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-   -   The Science of Nutrition (https://www.miataturbo.net/insert-bs-here-4/science-nutrition-75333/)

JasonC SBB 02-06-2015 04:21 PM

Before the 1950s, it was common wisdom that carbs tended to make one fat.
After grain-industry lobbying and government money backed Ancel Keys' hypothesis, there was a reversal.
Now it looks like his hypothesis was a long and lengthy diversion.

Joe Perez 03-26-2015 05:36 PM

For Jason:


mgeoffriau 03-26-2015 09:36 PM


Originally Posted by Joe Perez (Post 1218920)

Can I have a summary in text? I'm not an animal; I like to read information.

JasonC SBB 03-26-2015 11:34 PM

He's saying obesity is caused by insulin resistance rather than the other way around which was the old paradigm.

I believe insulin resistance is caused by eating beyond one's starch tolerance, which varies widely, for years and years. Eating "low fat" and "healthy whole grains" has been disastrous.

The number of copies of AMY1 genes (amylase production which digests starch) one has, is strongly correlated with blood sugar spikes after a starchy meal.

Joe Perez 04-02-2015 02:01 PM

4 Attachment(s)
According to a widely discredited paper published in a non-peer-reviewed journal, by Dr. Stephanie Seneff, a senior researcher at MIT who specializes in computer science and artificial intelligence (but not biology, toxicology, medicine, chemistry or agriculture), half of all children born in American will have Autism by the year 2025 because of Monsanto.

Autism Rates To Increase By 2025? Glyphosate Herbicide May Be Responsible For Future Half Of Children With Autism



I post this, as both the original paper and the ensuing debate make numerous claims of varying credibility about gut flora, which I know is a subject of keen interest to several in this thread.


Another scientist, who is somewhat less discredited, supports Seneff's conclusion by drawing the following correlation between the use of herbicides produced with glyophosate (the magic bullet chemical that Seneff predicts will kill us all) and the number of 6 years olds who benefit from the federal Individuals with Disability Act (IDEA) over the time period of 1993-2010:

https://www.miataturbo.net/attachmen...ine=1427997662




This study demonstrates, in a similar fashion, that a decrease in the number of honey-producing bee colonies in the US directly causes an increase in marijuana consumption by juveniles:

https://www.miataturbo.net/attachmen...ine=1427997662

JasonC SBB 04-02-2015 02:48 PM

Is there anyone in this thread that still takes Seneff's claims seriously?

Joe Perez 04-02-2015 03:12 PM


Originally Posted by JasonC SBB (Post 1220889)
Is there anyone in this thread that still takes Seneff's claims seriously?

A quick search of this thread shows that the name Seneff has only been mentioned once previously in this thread (on Jan 26 of this year), and the only response was from you claiming that her connections were "tenuous" and that more evidence was needed.

So, given that there's been virtually no discussion of the subject at all, I honestly don't know whether anyone takes her seriously or not.

I just figured you'd enjoy some more gut-flora-related things to warn us all about. The article does, after all, recommend avoiding a number of different food products which are generally recognized as safe.

Joe Perez 08-15-2015 10:20 PM

Scientists (sort of) settle debate on low-carb vs. low-fat diets

By Ariana Eunjung Cha August 14


Decisions, decisions. If you're looking to lose weight, should you go for the mango smoothie or the artisan cheese plate? The poppy-seed bagel or the cashew snack?

If you're unsure, join the crowd. For years nutritionists have debated the same kinds of questions -- with some arguing that a low-fat diet is the way to go, while others insisting that a diet with restricted carbohydrates is better.

With each academic study on the subject, public sentiment seemed to sway one way or the other. In the 1980s and ’90s, low-fat diets were the fad. In recent years, low-carb diets became the thing. It was enough to give the modern-day dieter whiplash.

Seeking to settle the debate, scientists from the National Institutes of Health set up a very detailed and somewhat unusual experiment.

They checked 19 obese adults (who were roughly the same weight and had the same body-mass index) into an inpatient unit at the NIH clinical center, for two-week increments.

For the first five days of each visit, the volunteers were given a baseline diet of 2,740 calories that was 50 percent carbohydrate, 35 percent fat and 15 percent protein. This wasn't very different from what they were eating before. But for the following six days, they were given either a low-fat diet or a low-carb diet, each having 30 percent fewer calories. Each participant was also asked to exercise one hour a day on the treadmill.

Then the researchers put the volunteers in metabolic chambers -- a sealed, climate-controlled room hooked up to a battery of recording and analyzing devices (kind of like the ones they use for lab rats) -- for five days to see what would happen.

After analyzing everything from how much carbon dioxide and nitrogen they were releasing to their hormone and metabolite levels, the researchers concluded that the calorie-per-calorie, low-fat diets beat out low-carb diets. During the study period, the minimum detectable difference in cumulative fat loss was 110 grams.

On average participants lost 463 grams on the low-fat diet vs. 245 grams on the low-carb diet by the end of the six-day diet period. The researchers projected out what might happen if they stuck to those diets for six months and found that the low-fat group would end up losing six more pounds on average than the low-carb group.

"In contrast to previous claims about a metabolic advantage of carbohydrate restriction for enhancing body fat loss our data and model simulations support the opposite conclusion," Kevin D. Hall, a senior investigator at NIH in biological modeling, and his co-authors wrote in Cell Metabolism on Thursday.

The study appeared to be a response to recent theories about how low-carb diets work. Proponents have said that decreasing carbs decreases insulin secretion, which leads to increased fat oxidation and burning of calories.

But, the researchers wondered, "While the first law of thermodynamics requires that all calories are accounted, could it be true that reducing dietary fat without also reducing carbohydrates would have no effect on body fat? Could the metabolic and endocrine adaptations to carbohydrate restriction result in augmented body fat loss compared to an equal calorie reduction of dietary fat?"

Does this mean that if you're on a low-carb diet that you should switch to a low-fat diet? Not necessarily.

The researchers acknowledge that "translation of our results to real-world weight-loss diets for treatment of obesity is limited." The design of their experiment relies on strict control of food intake -- which "is unrealistic in free-living individuals," they said.

Likewise Frank Hu, a professor of nutrition and epidemiology at Harvard T.H. Chan School of Public Health, told Healthline News that while the study was “rigorously conducted,” it “doesn't really portray real life situations.”

David L. Katz, founder of Yale University's Prevention Research Center, emphasized that despite the fact that the study is down on fats, scientists still believe fats aren't nearly as bad for us as we once thought.

“In my view, this is a reality check,” Katz told Forbes. “It does not invite us to go back to preferential fat-cutting, but it does invite us to get past the new folly of preferential carb-cutting. My hope is this study provides a nudge not from one nutrient fixation to another, but in that direction: Food, not nutrients.”

The takeaway: The most important part of dieting isn't necessarily the kind of diet you chose when it comes to low-carb vs. low-fat, it's whether you stick to it.

Scientists (sort of) settle debate on low-carb vs. low-fat diets - The Washington Post

patsmx5 08-16-2015 12:39 AM

LOL at the reporting. I've read it (the study, not the BS reporting on it). It's sad the testing was so short. Also would have been nice to include a very low carb (less than 50g/day) group to compare to as well.

Joe Perez 08-16-2015 08:50 AM

There's something I've found to be true among pretty much all proponents of "non-traditional" self-improvement methods, be they diet programs, multi-level-marketing systems, etc. That thing is that whenever a new study or paper is published by a scholarly source which in some way wholly or partially contradicts the claims of these proponents, no matter how solid the science, there's always "one little thing" that the researcher got wrong which would have somehow changed the whole outcome.

