (hyperinsulinemia).

[typ3z3r0]

He accidentally wrote "downloaded" instead of "downvoted".

[blood]

He accidentally wrote "downloaded" instead of "downvoted".

It was the autocorrect on my ipad. I misspelled "downvoted" and it got changed to "downloaded" without my noticing.

[misterE]

Well if that is the question, let me answer it. I think many people are confused about the whole insulin-resistance theme and think of insulin as an evil villain, when in fact the opposite is true. My post are contradictory to what many here believe, and as a way of protest, I presume they downvote it.

[JohnD60]

Well if that is the question, let me answer it. I think many people are confused about the whole insulin-resistance theme and think of insulin as an evil villain, when in fact the opposite is true. My post are contradictory to what many here believe, and as a way of protest, I presume they downvote it.

I am not confused by it, I just don't agree with some things you say regarding insulin. And yes, I do think hyper insulin production is an evil villian, and I think that is mainstream. If you are going to make extraordinary non mainstream claims I think you need to provide some references/links, but I am not a moderator.

[blood]

If you are going to make extraordinary non mainstream claims I think you need to provide some references/links, but I am not a moderator.

Yes, references should be provided.

However, it is also bad sport to downvote someone without decloaking and offering a reason for your objections. Even if your critique amounts to little more than "please provide references".

[misterE]

This is probably my favorite reference to cite on the subject:


Int J Clin Pract Suppl. 2004 Oct;(143):9-21.
Dysfunctional fat cells, lipotoxicity and type 2 diabetes.
DeFronzo RA.
Abstract
Type 2 diabetes is characterized by insulin resistance and impaired insulin secretion. Considerable evidence implicates altered fat topography and defects in adipocyte metabolism in the pathogenesis of type 2 diabetes. In individuals who develop type 2 diabetes, fat cells tend to be enlarged. Enlarged fat cells are resistant to the antilipolytic effects of insulin, leading to day-long elevated plasma free fatty acid (FFA) levels. Chronically increased plasma FFA stimulates gluconeogenesis, induces hepatic and muscle insulin resistance, and impairs insulin secretion in genetically predisposed individuals. These FFA-induced disturbances are referred to as lipotoxicity. Enlarged fat cells also have diminished capacity to store fat. When adipocyte storage capacity is exceeded, lipid 'overflows' into muscle and liver, and possibly the beta-cells of the pancreas, exacerbating insulin resistance and further impairing insulin secretion. In addition, dysfunctional fat cells produce excessive amounts of insulin resistance-inducing, inflammatory and atherosclerosis-provoking cytokines, and fail to secrete normal amounts of insulin-sensitizing cytokines. As more evidence emerges, there is a stronger case for targeting adipose tissue in the treatment of type 2 diabetes. Peroxisome-proliferator activated receptor gamma (PPARgamma) agonists, for example the thiazolidinediones, redistribute fat within the body (decrease visceral and hepatic fat; increase subcutaneous fat) and have been shown to enhance adipocyte insulin sensitivity, inhibit lipolysis, reduce plasma FFA and favourably influence the production of adipocytokines. This article examines in detail the role of adipose tissue in the pathogenesis of type 2 diabetes and highlights the potential of PPAR agonists to improve the management of patients with the condition.

[blood]

I am taking telmisartan, metformin, and various herbal extracts (in conjunction with a reduced calorie, but so far not a low fat, diet) in the hope of whittling away my visceral fat and gradually reducing my overall body fat %. Breakfast is a piece of fruit and a handful of pills. Dinner is some carbs, some vegetables, and also some fats: olive oil, nuts, chocolate. My diet is mostly vegetables & grains, plus small amounts of fat-rich foods. I've tried eating some meat recently (after not eating any for a long time). The first one or two times, the meat (kangaroo) was insanely delicious. I couldn't get enough. Then I bought more, ate it every night for a week, and now feel sick at the thought of consuming any more.

I am seeing a slow drop in overall body fat %. Of course that drop may have happened eventually just with a reduction in calories.

Edited by blood, 22 November 2013 - 02:23 AM.

[TheFountain]

I think the bigger question is why does he get downvoted despite providing references?

I think the bigger question is why does he get downvoted despite providing references?

[misterE]

Prolonged fasting and low-carb diets reduce subcutaneous-fat but increase visceral-fat. Whereas refeeding on highly insulinogenic foods (milk, beans, potatoes, flour and sugar) do the opposite; increase subcutaneous-fat and decrease visceral-fat.



