As is so often the case, I was looking up one thing and ran headlong into another a bit more interesting. I’d started once again on the “marijuana and cannabinoid” posting that was put off when the topic got forced at me too much. Time had passed. It was interesting again… And I ran smack into an issue strongly related to it (involves cannabinoid receptors) but complicated enough to not be just a chapter in another posting.
We’ll do this one sort of “middle out” with some jumping around. It just doesn’t lend itself to a linear approach, nor to a ‘surprise ending’. So just try to wade through it.
First off, what is “Metabolic Syndrome”? Well, it’s a bunch of things. Mostly you get fat around the middle and your insulin response gets off so pre-diabetic (god I hate that term… you either are, or are not, diabetic… it ought to be “insulin reduced sensitivity” or some such). There are some other bits involving depressive feelings and more. The wiki looks OK on it:
Metabolic syndrome is a disorder of energy utilization and storage, diagnosed by a co-occurrence of three out of five of the following medical conditions: abdominal (central) obesity, elevated blood pressure, elevated fasting plasma glucose, high serum triglycerides, and low high-density cholesterol (HDL) levels. Metabolic syndrome increases the risk of developing cardiovascular disease and diabetes. Some studies have shown the prevalence in the USA to be an estimated 34% of the adult population, and the prevalence increases with age.
Metabolic syndrome is also known as metabolic syndrome X, cardiometabolic syndrome, syndrome X, insulin resistance syndrome, Reaven’s syndrome (named for Gerald Reaven), and CHAOS (in Australia).
Metabolic syndrome and prediabetes appear to be the same disorder, just diagnosed by a different set of biomarkers.
We get the usual set of overlapping and alternate names too. But at least one can dump “prediabetes” and call it “metabolic syndrome”…
It is basically that thing that Madam Obama is all worked up about, and for which she wishes to institute Green Nazi Food Police in schools and restaurants near you along with demanding that your Doctor harangue you about eating habits and maybe get your insurance companies (health, life, and auto…) to raise your rates. The “obesity epidemic” in technical dress.
But what if it isn’t related to how much you eat and drink, nor to food decisions YOU make, but rather those made for you by the food manufacturers? None of the proposed “fixes” would fix it. Not treadmills nor having more bread and less meat.
The wiki goes into the litany of “the usual suspects” with sedentary life style and food choices and all. I’ll quote it for context, but don’t need to read it; a quick “scan” will do.
The exact mechanisms of the complex pathways of metabolic syndrome are under investigation. The pathophysiology is very complex and has been only partially elucidated. Most patients are older, obese, sedentary, and have a degree of insulin resistance. Stress can also be a contributing factor. The most important factors are genetics, aging, diet (particularly sugar-sweetened beverage consumption), sedentary behavior or low physical activity, disrupted chronobiology/sleep, mood disorders/psychotropic medication use, and excessive alcohol use. There is debate regarding whether obesity or insulin resistance is the cause of the metabolic syndrome or if they are consequences of a more far-reaching metabolic derangement. A number of markers of systemic inflammation, including C-reactive protein, are often increased, as are fibrinogen, interleukin 6, tumor necrosis factor-alpha (TNFα), and others. Some have pointed to a variety of causes, including increased uric acid levels caused by dietary fructose.
It is generally accepted that the current food environment contributes to the development of metabolic syndrome: our diet is mismatched with our biochemistry. Weight gain is associated with metabolic syndrome. Rather than total adiposity, the core clinical component of the syndrome is visceral and/or ectopic fat (i.e., fat in organs not designed for fat storage) whereas the principal metabolic abnormality is insulin resistance. The continuous provision of energy via dietary carbohydrate, lipid, and protein fuels, unmatched by physical activity/energy demand, arguably creates a backlog of the products of mitochondrial oxidation, a process associated with progressive mitochondrial dysfunction and insulin resistance.
Recent research indicates prolonged chronic stress can contribute to metabolic syndrome by disrupting the hormonal balance of the hypothalamic-pituitary-adrenal axis (HPA-axis). A dysfunctional HPA-axis causes high cortisol levels to circulate, which results in raising glucose and insulin levels, which in turn cause insulin-mediated effects on adipose tissue, ultimately promoting visceral adiposity, insulin resistance, dyslipidemia and hypertension, with direct effects on the bone, causing “low turnover” osteoporosis. HPA-axis dysfunction may explain the reported risk indication of abdominal obesity to cardiovascular disease (CVD), type 2 diabetes and stroke. Psychosocial stress is also linked to heart disease.
