What's the difference between adenosine monophosphate and the nucleotide for RNA/DNA with adenine base?

Just finishing up for my final A-Level exams, and it hit me that the nucleotide used in RNA or DNA with adenine as the nitrogenous base is supposed to be composed of the nitrogenous base adenine, a ribose or deoxyribose sugar, and a single phosphate group. Similarly, when the energy molecule ATP is hydrolyzed to ADP and then to AMP, we are left with adenosine monophosphate, which is again composed of the nitrogenous base adenine, a ribose sugar, and a phosphate group. So what's the difference between the two? Or are they the same?

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👤︎ u/wankerkid
📅︎ Jan 31 2017
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Melatonin protects against chronic intermittent hypoxia-induced cardiac hypertrophy by modulating autophagy through the 5′ adenosine monophosphate-activated protein kinase pathway sciencedirect.com/science…
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Can the human body remove the phosphate group in adenosine monophosphate for energy?

I know that a phosphate group is removed from ATP to produce energy and another can be removed from the resulting ADP molecules for more energy, but I did not know if the body could gain any energy from removing the last phosphate group from AMP.

Thank you for your explanations!

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Amino acids regulate energy utilization through mammalian target of rapamycin complex 1 and adenosine monophosphate activated protein kinase pathway in porcine enterocytes. - March 2020

https://www.ncbi.nlm.nih.gov/pubmed/32211535 ; https://www.sciencedirect.com/science/article/pii/S2405654519301970?via%3Dihub

Xiao H1,2, Zha C1, Shao F3, Wang L1, Tan B2,4.

Abstract

As major fuels for the small intestinal mucosa, dietary amino acids (AA) are catabolized in the mitochondria and serve as sources of energy production. The present study was conducted to investigate AA metabolism that supply cell energy and the underlying signaling pathways in porcine enterocytes. Intestinal porcine epithelial cells (IPEC-J2) were treated with different concentrations of AA, inhibitor, or agonist of mammalian target of rapamycin complex 1 (mTORC1) and adenosine monophosphate activated protein kinase (AMPK), and mitochondrial respiration was monitored. The results showed that AA treatments resulted in enhanced mitochondrial respiration, increased intracellular content of pyruvic acid and lactic acid, and increased hormone-sensitive lipase mRNA expression. Meanwhile, decreased citrate synthase, isocitrate dehydrogenase alpha, and carnitine palmitoyltransferase 1 mRNA expression were also observed. We found that AA treatments increased the protein levels of phosphorylated mammalian target of rapamycin (p-mTOR), phosphorylated-p70 ribosomal protein S6 kinase, and phosphorylated-4E-binding protein 1. What is more, the protein levels of phosphorylated AMPK α (p-AMPKα) and nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase sirtuin-1 (SIRT1) were decreased by AA treatments in a time depending manner. Mitochondrial bioenergetics and the production of tricarboxylic acid cycle intermediates were decreased upon inhibition of mTORC1 or AMPK. Moreover, AMPK activation could up-regulate the mRNA expressions of inhibitor of nuclear factor kappa-B kinase subunit beta (Ikbkβ), integrin-linked p

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👤︎ u/Ricosss
📅︎ Mar 27 2020
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ELI5 What is the sAC (Soluble adenylyl cyclase) enzyme? Why is it so important for the human body? How is it related to cAMP (Cyclic adenosine monophosphate)?
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Adenosine monophosphate-activated protein kinase activation mediates the leptin-induced attenuation of cognitive impairment in a streptozotocin-induced rat model spandidos-publications.co…
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What causes a raise in cAMP (cyclic adenosine monophosphate) levels?

Could it be a certain diet, and/or stress or something else?

Also, does cAMP flow freely throughout the body or is the cAMP in the brain separate from cAMP in the rest of the body? Thanks.

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A cup of insecticide - straight talk

A pal of mine who has only recently started drinking coffee and believes all the legacy marketing hype said to me, “I believe the bad things coffee does to you are from the insecticides.”

Obviously he wasn’t aware that caffeine is the main insecticide.

