You folks really need to try harder.
I do like Bill Davis and have had some nice exchanges with him going way back and most importantly, he was very friendly to the revolutionary work Tim Steele and I did here on Resistant Starch. I got notice of a post on a new study a couple of days ago that strikes me as a bit bright eyed.
Here’s the study. In fairness, it’s not yet published and so might be different in the final.
Wheat gluten intake increases weight gain and adiposity associated with reduced thermogenesis and energy expenditure in an animal model of obesity
BACKGROUND/OBJECTIVES. The association between gluten and body weight is inconsistent. Previously, we showed that a gluten-free diet reduces weight gain without changing food intake in mice fed high-fat diets. In the present study, we investigated the effects of gluten intake on fat metabolism, thermogenesis and energy expenditure in mice fed a standard or high-fat diet.
METHODS. Mice were fed four different experimental diets during eight weeks: a control-standard diet (CD), a CD added with 4.5% of wheat gluten (CD-G), a high-fat diet (HFD) and a HFD added with 4.5% of wheat gluten (HFD-G). After the eight weeks, the mice received 99mTc-radiolabeled gluten orally to study gluten absorption and biodistribution or they underwent indirect calorimetry. After euthanasia, subcutaneous (SAT) and brown (BAT) adipose tissues were collected to assess thermogenesis-related protein expression. Lipid metabolism was studied in adipocyte cultures from the four groups.
RESULTS. Despite having had the same energy intake, CD-G and HFD-G mice exhibited increased body weight and fat deposits compared to their respective controls. 99mTc-GLU or its peptides were detected in the blood, liver and visceral adipose tissue (VAT), suggesting that gluten can even reach extra-intestinal organs. Uncoupling protein 1 (UCP1) expression was reduced in the BAT of HFD-G and in the SAT of CD-G and HFD-G mice. Indirect calorimetry showed lower oxygen volume consumption in CD-G and HFD-G groups compared with their controls. In HFD mice, daily energy expenditure was reduced with gluten intake. Gluten also reduced adiponectin, peroxisome proliferator-activated receptor (PPAR) α and PPARγ and hormone-sensitive lipase in cultures of isolated adipocytes from HFD mice, while in the CD-G group, gluten intake increased IL-6 expression and tended to increase that of TNF.CONCLUSIONSWheat gluten promotes weight gain in animals on both HFD and CD, partly by reducing the thermogenic capacity of adipose tissues.
International Journal of Obesity accepted article preview online, 07 October 2015. doi:10.1038/ijo.2015.204.
OK, let’s take a look.
The gluten used in this study is not in the composition one finds in freshly-baked bread or other sources of gluten, which are varied. It’s isolated; not in whole food form, which is an issue for me. This sort of methodology seems to be pervasive and goes back a long time. I’ve called it unbridled deconstruction and reductionism in the past, and that’s because it is.
For instance, eating fruit is not the same as taking a multivitamin with a glass of sugar water. And with all of the knowledge building on more knowledge and understanding over the gut biome, the glaring omission beyond the balances of nutrients in whole foods is the lack of fiber (and maybe even probiotics on your food), and fiber feeds gut bugs and gut bugs are important in body fat homeostasis and probably appetite control: 52% Reduced Fat Gain Over 4 Weeks of Overfeeding Twenty Young Men W/ 1000 kCal/Day on a High Fat (55%) Diet Due to Double Dose of a Commercial Multistrain Probiotic. That’s in isolation too, but it has the advantage of at least using “whole organisms.” And if that’s not enough, other research suggests that certain gut bugs are critical in dealing with gluten.
Celiac disease and non-celiac gluten sensitivity may be all about the microbiome and begin at the very moment you’re born via cesarean section and worsen when you’re not breastfed – In a soon-to-be-published review in Nutrients Cenit et al. try to elucidate whether gluten intolerance and celiac disease are consequences or triggers of significant imbalances in the bacterial composition of the human microbiome and how one or the other may eventually come about.
As the authors point out, there are in fact studies which suggest that the early colonization of the infant’s gut in conjunction with environmental factors (e.g., breast-feeding, antibiotics, etc.) could influence the development of our kids’ oral tolerance to gluten.
