Elevated Free Fatty Acids: Detrimental?

As many of my readers know, I've been challenged lately on my beliefs on NEFA.  So I thought I would summarize my thinking on this in a post rather than having several comments scattered amongst a few threads.   I'm not going to be referencing my post here at this time (it's too time consuming to do so at the moment).  If/when I have the opportunity to do so in the future, I'll do a bumped update.  

These are my thoughts based on extensive research of the peer review literature on this topic, in almost all cases, considered review of full text articles including reading as many supporting citations in major reviews as possible.  Over the past year I have read at least a hundred such articles.

Elevated non-esterified or free fatty acids (NEFA/FFA) are a symptom associated with insulin resistance, Metabolic Syndrome (aka Syndrome X) and Type II diabetes.  The overwhelming evidence in the literature points to elevated NEFA being more than just associated with these conditions, but rather the initiating step in their development..   

It seems that each of us, lean and obese, have a limit to our fat storage capacity, and there is evidence to support the theory that it is more the limits of our visceral adipose tissue (VAT) than our subcutaneous adipose tissue (SCAT) that cause us trouble.  The reasons for this are twofold:
1.  Adipocyte Turnover & Insulin Sensitivity v. Adipocyte Size:  Although the number of fat cells we have seems to be determined by the time we reach adulthood, there is still turnover of fat cells where pre-adipocytes are differentiated into mature adipocytes and old adipocytes die off.  There is a distinct difference between the behavior of VAT and  SCAT in  this regard.  Adipogenesis (formation of new fat cells by differentiation of pre-adipocytes) is greater in SCAT than VAT.   It has also been established that as fat cells are filled and grow larger, they lose their sensitivity to the action of insulin on hormone sensitive lipase (HSL) which regulates NEFA release.  Although at least one study I read showed larger cells in SCAT vs. VAT, the ability of SCAT to produce young insulin-sensitive cells is protective against excess NEFA release.  Indeed, one effective diabetes drug does just that:  stimulates adipogenesis generally accompanied by weight gain, but improved metabolic function.
2.  Lipolytic Rates:   The process of lipolysis (breaking down triglycerides into glycerol + fatty acids) occurs at higher rates in VAT.  Elevated NEFA are the result of increased or excessive lipolysis without a concurrent increase in energy needs.   One encouraging thing about this characteristic of VAT is that, when we lose fat, we tend to lose proportionally more from VAT.  This phenomenon is often cited as the reason why only modest weight reduction (10%) even in the severely obese is often accompanied by significant amelioration of MetS/IR/T2.

Fat cells, regardless of location, become less sensitive to insulin as they get bigger.  When they do, insulin is unable to properly suppress HSL resulting in increased mobilization of fatty acids from it's appropriate storage depots.  This condition is called adiposopathy, or "sick fat" by some.  At the risk of being repetitive, we each seem to have our own individual threshold for this condition to develop.  Lean or those suffering from some degree of lipodystrophy can have insufficient fat to buffer dietary intake or store much before getting over-full.  In such a person, a little paunch can be all that's required to set things in motion.  The gynoid, "female pattern" obese, aka "pears", who have large amounts of below-the-waist SCAT in hips and thighs tend to have lower rates of MetS.  Thigh/butt SCAT in particular, however we feel about it aesthetically, is generally considered protective for this reason.  The android, "male pattern", centrally obese, aka "apples" lack this buffer, tend to have exceeded their threshold and exhibit MetS.

Regardless of if a person is lean or obese, chronic/pathological insulin resistance initiates in the fat cells.   And the initial factor is the excessive release of fatty acid resulting in increased/elevated levels of circulating NEFA.    It should be pointed out that Type 1 diabetics also have elevated NEFA because of lacking basal insulin.  Even those who believe in the carb/insulin hypothesis can accept this.  Just go ahead and blame the carb-induced postprandial insulin for fat accumulating in your body, the result is the same.  Once you've reached your storage limit, your fat becomes insulin resistant, HSL is insufficiently suppressed and NEFA flow out.  

