podgaj

You are the Ponzi schemer. It is a combination of Pump and Dump and Ponzi. That's why it "comes back bigger".

Bitcoin is the stock market. Just more volatile. Prove me wrong.

I want to push the cause further back. The problem is not that rates are going up, the problem is that rates were close to zero for so long,

"to make it almost always increase in value"

To any investor this should be the biggest red flag that you are in a Ponzi/pump and dump scheme. "You can't lose!"

And rather than you are "buying electricity" I would say you are buying used electricity, which is useless.

Bitcoin is probably the first Ponzi scheme where everyone in it knows it is a Ponzi scheme. So I agree with your take here.

The moment you say the cat is "alive" you create time and you also start killing your cat.

In Buddhism there is no birth, no death. Both are illusions.

Time is objective? The measurement of time is objective but the feeling of time is not.

But in the same breath you can dismiss what the human body can do given a sufficient balance of omega-3 to omega 6?

Did you even try to see if omega 3 endocanibinols effected the g coupled protein receptors as well?

Yes, it is. They are not explaining HOW IRE1a is triggered by CDB, and it is because CDB triggers the CB1/2 receptor which activates these pathways.

https://journals.plos.org/plosone/article?id=10.1371/journal...

"Overall, our study investigates for the first time the effects of the endocannabinoid AEA on primary human T-lymphocytes, demonstrating that it is a powerful modulator of immune cell functions. In particular, not only we clarify that CB2R mediates the immunosuppressive activity of AEA, but we are the first to describe such an immunosuppressive effect on the newly identified Th-17 cells. These findings might be of crucial importance for the rational design of new endocannabinoid-based immunotherapeutic approaches."

The only way CBD can trigger these pathways is by effecting a cell receptor The only cell receptors for CBD are CB1r and CB2R. There is literally no other way this can happen.

If y9ou can explain how CBD increases IRE1α activity any other way I am all ears,

It’s about controlling the out of control inflammation caused by the body fighting the infection.

Correct, you also need to lower Omega 6 fats dramatically, and probably focus on long chain Omega 3.

while it can lead to more robust synthesis of endocannabinoids, really has nothing to do with the study at hand. Generally we use drugs because they have different or greater degrees of their mechanism than the endogenous compounds.

You can either excite these receptors or not. Exciting the receptor more than needed, which is what these overly high levels of exogenous cannabinols do, leads to degraded receptor sensitivity (dependance) and probably a rebound effect when the drug is stopped. It is not that I feel the drugs do not work, but they are not needed and are lacking the sensitivity.

Not to mention we don't know if endocannabinoids such as anandamide or 2-AG even have the same effect as high doses of CBD shown in this study. Also the concentrations of the endogenous molecules are likely nowhere near high enough

The arachidonic acid (Omega 6) derivatives (anandamide) are known to not be as anti-inflammatory and is more in line with THC, not CDB, in its action. Which is my point of having to get the 3/6 ratio much higher, and has nothing to do with this study other than showing that we need LESS anandamide and more docosahexaenoyl and eicosapentaenoyl ethanolamides.

If someone has enough omega 3 endocannabinoids it is likely that they would not need the heavy hammer of CBD to get them out of the inflammation. I am not saying CBD does not work, but endocannabinoids are more than just one molecule, and CBD cannot compare.

For a overall robust immune system we should be studying Omega 3's/Omega 6 balance more deeply.

Oh, that makes it OK I guess.

Endocannabinoids have been known for a while, but how Endocannabinoids are made in the human body is a newer discovery (~2016).

What should be being broadcast is how important Omega 3 is for increasing CB1R and CB2R activity to reduce inflammation and disease. This has everything to do with COVID and learning to live with SARS2 without people dropping dead or having to stay home from work. This is something everyone can do now, without waiting for legalization, working about dosing, or giving money to yet another 3rd party.

Why is there so little talk about Omega 3 and lowering COVID complications?

Because people are trained by the media everyday that drugs are the answer to everything and diet does not matter.

The global cannabidiol market size was valued at $2.8 billion in 2020 and is expected to expand at a compound annual growth rate of 21.2% from 2021 to 2028. Do you think these people want you to know that the same anti-inflammatory action can be achieved by lowering Omega 6 and increasing Omega 3 in your diet?

Let me fix that for you:

"Yemen has lost internet after U.S. Funded, Saudi-led, airstrikes"

Eat more Omega 3:

https://pubmed.ncbi.nlm.nih.gov/31085370/

https://www.sciencedaily.com/releases/2017/07/170718142909.h...

https://www.intechopen.com/chapters/50397

I think dehumanizing people is harmful regardless of the reason. And I agree, the holocaust equivalencies are just as harmful.

You're overlooking the somewhere between 1% and 30% chance of becoming disabled from Long Covid.

As a Daoist how can I not see the good in this? Maybe now now that everyone knows they can suffer a chronic disease they will find a cure for those of us suffering with ME/CFS for all these years?

This is the arrogance that amazes me. Suddenly everyone cares about chronic disease. the ME/CFS community has been crying for help for years. Am I glad this happened to you or anyone? No. But as I said, maybe some good will come out of it.

By the way, if you want to get out of your situation the only answer is nutrition.

I am disabled.

What have we become? This fear and alienation over less than 1% chance of dying?

Where did the study say that? They did the genetic study on mice, not humans. And they only said it gave them a better BMI, which is only one indicator of health.

In this case, for the Inuit, the common allele (for Caucasians) presents as a disadvantage.

They needed this polymorphism to survive on a diet with low sucrose.

