Polysorbate, Metabolic Syndrome, Obesity, and You

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.

Sedentary lifestyle

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


A study in Nature suggests that common food additives could be contributing to the development of chronic inflammatory diseases. Chassaing et al.[1] 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.[2]

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.


[1] 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

[2] 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.
Food use

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:

Crohn’s disease

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.

Decreased fertility

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…

The Papers


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.

In Conclusion

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.

Subscribe to feed

About E.M.Smith

A technical managerial sort interested in things from Stonehenge to computer science. My present "hot buttons' are the mythology of Climate Change and ancient metrology; but things change...
This entry was posted in Science Bits. Bookmark the permalink.

11 Responses to Polysorbate, Metabolic Syndrome, Obesity, and You

  1. Alexander K says:

    In the last few weeks, my wife and I have at last been successful at baking ACCEPTABLY FLAVOURED AND TEXTURED Gluten-free bread for my wife, a medically-assessed Celiac. Because I work at home, I have long ago taken over catering duties for our household, so in view of our success baking acceptable bread, I decided to eat Gluten free bread rather than the commercially-baked bread and have eaten none of the latter for about 3 weeks now; the tape measure tells me that my belly is shrinking, which is great as I have been conscious of my big belly since I was a small boy – at school my nickname was ‘Jellybelly’.
    As I said earlier on the topic of Glycophates, I have T2 diabetes, diagnosed at age 60. Since age 72, I have followed a weights and general fitness workout 3 times per week. I am now aged 75, the T2 diabetes is no longer identifiable in blood tests and my muscle mass and bone demsity have increased markedly.
    Not ingesting wheat products along with all their hidden ‘extras seems another step toward good health.

  2. tom0mason says:

    Uuummm, carboxymethylcellulose (aka CMC), just so delicious and also used as glue! (Especially as wood and paper adhesive, used in the building trade.)

    Syrup too thin, sauce not the correct consistency? Just add wallpaper glue for that perfect mouth-feel.

  3. sabretoothed says:

    It’s just low Iodine, that’s all. Also low Vit A, low mag, causing unbound copper to accumulate in the tissues.

    These are all symptoms of a cause.

  4. Gary P Smith says:

    E.M. Thank you for the article. I’ve been wondering the same thing for a while now, what has changed? My own research into the topic led to much of the same conclusions, micro-nutrients in the gut getting out of balance, and there is no way to avoid these ‘issue ingredients’ short of growing your own food.

    One of the most interesting books I’ve come across is by Dr. Joel Fuhrman who has published several books in his Eat To Live series. I read “The End of Diabetes” version as I have been Type 2 for a decade but am getting close to eliminating all my symptoms. I had to work hard to get past the first few chapters as he spends a lot of time repeating himself that the medical profession is not doing its job, and we can cure ourselves of diabetes, high blood pressure, risk of cardio-vascular diseases which are mostly caused by inflammation, risk of strokes, etc. IF WE JUST EAT RIGHT. He also shares your sentiments that when you eat the right stuff, you are truly satiated.

    I’m not ready to give all his recommendations a go as his recommended diet is almost vegan, and I would need to give up coffee. He has something I don’t quite understand against animal proteins as the amino acid chains are “too complete”. He states it is better to get our proteins from plant sources. He backs up his claims with references to published medical research, about 20 pages of references alone.

    I am getting good results with just traditional calorie counting, increasing exercise, and following some of the recommendations Fuhrman has as well as others to try and get more of the junk out of my diet.

    I would be very interested in your analysis of his claims. I will gladly pay for the book for you if you are interested in reading it.

  5. p.g.sharrow says:

    This homemade verses store bought also has me wondering. Tomato sauce that I make, used in dishes at home, cause me no problems but modern creations from the store cause me upset for days. I tell my lady Read the Ingredients before buying prepared sauces, a thing she loves to use, and then she complains for 5 days about her IBS.
    A manufactured food additive that is used in everything to make it “Better” could be the root cause of this health epidemic. It is certain that something in our modern diet is not right. Making dinner from scratch seems to avoid the problem but even that gets harder to attain. pg

  6. Petrossa says:

    and there is this:
    “40 years of federal nutrition research fatally flawed

    University of South Carolina study shows flaws in NHANES data

    Four decades of nutrition research funded by the Centers for Disease Control and Prevention (CDC) may be invalid because the method used to collect the data was seriously flawed, according to a new study by the Arnold School of Public Health at the University of South Carolina.