Overweight and obesity
Main article: Central obesity
Central obesity is a key feature of the syndrome, reflecting the fact that the syndrome’s prevalence is driven by the strong relationship between waist circumference and increasing adiposity. However, despite the importance of obesity, patients who are of normal weight may also be insulin-resistant and have the syndrome.
Physical inactivity is a predictor of CVD events and related mortality. Many components of metabolic syndrome are associated with a sedentary lifestyle, including increased adipose tissue (predominantly central); reduced HDL cholesterol; and a trend toward increased triglycerides, blood pressure, and glucose in the genetically susceptible. Compared with individuals who watched television or videos or used their computers for less than one hour daily, those who carried out these behaviors for greater than four hours daily have a twofold increased risk of metabolic syndrome.
It also goes into age and gender and diabetic connections and more. Now I’m not going to advocate for tossing out the whole suite of ‘this causes that’ and ‘a leads to b that changes c’. Much of it is undoubtedly accurate (especially where they have metabolic pathways identified). No, what I’m looking for is “What is the root cause that STARTS this process?”. It didn’t exist nearly so much when I was a kid. We didn’t all suddenly become insatiable gluttons without cause. I knew plenty of very sedentary folks before who didn’t have the syndrome. So what is the root causality? THEN many of those levers of metabolism start shifting and you end up in the dysfunctional metabolic state. At least, that’s my hypothesis…
I do want to mention the “controversy” part of it, since it irritates the hell out of me ;-) I’ve bolded one bit that I have seen in the small town where I grew up. Fat folks had no more problems than skinny folks, then. We knew all our customers (small very small town) and when anyone was sick or died everyone knew. We had ONE diabetic who needed saccharine a couple of ‘maybees’ and a bunch of women who were dieting that wanted it. There was much less “issue” then. So again, what changed?…
The clinical value of using “metabolic syndrome” as a diagnosis previously has been debated due to different sets of conflicting and incomplete diagnostic criteria. These concerns have led the American Diabetes Association and the European Association for the Study of Diabetes to issue a joint statement identifying eight major concerns on the clinical utility of the metabolic syndrome diagnosis. The principal argument has been that when confounding factors such as obesity are accounted for, diagnosis of the metabolic syndrome has a negligible association with the risk of heart disease.
Naturally, since the metabolic syndrome is a disorder of energy distribution and storage, fat accumulation explains for a significant proportion of cardiovascular risk. However, obesity without metabolic syndrome does not confer a significant cardiovascular risk, whereas metabolic syndrome without obesity is associated with a significant risk of diabetes and cardiovascular disease. This association of metabolic syndrome with diabetes can be illustrated by generalized lipodystrophy (near complete absence of adipose tissue). The animals and humans with generalized lipodystrophy develop signs of metabolic syndrome in the absence of adipose tissue; and the metabolic syndrome progresses to type 2 diabetes. Adipose tissue transplantation in transgenic mice with lipodystrophy can cure the type 2 diabetes. It has not been contested that cardiovascular risk factors tend to cluster together; the matter of contention has been the assertion that the metabolic syndrome is anything more than the sum of its constituent parts.
Phenotypic heterogeneity (for example, represented by variation in metabolic syndrome factor combinations among individuals with metabolic syndrome) has fueled that debate. However, more recent evidence suggests that common triggers (for example, excessive sugar-intake in the environment of overabundant food) can contribute to the development of multiple metabolic abnormalities at the same time, supporting the commonality of the energy utilization and storage pathways in metabolic syndrome.
IMHO, it all comes down to those energy utilization and storage pathways, along with some gut interaction issues. (Especially as it relates to the inflammation aspects). But is it really just “eat sugar and die”? I don’t think so… I think the sugar response is after the fact of onset.
This next bit largely just lays out in detail how some of the feedback loops work. More fat makes more enzymes that cause inflammation and insulin resistance that makes more metabolic syndrome that makes more fat that… Personally, I was more interested in the inflammation connection. We already know that a diet high in Omega-6 fats and low in Omega-3 fats cause more inflammation (and trans-fats screw it all up); so they might feed into this part of the feedback loop too. I’d also note in passing my hypothesis that trans-fats clog up the fat metabolism enzymes as they are something like 50 times slower to metabolize, so would tend to make you feel starved for energy and resort to sugars and starches, so even more feedback loop. Until this article, that was about as far as I’d gotten. Add Omega-3, remove Omega-6 where easy to do (olive oil instead of soy or corn, for example) and in all cases avoid hydrogenated fats, trans-fats, and since they now hide those in “mono and di-glycerides”, those too. But this has the potential for more. Much more.