Indeed, the optimistic idea that changing just "one little thing" can turn "the whole system" on its head is so deeply ingrained in the popular psyche that internet marketers have been exploiting it for year in the forum of clickbait ads. How many times* have you loaded a webpage and seen a crudely-drawn add jiggling at you from the sidebar, promising that you can boost your credit score, eliminate acne, slash your car insurance bill, decrease belly fat, pay off your mortgage in half the time, increase testosterone, reverse hair loss, or prepare for the upcoming tyranny under whatever president was just elected, simply by following "This One Weird Old Trick!"
* = hopefully none, if you use a reliable ad-blocking mechanism such as ABP.
Modern organized religion works in pretty much the same way. Each religious sect is the "true belief" above all others, because they either do or do not eat certain foods, or attend worship services on a certain day of the week, or pray to a certain saint or another, or wear a certain type of underwear, or baptize their faithful by a certain method, or clip the foreskin from male infants, or whatever.

Same idea. We like to believe that whatever system we adhere to works better than any other, because we understand the one crucial detail which the rest of the professional and academic world has either overlooked or ignored.



In this case, the study was (to the best of my knowledge), the first to be carried out in a completely controlled clinical environment, where the participant's food intake and chemical output could be monitored with absolute precision. As it was, the participants were required to spend one full month (in two two-week segments) in this sealed environment. How much longer would have been reasonable?

A similar article in Runners World expressed the exact same concern as you regarding a desire to see carb reduction to 50g/day (as opposed to 140 g/day as was done,) but also noted that "The enhanced weight loss seen by low-carb dieters jibes with prior studies that have shown rapid results from such dieting. Experts believe this effect is related to the large amount of water lost from the body when carbohydrates are restricted. Hence, this loss doesn’t represent a true change in body tissue. Also, the low-carb weight-loss advantage generally disappears after six to 12 months."


For those who wish to read the original paper, it is here: http://www.cell.com/cell-metabolism/...131(15)00350-2

mgeoffriau 08-16-2015 10:42 AM

You're projecting. Nobody is discussing raspberry ketones.

Joe Perez 08-16-2015 10:52 AM

1 Attachment(s)

Originally Posted by mgeoffriau (Post 1257251)
You're projecting.

https://www.miataturbo.net/attachmen...ine=1439736739

Joe Perez 08-16-2015 11:58 AM

Contrarian nonsense deleted.

By the power of Greyskull, I have the power.

sixshooter 08-16-2015 12:06 PM

The hypochondria and pseudoscience thread
 

Originally Posted by Joe Perez (Post 1257263)
By the power of Greyskull, I have the power.

Lol.

Diet fads are much like politics in the way they are defended and contrarians are vilified.

JasonC SBB 08-16-2015 12:11 PM

Over the months and years I've found more and more evidence (such as the study Joe posted) that falsifies Gary Taubes' simplistic "carbs drive insulin drives obesity".

The simplistic hypothesis appears to be wrong; either it's completely wrong, or there's more nuance to it.

Couple of things I noticed with the linked study. First is that the subjects had healthy morning blood sugar and insulin levels. It's possible that the success some people have with reducing carbs instead of fat are among those with some degree of blood sugar dysregulation - and in those people reducing carbs is the most important first step towards health.

Second is that the study didn't report the subjects' reported hunger levels (or I missed it). This is very important for being able to stick to a diet (as Joe pointed out). A lot of low-carb dieters report reduced hunger, making it easy to continue long enough to lose significant amounts of weight.

And 3rd, FWIW 140g carbs/day is "moderate carb" not low carb. That's about 3 cups of rice a day. This study tested "reduced carb" not "very low carb" (ketogenic), which is a whole 'nother kettle of fish. Typical threshold is 50g/day with moderate protein. Ketosis is well studied and is known to be very effective in the *short term* for rapid weight loss and improving blood sugar regulation, as well as for treating seizures and some other nervous system issues. It's also well known that switching to a ketogenic diet can produce discomfort in some people for the first week, making it difficult for them.

Individuals vary significantly in how many carbs they can metabolize properly. The # of copies of the "AMY1" gene one has has a big effect. Indeed individuals in cultures that historically ate a lot of starch tend to have more copies.

And intense exercise greatly increases the # of carbs an individual needs and can metabolize well.

Lastly FWIW, (and this has little to do with the hypothesis being tested in the study), the reduced-carb group had over double the recommended Omega-6 intake (probably from crappy "vegetable" oils), the low-fat group had insufficient Omega-3, the reduced-fat group ate a lot of sugar and probably refined grains too (which promotes unhealthy gut flora). Not good in the long term.

(Low-carb dieters should probably supplement with prebiotic fiber such as Inulin and Resistant Starch)


In this talk "Lessons From the Vegans", Denise Minger has an interesting hypothesis. That there are benefits in both very low fat and very low carb diets (in the short term), with some similarities between them:


Joe Perez 08-16-2015 12:22 PM

^ I wish we still had props. As it is, all I can give you is :likecat:.

Joe Perez 08-16-2015 01:53 PM

1 Attachment(s)
More antagonizing, content-free flamebait from mgeoffriau deleted.

https://www.miataturbo.net/attachmen...ine=1439747651

sixshooter 08-16-2015 02:13 PM

http://Eliminate Hairy Ballsack Perm... Simple Trick!

patsmx5 08-17-2015 08:53 PM


Originally Posted by Joe Perez (Post 1257243)
There's something I've found to be true among pretty much all proponents of "non-traditional" self-improvement methods, be they diet programs, multi-level-marketing systems, etc. That thing is that whenever a new study or paper is published by a scholarly source which in some way wholly or partially contradicts the claims of these proponents, no matter how solid the science, there's always "one little thing" that the researcher got wrong which would have somehow changed the whole outcome.

Indeed, the optimistic idea that changing just "one little thing" can turn "the whole system" on its head is so deeply ingrained in the popular psyche that internet marketers have been exploiting it for year in the forum of clickbait ads. How many times* have you loaded a webpage and seen a crudely-drawn add jiggling at you from the sidebar, promising that you can boost your credit score, eliminate acne, slash your car insurance bill, decrease belly fat, pay off your mortgage in half the time, increase testosterone, reverse hair loss, or prepare for the upcoming tyranny under whatever president was just elected, simply by following "This One Weird Old Trick!"
* = hopefully none, if you use a reliable ad-blocking mechanism such as ABP.
Modern organized religion works in pretty much the same way. Each religious sect is the "true belief" above all others, because they either do or do not eat certain foods, or attend worship services on a certain day of the week, or pray to a certain saint or another, or wear a certain type of underwear, or baptize their faithful by a certain method, or clip the foreskin from male infants, or whatever.

Same idea. We like to believe that whatever system we adhere to works better than any other, because we understand the one crucial detail which the rest of the professional and academic world has either overlooked or ignored.



In this case, the study was (to the best of my knowledge), the first to be carried out in a completely controlled clinical environment, where the participant's food intake and chemical output could be monitored with absolute precision. As it was, the participants were required to spend one full month (in two two-week segments) in this sealed environment. How much longer would have been reasonable?

A similar article in Runners World expressed the exact same concern as you regarding a desire to see carb reduction to 50g/day (as opposed to 140 g/day as was done,) but also noted that "The enhanced weight loss seen by low-carb dieters jibes with prior studies that have shown rapid results from such dieting. Experts believe this effect is related to the large amount of water lost from the body when carbohydrates are restricted. Hence, this loss doesn’t represent a true change in body tissue. Also, the low-carb weight-loss advantage generally disappears after six to 12 months."


For those who wish to read the original paper, it is here: http://www.cell.com/cell-metabolism/...131(15)00350-2

Damn that's a hell of a reply. Maybe this is a touchy subject.

Anyways, you said,


As it was, the participants were required to spend one full month (in two two-week segments) in this sealed environment. How much longer would have been reasonable?
And the study said,


We selectively
restricted dietary carbohydrate versus fat for
6 days following a 5-day baseline diet in 19 adults
And then a rest period, switch the groups and repeat. I've read that article as I'm sure you have too.