Fatty acid flow is essentially a one-way street for all cells in the body except for fat and the liver.  Fatty acids are transported into cells by diffusion so that the higher the concentration in circulation, the more flow into non-adipose tissue (ectopic) cells.  Once in, they are either oxidized for energy or esterified and stored as triglycerides in lipid droplets.  This lipid content in muscle cells is often called intra myocellular lipid or triglyceride (IMCL or IMCT) and high levels cause insulin resistance in most cases.  When do they not?  There is a paradox whereby insulin resistant obese and insulin sensitive trained athletes both exhibit high levels of IMCT, so it can't be the lipid itself that is the culprit here.  The evidence points to metabolic intermediaries in lipid oxidation - diacylglycerols, ceramides - building up in cells when oxidation rates aren't sufficiently high.  These interfere with overall cell metabolism, and increase reactive oxidative species (ROS) formation.  The ROS are the "toxic" culprits in lipotoxicity and the effects can range from functional impairment to cell death.   So the athlete may have high IMCL/T levels, but the turnover is sufficiently rapid so that the molecules aren't hanging around long enough to form ROS, whereas the obese person has lipid intermediary metabolites hanging around, forming ROS and causing insulin resistance.

Now, IMCL/T accumulation is also associated with a high fat Western style diets.   So, unfortunately, the introductions and discussions in much of the "lipotoxicity" studies is littered with statements indicating bias or adherence to the lipid hypothesis.  I see that too, but I read past it and look at the actual results.  IOW if they infuse free fatty acids into circulation and those disproportionately infiltrate ectopic tissues instead of being taken up and stored in adipose tissue, I don't care if the investigator is biased.  It shows me that the concentration of fatty acids alone, coupled with an inability of the fat tissue to properly sequester the excesses CAN lead to accumulation of IMCL/T in ectopic tissues, which CAN, in turn lead to disruption of cell function that may or may not be associated with insulin resistance.  Please note my qualifiers here.  

In this regard I have come across too many studies implicating either absolute NEFA levels, NEFA turnover rates or both directly interfering with proper cell function/insulin action in pancreatic beta cells, vascular endothelium (blood vessel lining), liver cells, etc.   The progression/causality of what we might refer to as chronic, metabolic or pathological IR (as opposed to transient IR due to dietary state) is pretty clearly established in the literature:  NEFA --> (a)Muscle IR & (b) Liver IR --> (a) reduced clearance of glucose from blood & (b) increased glucose production - gluconeogenesis --> hyperglycemia.

VLC diets seem to cause fat cells to behave like those that start this whole progression above.  NEFA levels rise to fasting levels and stay close for the entire day.  Both the T2 and the IR individual, fasting NEFA and postprandial NEFA release is elevated.   By keeping exogenous glucose (dietary carb) low to non-existent, hyperglycemia is ameliorated.   But if dietary carb were the only contributing factor to hyperglycemia, this control should be immediate but it's not.  Yes, postprandial glucose excursions are reduced, but elevated fasting BG is reduced much more slowly.  On the bright side, even elevated fasting levels are below levels normally implicated in glycation or under the umbrella term glucotoxicity.  But on the other hand, in exchange for this improvement, the other circulating energy substrate - NEFA - is released.  Now folks often point to the elevated ppBG lasting longer, essentially overlapping = chronic hyperglycemia.  This is fair enough for someone who is in what I would call advanced stage IR or full-blown T2.   

For a goodly portion of people, especially the very obese, VLC leads to substantial rapid weight loss coinciding with significant caloric deficit.  The combination of glycogen depletion and caloric deficit ameliorates insulin resistance as measured by glucose disposal.  Adding the glycogen depletion to the equation, one might expect the improvements to be better for VLC vs. conventional calorie restricted diets (CRD) in the short run because of the extra "sink".  But what of the long run?  What of those who lose weight but remain obese or significantly overweight?  What of those who do not lose much doing low carb?   There are many whose diabetes progresses on low carb diets.  They become more and more intolerant of any carbohydrate.  These people will even see their blood glucose levels soar after eating low carb bread products and fasting FBG's slowly rise over time.  If someone can't eat a cup of white rice with a pat of butter and a splash of soy sauce without their blood sugar levels going all out of whack they simply have not re-established normal metabolic control.   

The lipid profile of IR/MetS/T2 is characterized by high triglyceride levels.  These are usually attributed to carbs and DNL (that do contribute), but a goodly portion of the fatty acids the liver packages up and exports as triglycerides (VLDL) are *excess* NEFA the liver "filters" from circulation!  In a low carb state triglycerides tend to go down rather dramatically.  The reasons for this may well relate to lower insulin 24-hour exposure, but this means NEFA is not being properly removed from circulation.   The fasting triglycerides as major biomarker for CVD are likely associated with elevated NEFA (that is not commonly  measured and reported unfortunately) for those consuming sufficient carb (say >100g/day).  On VLC inefficient esterification means fewer circulating trigs but more NEFA.  

