#sam-e

Methylation risk variant results MTHFR, CBS, COMT, MTR and MTRR I had a DNA test done through ancestry. I sent the results to Life DNA and got some information. They had an offer on methylation genes so I had that analyzed. Out of 10 genes, 7 had risk variants. The variants are not unusual. Some of them lead to an increase in homocysteine which when increased can be a heart attack risk.  I …

Little to nothing is known about the Benefactor save for a few details:

They hide behind a shifting guise of multiple species and gender, while using a female voice

They were able to provide the Initiative with apparently unlimited resources to supplement Garson’s fortune

They knew the Reapers were coming which is their supposed motivation for funding the Initiative

Only a handful of individuals were aware of the Benefactor’s involvement; Jien Garson, Alec Ryder, and (presumably) the first six successors for the position of Initiative Director. All of whom are now dead. Alec was killed in the accident on Habitat 7, Garson was murdered to silence her, and the successors were reported as casualties of the Scourge. But considering Garson was also presumed a casualty of the Scourge, it’s much more likely that they were also murdered to ensure no one in Andromeda knew about the Benefactor’s existence, which left Tann (the eighth-in-line, and someone with no knowledge of the Benefactor) to take up the role of Director.

Now onto why I think the Benefactor is a Rogue AI.

In the novel Mass Effect: Andromeda - Initiation, a kernel of SAM’s AI data is stolen and Cora Harper is sent to retrieve it or see it destroyed before it has the chance to be disseminated throughout the Milky Way. In the end the data is destroyed, but it’s revealed that one of the thieves may have been able make a copy of the data which they could then sell regardless.

Towards the end of the novel, Jien Garson appears in hologram form to Cora Harper where she reveals that there are other groups that want to get their hands on the AI tech and have it be available in the Milky Way. AI is the core of the Andromeda Initiative after all. And Garson states that the one behind it all, the one pulling all the strings and manipulating events surrounding the Initiative, ‘wants it more than any of us, and is willing to do anything to see it come to life.’

Organic-AI integration first appeared in Mass Effect 2′s Project Overlord DLC, which also served as the driving motivation behind Katherine Nigh, or Knight, in the Firefighters sidequest. It’s also an overarching theme in Initiation, which multiple examples of Organic-AI integration ranging from beneficial (Cora and SAM-E) to horrifying (Medea and the Augments). So we can guess that universal acceptance of this integration is key to the Benefactor’s ultimate goal; fleeing the Reapers wouldn’t exactly be unique or interesting, and if all they wanted was to escape the Reapers, why try to leak SAM’s AI data in the Milky Way? Initiation takes place after the Battle of the Citadel and around the time that the Collectors were abducting colonies, so its not like that those events happened before the Benefactor’s ‘suspicions’ about the Reapers were confirmed. They knew the Reapers were coming, and still tried to leak SAM’s data.

As Garson said, the Benefactor is willing to do anything to ensure the dispersal of SAM’s technology and see it fully realised with no restrictions. And probably not for altruistic purposes. More likely the Benefactor has recognised that AI like the Geth would never be accepted by organics (whether this is true or not depends on Shepard’s choices in ME2 and ME3), and that AI needed to try a different tact to have any real and unrestrained presence in the galaxy. So they’re pushing for the Organic-AI integration seen in Andromeda, but they likely have more sinister designs than the co-existence we’ve seen so far between SAM and Ryder.

Their plans are probably more aligned with Medea’s actions, though not in the exact same way. While Medea wanted to kill the personnel of Quiet Eddy and altered lab-grown, cybernetically-enhanced humans into weapons to do so, the Benefactor is likely looking to use organics as physical hosts for AI, enabling them to interact with the world directly.

Additionally, a rogue AI could hack all number of accounts for funds and resources and sufficiently cover their tracks, which accounts for their ‘unlimited’ resources.

The Internet Explorers | 1.01

— The Internet Explorers —

“Its not all about finding the memes out there, its about coming to terms with the memes that are ourselves.”