I said,


It's sad the testing was so short. Also would have been nice to include a very low carb (less than 50g/day) group to compare to as well.
And that's what I meant.

I'm not discounting the study, I think it's awesome they did it. I just wished it was more than 6 days of monitoring them on there new diet. And it would have been nice to compare to a very low carb group too. If this is insulting, or a bad question, or anything like that then my bad!

JasonC SBB 08-19-2015 01:19 PM

Here's an article discussing the study Joe posted:

Whole Health Source: More Thoughts on the Recent Low-fat vs. Low-carb Metabolic Ward Study

Mostly what's already been mentioned, plus 1 more:

- The reason the low-fat group lost more fat in the 6 day test is probably that the low-carb group was burning through their glycogen stores. A longer test may have shown different results. This reasoning is based on deduction from earlier studies.

Joe Perez 10-15-2015 11:35 PM

Scientists Have Developed a Pill to Help Gluten-Intolerant People -- Grub Street


Scientists Have Developed a Pill to Help Gluten-Intolerant People
By Clint Rainey

Canadian scientists are working on a pill that could help people who can't digest gluten. This might cause some panic for actual gluten-free people, half of whom do actually get sick, and half of whom just read Goop. ("I've only been gluten-free for a week, but I'm already really annoying," as that New Yorker cartoon quips.)

Hoon Sunwoo, a professor at the University of Alberta, says that he and his team have developed an antibody out of chicken yolks that prevents the absorption of the troublesome component of gluten known as gliadin. "This supplement binds with gluten in the stomach and help to neutralize it," Sunwoo explains, "therefore providing defense to the small intestine, limiting the damage gliadin causes."

Celiacs and gluten-senstives can swallow the pill a few minutes before eating, and researchers say it opens a one- to two-hour window where they can gorge on bread, pasta, and beer with impunity (side effects to their waistlines perhaps notwithstanding). Clinical trials are supposed to kick off within the year, and the pill could be for sale in Canada as soon as three years from now. Sunwoo tells Quartz that it's expected to be sold as a simple over-the-counter med, just like Tylenol.

[UPI, Quartz]

mgeoffriau 10-19-2015 09:45 AM

1 Attachment(s)
https://www.miataturbo.net/attachmen...ine=1445262334

Joe Perez 11-05-2015 09:15 PM

Processed white bread promotes healthy gut biome:

New Study Suggests Some People Still Think White Bread Is Awesome

http://pixel.nymag.com/imgs/daily/gr....w529.h352.jpg
Booyah, whole wheat! In your face! Photo: Shutterstock


Entry-level plain white bread, with all its bleached flour, trouble-making gluten, and uncouth carbohydrates, really lost a lot of love from the good sandwich-making people of the United States during the last few years. It's been a victim of local food movements and fad diets, on a clear decline since 2010 when whole wheat surpassed white for the first time ever and everybody basically cheered. Sales are down again this year; 56 percent of shoppers say they want nothing at all to do with white bread; and hell, we even almost lost Wonder Bread when parent company Hostess foundered. But a new study conducted at the University of Oviedo in Spain says, essentially, maybe it's time to stop the hate.

A team of seven researchers looked at fibers and polyphenols found in white bread and oranges, respectively, with relation to production of intestinal microbiota, the vast bacterial colonies that do the heaviest lifting of your digestive process. "In terms of food consumption," researchers write, "probably the most novel finding of our study was the positive association between the intake of white bread and Lactobacillus levels." Specifically, people who ate more white bread had higher numbers of Lactobacilli, which is generally believed to be a good thing and runs contrary to the notion that a favored "prebiotic effect of cereals" comes from whole grain foods. In other words: Up yours, whole wheat.

While the authors of the paper, which appeared in the Journal of Agricultural and Food Chemistry last month, write that a number of other factors — everything from mastication to more variables of the other stuff that gets eaten with white bread, like good pickles and fatty brisket — need consideration in subsequent experiments, let's just call it peanut butter jelly time. "[O]ur results reveal that the consumption of refined grains, often undervalued in this regard, could beneficially modulate intestinal microbiota," the researchers write.
Article: New Study Suggests Some People Still Think White Bread Is Awesome -- Grub Street

Study: An Error Occurred Setting Your User Cookie

mgeoffriau 11-08-2015 08:10 PM

Effect of low-fat diet interventions versus other diet interventions on long-term weight change in adults: a systematic review and meta-analysis


Summary

Background


The effectiveness of low-fat diets for long-term weight loss has been debated for decades, with many randomised controlled trials (RCTs) and recent reviews giving mixed results. We aimed to summarise the large body of evidence from RCTs to determine whether low-fat diets contribute to greater weight loss than participants' usual diet, low-carbohydrate diets, and other higher-fat dietary interventions.

Methods

We did a systematic review and random effects meta-analysis of RCTs comparing the long-term effect (≥1 year) of low-fat and higher-fat dietary interventions on weight loss by searching MEDLINE, Embase, Cochrane Central Register of Controlled Trials (CENTRAL), and Cochrane Database of Systematic Reviews to identify eligible trials published from database inception up until July 31, 2014. We excluded trials if one intervention group included a non-dietary weight loss component but the other did not, and trials of dietary supplements or meal replacement drink interventions. Data including the main outcome measure of mean difference in weight change between interventions, and whether interventions were intended to lead to weight loss, weight maintenance, or neither, were extracted from published reports. We estimated the pooled weighted mean difference (WMD) with a DerSimonian and Laird random effects method.

Findings

3517 citations were identified by the search and 53 studies met our inclusion criteria, including 68 128 participants (69 comparisons). In weight loss trials, low-carbohydrate interventions led to significantly greater weight loss than did low-fat interventions (18 comparisons; WMD 1·15 kg [95% CI 0·52 to 1·79]; I2=10%). Low-fat interventions did not lead to differences in weight change compared with other higher-fat weight loss interventions (19 comparisons; WMD 0·36 kg [−0·66 to 1·37; I2=82%), and led to a greater weight decrease only when compared with a usual diet (eight comparisons; −5·41 kg [−7·29 to −3·54]; I2=68%). Similarly, results of non-weight-loss trials and weight maintenance trials, for which no low-carbohydrate comparisons were made, showed that low-fat versus higher-fat interventions have a similar effect on weight loss, and that low-fat interventions led to greater weight loss only when compared with usual diet. In weight loss trials, higher-fat weight loss interventions led to significantly greater weight loss than low-fat interventions when groups differed by more than 5% of calories obtained from fat at follow-up (18 comparisons; WMD 1·04 kg [95% CI 0·06 to 2·03]; I2=78%), and when the difference in serum triglycerides between the two interventions at follow-up was at least 0·06 mmol/L (17 comparisons; 1·38 kg [0·50 to 2·25]; I2=62%).

Interpretation

These findings suggest that the long-term effect of low-fat diet intervention on bodyweight depends on the intensity of the intervention in the comparison group. When compared with dietary interventions of similar intensity, evidence from RCTs does not support low-fat diets over other dietary interventions for long-term weight loss.

Joe Perez 11-18-2015 06:59 PM


sixshooter 11-18-2015 07:35 PM

This is absolutely amazing research.


Joe Perez 11-18-2015 11:30 PM


Originally Posted by sixshooter (Post 1285050)
This is absolutely amazing research.

That was an extremely interesting and informative lecture. I'm not being the least bit sarcastic.

But it was more than a trifle abstract.

Serious question: how do I sterilize my innards and populate my gut with skinny-mouse biome? What factors determine, in the aforetomentioned identical-twin studies, which twin develops "obese" gut flora vs. "skinny" gut flora?

Or, how does one apply these findings?

y8s 11-19-2015 03:25 PM

Get the skinniest person your age to vomit into your mouth. This doesn't count if their skinny is due to anorexia nervosa or marathoning.

..



No idea if it'll work, but please film it.