Now I can’t stop seeing everything for what it is:

  • Black coffee: a cup of addictive insecticide.
  • Latte: a high-dose insecticide with flavouring, sugars and a soporific to make it more addictive and reduce insecticide-induced anxiety.
  • Tea: Insecticide with a natural soporific (theanine).
  • Chocolate: Insecticide mixed with fat and sugar to hide taste/increase addiction.
  • Caffeine pills: Insecticide pills without flavour or diuretic effect.
  • Etc.

Makes for a useful frame of reference.

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👤︎ u/WinstonFox
📅︎ Jan 12 2022
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Potential alternatives to beta blockers for physical anxiety [list]

I have done a few days research about natural alternatives to beta blocker.

I havent tested any of the following alternatives efficacy, aswell i cant tell you if one of them work or are safe to take.

They might work through a different mechanism but can lead to a similar result.

Some of them do the opposite, those i have included for a potential downregulation or just because they act on the same receptor system.

I will try to edit the list with any new find.

St. John's wort (weak MAO-A and MAO-B inhibition; glutamate, GABA-A, and GABA-B affinity; downregulation of beta-adrenergic receptors and upregulation of 5-HT2 receptors)

https://pubmed.ncbi.nlm.nih.gov/14672758/

HAWTHORN (CRATAEGUS SPP) (The mechanism is attributed to a slight inhibition of sodium/potassium adenosine triphosphatase (Na+/K+-ATPase), which might be responsible for the positive inotropic action. Evidence also reveals inhibition of angiotensin-converting enzymes (ACEs) and of interactions with the cyclic adenosine monophosphate (cAMP)-mediated β-adrenergic system)

https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC7151902/

Apium graveolens (celery) (apigenin - possibly by lowering levels of circulating catecholamines and decreasing vascular resistance)

https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC4717468/

Coriandrum sativum (cilantro or coriander) - (coriander extract (200 and 300 mg/kg) inactivated β-adrenoceptor-induced ROS production and also prevented MI by inhibiting myofibrillar damage)

https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC4717468/

Crocus sativus (saffron) - (guinea-pig isolated perfused hearts (Langendorff procedure) by blocking Ca2+ channels, opening potassium channels, and antagonizing β-adrenoceptors)

https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC4717468/

Rauwolfia serpentina (reserpine - depletes adrenergic neurotransmitters)

https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC4717468/

Melothria maderaspatana (melon-gubat) (Importantly, M. maderaspatana seems to decrease levels of ET-1, epinephrine and norepinephrine)

[https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC478210

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📅︎ Dec 26 2021
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Nootropics that upregulate dopamine (V2.0)

Increasing dopamine without tolerance or addiction:

Hey guys. I've been hoarding all this information for the past year, and I think it's time I release it to the public. Bromantane and ALCAR are some of the most promising dopaminergics on the market, and this post will explain why.

For those of you confused about dopamine:

To put it simply, it's the motivating neurotransmitter. And this bleeds into things such as optimism, confidence, social interaction, mood, learning etc. It would take 10 posts to go over everything dopamine does, so hopefully you accept the generalization.

Here's a simplified version of the dopamine/ CREB cascade:

Dopamine --> D1 activation --> Adenylate Cyclase --> Cyclic Adenosine Monophosphate (cAMP) production --> Protein Kinase A --> CREB (key factor in learning and memory) --> (ΔFosB --> inhibits C-Fos), Dynorphin (inhibits dopamine release), (Tyrosine Hydroxylase activation --> more dopamine), and so much more.

Your idea of dopamine receptor upregulation may be wrong.

So many things are said to "upregulate dopamine receptors", but what does that truly mean? Well it's not so simple. Usually receptor upregulation just hints at temporarily lowered neurotransmitter causing increased sensitivity to maintain homeostasis. So keep that in mind when discussing Uridine. This source for instance. Or Sulbutiamine. So besides Uridine being GABAergic, that has to be part of Nootropic Depot's motivation to include it in the sleep support stack. Reviews are mixed, but I felt sedated by Uridine Monophosphate.