It is common for there to be a development of visceral fat, after which the adipocytes (fat cells) of the visceral fat increase plasma levels of TNFα and alter levels of a number of other substances (e.g., adiponectin, resistin, and PAI-1). TNFα has been shown not only to cause the production of inflammatory cytokines, but also possibly to trigger cell signaling by interaction with a TNFα receptor that may lead to insulin resistance. An experiment with rats fed a diet with 33% sucrose has been proposed as a model for the development of metabolic syndrome. The sucrose first elevated blood levels of triglycerides, which induced visceral fat and ultimately resulted in insulin resistance. The progression from visceral fat to increased TNFα to insulin resistance has some parallels to human development of metabolic syndrome. The increase in adipose tissue also increases the number of immune cells present within, which play a role in inflammation. Chronic inflammation contributes to an increased risk of hypertension, atherosclerosis and diabetes.
Here comes the part M. Simon will be excited about, and that lead me here while doing searches on cannabinoids… I’ve bolded a bit.
The central role of the cannabinoid system in the development of metabolic syndrome is indisputable. Endocannabinoid overproduction and dysbalance may exacerbate corticolimbic reward system dysfunction, and contribute to executive dysfunction (e.g., impaired delay discounting), perpetuating unhealthy behaviors. The brain is crucial in development of metabolic syndrome, modulating peripheral carbohydrate and lipid metabolism.
It is interesting to me that what they describe is remarkably close to saying “you get the munchies and snack to fatness”… but in much fancier terms. I can certainly attest that when I eat too much “junk food”, I crave a lot more of it and feel hungry and slightly unhappy unless I’m snacking away on it… So there is some involvement like that going on. Salad, pork chop, applesauce and peas, side of bread and butter? Eat it, done, not hungry for hours. What’s the difference? I’m going to assert that it is the processing more than the sugar.
Metabolic syndrome is a risk factor for neurological disorders.
The metabolic syndrome can be induced by overfeeding with sugar or fructose, particularly concomitantly with high-fat diet. The resulting short-chain fatty acid production, and general oversupply of n-6 fatty acids are important determinants of metabolic syndrome. In particular, arachidonic acid metabolism appears to be a factor in the pathogenesis of metabolic syndrome: arachidonic acid (with its precursor – linoleic acid) serve as a substrate to inflammatory factor production (prostaglandins and leukotrienes), whereas arachidonic acid-containing diacylglycerol (DAG) is a precursor to the endocannabinoid (2-arachidonoylglycerol) and is a by-product of fatty acid amide hydrolase (FAAH)- mediated metabolism of anandamide (produced from N-arachidonoyl phosphatidylethanolamine).
Metabolomic studies suggest an excess of organic acids, impaired lipid oxidation byproducts, essential fatty acids and essential amino acids in the blood serum of affected patients. However, it is not entirely clear whether the accumulation of essential fatty acids and amino acids is the result of excessive ingestion or excess production by gut microbiota.
Here we have the first hint of a connection to “gut microbiota”. What you feed your bugs, and which ones live inside you, in many ways determine your health and fat status. That’s a key bit, and we get just a couple of words on it way down here nearly at the bottom of the wiki. Sigh.
Also note that linoleic acid is one of those Omega-6 fatty acids we get to very large excess in our seed-oil heavy diets. It not only enters into direct inflammation enhancement, but contributes to this metabolic syndrome feedback loop too. Historically we ate a lot of saturated fats (now having been absolved of any ‘bad cholesterol’ effects, so about 50 years of propaganda to be undone…) and NOT seed oils. We did have much more flax in the diet centuries past (high in Omega-3) and more olive oil (neutral). While eating a lot more grass fed meat (good Omega-3 intake) and fish from the sea (good Omega-3 intake). Now we have much more grain fed beef, and “pig chow” fed pork, all taking in tons of soy and corn (high in Omega-6 with linoleic acid). “You are what you eat”, and what THEY ate too… Now also note that “anandamide” it is your own natural cannabinoid. That’s where the process starts to hit your brain centers.