Joe Perez 11-19-2015 04:52 PM

1 Attachment(s)

Originally Posted by y8s (Post 1285249)
Get the skinniest person your age to vomit into your mouth.

If I understand the science correctly, I'd actually need for them to shit into my mouth.



To paraphrase XKCD, I'm assuming there's an easier way.

https://www.miataturbo.net/attachmen...ine=1447970026
"I know it seems unpleasant, but of the two ways we typically transfer them, I promise this is the one you want."

y8s 11-19-2015 06:11 PM

You might be right.

And you can wash it down with this guy's vomit:

Beer Gut: Man?s Belly Brews Own Beer | National Geographic (blogs)

sixshooter 11-19-2015 07:01 PM

This is amazing research with huge implications.

I hope the islamic caliphate doesn't blow them up for being Jews before they can finish their research. /isis rant

Leafy 11-19-2015 07:43 PM

No no, you need them to shit in your anus. It might be easier to just do an alaskan pipeline.

mgeoffriau 11-19-2015 07:48 PM

Fecal transplant therapy is about to get a lot less icky*.

$635 poop pills cure deadly gastrointestinal infection | Ars Technica




*Still pretty icky, but then if you can't eat without shitting your pants 30 minutes later, you're probably not so concerned with the ickiness of the treatment.

Joe Perez 11-20-2015 08:59 AM

Six's video led me down an interesting path of Googling. Specifically, there's a fair bit of work being done in both identification of the functions of various gut flora, as well as the transplantation of said critters not just for disease-prevention as MG notes, but also specifically to combat obesity.
How Gut Bacteria Help Make Us Fat and Thin
Intestinal bacteria may help determine whether we are lean or obese
By Claudia Wallis | Jun 1, 2014

For the 35 percent of American adults who do daily battle with obesity, the main causes of their condition are all too familiar: an unhealthy diet, a sedentary lifestyle and perhaps some unlucky genes. In recent years, however, researchers have become increasingly convinced that important hidden players literally lurk in human bowels: billions on billions of gut microbes.

Throughout our evolutionary history, the microscopic denizens of our intestines have helped us break down tough plant fibers in exchange for the privilege of living in such a nutritious broth. Yet their roles appear to extend beyond digestion. New evidence indicates that gut bacteria alter the way we store fat, how we balance levels of glucose in the blood, and how we respond to hormones that make us feel hungry or full. The wrong mix of microbes, it seems, can help set the stage for obesity and diabetes from the moment of birth.

Fortunately, researchers are beginning to understand the differences between the wrong mix and a healthy one, as well as the specific factors that shape those differences. They hope to learn how to cultivate this inner ecosystem in ways that could prevent—and possibly treat—obesity, which doctors define as having a particular ratio of height and weight, known as the body mass index, that is greater than 30. Imagine, for example, foods, baby formulas or supplements devised to promote virtuous microbes while suppressing the harmful types. “We need to think about designing foods from the inside out,” suggests Jeffrey Gordon of Washington University in St. Louis. Keeping our gut microbes happy could be the elusive secret to weight control.


An Inner Rain Forest

Researchers have long known that the human body is home to all manner of microorganisms, but only in the past decade or so have they come to realize that these microbes outnumber our own cells 10 to one. Rapid gene-sequencing techniques have revealed that the biggest and most diverse metropolises of “microbiota” reside in the large intestine and mouth, although impressive communities also flourish in the genital tract and on our skin.

Each of us begins to assemble a unique congregation of microbes the moment we pass through the birth canal, acquiring our mother's bacteria first and continuing to gather new members from the environment throughout life. By studying the genes of these various microbes—collectively referred to as the microbiome—investigators have identified many of the most common residents, although these can vary greatly from person to person and among different human populations. In recent years researchers have begun the transition from mere census taking to determining the kind of jobs these minute inhabitants fill in the human body and the effect they have on our overall health.

An early hint that gut microbes might play a role in obesity came from studies comparing intestinal bacteria in obese and lean individuals. In studies of twins who were both lean or both obese, researchers found that the gut community in lean people was like a rain forest brimming with many species but that the community in obese people was less diverse—more like a nutrient-overloaded pond where relatively few species dominate. Lean individuals, for example, tended to have a wider variety of Bacteroidetes, a large tribe of microbes that specialize in breaking down bulky plant starches and fibers into shorter molecules that the body can use as a source of energy.

Documenting such differences does not mean the discrepancies are responsible for obesity, however. To demonstrate cause and effect, Gordon and his colleagues conducted an elegant series of experiments with so-called humanized mice, published last September in Science. First, they raised genetically identical baby rodents in a germ-free environment so that their bodies would be free of any bacteria. Then they populated their guts with intestinal microbes collected from obese women and their lean twin sisters (three pairs of fraternal female twins and one set of identical twins were used in the studies). The mice ate the same diet in equal amounts, yet the animals that received bacteria from an obese twin grew heavier and had more body fat than mice with microbes from a thin twin. As expected, the fat mice also had a less diverse community of microbes in the gut.

Gordon's team then repeated the experiment with one small twist: after giving the baby mice microbes from their respective twins, they moved the animals into a shared cage. This time both groups remained lean. Studies showed that the mice carrying microbes from the obese human had picked up some of their lean roommates' gut bacteria—especially varieties of Bacteroidetes—probably by consuming their feces, a typical, if unappealing, mouse behavior. To further prove the point, the researchers transferred 54 varieties of bacteria from some lean mice to those with the obese-type community of germs and found that the animals that had been destined to become obese developed a healthy weight instead. Transferring just 39 strains did not do the trick. “Taken together, these experiments provide pretty compelling proof that there is a cause-and-effect relationship and that it was possible to prevent the development of obesity,” Gordon says.


Gordon theorizes that the gut community in obese mice has certain “job vacancies” for microbes that perform key roles in maintaining a healthy body weight and normal metabolism. His studies, as well as those by other researchers, offer enticing clues about what those roles might be. Compared with the thin mice, for example, Gordon's fat mice had higher levels in their blood and muscles of substances known as branched-chain amino acids and acylcarnitines. Both these chemicals are typically elevated in people with obesity and type 2 diabetes.

Another job vacancy associated with obesity might be one normally filled by a stomach bacterium called Helicobacter pylori. Research by Martin Blaser of New York University suggests that it helps to regulate appetite by modulating levels of ghrelin—a hunger-stimulating hormone. H. pylori was once abundant in the American digestive tract but is now rare, thanks to more hygienic living conditions and the use of antibiotics, says Blaser, author of a new book entitled Missing Microbes.

Diet is an important factor in shaping the gut ecosystem. A diet of highly processed foods, for example, has been linked to a less diverse gut community in people. Gordon's team demonstrated the complex interaction among food, microbes and body weight by feeding their humanized mice a specially prepared unhealthy chow that was high in fat and low in fruits, vegetables and fiber (as opposed to the usual high-fiber, low-fat mouse kibble). Given this “Western diet,” the mice with obese-type microbes proceeded to grow fat even when housed with lean cagemates. The unhealthy diet somehow prevented the virtuous bacteria from moving in and flourishing.

The interaction between diet and gut bacteria can predispose us to obesity from the day we are born, as can the mode by which we enter the world. Studies have shown that both formula-fed babies and infants delivered by cesarean section have a higher risk for obesity and diabetes than those who are breast-fed or delivered vaginally. Working together, Rob Knight of the University of Colorado Boulder and Maria Gloria Dominguez-Bello of N.Y.U. have found that as newborns traverse the birth canal, they swallow bacteria that will later help them digest milk. C-section babies skip this bacterial baptism. Babies raised on formula face a different disadvantage: they do not get substances in breast milk that nurture beneficial bacteria and limit colonization by harmful ones. According to a recent Canadian study, babies drinking formula have bacteria in their gut that are not seen in breast-fed babies until solid foods are introduced. Their presence before the gut and immune system are mature, says Dominguez-Bello, may be one reason these babies are more susceptible to allergies, asthma, eczema and celiac disease, as well as obesity.