Whatever folks think about my treatment of  a certain author, this blog remains largely a labor of love for me born out of my desire to assure myself that my diet is a healthy one for me.  That's why I started looking into this stuff and why so much of my research (yes, folks, by definition what I do fits well within the definition of that word) has ended up focusing on NEFA.  The cluster of metabolic diseases seem to all point to one culprit:  resistance to the appropriate action of insulin by various tissues.  And, to repeat, the evidence strongly supports that this process initiates in the adipocytes with excessive release and/or inefficient trapping of NEFA/FFA leading to elevated circulating levels of free fatty acids.  Just as the concentration of glucose in blood is directly linked to deleterious consequences, so, too, are NEFA levels.  Not just a "biomarker associated with" (although there are those indications too), but a direct effect. 

So, does VLC cause a detrimental NEFA level?  Well, I compare some of the levels reported following a single large meal as well as the consistent levels reported after 6 weeks of VLC reducing diet, and they are comparable to those exhibited by those with active diabetes and such.  And sustained far more than abnormal  blood glucose incursions I might add.  The chance of a diabetic who has a heart attack (myocardial infarction) subsequently going into sudden cardiac arrest and dying (SCD) is about 3X higher and this is attributable to circulating NEFA concentrations.   So at least in this instance, it matters not what elevates the NEFA, only that they are high.  I'm going to inject a little sarcasm here:  This is, of course, nothing any of us have anything to worry over if we've been extremely overweight, eating a crappy diet, and possibly been diabetic for years.  Because we know none of us have even a risk, let alone an elevated one, of having a heart attack or any issues with hypertension  or arrhythmia or racing hearts.  Right? 

Control hyperglycemia through removing exogenous glucose, and you still don't address the risks of NEFA.  My personal advice for the long term (and take it for what you will based on your assessment of what I write here, I'm not a medical doctor!):  Focus, instead, on long term improvements in sensitivity to insulin and controlling the NEFA, and the hyperglycemia will fix itself.  Provided your beta cells haven't sustained permanent damage (and the diabetes cure rate with gastric bypass provides reason to be optimistic that this is actually not the case for some 85% of morbidly obese diabetics)  this should ultimately be reversible with lifestyle change.  I mean reversible to the point that you CAN enjoy moderate carbohydrate consumption (of whole fruits and "safe starches") with normal glycemic control.  Couple this approach with eliminating foods you can identify an intolerance to and avoiding/cutting back on foods that are potentially toxic, and get healthy.

I am planning a series on IR that will include an installment on why I think VLC diets are so effective for weight loss in so many with some significant degree of this condition.  I have no idea when that will be.  In retrospect, I have reservations on the safety of this approach, but if one can reduce and MAINTAIN weight, the benefits do definitely, in my considered opinion, outweigh the risks.   


MM said…

Thanks for this explanation. I have what is probably a ridiculously stupid question.

You say, "The evidence points to metabolic intermediaries in lipid oxidation - diacylglycerols, ceramides - building up in cells when oxidation rates aren't sufficiently high. These interfere with overall cell metabolism, and increase reactive oxidative species (ROS) formation."

However, in the 6WC book Eades recommends DAG oil (diacylglycerols) for "better B-oxidation (fat burning)" and "to clear fat out of the liver cells" (pg 73 hardbound). His references are just listed in alphabetical order in the back, so I'm not sure which one(s) he got this out of (annoying!). Perhaps the difference is the DAG oil is ingested as opposed to being produced inside cells. Or maybe this is just one of the mistakes you mentioned 6WC being littered with. Thanks.
CarbSane said…
Hi MM, this is "off the cuff" but the rub I get on DAG oil is that it is less likely to be stored as body fat (just as MCT's are even less likely to be ultimately stored in body fat). I can only surmise that some of the DAG makes it intact into our systems and into our cells in DAG form. For this to happen, the DAGs must not be hydrolyzed for incorporation into triglycerides in chylo and aren't converted to TAG either. (Perhaps DAGs do not enter the esterification process midway while the single FA's that enter the esterification process are committed to a TAG endpoint). Then those DAG must also make it into the cells intact because, again, if not and they were hydrolyzed to single FA's what's to keep them from becoming TAG? So ... intact DAG that make it to cells would feed into the oxidative pathway midway rather than being packaged up in the non-oxidative disposal (TAG synthesis). Much like MCT's do not seem to feed into a later step in de novo lipogenesis.