Cocaine upregulates dopamine receptors. And I'll reference this study later. But basically the transition of CREB to ΔFosB and Dynorphin, leading to a depletion of CREB and dopamine is evidence of tolerance to cocaine. So looking at receptors alone is SIMPLISTIC, especially when you consider the inhibitory role of D2 receptors which people here misconceive to be a good thing. It's almost as simplistic as assuming Tyrosine Hydroxylase upregulation is why Bromantane is so great, which is one of many misconceptions I had in the past. It's the mechanism that makes it great, not just downstream activity.

And by

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👤︎ u/sirsadalot
📅︎ Oct 09 2021
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Effect of Inonotus obliquus (Chaga) extract on the regulation of glycolipid metabolism via PI3K/Akt and AMPK/ACC pathways in mice , study [06 - 2021]

Aim of the study

I. obliquus contains abundant functional components, which provide potential medicinal value. The purpose of this study was to investigate compositions of I. obliquus extract with a high-pressure water extraction method, and investigate the anti-type 2 diabetic effects of I. obliquus extract and the possible underlying mechanisms involved.

Materials and methods

The I. obliquus was extracted by a high-pressure water extraction method, and tested its main components by special assay kit and instrumental analysis. Type 2 diabetic C57BL/6 mice were induced by high-fat diet with low-dose STZ injection, and were daily gavaged with different doses of I. obliquus extract for 8 weeks. Glycemic, blood lipid profile, and histopathology of liver and pancreas were assessed. Underlying mechanisms related to glycemic control in liver were further performed.

Results

The I. obliquus extract main compounds were β-Glucans, triterpenoids and polyphenol by determination. Oral administration of 250 mg/kg and 500 mg/kg I. obliquus extract significantly alleviated blood glucose and insulin resistance. Moreover, 250 mg/kg and 500 mg/kg of I. obliquus extract increased liver glycogen content and high-density lipoprotein cholesterol (HDL-C) levels while decreased total cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C) levels. Furthermore, the protein expression levels of phosphatidylinositol-3 kinase (PI3K), p-protein kinase B (Akt), p-adenosine monophosphate activated protein kinase (AMPK), and p-acetyl-CoA carboxylase (ACC) were upregulated, whereas sterol regulatory element-binding protein-1c (SREBP-1c) and fatty acid synthase (FAS) were downregulated after supplement with 250 mg/kg and 500 mg/kg of I. obliquus extract. Interestingly, I. obliquus extract was a dose-effect relationship within a certain range. 250 mg/kg had obvious anti-diabetes effect, and the effect of 500 mg/kg dose was the same as that of metformin.

Conclusion

I. obliquus extract ameliorated insul

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👤︎ u/Sorin61
📅︎ Jan 18 2022
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LLLT and ATP metabolism -> Thermogenesis/ROS

Since LLLT (low-level laser therapy aka red light therapy aka photobiomodulation) is poorly understood, I wanted to share some information about it and how it might be useful for healing our PUFA-damaged metabolisms.

LLLT is typically used in medicine for three main purposes: to promote wound healing, tissue repair, and the prevention of tissue death; to relieve inflammation and edema because of injuries or chronic diseases; and as an analgesic and a treatment for other neurological problems. Modern LLLT devices are LED-based and generally use a combination of infrared and near-infrared wavelengths (600–1070 nm).

My interest with LLLT started with sunbathing in the winter, trying to counter my seasonal depression. I found that morning sunlight made me feel better and more energetic than sunlight from later in the day, and research revealed that morning light has the more red light wavelengths. I bought an inexpensive red light device and started using it in the mornings, and found it gave me a strong boost. Researching the science of why it helped, I found out about LLLT.

The primary mechanism I’m interested in is how LLLT interacts with the mitochondria and ATP cycles. The simple version is here, and the complicated version below.

When red light wavelengths reach the mitochondria, there is a photochemical reaction. This happens in the electron transport chain at complex IV, also known as cytochrome c oxidase (CCO). The exact mechanisms are still being studied, but two significant things happen: one is that Nitric Oxide (NO) is released from the CCO, increasing NO in the bloodstream and lowering blood pressure, while also freeing up the CCO for oxygen; cellular respiration functioning is increased and more ATP is produced. The other result is that the successful creation of ATP released Reactive Oxygen Species (ROS). Red light produces a significant boost to ATP production, and therefore a significant amount of NO and ROS.