A new appreciation for the impact of gut microbes on body weight has intensified concerns about the profligate use of antibiotics in children. Blaser has shown that when young mice are given low doses of antibiotics, similar to what farmers give livestock, they develop about 15 percent more body fat than mice that are not given such drugs. Antibiotics may annihilate some of the bacteria that help us maintain a healthy body weight. “Antibiotics are like a fire in the forest,” Dominguez-Bello says. “The baby is forming a forest. If you have a fire in a forest that is new, you get extinction.” When Laurie Cox, a graduate student in Blaser's laboratory, combined a high-fat diet with the antibiotics, the mice became obese. “There's a synergy,” Blaser explains. He notes that antibiotic use varies greatly from state to state in the U.S., as does the prevalence of obesity, and intriguingly, the two maps line up—with both rates highest in parts of the South.


Beyond Probiotics

Many scientists who work on the microbiome think their research will inspire a new generation of tools to treat and prevent obesity. Still, researchers are quick to point out that this is a young field with far more questions than answers. “Data from human studies are a lot messier than the mouse data,” observes Claire Fraser of the University of Maryland, who is studying obesity and gut microbes in the Old Order Amish population. Even in a homogeneous population such as the Amish, she says, there is vast individual variation that makes it difficult to isolate the role of microbiota in a complex disease like obesity.

Even so, a number of scientists are actively developing potential treatments. Dominguez-Bello, for example, is conducting a clinical trial in Puerto Rico in which babies born by cesarean section are immediately swabbed with a gauze cloth laced with the mother's vaginal fluids and resident microbes. She will track the weight and overall health of the infants in her study, comparing them with C-section babies who did not receive the gauze treatment.

A group in Amsterdam, meanwhile, is investigating whether transferring feces from lean to overweight people will lead to weight loss. U.S. researchers tend to view such “fecal transplants” as imprecise and risky. A more promising approach, says Robert Karp, who oversees National Institutes of Health grants related to obesity and the microbiome, is to identify the precise strains of bacteria associated with leanness, determine their roles and develop treatments accordingly. Gordon has proposed enriching foods with beneficial bacteria and any nutrients needed to establish them in the gut—a science-based version of today's probiotic yogurts. No one in the field believes that probiotics alone will win the war on obesity, but it seems that, along with exercising and eating right, we need to enlist our inner microbial army.
How Gut Bacteria Help Make Us Fat and Thin - Scientific American

Joe Perez 11-23-2015 10:24 PM

Watch from 5:30-10:30 for information regarding Hitler's dietary habits, the color and consistency of his feces, his general health and medical problems, and how a little-known Nazi physician by the name of Theodor Morell used fecal bacteriotherapy (poop transplantation) to treat the Führer's digestive ailments.



I post this purely to shine light on the rather interesting fact that such diagnoses and treatments as are being hailed as "revolutionary" over the past few years were, in fact, known to German medicine (if, admittedly, on the fringes of then-credible science) in the 1930s.

y8s 11-24-2015 10:16 AM

Related:


JasonC SBB 11-24-2015 11:23 AM

Gut flora appears to play a huge role in autoimmune disease:
Does the Gut Microbiome Play a Role in Autoimmune Disease?

Braineack 11-24-2015 11:53 AM

I liked this thread when it wasnt so shitty.

Joe Perez 12-11-2015 11:28 AM

1 Attachment(s)
A Protein In The Gut May Explain Why Some Can't Stomach Gluten
December 9, 20156:01 PM ET

https://www.miataturbo.net/attachmen...ine=1449851329
Those who avoid gluten may not be food faddists after all. Researchers are finally homing in on markers for gluten sensitivity in the body.

If you've found that you are sensitive to gluten — the stretchy protein that makes wheat bread fluffy and pie crusts crisp – perhaps you've had to bear the brunt of the gluten-free backlash.

Some 47 percent of American consumers say the gluten-free diet is a fad, according to Mintel research. And that's partly because there's been scant proof of what causes non-celiac gluten sensitivity. As far as diagnosing it goes, there's nothing akin to the gold standard tests that help diagnose the one percent of the population that has celiac disease.

But those who shun gluten (and don't have celiac disease) may not be food faddists after all. Researchers are finally homing in on markers for gluten sensitivity in the body. A study from Giovanni Barbara and his team at the University of Bologna, Italy, suggests that gluten sensitive individuals may harbor high levels of a molecule called zonulin that is linked to inflammation.

Levels of zonulin in the blood have already shown to be high in celiacs. In Barbara's study, levels in gluten-sensitive individuals almost matched those of celiacs. Though the results are preliminary, they point in a hopeful direction for future tests to help diagnose this controversial condition.

About 6 percent of the global population may be sensitive to gluten, according to gastroenterologist Alessio Fasano of Massachusetts General Hospital in Boston. Symptoms can be similar to irritable bowel syndrome, with abdominal pain, bloating, alternating diarrhea or constipation. And there can be other symptoms, including "brain fog", headache, fatigue, joint and muscle pain.

Enter zonulin, stage left. Zonulin is an inflammatory protein first discovered by Fasano and his team in 2000. It helps regulate leakiness in the gut by opening and closing the spaces or "junctions" between cells in the lining of the digestive tract. Zonulin is triggered by harmful bacteria, and offers important protection to the body: If you accidentally eat a food contaminated with salmonella, you rely on zonulin to help trigger diarrhea and flush out the bugs.

Once the pathogen is gone, zonulin levels drop and the junctions close.

So what does it have to do with gluten? It turns out that gluten is a strong trigger of zonulin in some individuals. "No human being completely digests gluten," says Fasano. "And in a small percentage of us, that undigested gluten triggers the release of zonulin," leading to high levels of it.

To test the theory, Giovanni Barbara and a team of researchers at the University of Bologna measured blood levels of zonulin in four groups of individuals: those with celiac disease, those with irritable bowel syndrome marked by diarrhea, those with self-diagnosed gluten sensitivity and healthy volunteers. Both celiacs and gluten sensitives turned up with remarkably high levels of zonulin in their blood. Those with IBS had elevated levels but less than half of celiacs or gluten sensitive individuals. Healthy volunteers had negligible blood levels of zonulin.

The results were presented in October as an abstract at the 23rd United European Gastroenterology Week in Barcelona, Spain. "I was very surprised, but not only by the zonulin levels," says Barbara. "In our study, gluten-sensitive individuals who responded to a gluten-free diet had a genetic predisposition to celiac disease. They had no evidence of celiac, but they did have the vulnerable genes that put a person at risk of celiac."

Despite having found two potential biomarkers, Barbara cautions that it's far too soon to recommend any kind of clinical testing. "We need more research to determine the clinical usefulness of these markers .... Other laboratories need to reproduce our data, and we need to repeat our own experiment with gluten sensitive patients who have been identified by strict criteria in double blind studies." Barbara adds that his center only sees the most severe patients who been unsuccessful finding treatment elsewhere, which may have influenced the results.

Fasano, who was not involved in Barbara's study, says the discovery of zonulin is part of a larger evolving picture. "This molecule is extremely important in a lot of illness, from Type 1 diabetes to other autoimmune diseases. Many illnesses link back to loss of barrier function in the gut." Soon, a trial will begin to test whether it's possible to shut down zonulin production in the gut for a few hours.

"It would be really great," says Fasano, "if we had a safe medication that could keep this molecule at bay and offer help for celiac disease, gluten sensitivity, and perhaps other conditions."


A Protein In The Gut May Explain Why Some Can't Stomach Gluten : The Salt : NPR

JasonC SBB 12-19-2015 12:04 PM

"10 Incredible Things We Learned About Our Health in 2015"
https://www.facebook.com/notes/max-l...92814777691610

JasonC SBB 05-12-2016 10:42 AM

Since potatoes got discussed in another thread...