When you remove carbohydrates from the diet, the Randle-Cycle becomes altered and the stored fat in the subcutaneous regions gets summoned as energy substrate. When regularly eating starchy foods, stored fat isn’t needed as energy, thus it is kept locked away in subcutaneous regions.



This phenomenon is why older people who become resistant to the effects of insulin have what I call “fat migration”. Women lose their curves, their breasts, and that plump bubble-butt; because the fat in those areas is now being used as energy (the fat from the breast and buttocks migrates to the mid-section to be used as food for the vital organs located there, because their body has lost the ability to metabolize carbohydrates).

Edited by misterE, 22 November 2013 - 07:37 PM.

[Mind]

Mister E has a religious devotion to veganism, which is fine, but it introduces extreme bias into his reasoning. That is probably why he gets down-voted often. Many people have joined into Mr. E's discussions about lipid/metabolic science, krebs cycle, macronutrients, only to be ignored. It is pointless to provide counter-points/references.

As an aside, I am fairly certain that animal-based foods are on their way out in the near future, which is fine as well, even though I enjoy being an omnivore.

[misterE]

I think the bigger question is why does he get downvoted despite providing references?

I think it’s because I challenge people’s belief about nutrition. And many folks become uncomfortable when evidence emerges that cause them to reevaluate their dietary-philosophy and as a way of protest, they downvote me.



I have had some very uncomfortable paradigm-shifts and I probably will have many more. And although uncomfortable at first, these paradigm-shifts are actually a good thing, because it means that you are refining or concentrating your beliefs and accelerating their evolution.

[misterE]

Mister E has a religious devotion to veganism, which is fine, but it introduces extreme bias into his reasoning.

Not necessarily to veganism per say… rather the “optimal-diet” for the human frame, that diet in my opinion is mostly vegan. There are certainly plant-based foods that don’t fit into my idea of an optimal-diet, like nuts and avocadoes for instance. If I were bias and if veganism is my agenda, then I wouldn’t care if people ate nuts, used vegetable-oils and didn’t eat starch, as long as they didn’t eat animal-products… but anyone familiar with me and my posts knows that I promote a highly insulinogenic diet that is based on starch.

Many people have joined into Mr. E's discussions about lipid/metabolic science, krebs cycle, macronutrients, only to be ignored. It is pointless to provide counter-points/references.

That’s not entirely true because I have had many debates here on the forum, which both sides bringing forth their best references. Now I don’t respond to everyone’s counter-point, but that doesn’t mean I don’t acknowledge and appreciate them. These counter-points (among other things) are what help me evolve my beliefs about nutrition.

I am fairly certain that animal-based foods are on their way out in the near future,

I agree. The rich western-diet which is a very meat centric type of diet is flat-out non sustainable and promotes the death of humans, animals and mother-earth. It’s almost as if the western-diet was orchestrated intentionally to destroy the world, but that’s another discussion.

[TheFountain]

Mister E has a religious devotion to veganism, which is fine, but it introduces extreme bias into his reasoning. That is probably why he gets down-voted often.

Is that a reason to downvote his provided references?

As an aside, I am fairly certain that animal-based foods are on their way out in the near future

What do you mean by this?

[nowayout]

I am taking telmisartan, metformin, and various herbal extracts (in conjunction with a reduced calorie, but so far not a low fat, diet) in the hope of whittling away my visceral fat and gradually reducing my overall body fat %.

Wouldn't exercise be preferable to drugs?

[blood]

I am taking telmisartan, metformin, and various herbal extracts (in conjunction with a reduced calorie, but so far not a low fat, diet) in the hope of whittling away my visceral fat and gradually reducing my overall body fat %.

Wouldn't exercise be preferable to drugs?

Possibly/ probably. I do walk around 10,000 steps/ day.

The metformin obliterated my appetite - I lost around 10 kg when I commend taking it. I like it because it lets me eat a reduced calorie diet without any cravings. It also allows me to go longer without eating, without feeling like crap.

The telmisartan I can justify because I had "prehypertension" which I wanted to nip in the bud before it progressed to full blown hypertension. Hopefully that will go away once I've lost more weight. I'm also doing other things (magnesium supplements, less salt, etc).

Edited by blood, 24 November 2013 - 10:38 AM.

[misterE]

The metformin obliterated my appetite

Metformin is an insulin-sensitizer; it makes insulin more potent or effective at binding to its receptors. One of the main roles of insulin is to stimulate satiety in the brain. So since metformin increases the effectiveness of insulin… that means your insulin is more effective at regulating satiety. Insulin also lowers triglycerides and FFA’s in the blood which enables leptin (another appetite regulatory hormone) to cross the blood-brain-barrier and promote satiation.

