Gut ecosystem management

This topic contains 6 replies, has 4 voices, and was last updated by quizzle 10 years, 1 month ago.

Viewing 7 posts - 1 through 7 (of 7 total)

dlroseberry

12:39 am
20 Sep 14
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Just reading an article in this weeks Science that explains that intestinal epithelial cells produce a complex carbohydrate in order to feed mutualistic bacteria which have evolved to breakdown complex carbohydrates for our benefit and their own. Pathogenic gut bacteria, lacking machinery to digest this (and many other) complex carbohydrate, rely on simple carbohydrates. So in times of a shortage of dietary simple carbohydrate, the good bacteria have an advantage, relative to the bad bacteria, of food being available from the gut itself to get through the lean times.

I would think intermittent fasting should provide this shortage of simple carbohydrates, especially if, like everyone I hope, you’re not eating any simple carbohydrates on fast days (that would be silly anyway).

quizzle

5:30 pm
22 Sep 14
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This is an interesting topic – just recently a new nature paper draw my attention. The guys stated that taking sugar replacement like sucralose, saccharin and others give your carb-using bacteria a head start and leads to first signs of insulin resistance within 4 days!

I felt guilty since I was drinking a bottle of that stuff a day and stopped this immediately.
I think, those “microbiomics” will lead us into a new era of understanding…we’re not allone and we don’t eat allone. Counting calories is a joke – the source of the calories is more important than their amount!

Q.

simcoeluv

5:49 pm
22 Sep 14
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quizzle:

‘Counting calories is a joke – the source of the calories is more important than their amount!’

Are you suggesting that if your TDEE is 2000, you could eat 3000 per day of calories from the ‘right source’ and still lose weight?

ChicitaGatita

8:35 pm
22 Sep 14
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I’m so interested in all this research. I just realised that the reason I’d plateaued for 3 weeks and put on 3-4kg was because I’d started drinking 1-3 litres of diet cordial. I stopped 2.5 days ago & fasted and I’m already down from 71.3kg – 66.8kg!

simcoeluv

9:36 pm
22 Sep 14
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Chicita:

How many calories were in your diet cordial?

dlroseberry

12:38 am
23 Sep 14
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The study I was reporting on in the first post was actually about the intricate details of the control mechanisms involved in the process of maintaining gut biota with immune system cells that, besides attacking pathogens, also stimulate production of carbohydrate by epithelial cells to maintain our good bacteria. While the idea that gut bacteria is important to health is fairly new, there’s been a lot of research because of all of the serious diseases that could be impacted by the findings.

The story in the papers about a study in Israel that points a finger at artificial sweeteners is just an early, unverified little study of they type commonly used by researchers to use in future grant applications and needs to be taken with a grain of salt at this point because there are no details, no suggestion of any biochemical mechanism (and in this case, since the chemicals are very different, this is going to be especially hard) and no corroborating evidence. Distrust of artificial sweeteners though, is hardly new, and this doesn’t really change anything yet.

I’ve noticed that a lot of people refer to sugar alcohols like sorbitol and mantitol and many others, as “artificial sweeteners” and they are that, but they aren’t low calorie sweeteners, let alone zero cal sweeteners. They’re used in sugarless gum for instance because they’re less likely to cause caries than sugar and they’re used in some products because they’re purportedly better for diabetics. I’ve noticed they now use them so that they can say “no sugar added” on labels, especially on ice cream products, which have texture issues with the no-calorie artificial sweeteners. That’s something to watch out for in “diet” products.

quizzle

11:02 am
24 Sep 14
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It *is* something new; Nature doesn’t publish “early, unverified little studies” without having good reasons. I believe it’s just the head start of a new obesity-research putting the fingers of the microbiome.

Citing from a recent review:

“Different changes in the gut microbiota composition as well as a
reduced bacterial diversity have been associated with obesity by
human and mice studies. An enrichment of Firmicutesand a decrease
in Bacteroidetes levels has been reported in obese individuals compared
to lean individuals.
This was found both in humans[122]and in mice
genetically predisposed to obesity[123].
Interestingly, the Firmicutes/
Bacteroidetesratio was normalized to that observed in lean individuals
after weight loss[122]. More recently, Kalliomäki et al. have showed
that early differences in gut microbiota composition in children, higher
levels of Staphylococcus aureus, and lower levels of Bifidobacteriamay
predict overweight[124].
So far, different studies have been performed to investigate whether the altered gut microbiota contribute to obesity or whether obesity alters the gut microbiota.

These studies have suggested a causal relationship between changes in microbiota composition and obesity development, showing that the obese phenotype can
be transferred by the microbiota and also that the obese microbiome
has an increased capacity to harvest energy from the diet[125,126].

Analysis of the metagenome of twins concordant for obesity showed
altered representation of bacterial genes and metabolic pathways in
obese individuals, who harbored more genes for phosphotransferase
systems involved in carbohydrate processing[38]. It has been demonstrated that prevention of obesity by the microbiota in mice was diet dependent, Punkting to the connection between gut microbes and diet as a key factor in the path to obesity[127].

It is remarkable to note that the intestinal microbiota metabolism may also contribute directly to other phenotypes associated with obesity, such as CVD risk[128], while inflammasome-mediated microbiota dysbiosis also seems to
exacerbate more processes associated with the metabolic syndrome,
such as obesity and non-alcoholic fatty liver disease (NAFLD)[129].”

(taken from Cenit et al., Biochimica et Biophysica Acta 1842 (2014) 1981–1992)

So I guess it’s time to take your microbiome into account when simple caloric-restriction doesn’t make it (any more).

Q.