It looks like the "carb-insulin-obesity" hypothesis has been soundly falsified:
That is, the simple hypothesis that carbs drive insulin production drives fat storage has been falsified, by a study that was organized by "Mr. Insulin" himself, Gary Taubes.
The hypothesis of the "metabolic advantage" (metabolism is raised in a person doing a ketogenic diet), has been been falsified.
However it did show that the first 5 days of a ketogenic diet caused rapid fat loss, but the rate of loss slowed down over time. So maybe the bodybuilders who do a "cyclic ketogenic diet" have it right all along.

What was not tested, was the hypothesis that appetite is suppressed when a person goes very low carb, making it easier to eat less and go into calorie deficit. This hypothesis has been supported by other studies.





JasonC SBB 05-12-2016 10:18 PM

Also in recent news, if your study shows that vegetable oil (actually high-linoleic-acid industrial processed seed oils) is bad and saturated fat isn't, bury it:
Is Vegetable Oil Really Better for Your Heart? - The Atlantic

JasonC SBB 06-12-2016 07:08 PM

Interesting hypothesis: Iron and B vitamin fortification of refined flour is a major contributor to obesity:
How Food Enrichment Promotes Obesity ("The Theory of Everything" Wider and Deeper)

Joe Perez 10-11-2016 01:20 PM

Posting this here not as a response to Jason, but simply because it was today's XKCD and reminded me of this thread:


https://cimg3.ibsrv.net/gimg/www.mia...644389fc59.png

mgeoffriau 10-11-2016 01:38 PM

Hovertext:


I have this weird thing where if I don't drink enough water, I start feeling bad and then die of dehydration.

Joe Perez 10-28-2016 10:10 AM

This one's for Jason. Turns out it's not your guy microbiome, it's your DNA. (Or, at least, that's the trend we're trying to start at the moment.)


HABIT WILL OFFER PERSONALIZED DNA-BASED DIETS DELIVERED TO YOUR DOOR

Habit will be launching its healthy meal service in January of 2017 and all their recipes will contain one special ingredient: your genetics.

Charles Costa Oct 27, 2016

Dieting is one of the hottest industries in the world, filled with tens of thousands of products promising to help users live longer, longer lives and lose significant amounts of weight. The common goal, when it comes to most people’s diets, is pretty simple: they’re looking to become “healthier.” How they go about reaching their goals, however, varies wildly in both style and complexity. For most, dieting is significant challenge, made even more challenging by the one thing we’re stuck with: our genetics.

To address this often-overlooked layer of complexity, there is a developing field of science known as, nutrigenomics. Eating Well has a good in-depth discussion on the topic, but the science boils down to an appreciation and application of the fact that genetics have a significant impact on metabolism, appetite, and other characteristics critical to the necessary inputs and eventual outputs of dieting.

A new startup is placing this science at the heart of its service: Habit. Their plan is to provide personalized diets to people using their DNA to drive the menus. Their offering also tries to boil down the science to bits and bites, allowing users to discover their unique scientific characteristics in a language they speak—like ideal ratios of carbs, fats, and proteins, and general nutritional statuses via biomarkers such as Vitamin A, carotenoids, and omega-3 fatty acids.

To use the service, users first collect their own DNA sample (don’t worry, there are instructions and timers and stuff). The sample is sent over to a partner company that processes the specimen in a CLIA and CAP certified lab. Applying proprietary algorithms, Habit’s Nutrition Intelligence Engine identifies the user diet type and recommends foods and nutrients based on the profile. From there a team of chefs creates fresh meals and delivers them to each doorstep.

If they so choose, users can download and use Habit’s companion mobile app to share details of their meals, experience and progress. Fact: People on health kicks love to share (their thoughts, not their food).

Habit’s program is based on a few key elements:
  • DNA: Genotype determines whether genes are turned on or off. When they’re expressed, the genetic information is used to make proteins, including enzymes and polypeptide hormones which impact metabolism.
  • Phenotype: The observable expression of user genes, it describes how internal (physical) and external influences (food) affect the body’s biology. Weight, activity levels, age, and core measurement are just a few essential metrics.
  • Phenotype Flexibility: This is an analysis used to understand how the body responds to food. Habit replaces a user meal with the shake, and then measures several nutrition biomarkers after consumption. This provides more granular insight into how the body reacts to fats, carbs, and protein.
  • Habits and Goals: Habit not only works with your DNA but with your personal goals, employing registered dietitians and offering “coaching” services to achieve a generally healthy lifestyle.
  • Nutrition Intelligence Engine: Proprietary algorithms and decision trees are applied based on nutrition biomarkers, body basics, genetic variations in the user DNA, activity level, health goals, and food preferences. This is the brain that creates the personalized diets for each end user.
There’s a lot going on there, but at the end of the day, the company promises a pretty straight forward final product: a delicious meal.

Habit was founded by Neil Grimmer (who also founded Plum Organics back in 2005) and has an advisory board that includes a few members of the Institute of Systems Biology and the Vice President of Global Nutrition and Health at Campbell Soup Company. Habit will be launching their Beta program in select locations in January 2017. You can sign up for the waitlist on their website.

https://www.snapmunk.com/personalized-dna-diets-habit/

JasonC SBB 10-28-2016 10:50 AM

"Phenotype"... is epigenetics. The gut biome affects epigenetics.

Here's one example:

Pubmed:

Gut Bacteria May Override Genetic Protections against Diabetes

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3232188/

Joe Perez 02-27-2017 09:29 PM

I'll have the "chicken," please.

What's in your chicken sandwich? DNA test shows Subway sandwiches could contain just 50% chicken

Marketplace had chicken from 5 major fast food restaurants tested

By Pete Evans and Eric Szeto, CBC News Posted: Feb 24, 2017 8:00 PM ET Last Updated: Feb 24, 2017 8:00 PM ET



https://cimg8.ibsrv.net/gimg/www.mia...ef136f8985.jpg
Subway's oven-roasted chicken sandwich patty contained about 50 per cent chicken DNA, according to Marketplace's tests.

If you're one of many Canadians who opt for chicken sandwiches at your favourite fast food restaurant, you may find the results of a CBC Marketplace investigation into what's in the meat a little hard to swallow.

A DNA analysis of the poultry in several popular grilled chicken sandwiches and wraps found at least one fast food restaurant isn't serving up nearly as much of the key ingredient as people may think.

In the case of two popular Subway sandwiches, the chicken was found to contain only about half chicken DNA.

Will Mahood, a loyal customer who considered Subway chicken sandwiches a lunchtime staple, was alarmed by the findings. To Mahood, messages from fast food companies can make it sound like "you're taking it straight from a farm and it's just a fresh piece of meat."

DNA researcher Matt Harnden at Trent University's Wildlife Forensic DNA Laboratory tested the poultry in six popular chicken sandwiches.

An unadulterated piece of chicken from the store should come in at 100 per cent chicken DNA. Seasoning, marinating or processing meat would bring that number down, so fast food samples seasoned for taste wouldn't be expected to hit that 100 per cent target.

The Peterborough, Ont.-based team tested the meat in:
  • McDonald's Country Chicken - Grilled
  • Wendy's Grilled Chicken Sandwich
  • A&W Chicken Grill Deluxe
  • Tim Hortons Chipotle Chicken Grilled Wrap
  • Subway Oven Roasted Chicken Sandwich
  • Subway Sweet Onion Chicken Teriyaki (chicken strips)
NOTE: The tests were on the meat samples alone, without sauces or condiments.
In the first round of tests, the lab tested two samples of five of the meat products, and one sample of the Subway strips. From each of those samples, the researchers isolated three smaller samples and tested each of those.

