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

Blossom

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Here’s the old chicken coup. I think we could repair it and extend the run and hopefully be in for a decent supply of eggs.
 
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David PS

David PS

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Blossom

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It looks like a great setup. I do not know very much about raising chickens,
I have a couple friends who do it so it should work out with their guidance. Provided all goes well I’ll share my experience on the forum.
 
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David PS

David PS

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I have a couple friends who do it so it should work out with their guidance. Provided all goes well I’ll share my experience on the forum.
That will be great. Teamworking and networking is the way to survive.
 

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  1. DMAE and PABA – An Alternative to Gerovital (GH3), the “Romanian Youth Drug” (9/01/2001)
In Romania, Gerovital, or GH3, has been used for over 50 years to help people look and feel younger. It has attracted thousands of people each year to the spas of Romania and Western Europe where this therapy has been widely used. GH3 is a modification of the local anesthetic, procaine. It was developed for anti-aging uses by Professor Ana Aslan in Romania in the 1940s. The discovery of procaine's potential anti-aging properties was a serendipitous finding. Prof. Aslan was experimenting with the pain-relieving effects of procaine on patients with severe arthritis by injecting it into the arteries which supplied blood to the area of the affected joints. She logically theorized that procaine, being an anesthetic, would relieve the joint pain. She was surprised to find that in addition to dramatic relief of joint pains, many patients also noted (1) improved memory, (2) less depression, (3) more energy, (4) restoration of normal hair color, (5) improved skin tone, and (6) a generalized feeling of well-being.

When procaine enters the body, it is broken down into para-aminobenzoic acid (PABA, a para B-vitamin), and diethylaminoethanol (DEAE), both of which are naturally present in the body. Both of these substances are biologically active and have numerous beneficial effects of their own. Although the majority of the research involving Gerovital and Aslavital attribute the benefits to the procaine molecule, there is still controversy as to whether the effects are due to the procaine molecule itself, or to its breakdown products, PABA and DEAE.


PABA
One very interesting application for this versatile substance is its potential to restore hair to its natural color. In 1941, Dr. B. F. Sieve reported that administration of 200 mg of PABA per day for two months resulted in marked darkening of the hair in 30 patients with gray hair.

It has been well established that PABA is a potent neutralizer of singlet molecular oxygen, a potent free radical which is a common by-product of normal metabolism.

The crosslinkage theory of aging was proposed by Professor Johan Bjorksten in 1974. PABA appears to slow and in some cases even reverse crosslinking in the protein structures of connective tissues such as collagen.


DMAE
Dimethylaminoethanol (DMAE) is a substance that is closely related to DEAE.
DMAE is a mild cerebral stimulant, which was at one time approved by the FDA as being possibly effective for the following conditions:

  1. Learning problems associated with underachieving and shortened attention span.
  2. Behavior problems associated with hyperactivity.
  3. Combined hyperkinetic behavior and learning disorders with underachieving, reading and speech difficulties, impaired motor coordination, and impulsive/compulsive behavior, often described as asocial, antisocial, or delinquent.
In 1958, Dr. Leon Oettinger, Jr., found that DMAE:
  • Accelerated mental processes
  • Improved concentration span
  • Abolished early morning fogginess
  • Relieved lassitude and mild depression with obvious letdown when it was discontinued
  • Was useful in schizophrenia of long duration (with prolonged treatment)
  • Decreased irritability and reduced overactivity, leading to a much better overall social adaptation and improved scholastic functioning
  • Increased attention span
  • Did not cause drowsiness
  • Improved IQ!
Furthermore, he found that DMAE had numerous advantages over the amphetamines (like Ritalin) in that there were no effects on heart rate or blood pressure and no induced jitteriness. Instead of causing anorexia (loss of appetite) like the amphetamines, he found that DMAE actually improved appetite in many patients and caused no interference with sleep. In fact, he found that DMAE actually reduced sleep requirements.

In 1960, Dr. Stanley Geller reported on a double-blind study of 75 children, that DMAE in doses of 50 mg twice daily resulted in improved functioning capacity, puzzle-solving ability and organization of activity.

Kugel and Alexander reported that DMAE had also been demonstrated to be useful in the treatment of chronic fatigue and depression in children, and Sergin reported the phenomena of DMAE-induced lucid dreaming, and speculated on its effects in normalizing brain function and mood.

In 1974, Dr. Edith Miller added DMAE in doses ranging from 300-900 mg per day to the regimen of Parkinsons patients who had begun to exhibit adverse effects from high dosages of L-DOPA. DMAE administration resulted in a complete resolution of the L-DOPA-induced abnormal movements in a majority of the patients.

One of the most dramatic and well-documented effects of DMAE is its ability to inhibit the formation of aging pigment (lipofuscin).

DMAE not only can prevent the formation of lipofuscin, but it also actually flushes it from the body. Many people gauge the rate of lipofuscin removal from their hearts and brains by watching their liver spots disappear with long-term supplementation of DMAE. It usually takes about six months for significant changes to take place — many spots resolving completely.
 

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The current study reported an elevated level of glycerylphosphorylcholine (GPC) after the RDIF. While GPC was not itself signicantly dysregulated (P < 0.1), glycerophospholipid metabolism, as a pathway, was signicantly enriched for dysregulation (see Fig. 4). GPC is a natural brain choline compound that inuences Alzheimer's disease and dementia treatment [42; 43]. Also, GPC accumulation has a protective effect from the high interstitial concentrations of NaCl and urea in renal medullary cells during the renal concentrating mechanism [44]. Moreover, GPC metabolites play a role in modulating the risk of cardiovascular disease via the atherosclerosis pathway [45].
 
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David PS

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If your eating alot of eggs don't forget about the benefits of eggshell membrane.