Reading through fireinabottles’s blog, with the ROS theory of obesity, the basic problem is that bodies with too much (poly)unsaturated fats become stuck in a low-ROS generating state. We need a way to switch our bodies back to a high-ROS generating state, with a healthy saturated fat-based feedback system. FIAB has been focused on enzyme management (targeting SCD1) through various supplements, but if the essential problem is the need for more ROS, LLLT may be able to provide that without risk of side effects.

https://fireinabot

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Are protein powders like steroids?

The steroids that were found in the protein powders seized by the FDA in Pune were me phentermine sulphate and adenosine monophosphate used to treat blood pressure and improve blood circulation to the skeletal and cardiac muscles.

https://preview.redd.it/nqs4m7184u381.png?width=602&format=png&auto=webp&s=bf5150a39c1dfe449d98d9ae32a68b3e2ff6b0b7

Protein is one of the building blocks of bone, muscle, and skin. The body needs it to produce hormones, enzymes, and other chemicals.

Commonly referred to as steroids, corticosteroids are a type of anti-inflammatory drug. They are typically used to treat rheumatologic diseases, like rheumatoid arthritis, lupus or vasculitis (inflammation of the blood vessels).

The possible health benefits of protein powders include the following:

Eating protein-rich foods and taking protein supplements may help people feel fuller for longer. Feeling full tends to result in smaller portion sizes and less frequent snacking, which can help a person maintain a healthy weight or lose weight if necessary.

Protein is essential for muscle growth. Many athletes and gym enthusiasts consume protein shakes because they believe that these drinks will help them bulk up after strength training. Protein supplementation was equally effective in men and women. However, the effectiveness may decrease with age, as older adults have higher protein requirements than younger people.

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Ketotifen 1mg 30 tablets

Ketotifen belongs to the group of cycloheptothiophenones and has a pronounced antihistamine effect. It is a non-bronchodilating anti-asthma drug. Its mechanism of action is associated with inhibition of the release of histamine and other mediators of mastatsitam, with blocking of histamine H1 receptors and inhibition of the phosphodiesterase enzyme, resulting in an increase in the level of cyclic adenosine monophosphate in mast cells. Suppresses the effects of TAF (platelet-activating factor). When used alone, it does not stop attacks of bronchial asthma, but prevents their occurrence and reduces their duration and intensity, while in some cases they completely disappear. https://pharmasstore.com/product/ketotifen-1mg-30-tablets/

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Usual and alternative treatments for herpes:

I am a male and I was diagnosed with herpes (hsv2) since April 2020. Had 1 OB every 2 months but it looks like the fucker is getting resistence to Valtrex (500mg a day, 1000mg on OB) and the OB are getting more frequent.. But to be fair I am living a really stressed time… As I saw that usually it intends to get better after 1 year or 2 I hope I will be ok. Now I have this outbreak for a week now. Trying to fight it with just 1 pill… but now rise to 2. Any advices or similar experiences? What do you think is better :

1- try to take a higher dosage of medicine during OB until no sores are left and no itchy, and get more side effects in the future?

2- or just take 500mg daily usual dosage and wait with a bit pain and just double dosage for 2 or 3 days max during outbreak, with a bit less efects?

Meanwhile I see that is hard to find a post that organize a generic treatment, or kind of a receipt we could try and see what´s best for us . Here is my research of many reading hours and my guinea pig experience for you:

Usual stuff:

- Valtrex, acyclovir, famvir - famvir didn´t tried yet

- Boric Acid for cleaning – prescribed by doctors so ok, don’t use it regularly

- Practice Yoga, Sports and meditation

- Abreva or Zovirax

Alternatives:

Food and supplements:

- Alcaline food (Quit coffee, sugars, almonds, trying to shorten meat) – hard to quit meat… but still didn´t saw such a diference as I started 2 weeks ago because of this OB and I don´t want to keep taking 2 pills of Valtrex

- Lot of water lot of teas

- Lysine (started 2 weeks ago 500mg a day)- still on outbreak, so let´s see after this one OB