They were all DNA tested and the score was then averaged for each sandwich. Most of the scores were "very close" to 100 per cent chicken DNA, Harnden says.
  • A&W Chicken Grill Deluxe averaged 89.4 per cent chicken DNA
  • McDonald's Country Chicken - Grilled averaged 84.9 per cent chicken DNA
  • Tim Hortons Chipotle Chicken Grilled Wrap averaged 86.5 per cent chicken DNA
  • Wendy's Grilled Chicken Sandwich averaged 88.5 per cent chicken DNA

Subway's results were such an outlier that the team decided to test them again, biopsying five new oven roasted chicken pieces, and five new orders of chicken strips.

Those results were averaged: the oven roasted chicken scored 53.6 per cent chicken DNA, and the chicken strips were found to have just 42.8 per cent chicken DNA. The majority of the remaining DNA? Soy.

"That's misrepresentation," Irena Valenta, a Toronto resident who participated in a Marketplace taste test, said after seeing the test results.

Subway said in a statement that it disagrees with the test results.

"Our recipe calls for one per cent or less of soy protein in our chicken products."

"We will look into this again with our supplier to ensure that the chicken is meeting the high standard we set for all of our menu items and ingredients."

What else is in there?

On the whole, Marketplace's testing revealed that once the ingredients are factored in, the fast food chicken had about a quarter less protein than you would get in its home-cooked equivalent. And overall, the sodium levels were between seven and 10 times what they would be in a piece of unadulterated chicken.

https://cimg3.ibsrv.net/gimg/www.mia...7c7eb96028.jpg
Grilled chicken products are often marketed as the healthy alternative, but consumers may not always know what they are biting into.

Ben Bohrer, a food scientist at the University of Guelph, doesn't know exactly how the chicken products Marketplace tested are made, but he's very familiar with what the fast food industry calls "restructured products".

Restructured products are essentially smaller pieces of meat or ground meat, bound together with other ingredients to make them last longer, taste better and, as Bohrer puts it, "add value" — restaurant speak for cheaper.

The sandwiches tested contain a combined total of about 50 ingredients in the chicken alone, each with an average of 16 ingredients. The ingredients run the gamut from things you would find in your home such as honey and onion powder to industrial ingredients — all of which, Bohrer insists, are safe and government approved for human consumption.

McDonald's, A&W and Wendy's wouldn't break down exactly what ingredients are used in what proportions, citing proprietary information. Tim Hortons had no comment and directed Marketplace to their website.

Healthy alternative?

Nutritionist and registered dietitian Christy Brissette notes that most products in that alphabet soup ingredient list are simply variants on salt or sugar, the latter of which can elevate the carbohydrate level of a chicken breast to well above where it should be: zero per cent.

Before they saw the test results, both Valenta and Mahood said they chose chicken because they thought they were making a healthier choice — "the chicken is supposed to be the healthier type of meat," as Valenta put it.

But Brissette says it's important for consumers to not allow themselves to buy into the "halo" of health around such products.

"People think they're doing themselves a favour and making themselves a healthy choice," she says. "But from a sodium perspective you might as well eat a big portion of poutine."

What's in your chicken sandwich? DNA test shows Subway sandwiches could contain just 50% chicken - Business - CBC News

Never been a fan of Subway. There are just so many other sandwiches at the same price point which are better in every conceivable way.

y8s 02-28-2017 09:52 AM

Science.


Originally Posted by Trump on Fast Food
“I’m a very clean person. I like cleanliness. I think you’re better off going there than someplace you have no idea where the food is coming from. It’s a certain standard,” Trump explained.

secret sauce:
Donald Trump claims people are 'better off' eating at McDonalds and Burger King | The Independent

shuiend 02-28-2017 09:55 AM


Originally Posted by y8s (Post 1395824)

"Better Off" can be defined in a lot of different ways. I don't think they are defining it as healthier. I can say my wallet it better off after eating at McDonalds then Black Bean Company.

Joe Perez 04-08-2017 06:02 PM

When Gluten Is The Villain, Could A Common Virus Be The Trigger?

April 8, 2017 Allison Aubrey


https://cimg0.ibsrv.net/gimg/www.mia...befbaeb5b5.png
For people with celiac disease gluten-free food is a must. A new study suggests that a common virus may trigger the onset of the disease.

A new study raises a novel idea about what might trigger celiac disease, a condition that makes patients unable to tolerate foods containing gluten.

The study suggests that a common virus may be to blame.

For people with celiac disease, gluten can wreak havoc on their digestive systems. Their immune systems mistake gluten as a dangerous substance.

Scientists have known for a while that genetics predisposes some people to celiac. About 30 percent of Americans carry the genes that make them more susceptible to the disease. And yet, only about one percent of Americans have celiac.

Researchers wondered why not everyone with the risk genes gets the disease.

The answer is likely complicated, but one theory has emerged. Perhaps a "viral infection can serve as a trigger to celiac," explains Dr. Terence Dermody, who chairs the Department of Pediatrics at the University of Pittsburgh, and is an author of the new study published in Science.

He and a team of collaborators, led by Bana Jabri of the University of Chicago, decided to test this in experimental mice. They had been studying reovirus – a common virus that infects most Americans beginning in childhood, yet isn't considered dangerous. The researchers genetically engineered the mice to be more susceptible to celiac disease. Then they exposed mice to reovirus. At the same time they also fed gluten to the mice.

It turns out their hunch had been right. The mice developed "an immunological response against gluten that mimics the features of humans with celiac disease," Dermody says. The symptoms of celiac disease include diarrhea and other signs of gastrointestinal distress.

"It's all about the timing," Dermody says. The idea is that when the virus and gluten are introduced at the same time, the immune system mistakes the gluten-containing food as dangerous.

https://cimg3.ibsrv.net/gimg/www.mia...377ada408d.png
Transmission electron micrograph of a cell infected with reovirus (red). The virus is very common and not considered dangerous. Scientists now think it may have a role to play in triggering celiac disease.

But could this be true in humans too?

The second phase of the new study suggests an answer. Dermody and his collaborators analyzed the antibody levels to various viruses in a group of people. They found people who have celiac disease have two- to five-fold higher levels of reovirus-specific antibodies.

"It's a clue that people who have celiac may have been exposed to reovirus before the development of their disease," Dermody says. But, he stresses that "it's just a clue."

It will take a long time to figure out if there's a causal link between reovirus infections and the onset of celiac disease. Dermody envisions a study involving thousands of children who would be followed for several years. For now, he and his collaborators have some grant funds from the National Institutes of Health to continue their research.

The upside of understanding this possible connection is significant, explains Dr. Bana Jabri, of the University of Chicago, who is a co-author of the new study.

If it's true that the virus can trigger celiac disease, then young children who carry the risk genes for celiac could be vaccinated against Reovirus. "It may be useful to start thinking about vaccinating people who are at a high risk of celiac disease against [these] types of viruses," she says.

Links between viral infection and the development of auto-immune disorders such as celiac disease have been proposed before, "but this is the first tractable experimental model to tackle this question," says Julie Pfeiffer, an Associate Professor of Microbiology at University of Texas Southwestern, who has followed the research, but is not involved in the new study. Given the interest and the findings, "more studies in humans are warranted," she says.

As awareness of celiac disease has grown, so too has the number of people experimenting with gluten-free diets due to concerns about gluten sensitivities. This is evident from the growth in gluten-free food sales and most recently, the introduction of gluten-free dining halls on two college campuses.

For People With Celiac Disease, A Common Virus May Be The Trigger : The Salt : NPR

Joe Perez 07-16-2017 09:20 AM

Thought JasonC might enjoy this. It continues to demonize grains, while involving gut microbiome and a conspiracy theory which hinges upon the US Parent & Trademark Office being used as intended to explain why:




Gluten Intolerance is really GLYPHOSATE POISONING

What if...."gluten intolerance" is really "glyphosate poisoning"?

