Dietary choline intake is necessary to prevent systems-wide organ pathology and reduce Alzheimer's disease hallmarks

[AlphaCog]

Abstract​

There is an urgent need to identify modifiable environmental risk factors that reduce the incidence of Alzheimer's disease (AD). The B-like vitamin choline plays key roles in body- and brain-related functions. Choline produced endogenously by the phosphatidylethanolamine N-methyltransferase protein in the liver is not sufficient for adequate physiological functions, necessitating daily dietary intake. ~90% of Americans do not reach the recommended daily intake of dietary choline. Thus, it's imperative to determine whether dietary choline deficiency increases disease outcomes. Here, we placed 3xTg-AD, a model of AD, and non-transgenic (NonTg) control mice on either a standard laboratory diet with sufficient choline (ChN; 2.0 g/kg choline bitartrate) or a choline-deficient diet (Ch-; 0.0 g/kg choline bitartrate) from 3 to 12 (early to late adulthood) months of age. A Ch- diet reduced blood plasma choline levels, increased weight, and impaired both motor function and glucose metabolism in NonTg mice, with 3xTg-AD mice showing greater deficits. Tissue analyses showed cardiac and liver pathology, elevated soluble and insoluble Amyloid-β and Thioflavin S structures, and tau hyperphosphorylation at various pathological epitopes in the hippocampus and cortex of 3xTg-AD Ch- mice. To gain mechanistic insight, we performed unbiased proteomics of hippocampal and blood plasma samples. Dietary choline deficiency altered hippocampal networks associated with microtubule function and postsynaptic membrane regulation. In plasma, dietary choline deficiency altered protein networks associated with insulin metabolism, mitochondrial function, inflammation, and fructose metabolic processing. Our data highlight that dietary choline intake is necessary to prevent systems-wide organ pathology and reduce hallmark AD pathologies.

https://onlinelibrary.wiley.com/doi/10.1111/acel.13775

 

[BearWithMe]

bump

 

[Ras]

I like The Daily Egg.

 

[David PS]

Thanks for this thread. Choline is important and I consider adequate dietary choline to be essential to healthy aging.

Choline: An Essential Nutrient for Public Health that we’re not getting enough of in our diet

We were discussing choline at page 4 of another thread and we thought it was worthy of its own thread. According to the National Institutes of HealthTrusted Source, choline is an essential nutrient found in many foods. The brain and nervous system use it to regulate functions that include...

raypeatforum.com

 

[AlphaCog]

The interactive relationship of dietary choline and betaine with physical activity on circulating creatine kinase (CK), metabolic and glycemic markers, and anthropometric characteristics in physically active young individuals
Results
Increasing dietary betaine and total choline and betaine was positively related to weight, waist-to-hip ratio, fat-free mass and bone mass (P < 0.05). Increasing dietary betaine lowered total cholesterol (P = 0.032) and increased high density lipoprotein (HDL) (P = 0.049). The interaction effect of dietary choline and physical activity improved insulin resistance (P < 0.05). As well as dietary betaine interacted with physical activity increased HDL (P = 0.049). In addition, dietary total choline and betaine interacted with physical activity decreased FBS(fasting blood sugar) (P = 0.047).

The interactive relationship of dietary choline and betaine with physical activity on circulating creatine kinase (CK), metabolic and glycemic markers, and anthropometric characteristics in physically active young individuals - BMC Endocrine Disorder

Background There is conflicting evidence on the relationship between dietary choline and betaine with metabolic markers and anthropometric characteristics. The aim of this study is to investigate the relationship between the interaction effects of dietary choline and betaine and physical...

bmcendocrdisord.biomedcentral.com

 

[DanDare]

A lot in egg but decent amounts in beef and potatoes. Only low amounts in rice, but much more in corn, oats, barley, and a lot in wheat bran and wheat germ.

 

[BearWithMe]

Choline content per 3.5 oz / 100g:

Eggs, cooked: 293.8mg 53% RDA
Egg whites only, cooked: 1.1mg 0% RDA
Egg yolk, cooked: 820.2mg 149% RDA
Beef steak: 79.7mg 14% RDA
Potato, boiled with skin: 18.7mg 3% RDA
White rice: 2.1mg 0% RDA
Yellow corn, dry grain: 21.6mg 4% RDA
Oats, dry: 40.4mg 7% RDA
Barley, pearled, dry: 37.8mg 7% RDA
Wheat bran: 74.4mg 14% RDA
Wheat germ, crude: 143,2mg 26% RDA

Source: NCCDB

 

[ddjd]

correction- saturated choline is important

 

[DanDare]

I'm skeptical of the choline argument. Realistically choline RDA looks unattainable unless one is supplementing or eating eggs, and much of the world ( rice or bread eaters) should be severely deficient in it. I am also all too aware of people jumping to long term conclusions based on feelings and no actual evidence.

