Tracking Polynesian Roots

Posted on November 17, 2016 by gcochran9

That late-arriving ~25% Melanesian fraction of autosomal ancestry came from somewhere – somewhere in particular, some population from New Guinea or (more likely) the Solomon Islands. People have inhabited the Solomons for a long time, surely long enough to develop distinct genetics on different islands – so we may be able to find the source. Their language, whatever it was, may also have left a trace in the Polynesian languages.

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21 Responses to Tracking Polynesian Roots

  1. whyteablog says:
    November 17, 2016 at 10:33 pm

    A Polynesian language family of which some island is the Urheimat?

    Reply
  2. BRF says:
    November 17, 2016 at 10:41 pm

    Clickbait form the Daily Mail, but nicely photographed. Quite a variation in facial types or is that my euro centric view?
    http://www.dailymail.co.uk/news/article-3945366/Inside-isolated-Indonesian-Dani-tribe-women-expected-amputate-finger-relatives-die-men-eye-catching-outfits.html

    Reply
  3. whyteablog says:
    November 17, 2016 at 10:57 pm

    I remember you pointing out that Tonga was one of the first stops- and Tonga pretty much has its own branch of the Polynesian language family. This language family is so recent that different Polynesian languages even have a common term for their urheimat.

    Hm…

    Reply
  4. alcoholicwisdom says:
    November 18, 2016 at 3:55 am

    Why are Polynesians so strong physically?

    Reply
    • dearieme says:
      November 18, 2016 at 6:04 am

      So they can play rugby.

      Reply
      • syonredux says:
        November 18, 2016 at 2:57 pm

        Also American Football:

        “When University of Washington Defensive Tackle Danny Shelton arrived for the NFL Draft in Chicago wearing traditional Samoan dress and almost choked the life out of Commissioner Goodell in an on-stage hug, it symbolized the amazing dominance that one tiny island and its’ Polynesian neighbors have in NFL football. Five Polynesian players were selected in the first 66 picks of the 2015 NFL Draft, the most ever for the first three rounds. Over 70 players in the NFL are of Polynesian descent. There are 30 players from American Samoa in the NFL and more than 200 play Division I NCAA Football. A Samoan male is 56 times more likely to play in the NFL than an American non-Samoan.”

        http://www.forbes.com/sites/leighsteinberg/2015/05/21/how-can-tiny-samoa-dominate-the-nfl/#73e6d151d48e

        Please remember to close your eyes and say “HBD isn’t real” five times.

        Reply
        • silcon_valley_prole says:
          November 20, 2016 at 9:15 am

          I grew up in a part of the San Francisco Bay Area among a relatively high population of Tongans. You learn HBD on the street. I saw these guys in fights ripping out fence posts and hitting each other across the heads. I saw a 15 year old Tongan beat a grown white man ex-con with no problem. It was out of the question that I would ever fight a Polynesian growing up

          Reply
  5. Martin L. says:
    November 18, 2016 at 10:57 am

    Greg, admittedly this is a thread hijacking but you haven’t commented on transmissible cancers in quite some time. The mainstream leftist hivemind media is actually beginning to pick up on the topic–which shows that this is a biological reality that can’t be ignored:

    http://motherboard.vice.com/en_uk/read/to-understand-contagious-cancer-is-to-understand-cancer

    I think that this is happening a HELL of a lot more commonly than the MSM/SE is letting on to us.

    My strong hunch is that a whole lot of cancers are similar to prions–capable of spontaneously developing, but fully transmissible (under the right circumstances) after that, and quite likely able to jump species barriers in some cases. We have identifiable strains of breast, ovarian, colon, etc. cancer–what explanation for this is there other than that somehow, cancers have a life outside of their first host and are managing to propagate themselves in a sustainable fashion?

    Reply
    • dearieme says:
      November 18, 2016 at 11:03 am

      A friend suggested recently that Alzheimer’s may be the result of an infection.

      Reply
      • Martin L. says:
        November 19, 2016 at 2:18 am

        “A friend suggested recently that Alzheimer’s may be the result of an infection.”