Gluten has been in wheat since it was first grown. Sure, there have always been folks who have problems digesting wheat or grains with gluten. Today, about 50% of the world have problems with gluten. (1) Something has changed.

That "something" is glyphosate.

Glyphosate has only been on this planet since Monsanto patented it as "Roundup" in 1973. This chemical herbicide goes by 32 or more tradenames and, now that the patent protection expired in 2000, is made by nine chemical companies -- most of whom, not coincidentally, are also in the drug business. Over 200 million pounds of it is used all over the world every year. That's 100,000 tons! Roundup brings in half of Monsanto's yearly profits. Like vaccines, each manufacturer can add its own extra ingredients called adjuvants or surfactants. Some data suggests that the adjuvants are even more toxic than the glyphosate. (2)

The original use of glyphosate was to prevent weeds. Somewhere along the way, it was discovered that a pre-harvest spraying of glyphosate directly onto the crops made for an easier harvest, as it desiccates the material. WHEAT and CANE SUGAR are the two foods most often treated in this manner. What foods have wheat and sugar? Take a walk down the cereal aisle, the one with the pretty boxes that beckon to your children. See the cookies, crackers, breads, cakes -- all those things that have gluten -- as well as a double dose of glyphosate.

Nice.

And I really, really mean "nice." Etymology: Middle English, foolish, wanton, from Old French, from Latin nescius ignorant, from nescire not to know.

Monsanto applied for the patent on glyphosate with full knowledge that it worked by blocking the shikimate pathway of plants and certain bacteria. Therefore, since people are not plants or bacteria, glyphosate must be safe, they told the FDA.

What Monsanto did not disclose is that the bacteria in a human gut all have shikimate pathways. This is huge. Without gut bacteria, people become very ill and malnourished, develop antibodies to their own organs, mentally depressed, full of yeast and other pathogenic bacteria, and mineral deficient. Nerve transmission fails and energy is gone. The mind cannot focus. Children get labeled at school as having behavior problems. Adults think they are crazy and run to the Prozac. This could only have happened if the scientists at Monsanto and FDA are malevolent and the worst sort of facinorous psychopaths. They are not nice guys, not ignorant of their deeds; let us call them what they are: Murderers.

I submit: You do not have gluten intolerance; that is a symptom. You have been poisoned by glyphosate, therefore you have GLYPHOSATE POISONING. The first step to healing is calling something what it is. Using euphemisms and hiding wickedness behind medicalese and nebulous diagnoses does no one any good. The guilty go free and the victims are denied proper treatment and timely justice.

http://grannygoodfood.blogspot.com/2...osate.html?m=1

Footnotes:
(1) Dr. Ford, a pediatrician in Christchurch, New Zealand and author of The Gluten Syndrome, says he believes the percentage of people who are gluten-sensitive actually could be between 30% and 50%. Source: http://celiacdisease.about.com/od/gl...ensitivity.htm

(2) "...with respect to glyphosate formulations, experimental studies suggest that the toxicity of the surfactant, polyoxyethyleneamine (POEA), is greater than the toxicity of glyphosate alone and commercial formulations alone." https://en.wikipedia.org/wiki/Polyet...d_tallow_amine

For further study:
Monsanto's Roundup Causes Gluten Intolerance http://jonrappoport.wordpress.com/20...n-intolerance/

Glyphosate, pathways to modern diseases II: Celiac sprue and gluten intolerance
http://sustainablepulse.com/wp-conte...sel-Seneff.pdf


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JasonC SBB 07-16-2017 02:52 PM

Here's a more reliable article
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3945755/

I have seen the hypothesis that glyphosate and gluten act synergistically to increase gut permeability (the factor that causes all manner of immunogenic responses), but I haven't seen a study that shows that the trace amounts of glyphosate in produce result in a measurable effect on the gut's permeability.

Regarding carbs and obesity, I have seen a recent study that low-carbing is distinctly more effective at curbing *appetite* (and thus spontaneously reducing caloric intake), in individuals with blood sugar regulation issues; less so in those with good regulation.

y8s 07-17-2017 10:06 AM

The problem with technological farmery in the US is that we put things on the market THEN require proof of harm to have them removed.

In other places, they require proof that the stuff is safe before it gets to market.

So, you know, you don't end up with 45 years of glyphosate on your wheat and maybe free cancer.

Joe Perez 11-13-2018 07:34 PM

This thread kind of derailed last year (I'm largely to blame for that) and then sputtered out. Now that JasonC has gone inactive on the forum, I've pruned some of my more provocative (and less then useful) posts from the last page, as this actually is a topic which interests me.

Came across an interesting article in The Times recently, which seems to throw more fuel on the fire (and decrease clarity even further) insofar as answering the "which calories matter" question.
Which Kinds of Foods Make Us Fat?
https://cimg6.ibsrv.net/gimg/www.mia...cc53e141aa.png

By Gretchen Reynolds Sept. 25, 2018


One fundamental and unanswered question in obesity research is what kind of foods contribute most to the condition. Experts variously blame, for example, fatty or sugary fare or foods that lack protein, which may prompt us, unconsciously, to overeat. Plenty of anecdotal evidence can be marshaled against any of the culprits, but there has been little long-term, large-scale experimental research on people’s comparative eating habits. It is neither ethical nor practical to have healthy subjects gorge themselves on one diet for years until they are obese.

It is possible, though, to conduct this sort of experiment on mice. For a
diet study published this summer in Cell Metabolism, researchers randomly assigned one of 29 different diets to hundreds of adult male mice. (The scientists hope to include female mice in later experiments.) Some diets supplied up to 80 percent of their calories in the form of saturated and unsaturated fats, with few carbohydrates; others included little fat and consisted largely of refined carbohydrates, mostly from grains and corn syrup, although in some variations the carbs came from sugar. Yet other diets were characterized by extremely high or low percentages of protein. The mice stayed on the same diet for three months — estimated to be the equivalent of roughly nine human years — while being allowed to eat and move about their cages at will. The mice were then measured by weight and body composition, and their brain tissue was examined for evidence of altered gene activity.

Only some of the mice became obese — almost every one of which had been on a high-fat diet. These mice showed signs of changes in the activity of certain genes too, in areas of the brain related to processing rewards; fatty kibble made them happy, apparently. None of the other diets, including those rich in sugar, led to significant weight gain or changed gene expression in the same way. Even super-high-fat diets, consisting of more than 60 percent fat, did not lead to significant weight gains, and the mice on those diets consumed less food over all than their counterparts, presumably because they simply could not stomach so much fat. These findings were replicated in subsequent experiments with four other murine breeds. Male mice on relatively high fat diets became obese. The others did not.


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“It looks like consuming high-fat diets, if they aren’t extremely high fat, leads to weight gain, if you are a mouse,” says John Speakman, a professor at the Chinese Academy of Sciences in Beijing and at the University of Aberdeen in Scotland, who oversaw the study. Speakman and his co-authors believe that the fatty meals stimulated and altered parts of the brains, causing the mice to want fatty food so much that they ignored other bodily signals indicating that they had already consumed enough energy.

The study was focused on weight gain, not loss, and its subjects were mice, of course, not humans. But the results are suggestive. Sugar did not make the mice fat, and neither did protein deficits. Only fat made them fat.


https://www.nytimes.com/2018/09/25/w...ke-us-fat.html

It's interesting to see this data published in a reputable, peer-reviewed journal. Their conclusion, specifically that "It looks like consuming high-fat diets, if they aren’t extremely high fat, leads to weight gain, if you are a mouse," kind of supports the results which I observed during a highly unscientific, n=1 study in 2013-14.


Also, @IB Nolan , the[indent] function is still causing my text to grey out unless I specifically override it with a [color=#000000] tag.

Also, in the sentance above, there is a space between the word "the" and the word "[indent]", however it's vanishing in the actual post. Also, [noparse] is still broken.


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