If this occurs mostly in the liver I can see how it might possibly reduce liver fat but I'll have to look into that claim. The whole liver fat issue is a sticking point for me in that book because they tend to equate hepatic fat with overall visceral fat and that's simply not true.
MM said…
Ok, so just trying to understand.

I see what you mean about DAG not getting packaged into TAG, because then how would they make any difference? However, if DAG do enter cells intact and midway into the oxidative pathway, but a buildup of DAG interferes with cell metabolism then how could they have a positive affect? I realize you never claimed that. It seems to me that this buildup of DAG (and ceramides) in cells is a main crux of the problem. If they do indeed interfere with cell metabolism then this is going to be the primary adverse affect caused by high levels of NEFA and leading to all the other problems you mention. Yes? My background is engineering and I tend to be reductionist. Please correct me if I'm wrong!!!

Another thought just occurred to me. Eades said that the DAG oil was to replace some of the fat in the diet -- it was not in addition to. So, a DAG only has two fatty acids on the glycerol rather than three like in a TAG. That will reduce the calorie load by 1/3. Maybe that's all it is. How's that for simple! lol
MM said…
Re-read my post and realized I mixed up affect/effect. Bah! I'm fairly good with spelling but that one I mess up often.
Harry said…
Hi CarbSane,

I just wanted to register my thanks for this great summary of your stance on the NEFA issue. What with all the to and fro in the comments sections, my poor little noggin was starting to spin; this article will serve as a great reference from now on.

How do you feel about this hypothesis: "To the extent that one is losing weight (and thus in negative energy balance), selection of macronutrient ratios is inconsequential to health (assuming sufficient minimum levels of protein and micronutrients). However, if one is maintaining weight above a certain absolute value, or worse, gaining weight, then very high absolute levels of dietary fat can cause deleterious levels of circulating NEFA, which is a precursor to metsyn and Type 2 diabetes."

MM said…

I did some looking on my own, and I think I answered my question. I read several papers, but this one really stood out to me.


My apologies if you've already seen/commented on it. They infused FFA into normal, healthy subjects for 4 hours. They definitely did see an increase in ROS, as well as some other negative effects I'm not sure I entirely understand. I like this study because it doesn't confuse the effect of elevated FFA with diabetes, as those two things are usually seen together.
Stephan Guyenet said…
Hi CarbSane,

I'm not so sure that insulin resistance begins in adipose tissue. Kim et al. showed that in diet-induced obesity in mice, IR developed in vascular, muscle and liver tissue before AT. Adipose tissue was still insulin sensitive long after systemic hyperinsulinemia had developed. OK, those were mice not humans, but it does show that systemic insulin resistance does not require insulin resistant adipose tissue, at least early on. Mice have the advantage that you can directly test insulin sensitivity in various tissues at different fixed stages of obesity development.


I also think it's difficult to draw definitive conclusions about normal physiology from studies where researchers artificially increased FFA in humans using Intralipid and heparin. In those studies, increasing FFA decreased insulin sensitivity, but glucose did not decrease so overall energy exposure of cells was increased substantially. I think those results are probably relevant to diabetics and some obese people with elevated fasting FFA, but the relevance to normal FFA physiology and LC diets is less clear.

I do believe that pathologically elevated FFA are harmful and contribute to the negative effects of diabetes and some types of obesity.
CarbSane said…
@Harry: One of the issues I have with Kurt is that he repeatedly mischaracterizes NEFA as related to dietary fat per se. It doesn't under normal conditions. IOW, fat that's functioning normally appropriately traps fatty acids released by LPL in the fat tissue "buffer". Dysfunctional fat cells do not and in that context dietary fat adds to circulating NEFA that "escapes" (I have, yet another!, Frayn paper to discuss dealing with just this issue). I think there's reason to at least consider why a low fat version of low carb for weight loss might be safer (Dansinger is a bit too much of a low fattie for me, but he makes some good arguments on this point). We're getting plenty of NEFA release from fat. IMO, dietary fat doesn't cause diabetes unless it is consumed in a hypercaloric diet (and IMO a high fat diet in general makes it easier to do so) so that one's fat buffer capacity is exceeded.