- Vitamin C, B, Zinc – Haven´t tried

- Vitamin D, E, adenosine monophosphate – Haven´t tried

- Sauna? – Haven´t tried

- Alcohol, iodine, Neosporin to pass on sores - Iodine same as propolis or valaciclovir cream. Haven´t tried the others.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC266254/

Oils:

- Propolis extract - I usually combine it with Zovirax, has good effect but not enough

- Olive Leaf extract – Haven´t tried

- Oregano oil (made with coconut oil) – Haven´t tried

- Tee tree oil – Haven´t tried

- peppermint oil – Haven´t tried

Creams:

- Zinc Oxide – Haven´t tried

Future/recent treatments to try:

- Squaric acid dibutylester (SADBE)

[https://www.practiceupdate.com/content/single-dose-squaric-acid-dibutyl-ester-to-reduce-frequency-of-outbreaks-in-recurrent-he

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Man Greens Reviews |

Looking for Man Greens Reviews 2022 Reddit before making a decision ? In this article, we are going to provide you with the Man Greens Review 2022 Reddit, And give you a comprehensive detail it.

Man Greens Reviews

Greens supplements have become a crucial addition to one’s diet, as they can deliver antioxidants, vitamins, and minerals while freeing one’s system of inflammation. Other notable benefits include its convenience, value for the price, and its overall mess-free kind. On average, greens supplements are advertised as one-size-fits-all. Unfortunately, this is deemed inappropriate for male health, as most of the common ingredients used to trigger a testosterone deficiency.

On a mission to tailor greens so that men can attain its benefits without compromising their test levels is Chad Howse, who insists that his approach to greens called “Man Greens” is the way to go. To see why he firmly stands by this respective supplement, the following review breaks down Man Greens to unveil its motive, formula, and critical ingredients, among others.

What is Man Greens?

Man Greens is a dietary supplement formulated with male health in mind. Exclusively, this respective formula is said to contain ingredients that can potentially help to increase energy and libido levels, enhance sexual drive and athletic performance, boost testosterone and lower cortisol levels. To date, it is the only greens supplement in the market that is not one-size-fits-all. To better understand the consequences of taking traditional greens supplement, let’s further study how Man Greens has been formulated.

Click Here To Order A Man Greens Bottle From the Official Website (60 Days Money Back Guarantee)

How has Man Greens been formulated?

[Man Greens](https://www.reddit.com/r/WeightLossAtHome2022/comments/ql2ibg/man_greens_reviews_2022_warning_must_read_th

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Diets for Patients with Amyotrophic Lateral Sclerosis -- Pay Attention to Nutritional Intervention

Diets for Patients with Amyotrophic Lateral Sclerosis

Pay Attention to Nutritional Intervention

Yang, Li-Peng1,2; Fan, Dong-Sheng1,

Author InformationChinese Medical Journal: August 05, 2017 - Volume 130 - Issue 15 - p 1765-1767doi: 10.4103/0366-6999.211549

  • FREE

Metrics

INTRODUCTION

Amyotrophic lateral sclerosis (ALS) is characterized by the progressive degeneration of upper and lower motor neurons. Typical clinical features of ALS are limb paralysis, muscle atrophy, dysphagia, dysarthria, shortness of breath, and respiratory failure. Approximately 90% of ALS cases are classified as sporadic ALS, the remaining 10% are classified as familial.[12] Researchers have found that the survival of ALS patients is related to several factors, including clinical phenotype, age at onset, sex, early presence of respiratory failure, and treatment with riluzole. We recently found that there is a potential linear relationship in ALS between serum lactate and motor deterioration, and that slower lactate elimination rate might be associated with faster disease progression.[3] In addition, several studies have reported that nutritional status is closely related to the survival time of ALS patients, and there exists a U-shaped association between patients’ body mass index (BMI) and mortality.[14] The main cause of malnutrition (BMI ≤18.5 kg/m²) in ALS patients is an imbalance between intake and consumption, and some symptoms, such as dysphagia, can lead to insufficient energy intake. More importantly, recent studies have shown that ALS patients are in states of hypermetabolism.[56]