So, along the lines of it simply not being in whole food form, here’s an email from Jane Karlsoon, PhD (Oxford) who has studied whole mineral interaction in whole foods for over 30 years.
One effect of gluten in the papers you’ve linked is to lower PPAR alpha, which is important because PPAR alpha upregulates expression of genes for fat burning and browning of white fat. It’s also important in preventing oxidative stress.
In aged mice, the redox-regulated transcription factor nuclear factor-kappaB (NF-kappaB) becomes constitutively active in many tissues, as well as in cells of the hematopoietic system. This oxidative stress-induced activity promotes the production of a number of pro-inflammatory cytokines, which can contribute to the pathology of many disease states associated with aging. The administration to aged mice of agents capable of activating the alpha isoform of the peroxisome proliferator-activated receptor (PPARalpha) was found to restore the cellular redox balance, evidenced by a lowering of tissue lipid peroxidation, an elimination of constitutively active NF-kappaB, and a loss in spontaneous inflammatory cytokine production. Aged animals bearing a null mutation in PPARalpha failed to elicit these changes following treatment with PPARalpha activators, but remained responsive to vitamin E supplementation. Aged C57BL/6 mice were found to express reduced transcript levels of PPARalpha and the peroxisome-associated genes acyl-CoA oxidase and catalase. Supplementation of these aged mice with PPARalpha activators or with vitamin E caused elevations in these transcripts to levels seen in young animals. Our results suggest that PPARalpha and the genes under its control play a role in the evolution of oxidative stress excesses observed in aging.
So these effects can be prevented with vitamin E, which is very high in wheat germ.
The second paper you linked says this:
It has been previously demonstrated that gluten products may accumulate in the lysosomes of intestinal cells, leading to metabolic reactions that culminate in the proteosomal degradation of PPAR-γ . This may represent another mechanism by which gluten exclusion attenuates inflammation and glucose homeostasis.
Reference 38 says this:
After 24 h of challenge p31-43 [gluten fragment] but not palpha-2 or palpha-9, is still retained within LAMP1-positive perinuclear vesicles [lysosomes] and leads to increased levels of reactive oxygen species (ROS) that inhibit TG2 ubiquitination and lead to increases of TG2 protein levels and activation. TG2 induces cross-linking, ubiquitination and proteasome degradation of PPARgamma. Treatment with the antioxidant EUK-134 as well as TG2 gene silencing restored PPARgamma levels and reversed all monitored signs of innate activation, as indicated by the dramatic reduction of tyrosine and p42/p44 phosphorylation.
EUK-134 prevented all the bad stuff. It’s a manganese drug and MnSOD mimic. In other words, it looks like most or all of the bad things caused by gluten in these experiments can be prevented by vitamin E or manganese, the very things whole grains supply and isolated gluten does not.
This study does not represent the real world. For instance, the French, who have one of the highest levels of wheat consumption in the world (40% greater than the US according to FAOSTAT) also have one of the lowest obesity rates of any developed nation.
The idea that wheat or gluten causes obesity in healthy subjects is easily debunked by looking at the history of wheat, where both wheat and gluten were once considered to be health-promoting foods. And the 6th century Chinese added wheat gluten to their food as a meat replacement. There is no evidence in the historical record that this resulted in deleterious effects.
Isolated gluten is non-optimal, just as purified starch isn’t optimal. The isolated gluten came from a cereal laboratory, “granotec” in Brazil. And it’s not the first time that “granotec” gluten induced obesity from an overfeeding high fat diet. See this 2013 study:
Where it gets interesting is that the studies were done in Brazil/Argentina, which both happen to be fortified with… iron. So, could these researchers be paying attention to gluten free diets because they’re dealing with populations that may have gluten issues that arise in populations from fortification?
…Well, to bottom line it, the whole problem with both the grains and the gluten positions vis-a-vis a Paleo Diet is that it’s a falsified hypothesis from the get-go, since there’s so any examples of populations thriving on both, without the reports of sensitivity and outright celiac that have become so common.
You need a new hypothesis that scores well with all the available data. Like this one. You generally find those with no problems…
- Eat grains in whole food form (including germ and bran).
- Don’t fortify.
But even in the case of refined grains like white flour, the French example suggests that it’s doable absent fortification but with attention given to other foods containing the minerals that grain refining strips away.