And let's look at the side effects or consuming too much choline:

Getting too much choline can cause a fishy body odor, vomiting, heavy sweating and salivation, low blood pressure, and liver damage. Some research also suggests that high amounts of choline may increase the risk of heart disease.2 Jun 2022

Office of Dietary Supplements (ODS) › factsheets

Choline - Consumer - NIH Office of Dietary Supplements​

 

[Jabuger]

I'm skeptical of the choline argument. Realistically choline RDA looks unattainable unless one is supplementing or eating eggs, and much of the world ( rice or bread eaters) should be severely deficient in it. I am also all too aware of people jumping to long term conclusions based on feelings and no actual evidence.

And let's look at the side effects or consuming too much choline:

Getting too much choline can cause a fishy body odor, vomiting, heavy sweating and salivation, low blood pressure, and liver damage. Some research also suggests that high amounts of choline may increase the risk of heart disease.2 Jun 2022
View attachment 62218
Office of Dietary Supplements (ODS) › factsheets

Choline - Consumer - NIH Office of Dietary Supplements​

How much is too much. I’m guessing impossible to attain through diet.

 

[DanDare]

How much is too much. I’m guessing impossible to attain through diet.

In that study link it suggests 3500mg for an adult yes. However to get the RDA people supposedly need to eat 400 grams beef per day every day, and that's just the RDA. Meanwhile eggs and liver are a super high source of choline ... But also vitamin a, something smells fishy to me! No pun intended..

So if choline was so great at detoxing vitamin a as according to some people, EASILY making up for the vit A, then over consuming liver should not be a problem - yet it almost certainly is from a plethora of evidence

 

[DanDare]

The argument: 'Choline can cope with large amounts of retinol. The retinol prick in eggs is easily coped with.'

Ok so eat 20 eggs a day
Eat liver too as thats high in choline.
And then we have a high vit A diet again

 

[Jabuger]

The argument: 'Choline can cope with large amounts of retinol. The retinol prick in eggs is easily coped with.'

Ok so eat 20 eggs a day
Eat liver too as thats high in choline.
And then we have a high vit A diet again

Trying to relate everything back to VA detox is your first fault.

 

[DanDare]

Trying to relate everything back to VA detox is your first fault.

And what is the second?

This is the low toxin group looking into vit A, and choline is commonly quoted as being some kind of antidote to it, hence I am addressing that specifically ( however you can see I was speaking in general terms about choline in first comment). Would you like to make an actual argument that would be useful, something you have observed about dietary choline perhaps ?

 

[Jabuger]

something you have observed about dietary choline perhaps ?

Yea it’s great stuff

 

[AlphaCog]

Egg consumption improves vascular and gut microbiota function without increasing inflammatory, metabolic, and oxidative stress markers​

Abstract​

Egg consumption is one of the many inconsistencies in evidence linking dietary cholesterol to cardiovascular disease (CVD). In addition, the gut microbiota and its metabolite, trimethylamine-N-oxide (TMAO), have been shown to play a crucial role in the development of CVD. The fact that egg is rich in choline suggests that excessive egg consumption may increase TMAO production by altering the gut microbiota. However, the effects of egg consumption on vascular function and gut microbiota remain unclear. Here, the diet of nine young male subjects was supplemented with two boiled eggs daily for 2 weeks. Changes in vascular function, inflammation, metabolism, oxidative stress, and gut microbiota were examined. We found that egg consumption increased flow-mediated dilation and decreased brachial-ankle pulse wave velocity. Furthermore, egg consumption positively modulated the gut microbiota function but had no effects on the levels of C-reactive protein, glucose, lipid profile, malondialdehyde, superoxide dismutase, or TMAO. The current study provides evidence that egg consumption improves vascular function, which may be related to the alterations seen in the gut microbiota. Therefore, moderate egg consumption may help to improve vascular and intestinal function in individuals at low risk of developing CVD and other metabolic disorders.

https://onlinelibrary.wiley.com/doi/10.1002/fsn3.2671

Are eggs good again? A precision nutrition perspective on the effects of eggs on cardiovascular risk, taking into account plasma lipid profiles and TMAO​

3. Do eggs raise plasma TMAO?​

However, whereas there is a clear positive association between fasting plasma TMAO concentrations and CVD risk [15], and increased production of TMAO in many individuals in the hours immediately following the intake of eggs [14,16], studies have not shown a consistent link between the dietary intake of eggs and long-term fasting TMAO concentrations. Controlled intervention studies feeding 2-3 eggs per day have not shown increases in TMAO concentrations [17,18]. In comparison, observational studies show links between higher intakes of fish, and less so eggs, and circulating TMAO concentrations [19].