The study does not conclude that at all. They only concluded they might be able to trick some people to make money off a a drug they will make.

Limitations: We hypothesize that the healthier metabolic profile observed in homozygous c.273_274delAG carriers was mediated by acetate produced by gut bacteria; however, we lack data to firmly verify this hypothesis.

Impact: Our results suggest that sucrase-isomaltase constitutes a promising drug target for improvement of metabolic health, and in a broader perspective add to the debate about the health effects of sugar consumption.

You know, it could be that these people are healthier because they avoid sugar because sugar makes them feel like crap when they get overloaded with aceatate.

There is no evidence that higher levels of acetate are better for people. Because if that as so drinking would be healthy for everyone.

https://academic.oup.com/alcalc/article-abstract/23/2/123/96...

https://www.biorxiv.org/content/10.1101/2020.07.20.212597v1....

"Our guess is that as they age"

They are guessing and they are wrong. Higher levels of acetate are just as bad as lower levels of acetate. You know what also raises acetate levels? The metabolism of Alcohol.

The Inuit need a different diet. They do not "get used to" these sugars.

And why should someone who is lactose intolerant eat lactose? We have been getting around this for years by making yogurt and cheese.

The diets are the same and the Alaskan Inuit also carry the SI deficiency alleles.

https://pubmed.ncbi.nlm.nih.gov/25452324/

I agree with the first part of what you said.

(Note: I am an amateur Nutritional Geneticist)

They said:

"The results demonstrate that carriers of the genetic variation have what is known as sucrase-isomaltase deficiency, meaning that they have a peculiar way of metabolizing sugar in the intestine. Simply put, they do not absorb ordinary sugar in the bloodstream the way people without the genetic variation do. Instead, sugar heads directly into their intestine."

Ha! What? SI, the gene that they studied, ONLY exists in the intestine. The inability to break down sucrose leads to microbe imbalance that concerts the sucrose to acetate. They are using the word "sugar" to cover everything from sucrose to any other oligosaccaride. They just do not understand the science enough. If you read the study it is clear.

And in NO way doe sthis mean that eating sugar is healthy for them as the title implies!!!! Look at what happens when you have this deficiency!

https://medlineplus.gov/genetics/condition/congenital-sucras... "After ingestion of sucrose or maltose, an affected child will typically experience stomach cramps, bloating, excess gas production, and diarrhea. These digestive problems can lead to failure to gain weight and grow at the expected rate (failure to thrive) and malnutrition. "

So this is NOT a great mutation. There is no such thing as a universal "great" mutation. These genetic changes are just one change in a probably network of changes in the Inuit. Others would include genes like FADS1 and FADS2 and CPT1A.

(NOTE: I have Saami heritage, who are the Inuit of Finland.)

Next:

"'It is probably due to Greenlanders not having had very much sugar in their diet. For the most part, they have eaten meat and fat from fish, whales, seals and reindeer. A single crowberry may have crept in here and there, but their diet has had minimal sugar content,' "

Here the researchers are correct, this is not only a Greenlander trait, but a common trait in all Inuit, and very low sucrose is common in all Inuit diets. https://pubmed.ncbi.nlm.nih.gov/25452324/

And this absolutely is a fitness example. For people with the common allele, the lack of sucrose in the diet leads to lower levels of acetate and these people would die off leaving the survivors with the less common allele to flourish.

Yawn...

https://news.ycombinator.com/item?id=29592786

Yes I am. I am alone.

I am disabled, and homeless living in my van. I have a family history of mental illness and even they abandoned me. My friends, I get it, they just did not understand what happened to me. I make $1600 on disability but I still cannot find housing. Even when people

I love your sentiment but virtual hugs do not do it for me, nor for most people in my position.

What do we need? An understanding of Mental Illness stigma, housing for the 60% of us homeless who have a serious mood disorder, lower cost housing for the disabled. All of these would give me stability and a community again where I can feel like I am part of something instead of being an outsider.

There have been great people that helped me, and I hold no regrets because it reduces the stress and that helps me deal with my mental illness, but all the suffering comes right back, because here I am, alone again, in my van, in a vacant public park, on Christmas morning.

You want to really hug me? Start a revolution.

Distilled water can flush electrolytes from your body which is not what you want.

This could be a good thing, like for people with hyperkalemia and hypernatremia. Distilled water is usually given to patients with hypernatremia.

https://aspenjournals.onlinelibrary.wiley.com/doi/abs/10.117...

It is always best to know your body chemistry before listing to such blanket advice. (I suffer mild hyperkalemia and hypernatremia which is why I know this.)

I have linked some papers in a response to another comment, but here is a youtube video:

https://www.youtube.com/watch?v=0RIskTMLV40

I feel the research is lacking on this because there is a large genetic component. I do not feel LF-EMFs are a danger to everyone, but certain people, like me, with gene changes in CACNA1C, might be more affected by LF-EMFs. It is no coincidence that CACNA1C is also linked to pretty much all the mood disorders.

And I am in no way saying that LF-EMFs are the cause of all mood disorders.

If you have your genome from 23andme; https://promethease.com/

That is just a start, it is useful but incomplete. I usually end up searching for SNPs in my text file based on research I read. I made a bash program which I can use to run a bunch of SNPS of a specific gene.

Oh, also:

https://www.snp-nexus.org/v4/

https://www.uniprot.org/

https://www.ncbi.nlm.nih.gov/snp/

https://smpdb.ca/view/SMP0000017

http://slc.bioparadigms.org/