View: https://www.youtube.com/watch?v=1Q2HR-yzDLQ

 
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David PS

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I just read these blurbs from my news feed for the past week. I do not expect to find any double blinded placebo controlled studies on egg consumption. Purposefully depriving people of choline for an extended (like 6 years in the first study) time so that they are getting less than the offical adequate intake would not be ethical. So why do people do it to themselves?

Eggs Consumption in Relation to Lower Risk of Cognitive Impairment in Elderly: Findings from a 6-Year Cohort Study - J Nutr Health Aging 2022 - "Compared with non-consumers or less-than-weekly consumers, participants consuming 0.1-2.9 eggs/week and 3.0-5.9 eggs/week had 18% (RR=0.82, 95%CI 0.76-0.89) and 9% (RR=0.91, 95%CI 0.84-0.99) lower risks of cognitive impairment respectively, whereas no association was found in those consuming ≥6.0 eggs/week"

Is dietary choline intake related to dementia and Alzheimer's disease risk: results from the Framingham Heart Study - Am J Clin Nutr 2022 Aug 2 - "Dietary choline intake showed non-linear relationship with incident dementia and AD. After adjusting for covariates, low choline intake (defined as choline/100 ≤ 2.19 and choline/100 ≤ 2.15 in our sample) was significantly associated with incident dementia or incident AD"
 
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Guacamayo

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Eating a few eggs a day or even a few dozen is not going to help you with this, don't get your hopes up.
As someone who seems to be quite familiar with choline, could you let me know what you believe is the best way to raise choline levels?
I recently had a micronutrient blood test (they check the inside of your white blood cells) and was found to be deficient in Vitamin D, and borderline in choline, Vitamin B2, B5 and B12. That's why I'm very interested in discovering the most efficient way to increase choline stores.
 

LLight

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@Spartan300
You could be interested by this publication about glaucoma and the glymphatic system.

The authors hypothesized that glaucoma develops from restriction of normal glymphatic clearance at the lamina cribrosa, in combination with a low ICP.
There is much about the relationship between AQP4 and the impaired optic nerve that remains to be elucidated. These questions range from debris clearance, toxin removal, nutrient supply, IOP/ICP maintenance, to disease etiology and pathogenesis.
Future research into the glymphatic system should explore several different avenues, including noninvasive methods of imaging the glymphatic system, interactions between AQP4 and the cholinergic nervous system, the role that other aquaporins besides AQP4 play in the glymphatic system, and interactions between the glymphatic system and other waste clearance pathways.
Ps: the aquaporin AQP4 seems to be linked to vasopressin and hyperosmolarity (that may be both reachable from fluid restriction).
 

Vanset

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As someone who seems to be quite familiar with choline, could you let me know what you believe is the best way to raise choline levels?
I recently had a micronutrient blood test (they check the inside of your white blood cells) and was found to be deficient in Vitamin D, and borderline in choline, Vitamin B2, B5 and B12. That's why I'm very interested in discovering the most efficient way to increase choline stores.
I was talking about his exercise intolerance saying eating a few eggs a day will not help him as it's a steroid hormone / adrenal hormone / CNS problem. Eggs are an excellent way to get choline in your diet.
 
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Spartan300

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You could be interested by this publication about glaucoma and the glymphatic system.




Ps: the aquaporin AQP4 seems to be linked to vasopressin and hyperosmolarity (that may be both reachable from fluid restriction).
@LLight Many thanks for this. I'll take a more detailed look but interesting that this also seems to identify a choline/eye health connection
I was talking about his exercise intolerance saying eating a few eggs a day will not help him as it's a steroid hormone / adrenal hormone / CNS problem. Eggs are an excellent way to get choline in your diet.
One of my frustrations is that my steroid hormones are all good. High T and DHT, DHEA-s is above range. Prolactin mid-range
Cortisol high too though ..
 

Vanset

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@LLight Many thanks for this. I'll take a more detailed look but interesting that this also seems to identify a choline/eye health connection

One of my frustrations is that my steroid hormones are all good. High T and DHT, DHEA-s is above range. Prolactin mid-range
Cortisol high too though ..
Do you have insomnia after a workout?

Consider testing SHBG and free T.
 
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David PS

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My interest in choline is for its long term protection of my brain. The brain shrinkage associated with Alzheimer's may be the result of a long term (meaning lifelong) deficiency of choline and acetylcholine. We have known about the benefits of choline for decades.
The pharmaceutical industry has developed a class of cholinesterase inhibitor drugs which are based on this idea. They do not seem to work very well for Alzheimer's. They treat the disease but they do not cure the disease. They may slow the process but they do not halt the process.

The cholinesterase inhibitors are expensive and are prescribed as a last resort after cognitive decline is apparent.

The cholinesterase inhibitors slow down the loss of choline but if the choline is not there in the first place, what good are they? One of the hallmarks of Alzheimer's is the loss of brain tissue. The cholinesterase inhibitors were not designed to restore and regrow tissue. Once a critical mass of tissue is gone from the brain, the cholinesterase inhibitors are not the solution.

My analogy is the nursery rhyme, Humpty Dumpty. Once your brain has had the great fall, you will never put Humpty together again. The pharmaceutical industry will sell you drugs (if you can afford them), but they do not seem to work. Getting adequate choline in my diet is my plan to prevent the great fall (loss of brain tissue) and avoid the need to reassemble Humpty (the various networks in the brain for it to function).
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Choose wisely
 
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Peatness

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Way does adding more eggs to my diet cause my mood to tank? Been feeling a bit 'off' since I started about a week ago. I'm having 2 eggs a day, no egg whites. I am also increasing meat intake - very slowly.
 

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The glymphatic system and AQP4 seem to also be linked to Alzheimer's disease.
 
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