HYPERMETABOLISM IN AMYOTROPHIC LATERAL SCLEROSIS

It is difficult to explain the association between hypermetabolism and ALS, but it has been found in mutant Cu Zn-superoxide dismutase (SOD1) transgenic mice as well as in ALS patients. Resting energy expenditure (REE) is one reason for increased consumption for ALS.[6] Dupuis et al.[7] found that SOD1G86R and SOD1G93A mice have increased REE compared to control mice. Desport et al.[8] found that REE significantly increased by an average of 14% in 168 ALS patients compared to the calculated value, and 62.3% of ALS patients were considered hypermetabolic. Bouteloup et al.[5] confirmed that hypermetabolism existed in 48% of all AL

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Fructose Removal from the Diet Reverses Inflammation, Mitochondrial Dysfunction, and Oxidative Stress in Hippocampus

Fructose Removal from the Diet Reverses Inflammation, Mitochondrial Dysfunction, and Oxidative Stress in Hippocampus

https://www.mdpi.com/2076-3921/10/3/487/htm

Full free text - very complicated biochem - I posted the Discussion and Conclusion here.

Abstract

Young age is often characterized by high consumption of processed foods and fruit juices rich in fructose, which, besides inducing a tendency to become overweight, can promote alterations in brain function. The aim of this study was therefore to (a) clarify brain effects resulting from fructose consumption in juvenile age, a critical phase for brain development, and (b) verify whether these alterations can be rescued after removing fructose from the diet. Young rats were fed a fructose-rich or control diet for 3 weeks. Fructose-fed rats were then fed a control diet for a further 3 weeks. We evaluated mitochondrial bioenergetics by high-resolution respirometry in the hippocampus, a brain area that is critically involved in learning and memory. Glucose transporter-5, fructose and uric acid levels, oxidative status, and inflammatory and synaptic markers were investigated by Western blotting and spectrophotometric or enzyme-linked immunosorbent assays. A short-term fructose-rich diet induced mitochondrial dysfunction and oxidative stress, associated with an increased concentration of inflammatory markers and decreased Neurofilament-M and post-synaptic density protein 95. These alterations, except for increases in haptoglobin and nitrotyrosine, were recovered by returning to a control diet. Overall, our results point to the dangerous effects of excessive consumption of fructose in young age but also highlight the effect of partial recovery by switching back to a control diet.Keywords: hippocampus; mitochondria; fructose diet; young rat; inflammation; oxidative stress; haptoglobin; neurofilament-M; PSD-95

4. Discussion

Changes in dietary lifestyle, such as the dramatic abuse of processed foods (bakeries

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Anyone has a symptomatic AMPD1 deficiency?

https://en.m.wikipedia.org/wiki/Adenosine_monophosphate_deaminase_deficiency_type_1

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50 reason to quit caffeine.

Believe it or not these 50 points are not an exhaustive list, but just a few key points.

  1. Caffeine is a powerful drug with dangerous side effects and needs to be used with caution

  2. Caffeine accumulates in the body

  3. Damages the adrenals, blood vessels, breasts, brain, gastrointestinal tract, DNA, immune system and bones.

  4. Caffeine is very taxing on the liver and kidneys who are continuously removing caffeine and it’s many by-products

  5. Caffeine easily crosses the blood brain barrier and enters every organ, tissue and bodily fluid.

  6. Caffeine contains a large amount of chemicals, including polycyclic aromatic hydrocarbons (carcinogens)

  7. Caffeine is broken down into 25 by-products that all have detrimental effects on the body

  8. Caffeine contains aldehydes, alcohols and sulfides. All of which have to be removed by your poor liver

  9. Caffeine reduces the effectiveness of your prescription drugs.

  10. Prescription drugs reduce the livers effectiveness at removing caffeine from the body

  11. Some prescription drugs raise blood caffeine levels by as much as 600%.

  12. Caffeine disrupts your normal adenosine receptors, which control the brain, kidneys, gastrointestinal system, cardiovascular system and respiratory system. Caffeine triggers the neurons to fire uncontrollably throughout the body.