@MM: Regarding DAG, for some reason it is apparently no longer on the market. Much of the lit on it was put out by ADM so it was hard to judge if it was hype or not. Still, it seems that DAG were oxidized preferentally as MCT's are, and replacing TAG with DAG in a reducing diet did result in greater weight loss. It may well have been as simple as cal/g being less than 9 for the substitution. Glycerol is ~10% of a TAG but would be ~14% of a DAG. I also wonder if DAG would be more or less dense than TAG ~ I could give an argument for both options based on the same concept of polarity though :(

I found it interesting that those doing 6WC who followed the DAG advice were adding it to shakes along with the heavy cream and whatnot to make them rather than instead of it. I see this all the time with coconut oil and MCT oil. Studies demonstrating a weight loss advantage generally involve relatively low fat diets where MCT's make up a significant proportion of total fat consumption.
Muata said…
OK, I had to read it twice, but I think I got it CS.

Question for ya. How much effect does exercise (resistance/cardio) have on circulating NEFA?
CarbSane said…
@Stephan: Thanks for your input. I'm a bit backed up at the moment, so will have a more detailed/considered response in the coming days but one thing stuck out at me:

I also think it's difficult to draw definitive conclusions about normal physiology from studies where researchers artificially increased FFA in humans using Intralipid and heparin. In those studies, increasing FFA decreased insulin sensitivity, but glucose did not decrease so overall energy exposure of cells was increased substantially. I think those results are probably relevant to diabetics and some obese people with elevated fasting FFA, but the relevance to normal FFA physiology and LC diets is less clear.

Let's face it Stephan, isn't this a goodly portion of those undertaking LC diets?
LynMarie Daye said…
CarbSane wrote: "I have, yet another!, Frayn paper to discuss dealing with just this issue."

I think I recently read the Frayn paper you're referring to - published last month IIRC. It's a good one; very detailed and well done. I'm looking forward to your commentary
Anonymous said…
"One of the issues I have with Kurt is that he repeatedly mischaracterizes NEFA as related to dietary fat per se."

No, I most certainly do not. I object to your claim that elevated NEFA or relative rises in NEFA on LC have the same meaning. You have said that eating VLC, which is by definition relatively higher in fat, is a desired way to minimize dangerous NEFA elevations. I have challenged you on that.

Every paper I've read emphasizes that lipotoxicity is determined by cell utilization, not solely by serum NEFA level.

That is why talking about NEFA levels or even intracellular levels out of context (myocytes in athletes) as per se dangerous makes no sense. If you are running your metabolism on them, a NEFA level that might reflect cellular overload if you saw it on a high carb diet just reflects that you are running on fatty acids. And everyone, ceteris paribus, will have higher NEFA more of the time if they eat less glucose. The normal ones and the diabetics whose levels will fall if their livers heal. This is true for diabetics or normal people, when they drop their carb intake.

I would agree that if you hold carb intake and calories constant, that the AUC for NEFA could be inferred to be more inappropriate and reflect more pathology, but if you drop CHO consumption and NEFA goes up BECAUSE of that, you simply cannot make that conclusion.

It's the same with your beloved Jouven study. The elevated NEFA crowd are overrepresented by nascent diabetes. DIabetes predisposes to CAD. 90% of the time SCD is due to the same coronary disease that diabetics are more prone to get as well. The reason that NEFA did not correlate with MI is simply that the more diabetic you are, the worse your CAD and the worse your CAD the more likely you are to die quickly of an arrythmia from your heart attack - that could be due to the inappropriate NEFA on top of more massive heart attacks - but could also be due to larger areas of acute ischemia as well. Look carefully at the graph, and see how as SCD goes down, MI actually does up? That is because they are both ways to die from CAD, they are not at all independent. This paper only suggests it is worse to have worse diabetes, it says nothing at all about the danger of elevated NEFA all by itself, as that parameter cannot be separated from the

Finally, let's say that elevated NEFA in the context of ACS (acute coronary syndrome) does increase your risk of an arrythmia by 70% once you pop a vulnerable plaque. OK, what is the best way to prevent that? None of the papers you've cited says there is any effective strategy at all, even in those making it to the hospital, for dealing with the potential of arythmia due to NEFA. Not one suggests avoiding VLC or eating plenty of CHO to elevate insulin to keep lipolysis suppressed.

Why not focus on a non- atherogenic diet and lowering your A1c?

You simply cannot say that elevated NEFA in that population tells us we should fear elevated NEFA on VLC -that is just inappropriate.