Egg lipids as a source of choline in the form of phosphatidylcholine have been shown to result in increased concentrations of TMAO in the hours after consumption of 2 or more eggs [16]. Sphingomyelin is an additional source of choline from eggs, however, dietary sphingomyelin has been shown to have only modest effects on increasing circulating TMAO concentrations in mice [23]. There is high inter-individual variability in TMAO production following egg consumption, with the observation that individuals who follow a vegan diet do not produce TMAO whereas omnivores do [16]. Strikingly, although vegans do not produce TMAO at all after ingesting eggs and other sources of choline, omnivores are highly variable in their TMAO production ranging from near 0 μM, just as in the vegans, to as high as 30 μM [16]. It has now been shown that variation in the gut microbiome contributes to differences in TMAO production [24] and the gut microbes involved in this relationship include those belonging to the phyla Firmicutes and Proteobacteria [25,26], however the relationship between diet, the gut microbiome, and circulating TMAO concentrations is complex.

https://www.sciencedirect.com/science/article/pii/S0955286321003260#bib0016

Vitamin D Reduces TMAO From High-Choline Diet, Promotes Non-Atherogenic Microbiome​

Vitamin D Reduces TMAO From High-Choline Diet, Promotes Non-Atherogenic Microbiome

The role of trimethylamine n-oxide (TMAO) in human disease has been quite controversial. The carnitine/choline in red meat and eggs had been purported to generate trimethylamine (TMA) via bacterial metabolism, which then goes on to become TMAO via the action of hepatic FMO3. The often-promoted...

raypeatforum.com

Trimethylamine N-Oxide Improves Exercise Performance by Reducing Oxidative Stress through Activation of the Nrf2 Signaling Pathway​

Abstract​

Trimethylamine N-oxide (TMAO) has attracted interest because of its association with cardiovascular disease and diabetes, and evidence for the beneficial effects of TMAO is accumulating. This study investigates the role of TMAO in improving exercise performance and elucidates the underlying molecular mechanisms. Using C2C12 cells, we established an oxidative stress model and administered TMAO treatment. Our results indicate that TMAO significantly protects myoblasts from oxidative stress-induced damage by increasing the expression of Nrf2, heme oxygenase-1 (HO-1), NAD(P)H dehydrogenase (NQO1), and catalase (CAT). In particular, suppression of Nrf2 resulted in a loss of the protective effects of TMAO and a significant decrease in the expression levels of Nrf2, HO-1, and NQO1. In addition, we evaluated the effects of TMAO in an exhaustive swimming test in mice. TMAO treatment significantly prolonged swimming endurance, increased glutathione and taurine levels, enhanced glutathione peroxidase activity, and increased the expression of Nrf2 and its downstream antioxidant genes, including HO-1, NQO1, and CAT, in skeletal muscle. These findings underscore the potential of TMAO to counteract exercise-induced oxidative stress. This research provides new insights into the ability of TMAO to alleviate exercise-induced oxidative stress via the Nrf2 signaling pathway, providing a valuable framework for the development of sports nutrition supplements aimed at mitigating oxidative stress.
Previous research has shown a significant decrease in urinary TMAO levels in elite athletes and active women following acute exercise [34], with an approximate 20–21% reduction in TMAO levels one hour after exercise and a gradual return to baseline [35].

Trimethylamine N-Oxide Improves Exercise Performance by Reducing Oxidative Stress through Activation of the Nrf2 Signaling Pathway

Trimethylamine N-oxide (TMAO) has attracted interest because of its association with cardiovascular disease and diabetes, and evidence for the beneficial effects of TMAO is accumulating. This study investigates the role of TMAO in improving exercise performance and elucidates the underlying...

www.mdpi.com

Soluble Dietary Fiber Reduces Trimethylamine Metabolism via Gut Microbiota and Co-Regulates Host AMPK Pathways​

Abstract​

Scope: Evidence from animal experiments and clinical medicine suggests that high dietary fiber intake, followed by gut microbiota-mediated fermentation, decreases trimethylamine (TMA) metabolism, the mechanism of which, however, remains unclear. The objective of this analysis was to evaluate, using mice fed with red meat, the effects of soluble dietary fiber (SDF) intervention on TMA metabolism.
Methods and results: Low- or high-dose soluble dietary fiber (SDF) from natural wheat bran (LN and HN, low- and high-dose natural SDF), fermented wheat bran (LF and HF, low- and high-dose fermented SDF), and steam-exploded wheat bran (LE and HE, low- and high-dose exploded SDF groups) were used to examine whether SDF interventions in mice fed with red meat can alter TMA and trimethylamine N-oxide (TMAO) metabolism by gut microbial communities in a diet-specific manner. Results demonstrated that SDF-diets could reduce TMA and trimethylamine N-oxide (TMAO) metabolism by 40.6 and 62.6%, respectively. DF feeding, particularly fermented SDF, reshaped gut microbial ecology and promoted the growth of certain beneficial microflora species. SDF-diet decreased energy intake, weight gain, intestinal pH values, and serum lipid and cholesterol levels. SDF-diet also enhanced the production of short chain fatty acids with activation of the intestinal epithelial adenosine monophosphate-activated protein kinase (AMPK).
Conclusion: These findings suggest a central mechanism via which SDF-diet may control TMA metabolism by gut microflora and co-regulate the AMPK pathways of the host.

Soluble Dietary Fiber Reduces Trimethylamine Metabolism via Gut Microbiota and Co-Regulates Host AMPK Pathways - PubMed

These findings suggest a central mechanism via which SDF-diet may control TMA metabolism by gut microflora and co-regulate the AMPK pathways of the host.

pubmed.ncbi.nlm.nih.gov