But WHERE does this whole chain of events get kicked off?
Food Additives Feed the Fire via Microbiome Dysbiosis Induction
BY MICHAEL ASH / WEDNESDAY, 08 APRIL 2015 / PUBLISHED IN NEWS
A study in Nature suggests that common food additives could be contributing to the development of chronic inflammatory diseases. Chassaing et al. report that dietary emulsifiers induce low-grade inflammation in mice by disrupting the composition of their intestinal microbiota, thereby predisposing these animals to the development of metabolic syndrome and colitis. This builds on an earlier paper they published in the Journal of Toxicologic Pathology.
So TWO papers finding the same thing. Mess up your belly bugs, there’s hell to pay.
To explore the effects of emulsifying agents on the intestinal mucosa, the authors administered carboxymethylcellulose (CMC) or polysorbate 80 (P80), which are emulsifiers commonly used in human foods, to mice in their drinking water. Compared with control mice, animals that received the emulsifiers showed reduced mucus thickness and increased gut permeability.
Moreover, intestinal bacteria in these animals penetrated deeper into the mucus and were in closer association with the intestinal epithelium. Experiments using 16S sequencing indicated that CMC and P80 also altered the composition of the microbiota, and mice exposed to the emulsifiers had increased levels of bioactive lipopolysaccharide and flagellin in their faeces. Therefore, dietary emulsifiers seem to disrupt the protective mucus layer in the mouse intestine and induce the acquisition of a more pro-inflammatory microbiota.
Of note, the doses of CMC and P80 that were used in these studies were lower than those that are approved for use in human foods. The authors caution that current protocols for assessing food safety may be inadequate, in that they often only test for acute toxicity or cancer. They further suggest that dietary emulsifiers may have contributed to the increased incidence of inflammatory bowel disease and metabolic syndrome that has been seen in recent years.
 Chassaing B, Koren O, Goodrich JK, Poole AC, Srinivasan S, Ley RE, Gewirtz AT. Dietary emulsifiers impact the mouse gut microbiota promoting colitis and metabolic syndrome. Nature. 2015 Mar 5;519(7541):92-6 View Abstract
 Chassaing B, Gewirtz AT. Gut microbiota, low-grade inflammation, and metabolic syndrome. Toxicol Pathol. 2014 Jan;42(1):49-53 View Full Paper
Polysorbate is in damn near everything processed. Everything else processed seems to get carboxymethylcellulose. From soft drinks to ice cream and cookies. Even found it in Marie Callender’s Pot Pie. The use of such emulsifiers has grown dramatically over the years, more or less in step with “metabolic syndrome” and a bunch of other diseases. ( I note in passing that “leaky gut” and that relationship to Autism could easily be made much worse via this stuff…)
There are several Polysorbates. One is used in the lab to lyse cells. I.e. it is used to cause cells to burst.
Polysorbates are a class of emulsifiers used in some pharmaceuticals and food preparation. They are often used in cosmetics to solubilize essential oils into water-based products. Polysorbates are oily liquids derived from PEG-ylated sorbitan (a derivative of sorbitol) esterified with fatty acids. Common brand names for polysorbates include Scattics, Alkest, Canarcel, and Tween.
Polysorbate 20 (polyoxyethylene (20) sorbitan monolaurate)
Polysorbate 40 (polyoxyethylene (20) sorbitan monopalmitate)
Polysorbate 60 (polyoxyethylene (20) sorbitan monostearate)
Polysorbate 80 (polyoxyethylene (20) sorbitan monooleate)
The number 20 following the ‘polyoxyethylene’ part refers to the total number of oxyethylene -(CH2CH2O)- groups found in the molecule. The number following the ‘polysorbate’ part is related to the type of fatty acid associated with the polyoxyethylene sorbitan part of the molecule. Monolaurate is indicated by 20, monopalmitate is indicated by 40, monostearate by 60, and monooleate by 80.
That’s IT. That’s the whole wiki. You can dredge through the links to the Ps-20, 40, 60, 80, etc. and find a bit more. I’m not going to paste in the links (they are in that wiki linked above) but just quote a couple of interesting bits:
Polysorbate 20 is used as a wetting agent in flavored mouth drops such as Ice Drops, helping to provide a spreading feeling to other ingredients like SD alcohol and mint flavor.