    The study, led by Arnold School exercise scientist and epidemiologist Edward Archer, has demonstrated significant limitations in the measurement protocols used in the National Health and Nutrition Examination Survey (NHANES). The findings, published in PLOS ONE (The Public Library of Science), reveal that a majority of the nutrition data collected by the NHANES are not “physiologically credible,” Archer said.

    These results suggest that without valid population-level data, speculations regarding the role of energy intake in the rise in the prevalence of obesity are without empirical support, he said.”


  7. E.M.Smith says:


    It’s that kind of thing that causes me to always have some “reservation” about appeal to authority and peer reviewed literature. I’m always willing to at least listen to a “crank” and see if I can independently validate / refute their ideas, for the simple reason that they often have something of merit in there somewhere (even if it takes some digging…) and that The Authority is often peddling complete trash as God’s Own Wisdom. Yes, the balance is usually toward the well educated well researched Authority, but not always, and some fields are just entirely trash Authority be damned.

    But that attitude is sort of the definition of real science as I learned it. Always testing, never accepting blindly and never rejecting out of hand…

    @P.G. Sharrow:

    As of a couple of years back, the spouse and I both started to react to “tomato products”. I’ve not had the time yet to sort it all out, and find if it is “tomato-ness” or “commercial products only”. Maybe I will plant a tomato this year ;-) At this point, having a pot of spaghetti with commercial sauce, or a can of Chef B’s Ravioli (that I like quite a bit for historical reasons) results in 2 to 3 days of mild bowl discomfort ( more like ‘awareness’ and slight irritated feeling) and some joint discomfort (with, lately, a bit of a ‘flush’ that has that ‘immune reaction’ feeling…)

    I’ve been thinking to trying DIY tomato stuff, but figured it was just going to be the same, most likely. Maybe I was ignoring my own advice in the first paragraph above ;-)

    @Gary P. Smith:

    I’ll do an internet “dig here” on his stuff first. See what I can find for free and without reading the whole series ;-)

    On animal protein being “too complete”: Digestion is not perfect, and we tend to be ‘lowest energy path’ machines, so conserve what would have to be built some times. I see this with beef proteins. At about 26 I started to develop mild arthritis. It would show up when skiing as ‘creaky hands’. Over the years it got somewhat worse. There’s a long story of how I got to the solution, but I’ll skip it here. What I found was that “Cow Stuff” for a week or two would result in a flare up, but avoiding it for a week or two and all would be fine. The “thesis” is that as soon as digestion has broken down cartilage molecules into “small enough” chunks they are transported to the blood and then used to repair cartilage. Unfortunately, the digestion idea of “small enough” leaves some bits that the immune system sees as “that is cow” and attacks…

    So perhaps his “too complete” is the same as “digestion preserves some of the other species antigens”…

    This worked for me:

    Then I refined it a bit. Instead of a “only fish and vegetables with rice” starting point, I did an “elimination diet” and ate only chicken for a week… then started to branch out. Then, instead of “add one food at a time for one week”, I did a more efficient “binary search” where I’d add a block (say, lasagna) and if not problems, all ingredients were OK. IF there was a problem, you cut out half of the things in lasagna and find out which half. Repeat until Lasagna ingredients are sorted. ( I.e. do noodles and sauce vs sausage and cheese; then when it is the sausage and cheese to which you react, test sausage, then cheese…)

    What was very clear to me after that was the effect foods has on different folks varies by person and is often immune moderated. Yet there are patterns… Some things, like rice and squash, seem fine for everyone. Some, like beef and tomatoes cause more folks problems (enough that they are particularly called out in Dr. Dong’s book) Others, like wheat, are fine for most, but a few react very badly. And you must search to find what works and does not work for you.

    A friend with “hypoglycemia” (diagnosed, but in the end, wrongly) needed a special diet. I decided to “play with” my diet to see if I could “go where he could not” to gather information without making him sick. In short, after about a month of “crazy diet” with LOADS of noodles and sugar and very low meat and vegetables, I was having some near “hypoglycemic” episodes. Shakes and “the stupids” about an hour after a shot of sugary stuff. That kind of thing. Took me nearly 2 months to “recover”. Now I recognize that it was likely because the digestive bacteria need to change, not just my blood chemistry. But the result did help the friend (“yes, avoid carbs and eat meats). (Later it was chased down to an actual wheat allergy and not even a gluten intolerance, but avoiding carbs avoided the wheat…)

    So my “bottom line” even without reading the book is this: Try stuff. If it works, keep doing it. But test it a few times, not just one or two, as sometimes things are accidental coincidences.