  13. Because of this excess neuron activity, it triggers an “emergency’ response from the body. We’ve all heard of the “fight or flight” response. The adrenal glands pump out large amounts of stress hormones. EVERY DAY! This has very bad long-term effects on adrenal function, blood pressure, heart rate, and thyroid hormone levels.

  14. Caffeine’s by-products are reabsorbed into the blood stream. Living in the gastrointestinal tract and causing putrefaction, maldigestion, gas, bloating and increasing your risk of gastrointestinal disease.

  15. Caffeine significantly increases your chance of having a heart attack or stroke by causing vascular resistance (your peripheral blood vessels restrict) and damages blood vessels throughout the body.

  16. Caffeine causes your body to be less metabolically efficient. Less oxygen gets to the cells, therefore less waste is removed from the cells, increasing your risk of every type of cancer.

  17. Caffeine causes the blood vessels in the brain to constrict and blood flow to your brain is literally reduced. One study showed that a single 12 oz cup of coffee reduced cerebral blood flow by 40%.

  18. Caffeine reduces the qu

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SERIOUS: This subreddit needs to understand what a "dad joke" really means.

I don't want to step on anybody's toes here, but the amount of non-dad jokes here in this subreddit really annoys me. First of all, dad jokes CAN be NSFW, it clearly says so in the sub rules. Secondly, it doesn't automatically make it a dad joke if it's from a conversation between you and your child. Most importantly, the jokes that your CHILDREN tell YOU are not dad jokes. The point of a dad joke is that it's so cheesy only a dad who's trying to be funny would make such a joke. That's it. They are stupid plays on words, lame puns and so on. There has to be a clever pun or wordplay for it to be considered a dad joke.

Again, to all the fellow dads, I apologise if I'm sounding too harsh. But I just needed to get it off my chest.

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The glucose-mobilizing effect of glucagon at fasting is mediated by Cyclic AMP. (Pub Date: 2021-08-09)

https://doi.org/10.1152/ajpendo.00172.2021

https://pubmed.ncbi.nlm.nih.gov/34369821

Abstract

Glucagon is a fascinating peptide hormone. Since the discovery of a ‘glucose stimulatory factor’ from the pancreas (1), the physiological role of glucagon continues to be investigated and highly debated (2-5). This is exemplified by glucagon’s role in glucose control (5). From randomized clinical trials with glucagon receptor antagonists, we know that glucagon is a powerful regulator of fasting glucose in humans (6, 7) as previously demonstrated in preclinical studies (8, 9). However, the role of glucagon in postprandial glycemic control appears less clear, as those same studies did not observe any additional improvements in postprandial glucose once changes in fasting glucose had been considered. The main arguments made in this article are that

  1. cyclic adenosine monophosphate (cAMP) mediates glucagon glucose regulatory effects in (short-term) fasted conditions and
  2. glucagon role in postprandial metabolism is to regulate amino acid metabolism (termed the liver-alpha cell axis(2)) and secondly to circumvent the potential hypoglycemic effects of an amino acid-induced hyperinsulinemia (figure 1).

These arguments are placed in a context of glucagon resistance a new physiological terminology observed in patients with type 2 diabetes and non-alcoholic fatty liver disease(10).

------------------------------------------ Info ------------------------------------------

Open Access: True

Authors: Nicolai J. Wewer Albrechtsen -

Additional links:

https://journals.physiology.org/doi/pdf/10.1152/ajpendo.00172.2021

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👤︎ u/Ricosss
📅︎ Aug 10 2021
🚨︎ report
A science-based analysis on dopamine upregulation

Increasing dopamine without tolerance or addiction:

Hey guys. I've been hoarding all this information for the past year, and I think it's time I release it to the public. Bromantane and ALCAR are the most promising dopaminergics on the market, and this post will explain why.

For those of you confused about dopamine:

To put it simply, it's the motivating neurotransmitter. And this bleeds into things such as optimism, confidence, social interaction, mood, learning etc. It would take 10 posts to go over everything dopamine does, so hopefully you accept the generalization.