In biological techniques and sciences, Polysorbate 20 has a broad range of applications. For example, it is used:
as a washing agent in immunoassays, such as Western blots and ELISAs. It helps to prevent non-specific antibody binding. In this major application, it is dissolved in Tris-Buffered Saline or Phosphate buffered saline at dilutions of 0.05% to 0.5% v/v. These buffers are used for washes between each immunoreactions, to remove unbound immunologicals, and eventually for incubation solutions of immunoreagents (labeled antibodies) to reduce unspecific background.
to saturate binding sites on surfaces (i.e., to coat polystyrene microplates, generally combined with proteins such as BSA).
to stabilize proteins purified protein derivative (PPD) solution used in skin testing for tuberculosis exposure
as a solubilizing agent of membrane proteins
for lysing mammalian cells, at a concentration of 0.05% to 0.5% v/v, generally combined with other detergents, salts and additives.
Not real keen on the idea of eating something that is used for lysing mammalian cells. Yes, much higher quantities, but still…
Polysorbate 80 is a nonionic surfactant and emulsifier often used in foods and cosmetics. This synthetic compound is a viscous, water-soluble yellow liquid.
Polysorbate 80 is used as an emulsifier in foods.
For example in ice cream, polysorbate is added up to 0.5% (v/v) concentration to make the ice cream smoother and easier to handle, as well as increasing its resistance to melting. Adding this substance prevents milk proteins from completely coating the fat droplets. This allows them to join together in chains and nets, which hold air in the mixture, and provide a firmer texture that holds its shape as the ice cream melts.
Health and beauty use
Polysorbate 80 is also used as a surfactant in soaps and cosmetics, or a solubilizer such as in a mouthwash. The cosmetic grade of polysorbate 80 may have more impurities than the food grade.
Check your toothpaste. Guess what you will likely find. And your shampoo.
Oh, and now you also know why your ice cream no longer melts until quite warm and is full of foamed air. We used to eat healthy natural fruits and cream in ice cream. Now we are eating air and plastic wrapped around processed whatsit… I think this matters. But even further down, in a small section off by itself… at the bottom of a list of “maybe bad but we doubt it” that few folks will read through:
A small number of people may be sensitive to polysorbate 80, and it may be harmful to people with Crohn’s disease.
Lowered body weight of offspring
A 2008 animal study concluded no observable adverse effects were seen at doses per body weight up to 1.85 ml/kg·day, which is equivalent to a 70 kg person consuming about 140 g of this substance per day for 21 days. However, administration of 16.783 ml/kg·day to pregnant rats lowered body weight in male and female offspring. This is equivalent to a person consuming about 1.3 kg of polysorbate 80 per day for 21 days.
A 1956 study saw no effect on reproduction in rats during their lifetime at up to 5% of their diet being polysorbate 80. Reproduction decreased at 20% of their diet. A 1993 study raised concerns that polysorbate 80 might decrease fertility in rats.
Impact on mouse gut microbiota
Relatively low concentrations of two commonly used emulsifiers, namely carboxymethylcellulose and polysorbate-80, induced low-grade inflammation and obesity/metabolic syndrome in wild-type hosts and promoted robust colitis in mice predisposed to this disorder. Use of germ-free mice and fecal transplants indicated that such changes in microbiota were necessary and sufficient for both low-grade inflammation and metabolic syndrome.
So that’s the meat of it all. We have a substance shown in a couple of studies to cause metabolic syndrome and other gut related issues. It is ubiquitous in foods now. And at “relatively low” concentrations of about what we eat it messes up mice who are relatively close to us metabolically.
Houston, I think we have a problem here…
Nature. 2015 Mar 5;519(7541):92-6. doi: 10.1038/nature14232. Epub 2015 Feb 25.
Dietary emulsifiers impact the mouse gut microbiota promoting colitis and metabolic syndrome.
Chassaing B1, Koren O2, Goodrich JK3, Poole AC3, Srinivasan S4, Ley RE3, Gewirtz AT1.
The intestinal tract is inhabited by a large and diverse community of microbes collectively referred to as the gut microbiota. While the gut microbiota provides important benefits to its host, especially in metabolism and immune development, disturbance of the microbiota-host relationship is associated with numerous chronic inflammatory diseases, including inflammatory bowel disease and the group of obesity-associated diseases collectively referred to as metabolic syndrome.