[Chupo]

The metformin obliterated my appetite

Metformin is an insulin-sensitizer; it makes insulin more potent or effective at binding to its receptors. One of the main roles of insulin is to stimulate satiety in the brain. So since metformin increases the effectiveness of insulin… that means your insulin is more effective at regulating satiety. Insulin also lowers triglycerides and FFA’s in the blood which enables leptin (another appetite regulatory hormone) to cross the blood-brain-barrier and promote satiation.

It's triglycerides that keep leptin from crossing the blood brain barrier, not FFAs from what I've read. I don't buy the bit about insulin lowering triglycerides either. Want to see what happened to me after two months of McDougall? Here's my NMR after that experiment:








I did not eat fruit or drink alcohol and consumed no fat other than what was in the potatoes, sweet potatoes, beans, lentils, rice, greens, and veggies that I ate. I am an ApoE2 carrier however.


Previous basic lipid panel on low carb, moderate protein and high fat:

TC 177
TG 68
HDL 77
LDL Calc 86 (76.5 Iranian)

TC dropped a whopping 11 points.
Triglycerides went up 171 points and I lost 30 points of HDL.
LDL went down 15 points (4.5 points using the Iranian calculation) and everything was the wrong type - large VLDL, small LDL and small HDL.
My insulin resistance score was in the highest percentile at 79!

[Chupo]

What may seem paradoxical is that those on high fat diets almost always have rock bottom triglycerides. This is how. ASP (acylation stimulating protein) is produced by adipose tissue and is increased postprandially. This allows them to take fat out of the blood for storage and later release as FFAs. HDL, LDL, and VLDL have little to no effect on the stimulation of ASP. Insulin increases ASP production two fold. Chylomicrons (the lipoprotein dietary fat is packed into) stimulate the production of ASP 150 fold.

We have previously shown that in normolipidemic healthy adults, plasma acylation stimulating protein (ASP) increases postprandially and is produced in vitro by cultured differentiated human adipocytes. The present studies were undertaken to examine the influence of specific plasma components on endogenous ASP production in cultured human adipocytes. The results demonstrate that neither glucose nor fatty acids (over a wide range of concentrations) had any substantial effect on ASP production. Insulin increased ASP production up to 2-fold (208% +/- 18%, P < 0.01). However, the most profound increase in ASP was generated by the addition of chylomicrons to the cell culture medium. Chylomicrons (CHYLO) obtained from postprandial plasma increased ASP production in a time- and concentration-dependent manner, producing up to a 150-fold increase in ASP at the highest concentration of CHYLO tested (500 microg triacylglycerol/mL medium (P < 0.001)). By contrast, very low (VLDL), high (HDL), and low density lipoproteins (LDI) had only marginal effects. The effects on ASP parallelled the changes in adipocyte C3 secretion (the precursor protein of ASP). As with ASP, glucose, oleate, insulin, and hepatic lipoproteins (VLDL, LDL, and HDL) had little or no effect on C3 secretion. In contrast, CHYLO had an even greater effect on C3 secretion than on ASP generation. Finally, the effects of CHYLO on generation of ASP and C3 were not dependent on lipolysis of CHYLO by lipoprotein lipase (LPL). These results are consistent with the changes in plasma ASP seen postprandially, and suggests a role of ASP as a positive feedback regulator of triacylglycerol synthesis in adipose tissue.

http://www.ncbi.nlm..../pubmed/9034195


This Wikipedia entry is interesting.

Chylomicrons secreted from the intestinal enterocyte also contain apo A-I but it is quickly transferred to HDL in the bloodstream.^[3]

The study referenced is Impact of lipoproteins on the biological activity and disposition of hydrophobic drugs: implications for drug discovery. I don't have access to the full text and the abstract says nothing about it that I can tell. I think it makes sense though as apo A-I is what gives HDL its effectiveness. An apoE4 carrier would not see this. I'm unclear of the reason. Perhaps their chylomicrons don't have enough apo A-I on top of their VLDL (or chylomicrons?) being converted to LDL to quickly? I don't know what is at work there but I'd like to know.

Edited by Chupo, 25 November 2013 - 11:54 PM.

[HaloTeK]

I did not eat fruit or drink alcohol and consumed no fat other than what was in the potatoes, sweet potatoes, beans, lentils, rice, greens, and veggies that I ate. I am an ApoE2 carrier however.