I also agree with Stephan (and Peter as I know his views well) that the liver is the nexus for metabolic syndrome. Perhaps you have trouble with that as you are so certain that everything is passively driven by energy balance. I do think GT is absolutely correct that it is possible that things in our diet perturb our metabolic regulation, and we eat in response to inappropriate fat storage. Stephan's set point theory is compatible with this as well. So I think energy balance is usually perturbed as a result of of metabolic dysregulation, not the other way round. Notice I said usually. It is trivially obvious that one can override the setpoint with starvation or purposeful overeating.

You think: eat more, overload fat cells -metS

I think: Eat poisons - damage liver - metS
MM said…

In the study I link to in my previous comment they took normal, healthy subjects and infused them with FFA. Their blood glucose was measured throughout the study and ranged between 79 and 83 mg/dl. The FFA levels topped out at 732 μmol/l. This is about the level seen in subjects on the high fat, low carb diet CarbSane wrote about in this post:
The average blood glucose measured in those subjects was 83 mg/dl.

So, when you say, "glucose did not decrease so overall energy exposure of cells was increased substantially", I don't understand how the glucose level could have been realistically decreased further. Most people wouldn't want their blood sugar to get much below 80 mg/dl.
kds said…
MM- healthy fasting BG levels are typically below 80 with the median BG in studies being somewhere around 72-74mg/dl. Indeed, having a FBG equal to 87mg/dl or greater puts you at significantly more risk for developing DM compared to having a FBG below 81.

CarbSane said…
@kds: It's too bad they didn't look at NEFA in that study.

I think MM's point is that total energy exposure is not regulated entirely by the simple Randle cycle. For example, when NEFA are doubled, glucose levels don't drop proportionally.
CarbSane said…
@LMD: Can you possibly email me your paper through my profile? Thanks!
LynMarie Daye said…
I just sent it. If you didn't get it, let me know.
Anonymous said…
If you're really interested in your health, then you should read "Diet Evolution" by Steve Gundry MD (2009). He doesn't present much biochemical evidence, but he does present a strong case (to my mind) that low-fat, low-grain, high-vegetables, low-animal-protein is the way to go for long-term health. He see too much of either animal protein or fat as causing premature aging.

The idea is the the genes deliberately cause old people who eat rich foods to commit suicide via heart attack, cancer, or stroke, because old people who eat rich foods are taking away scarce resources from their grandchildren. Since genes are shared between grandparents and grandchildren, and grandparents are incapable further reproduction (at least in the old days), there will be selection pressure for a system whereby grandparents who eat too much rich food are forced out of the picture via unconscious suicide. Grandparents who eat a lean diet (mostly green "donkey food") are spared this fate, because they are not really competing for scarce resources. Unlike today, where meat and eggs are cheaper than fresh vegetables, in the ancestral environment, fresh vegetables were there for the taking and meat and fat were the hard-to-come-by foods.

Gundry sees low-carb and high-animal-protein as the best approach for losing excess weight, on the other hand.
Marcus R Williams MD said…
In my personal experience, having weighed over 500lbs with cardiometabolic syndrome and still not reaching goal, Only when I began to approach reduction of carb intake with a with careful discrimination between simple sugars, starches, and non-starch carbs did I find a remarkable decrease in the ravenous hunger induced by prolonged and excessive insulin peaks by starches. I currently maintain a 40% protein, 30% largely non-starch carb, and 30% "healthy fat" diet. As a result I have no difficulty losing and easily maintaining my weight loss. I did have a gastric bypass and lost to about 215 lbs, without ability to lose further, until I eliminated "sugared-fluids", most free sugars other than those naturally in fresh, canned, or frozen fruits (excluding juices and sugar added fruit preparations), and began to treat starches as a "condiment rather than a staple." While there are essential fats and amino acids, there are no essential starches. I would suspect that I have reduced starch intake by 80-90% in my daily diet. After approximately 6 months of such a diet and an easy loss to near normal BMI at 170 lbs, for the first time in years, and off all diabetes medications and insulin which had topped over 400u a day at one point only 6 months previously, my labs are essentially normal including fasting glucose and HgbA1c. No meds at all, and no vigorous exercise other than fast-walking 30 minutes to 60 minutes a day.
I would propose evaluation not of a VLCD, but a near VLCD which drastically limits starch intake as a method of decreasing FFA and insulin resistance, by reducing the prolonged insulin peaks which stimulate hunger and fat storage. My thoughts are clearly not research-based, but experiential and based on my personal experience and by empirically suggesting a similar approach to patients as a primary care MD.