A primary means by which the intestine is protected from its microbiota is via multi-layered mucus structures that cover the intestinal surface, thereby allowing the vast majority of gut bacteria to be kept at a safe distance from epithelial cells that line the intestine. Thus, agents that disrupt mucus-bacterial interactions might have the potential to promote diseases associated with gut inflammation.
Consequently, it has been hypothesized that emulsifiers, detergent-like molecules that are a ubiquitous component of processed foods and that can increase bacterial translocation across epithelia in vitro, might be promoting the increase in inflammatory bowel disease observed since the mid-twentieth century. Here we report that, in mice, relatively low concentrations of two commonly used emulsifiers, namely carboxymethylcellulose and polysorbate-80, induced low-grade inflammation and obesity/metabolic syndrome in wild-type hosts and promoted robust colitis in mice predisposed to this disorder.
Emulsifier-induced metabolic syndrome was associated with microbiota encroachment, altered species composition and increased pro-inflammatory potential. Use of germ-free mice and faecal transplants indicated that such changes in microbiota were necessary and sufficient for both low-grade inflammation and metabolic syndrome. These results support the emerging concept that perturbed host-microbiota interactions resulting in low-grade inflammation can promote adiposity and its associated metabolic effects. Moreover, they suggest that the broad use of emulsifying agents might be contributing to an increased societal incidence of obesity/metabolic syndrome and other chronic inflammatory diseases.
So yeah, cut out the “junk food” and “processed foods” and you can reduce the incidence. BUT, how about we just take the crap out of the food?
There is NOTHING wrong with a cookie, or with french fries, or with ice cream; as long as it is REAL and not a load of metabolic intoxicants.
Can I have my hamburger back now, please.
Toxicol Pathol. 2014 Jan;42(1):49-53. doi: 10.1177/0192623313508481. Epub 2013 Nov 27.
Gut microbiota, low-grade inflammation, and metabolic syndrome.
Chassaing B1, Gewirtz AT.
The intestinal tract is inhabited by a large diverse community of bacteria collectively referred to as the gut microbiota. Alterations in gut microbiota composition are associated with a variety of disease states including obesity, diabetes, and inflammatory bowel disease (IBD). Transplant of microbiota from diseased persons (or mice) to germfree mice transfers some aspects of disease phenotype, indicating that altered microbiota plays a role in disease establishment and manifestation.
There are myriad potential mechanisms by which alterations in gut microbiota might promote disease, including increasing energy harvest, production of toxic metabolites, and molecular mimicry of host proteins. However, our research indicates that an overarching mechanism by which an aberrant microbiota negatively impacts health is by driving chronic inflammation. More specifically, we hypothesize that the histopathologically evident gut inflammation that defines IBD is a severe but relatively rare outcome of an altered host-microbiota relationship, while a much more common consequence of such disturbances is “low-grade” inflammation characterized by elevated proinflammatory gene expression that associates with, and may promote, metabolic syndrome.
In this context, a variety of chronic inflammatory diseases may stem from inability of the mucosal immune system to properly manage a stable healthy relationship with the gut microbiota. While one’s ability to manage their gut microbiota is dictated in part by genetics, it can be markedly influenced by the composition of the microbiota one inherits from their early environment. Moreover, the host-microbiota relationship can be perturbed by instigator bacteria or dietary components, which may prove to play a role in promoting chronic inflammatory disease states.
There’s more if you chase it all down, but it is time for dinner and the family is starting to look at me… ;-) I’ll put up some more in other postings, but for now, this one is long enough.
The bottom line is simply that we are likely in an “obesity epidemic” not because we are bad people, have poor willpower, or “eat bad”, other than that we didn’t know the stuff the government approved to have put in our food by others was causing us to be made sick as it corrupted our gut flora.
The “fix” is not to demonize foods like pizza and ice cream, but to get the carboxymethylcellulose out of the bread and the polysorbate out of everything else.
But at least now I know why my home made bread makes me feel better and why the “store bought” stuff is a bit of a lump in the tummy and why I always feel hungry after a bag of Oreos or commercial potato chips; but always feel full and happy / content after home made ‘chips’, cookies, and such.
Unfortunately, I have no idea if buying “organic” bread at Whole Foods gets rid of these things too, so I’m still going to be stuck in the label reading duty. But at least now I know to watch out for “emulsifier” on the label.