Sorry I’m late in answering this! I read some parts of Initiation again to answer. Under a cut for spoilers.

http://open.spotify.com/user/miratunek/playlist/7zOrMzFtOWWk0O4a2zoSAR

ocean - Yaeger

Nuggets - Mura Masa ft. Bonzai

VIP Wet Dreams - Tella Viv

Ashanti - Unge ferrari

Keep My Head Up - LNKAY

Not Down 4 Whatever - IMAN

Don’t You Worry - Marlene

Dela På Hälften (RMH Remix) - Parham ft Adam Tensta, Eboi, Nebay Meles

Spela Över - Parham

0400 - Julia Adams

Litt for mye - Lovless ft. Philip Emilio

Champagne - Adoo, Baba Moe, Sam-E

Mirror - Hyuna

Rough Soul - Goldlink ft April George

NA B YA - Peejay ft Zion.T

Bad4U - Loveless ft Awa

Alene - Arif

Vi Burde Ha Vært På Film - No. 4

Blood Under My Belt - The Drums

Gamble - TOKiMONSTA

Ring Ring Ring - Somdef ft. Verbal Jint, Paloalto, DPR LIVE & CAR, THE GARDEN

Where - Laybacksound

MAKE YOU SAY - Rachel Foxx

Beautiful Little Fools - Jorja Smith

Nostalgia - JON VINYL

Froot - Marina and the Diamonds

Make You Love Me - Jarreau Vandal ft Zac Abel

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4439868/#b12

Progress in pharmacology

Historically, there has always been pharmacology; however it wasn't always termed as such. From prehistoric use of plants as medicines, such as aspirin-like compounds from the bark of willow trees or other salicylate-rich plants in ancient Egyptian and Greek times, man has used drugs to control our physiology. Pain management is a good example of how Pharmacology has developed over time – from medicinal products with unknown ingredients that helped, through to chemically-synthesised purified compounds with known structure and activity – pharmacological science has developed our understanding and creation of therapeutically-useful compounds.

The epigenetic era

With recent improvements in understanding of the actual function of the entire genome, pharmacology has to modify itself further to think of tackling diseases not in the conventional ‘drug-receptor’ sense, but in a more ‘global-response’ sense. Drugs may not be designed to be as exact to a particular ligand or specific to a particular gene or protein subtype, they may indeed have to be able to be more broad-acting over a range of epigenetic large-scale events. These larger-scale epigenetic regulatory mechanisms may span more than one gene or family of proteins, they may in fact regulate large groups of genes (Figure 1). Importantly, the advantage to this approach is that often, the epigenetic variations can be the underlying cause of a particular disease, and simply targeting one protein of the multiple pathways involved may be futile. Diseases such as cancer often have many different mutation variations that are difficult to detect, predict and effectively treat, leading too often to relapse. Epigenetics of cancers may be the key to more effective treatments.

Nutrition and the epigenome

There are several theories why a healthy balanced diet rich in fresh fruit and vegetables is good for your health. What may be undervalued as a mechanism by which our diet is able to stave off diseases of old age (cancer, cardiovascular diseases, dementia, etc.) is the role of epigenetics. Epigenetic modifications are heritable with simultaneous dynamics, plasticity and reversibility, and as such they are prone to changes upon external stimuli including diet. One of the strongest links between diet and the epigenome exists in one carbon metabolism where nutrients including methionine and folate are needed for synthesis of a methyl donor, S-adenosylmethionine (SAM) (Stefanska et al., 2012). Any imbalances in the intake of these nutrients will impact the rate of methylation reactions in the human body and consequently DNA methylation patterns and histone methylation marks followed by alterations in chromatin and gene expression. Recent studies of the genome-wide DNA methylation profiles in different cancers reveal that hypermethylation and silencing of genes is only one side of the story. An almost equal number of gene promoters is activated following loss of DNA methylation marks (demethylation) (Stefanska et al., 2011). These genes are putative drivers of carcinogenesis and metastasis. Using SAM as a tool to methylate and silence this group of genes appears to be a tailored way to impair metastasis (Shukeir et al., 2015). The function of SAM in increasing DNA methylation has been also used in treatment of Alzheimer's disease with promising results in animal models (Scarpa et al., 2006). Pharmacological intervention with SAM restores the epigenetic control of the β-secretase gene by hypermethylation and silencing followed by a decrease in formation of amyloid plaques.

The last decade of research has provided us with numerous pieces of evidence supporting the role of many other diverse groups of dietary compounds, particularly polyphenolics, in modifying the epigenetic marks. A few representatives of polyphenols, such as resveratrol, genistein, and curcumin, have been demonstrated to regulate gene expression through affecting several epigenetic components, from DNA methylation through histone modifications to microRNAs (Stefanska et al., 2012). Apart from catechol compounds that reduce intracellular SAM pools available for DNA and histone methylation, polyphenols lack a direct link with the epigenetic machineries and the mechanisms underlying their epigenetic action are yet to be determined. The importance of epigenetic mechanisms in shifting the disease phenotype towards the healthy phenotype will be crucial to the adaptation of these compounds in pharmacological therapeutic approaches. With technological advances and next generation sequencing, the future will allow us to switch from studying candidate genes and single pathways to exploring a comprehensive genome-wide view of epigenetic effects of diets and isolated compounds and elaborating on underlying mechanisms of their epigenetic actions.