    You will appreciate this…

    I have had NO symptoms of Vit. A deficit. Night vision is fine, etc. We eat a fair amount of butter and cheese, meat too. So it OUGHT to not be a problem. However….

    Due to your “push” on Animal Vit-A and high amounts of it too, I decided to “experiment”. (Anybody notice a habitual behaviour on my part? ;-) So I bought a tub of chicken livers. I love chicken livers if gently fried such that they don’t dry out too much and have a nice gooey texture. Ate a large plate of them. Next day had more for lunch.

    Now, despite my expectations, I’m feeling significantly more energetic and some “skin spots’ are resolving. ( Long duration lesions that were oh so slowly healing, but way too slow, about lentil sized and with a small scab in the middle. I’d picked up one on each forearm and one on my shoulder somewhere along the line. Sometimes I’m out in the rough and “stuff accumulates” ;-)

    So you’ve gotten me going “Hmmmm…..” and a deeper dive into Vit-A is on the cards ( I’ve accumulated a fair number of links already).

    I’ve also got another tub of chicken livers to work through…


    Yeah, the “industrial” uses of the stuff (and the polysorbates – lab ware cleaning and cell busting? Uh, and you want that in my food?…) is a bit off putting…

    @Alexander K:

    If you have a nice gluten free bread recipe, feel free to post it. I’ve got a couple of gluten free / wheat intolerant friends and can always use another bread recipe…

    I’ve been on a Rogues Gallery of diets with various friends over the years ( tendency to experiment mixed with ‘loyalty to friends’ and ‘why not’…). At the end of it all, a remarkable pattern emerged: Simple calorie reduction works, but at great emotional strain. Ketosis works, but is hard to reach and a meat only diet is boring, also I don’t feel great on it. Avoidance of carbs works. High Carbs can work, but ‘has issues’ IMHO involving blood sugar stability and the additives noted above. But what REALLY struck me was that “eating simple home prepared plain foods” resulted in my feeling overall my best, even if a bit ‘robust’ of form. (Not fat, I’ve been fat, but with a +5 to +10 lbs that does NOT get higher)… When doing regular karate training for a few years, my weight went UP (muscle is heavier) but my body form got better. My overall conclusions was: Look in the mirror, not at the scales.

    So largely I’ve gone back to eating the way I was raised. Meals are based around the “protein, starch, vegetable” pattern. Bias toward fish and birds, occasional red meats. Lots of bean and potato dishes. Occasional noodle dishes. Typical peas, green beans, carrots, side salads vegetables (but occasionally with pickles and beets and…) Starch most often rice, potatoes, home made bread, or a vegetable / starch dual purpose food like beans (or corn for the spouse); occasionally pasta. Sometimes Oats (breakfast and cookies ;-) or mixed grain Kashi mixes When I do that, I’m healthy even if I have the occasional dish of ice cream or sandwich with “store bought” bread. (Though with this article, I’m biasing much more away from “store bought”…)

    It does, also, seem to be getting harder to find “plain ingredients” and “plain foods”, though…

  8. tom0mason says:

    I’ve spent a while trying to find your recent article about growing cinnamon but with no success. Ho hum.
    I’ve just come across this interesting paper on cinnamon bark and it’s basically a review of reports on cinnamon in Pharmacological studies. Called ” From type 2 diabetes to antioxidant activity: a systematic review of the safety and efficacy of common and cassia cinnamon bark1 by Jean-Jacques Dugoua, Dugald Seely, Dan Perri, Kieran Cooley, Taryn Forelli,Edward Mills, and Gideon Koren” it really is an eye-opener.
    IMO Wow! is just an understatement


    Both bark and flower can be used medicinally; however,the bark is used more commonly. Levels of the active constituents vary depending on the method used in the extraction process. Extensive gas chromatography analysis of cinnamon leaf, stem bark, and root bark oils indicated a total of 72 compounds in varying proportions (Senanayake et al. 1978). Common and cassia cinnamon (C. verum and C. aromaticum) contain volatile oils (1%–4%) such as cinnamaldehyde (60%–80%, 1400–30000 ppm), eugenol (up to 10%), and trans-cinnamic acid (5%–10%); phenolic compounds (4%–10%) such as condensed tannins, catechins, and proanthocyanidins; monoterpenes and sesquiterpenes (pinene); calcium-monoterpenes oxalate; gum; mucilage; resin; starch; sugars; and traces of coumarin (Duke 1992; Bruneton 1995; Leung and Foster 1996; Anderson et al. 2004).