Previous basic lipid panel on low carb, moderate protein and high fat:

TC 177
TG 68
HDL 77
LDL Calc 86 (76.5 Iranian)

TC dropped a whopping 11 points.
Triglycerides went up 171 points and I lost 30 points of HDL.
LDL went down 15 points (4.5 points using the Iranian calculation) and everything was the wrong type - large VLDL, small LDL and small HDL.
My insulin resistance score was in the highest percentile at 79!

Here are my issues Chupo:

1: When you changed your diet, did you maintain your weight over 2 months or did it go up or down. I would almost say with certainty if you lowered your caloric intake, your stats would not have looked as bad.

2: What was your fructose intake/ refined grain intake? That would tell us a little more on why your trigs went so high. Inactivity is also a factor there.

3: Did you exercise at all? If you are completely sedentary, higher carbs diet might hurt at first <----- but once again, only if you are in a caloric excess!

4. Are you overweight at all or skinny? Both would effect your response to a change in diet.

5: You need to look at how your body responds over a longer period of time -- 2 months is just not enough.

6: We already know that adding some extra virgin olive oil 2-3 tbsps is better than a non-added fat diet and would improve your stats alot so please don't compare yourself to inferior diets like mcdougalls or 80-10-10 people.

[misterE]

TC 177
TG 68
HDL 77
LDL Calc 86 (76.5 Iranian)

TC dropped a whopping 11 points.
Triglycerides went up 171 points and I lost 30 points of HDL.
LDL went down 15 points (4.5 points using the Iranian calculation) and everything was the wrong type - large VLDL, small LDL and small HDL.
My insulin resistance score was in the highest percentile at 79!

The starch-based diet brought my cholesterol from 220 to 120mg/dl.
Triglycerides from 172 to 57mg/dl and:
LDL from 100 to 71mg/dl.

My doctor remarked that I had a better blood lipid panel than he did and asked me what I ate.

However, this blood test was taken four years after my first blood tests. So a four year adherence to a starch-based diet lowered my:

Total-cholesterol by: 45%
Triglycerides by: 66%
LDL by: 29%

Edited by misterE, 29 November 2013 - 06:44 PM.

[misterE]

Insulin increases ASP production two fold. Chylomicrons (the lipoprotein dietary fat is packed into) stimulate the production of ASP 150 fold.

Ah, so you agree that it is best to store fat within the adipocytes considering ASP activity is inhibited in insulin-resistant states?

[Chupo]

Here are my issues Chupo:

1: When you changed your diet, did you maintain your weight over 2 months or did it go up or down. I would almost say with certainty if you lowered your caloric intake, your stats would not have looked as bad.

I maintained my weigh. I wanted diet to be the only variable.

2: What was your fructose intake/ refined grain intake? That would tell us a little more on why your trigs went so high. Inactivity is also a factor there.

I didn't have any fructose. Even though McDougall does allow limited fruit, I wanted to keep it out of the picture so I only had whole starches. I had a quite physical job of unloading trucks at the time of both tests. Oddly, I was always hungrier on the days that I didn't work.

3: Did you exercise at all? If you are completely sedentary, higher carbs diet might hurt at first <----- but once again, only if you are in a caloric excess!

Aside from work, I didn't exercise.

4. Are you overweight at all or skinny? Both would effect your response to a change in diet.

My BMI is 24.4. It was over 36 at my heaviest five years ago.

5: You need to look at how your body responds over a longer period of time -- 2 months is just not enough.

That may be true but would it have kept getting worse?

6: We already know that adding some extra virgin olive oil 2-3 tbsps is better than a non-added fat diet and would improve your stats alot so please don't compare yourself to inferior diets like mcdougalls or 80-10-10 people.

The reason for the experiment was to test a low fat diet - the McDougall diet specifically as I am ApoE2/E3. Low fat diets aren't recommended for E2 carriers since VLDL and chylomicrons aren't cleared by the liver efficiently. This can lead to high trigs, small dense LDL and high LDL-P on a low fat diet. This is where chylomicrons and ASP come into the picture. By increasing the uptake of fat out of the blood, trigs are lowered and the liver doesn't have to pump out as many lipoprotein particles to carry cholesterol.

[Chupo]

TC 177
TG 68
HDL 77
LDL Calc 86 (76.5 Iranian)

TC dropped a whopping 11 points.
Triglycerides went up 171 points and I lost 30 points of HDL.
LDL went down 15 points (4.5 points using the Iranian calculation) and everything was the wrong type - large VLDL, small LDL and small HDL.
My insulin resistance score was in the highest percentile at 79!