Here's a simplified version of the dopamine/ CREB cascade:

Dopamine --> D1 activation --> Adenylate Cyclase --> Cyclic Adenosine Monophosphate (cAMP) production --> Protein Kinase A --> CREB (key factor in learning and memory) --> (ΔFosB --> inhibits C-Fos), Dynorphin (inhibits dopamine release), (Tyrosine Hydroxylase activation --> more dopamine), and so much more.

Your idea of dopamine receptor upregulation may be wrong.

So many things are said to "upregulate dopamine receptors", but what does that truly mean? Well it's not so simple. Usually receptor upregulation just hints at temporarily lowered neurotransmitter causing increased sensitivity to maintain homeostasis. So keep that in mind when discussing Uridine. This source for instance. Or Sulbutiamine. So besides Uridine being GABAergic, that has to be part of Nootropic Depot's motivation to include it in the sleep support stack. Reviews are mixed, but I felt sedated by Uridine Monophosphate.

Cocaine upregulates dopamine receptors. And I'll reference this study later. But basically the transition of CREB to ΔFosB and Dynorphin, leading to a depletion of CREB and dopamine is evidence of tolerance to cocaine. So looking at receptors alone is SIMPLISTIC, especially when you consider the inhibitory role of D2 receptors which people here misconceive to be a good thing. It's almost as simplistic as assuming Tyrosine Hydroxylase upregulation is why Bromantane is so great, which is one of many misconceptions I had when I wrote [this](https://www.reddit.com/r/Nootropics/comments/jhos16/the_resolution_to_dopamine_do

... keep reading on reddit ➡

👍︎ 167
💬︎
👤︎ u/sirsadalot
📅︎ Jul 31 2021
🚨︎ report
Usual and alternative treatments for herpes:

I am a male and I was diagnosed with herpes (hsv2) since April 2020. Had 1 OB every 2 months but it looks like the fucker is getting resistence to Valtrex (500mg a day, 1000mg on OB) and the OB are getting more frequent.. But to be fair I am living a really stressed time… As I saw that usually it intends to get better after 1 year or 2 I hope I will be ok. Now I have this outbreak for a week now. Trying to fight it with just 1 pill… but now rise to 2. Any advices or similar experiences? What do you think is better :

1- try to take a higher dosage of medicine during OB until no sores are left and no itchy, and get more side effects in the future?

2- or just take 500mg daily usual dosage and wait with a bit pain and just double dosage for 2 or 3 days max during outbreak, with a bit less efects?

Meanwhile I see that is hard for this group to organize a generic treatment we could try and see what´s best for us and lot of shitty posts from non-herpes people and repeated posts. Here is my research of many reading hours and my guinea pig experience for you:

Usual stuff:

- Valtrex, acyclovir, famvir - famvir didn´t tried yet

- Boric Acid for cleaning – prescribed by doctors so ok, don’t use it regularly

- Practice Yoga, Sports and meditation - in process, need to do everyday

- Abreva or Zovirax - Zovirax for me

Alternatives:

Food and supplements:

- Alcaline food (Quit coffee, sugars, almonds, trying to shorten meat) – hard to quit meat… but still didn´t saw such a diference as I started 2 weeks ago because of this OB and I don´t want to keep taking 2 pills of Valtrex

- Lot of water lot of teas

- Lysine (started 2 weeks ago 500mg a day)- still on outbreak, so let´s see after this one OB

- Vitamin C, B, Zinc – I will try it after Lysine

- Vitamin D, E, adenosine monophosphate – I will try it after above

- Sauna – Haven´t tried

- Alcohol, iodine, Neosporin to pass on sores - Iodine Haven´t tried the others.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC266254/

Oils:

- Propolis extract - I usually combine it with Zovirax, has good effect but not enough

- Olive Leaf extract – didn´t try yet

- Oregano oil (made with coconut oil) – didn´t try yet

- Tee tree oil – didn´t try yet

- peppermint oil – didn´t try yet

Creams:

- Zinc Oxide – didn´t try yet

Future/recent treatments to try:

- Squaric acid dibutylester (SADBE)

[https://www.practiceupdate.com/content/single-dos

... keep reading on reddit ➡

👍︎ 7
💬︎
📅︎ Jun 17 2021
🚨︎ report

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