    The polyphenolic polymers found in C. verum and C. aromaticum have antioxidant activity and have been shown to reduce oxidative stress in a dose-dependant manner through inhibition of 5-lipooxygenase enzyme (Anderson et al. 2004; Blomhoff 2004; Ranjbar et al. 2006).

    ***Antidiabetic ****

    Methylhydroxychalcone polymer (MHCP) in common and cassia cinnamon was found to be an effective mimetic of insulin (Jarvill-Taylor et al. 2001). MHCP demonstrated in vitro activation of glycogen synthase and inhibition of glycogen synthase kinase-3b as well as insulin receptor phosphorylation homologous to the effects of insulin in 3T3-LI adipocytes (Jarvill-Taylor et al. 2001). In vivo studies show an increase in insulin-stimulated IR-b and the IRS1 tyrosine phosphorylation treated with cassia cinnamon (Qin et al. 2003). Cinnamon acts as a synergetic agonist with insulin in vivo to decrease blood glucose levels after a glucose tolerance test (Verspohl et al. 2005) and in chronically high fructose diets(Qin et al. 2004).


    A natural medicine compendium reported that cinnamaldehyde is a central nervous system (CNS) stimulant in high doses, a CNS sedative in low doses, increases peripheral blood flow, slows heart rate, reduces blood pressure, and has antipyreticandhypothermiceffects(Jellin2006a, 2006b). Common cinnamon bark reduces the amplitude of penile somatosensory-evoked potentials in a mechanism that is not clearly understood, but may be useful in the treatment of premature ejaculation (Choi et al. 2000; Anderson et al.


    The essential oil has demonstrated strong antibacterial and antifungal activities in vitro. Antifungal, antiviral, bactericidal, and larvicidal actions have been reported for the volatile oil. Its constituents eugenol, eugenol acetate, and methyl eugenol have been reported to enhance trypsin activity in vitro (Bruneton1995).Cinnamaldehyde has broad spectrum gram-positive and gram-negative antibacterial activity in which it was shown to inhibit the growth of Clostridium perfringens, Bacteroides fragilis, Bifidobacterium bifidum (Lee and Ahn 1998), Staphylococcus aureus, Listeria monocytogenes, Escherichia coli, Enterobacter aerogenes, Proteus vulgaris, Pseudomonas aeruginosa, Vibrio cholerae, V.parahaemolyticus, and Salmonella typhimurium (OAI et al.2006) as well as broad-spectrum vaginal microflora (Arnal-Schnebelen et al. 2004). One mechanism that has been explored for this antibacterial activity is that cinnamaldehyde destroys the cytoplasmic membrane of both gram-positive and gram-negative bacteria and induces depletion of the intracellular ATP concentration (Oussalah et al. 2006).

    I downloaded the full report from

  9. tom0mason says:

    Further to what I’ve written above is this about cinnamon and diabetes —
    Cinnamon and Health DOI:10.1080/10408390902773052
    Joerg Gruenwalda, Janine Frederb & Nicole Armbruester

    From the Abstract —

    “…We found two prospective, randomized, double-blind, placebo-controlled, peer-reviewed clinical trials and one prospective, placebo-controlled, peer-reviewed clinical trial that evaluated the efficacy of cinnamon supplementation in patients with type 2 diabetes; a total of 164 patients were involved in these trials. Two of the studies reported modest improvements in lowering blood glucose levels with cinnamon supplementation in small patient samples. One trial showed no significant difference between cinnamon and placebo in lowering blood glucose levels. Overall, cinnamon was well tolerated. These data suggest that cinnamon has a possible modest effect in lowering plasma glucose levels in patients with poorly controlled type 2 diabetes. However, clinicians are strongly urged to refrain from recommending cinnamon supplementation in place of the proven standard of care, which includes lifestyle modifications, oral antidiabetic agents, and insulin therapy.”

    I wonder how cinnamon plays with those who have “pre-diabetic” conditions?

  10. E.M.Smith says:


    I think I mentioned cloves as what grew. You comment may explain why I don’t get a suger rush frm cinnamon toast… and like it so much :-)

  11. Pingback: Interesterified Fats – How Evil? | Musings from the Chiefio

Comments are closed.