The starch-based diet brought my cholesterol from 220 to 120mg/dl.
Triglycerides from 172 to 57mg/dl and:
LDL from 100 to 71mg/dl.

My doctor remarked that I had a better blood lipid panel than he did and asked me what I ate.

However, this blood test was taken four years after my first blood tests. So a four year adherence to a starch-based diet lowered my:

Total-cholesterol by: 45%
Triglycerides by: 66%
LDL by: 29%

Good for you! Do you know your ApoE?

Insulin increases ASP production two fold. Chylomicrons (the lipoprotein dietary fat is packed into) stimulate the production of ASP 150 fold.

Ah, so you agree that it is best to store fat within the adipocytes considering ASP activity is inhibited in insulin-resistant states?

I would certainly agree with that! What I don't agree with is your conflating pathological insulin resistance with peripheral insulin resistance.

Edited by Chupo, 29 November 2013 - 11:22 PM.

[misterE]

Good for you! Do you know your ApoE?

Thanks Chupo! I don’t know my ApoE. I think it is best to keep things simple. Ornish and Esselstyn are arguably the best cardiologists in the USA. Their protocol is the only one documented showing reversal of atherosclerosis. And both of them don’t put much weight into this whole Apo-whathaveyou.



They both agree that if you can get your total-cholesterol below 150mg/dl, then eventually over time, your atherosclerotic lesions will dissolve away. New research indicates that nitric-oxide also plays a crucial role. Esselstyn is very adamant about the beneficial role of nitric-oxide production in its ability to prevent and reverse atherosclerotic-plaque. Research shows that insulin (which is stimulated by eating potatoes, beans and flours) promotes nitric-oxide synthesis from the endothelium.

What I don't agree with is your conflating pathological insulin resistance with peripheral insulin resistance.

Can you elaborate on this please? An example would be helpful.

Edited by misterE, 30 November 2013 - 12:16 AM.

[drew_ab]

 

They both agree that if you can get your total-cholesterol below 150mg/dl, then eventually over time, your atherosclerotic lesions will dissolve away. New research indicates that nitric-oxide also plays a crucial role. Esselstyn is very adamant about the beneficial role of nitric-oxide production in its ability to prevent and reverse atherosclerotic-plaque. Research shows that insulin (which is stimulated by eating potatoes, beans and flours) promotes nitric-oxide synthesis from the endothelium.

 

I agree with the 150mg/dl golden cholesterol level.  And I'm inclined to believe that NO in the form of green vegetables could help prevent, arrest and reverse atherosclerotic plaque.  But could you cite some research on this?  Could you also cite some research on insulin promoting NO synthesis in from the endothelium?

 

I've been following a WFPD for a long period of time now, but am always interested in reading the science behind it. And I always enjoy reading your posts and the studies you cite.




 

 

Edited by Drew_ab, 07 December 2014 - 01:21 AM.

[misterE]

 

 

 Could you also cite some research on insulin promoting NO synthesis in from the endothelium?

 

 

 

J Clin Invest. 1994 Dec;94(6):2511-5.

 

Nitric oxide release accounts for insulin's vascular effects in humans.

 

Scherrer U¹, Randin D, Vollenweider P, Vollenweider L, Nicod P.

 

Abstract

 

Insulin exerts effects on the vasculature that (a) may play a role in the regulation of blood pressure; and (b) by boosting its own delivery to target tissues, also have been proposed to play an integral part in its main action, the promotion of glucose disposal. To study the role of nitric oxide (NO) in the mediation of insulin's effects on the peripheral vasculature, NG-monomethyl-L-arginine (L-NMMA), a specific inhibitor of the synthesis of endothelium-derived NO, was infused into the brachial arteries of healthy volunteers both before, and at the end of a 2-h hyperinsulinemic (6 pmol/kg per min) euglycemic clamp. L-NMMA (but not norepinephrine, an NO-independent vasoconstrictor) caused larger reductions in forearm blood flow during hyperinsulinemia than at baseline. Moreover, L-NMMA prevented insulin-induced vasodilation throughout the clamp. Prevention of vasodilation by L-NMMA led to significant increases in arterial pressure during insulin/glucose infusion but did not alter glucose uptake. These findings indicate that insulin's vasodilatory effects are mediated by stimulation of NO release, and that they play a role in the regulation of arterial pressure during physiologic hyperinsulinemia. Abnormalities in insulin-induced NO release could contribute to altered vascular function and hypertension in insulin-resistant states.

 

Edited by misterE, 07 December 2014 - 02:54 AM.