        This is highly likely and mainstream science is warming up to it, but so far I’ve never seen someone delineate whether the actual brain damage of Alzheimer’s is caused by the pathogens themselves, or the immune system’s overzealous reaction to them.

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        • dearieme says:
          November 19, 2016 at 8:23 am

          Her suggestion was that the old tend not to drink enough, to avoid getting up in the night to pee, or to avoid wetting themselves, and thereby are particularly prone to bladder infections and the like. (I have no idea whether that line of argument has any merit.)

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          • Martin L. says:
            November 19, 2016 at 10:25 am

            That sounds ridiculous to me. I thought that the current thinking is that Alzheimer’s could be the result of long-standing chronic infiltration of herpesviruses, etc. into the brain.

            Reply
            • dearieme says:
              November 20, 2016 at 5:46 am

              Until someone identifies the microorganisms responsible, who knows? It’s like the germ hypothesis for heart attacks: it’s in better agreement with the epidemiological evidence than the lipid hypothesis is, but until somebody identifies the hypothesised microorganisms, it’s all up in the air.

              Reply
    • gcochran9 says:
      November 18, 2016 at 11:51 am

      “We have identifiable strains of breast, ovarian, colon, etc. cancer”

      In the sense you mean, we don’t. At least no one has ever seen it.

      Probably the most interesting thing about a transmissible cancer is that it could well evolve to act in a way very different from a standard cancer. For example, limited virulence. Maybe chronic.

      Reply
      • Martin L. says:
        November 19, 2016 at 2:39 am

        Thank you for replying to me, Greg.

        “In the sense you mean, we don’t. At least no one has ever seen it.”

        Well, we have some very distinct subtypes of types of cancer that repeat themselves in recognizable form across the population–small-cell lung cancer, triple-negative breast cancer, etc. It’s hard for me to believe this can be so without some mechanism for the cells, or a genetic or chemical blueprint for these specific types of cancer, to exist outside of the host for awhile.

        “Probably the most interesting thing about a transmissible cancer is that it could well evolve to act in a way very different from a standard cancer. For example, limited virulence. Maybe chronic.”

        Greg, you’re a genius! I never even thought of this, and it makes perfect sense. Perhaps some of the chronic conditions that plague us today already are actually unrecognized low-grade cancers that function as a parasite rather than a parasitoid upon their host. Maybe we even have limited-potency prions out there. Possibly some non-fatal degenerative brain disorders (the aphasias, some of the frontotemporal dementias, some cases of schizophrenia, etc.) could actually be attenuated prion conditions?

        Then again, there is no real need for a ruthlessly effective pathogen to moderate itself if it can survive indefinitely outside of a host at full strength. Examples would be spore-forming bacilli and the prions. CWD particles persist basically forever in soil and plants that grow out of soil contaminated by infected urine, saliva, blood, or the decomposing corpses of herbivores that died from it and as far as we know do not degrade at all over time. If this were true of cancers, it would give extraordinarily lethal cancers such as glioblastoma, ovarian, etc. an unlimited free pass to kill all their hosts. (BTW, I see a good chance that glioblastoma could be yet another unrecognized prion disease, but I digress.)

        Alternately, transmissible cancers could carry on through carriers, or intermediate hosts that are affected in a different way than the end host, similar to the life cycle of numerous parasites. For instance, a very aggressive infectious breast cancer could effectively spread to men, who only get a relatively mild form of prostate cancer late in life as their manifestation of it, but who nonetheless can spread it to women (during sex?) who get it in its original full-strength manifestation. Or, possibly, a transmissible pancreatic cancer cell (highly lethal) only causes type II diabetes in some “lucky” folks who catch it? Or, a household pet could catch a cancer cell, have it replicate to some extent but never develop clinical disease from it at all because their immune systems can corral it to a good degree, but then give it to an unsuspecting child with a slobbery lick, with his or her underdeveloped immune system, who then goes on to come down with osteosarcoma as a teen, etc. (I seem to recall osteosarcoma is pretty common in dogs.)

        So many huge questions that the establishment is completely ignoring…

        Reply
        • gcochran9 says:
          November 19, 2016 at 1:15 pm

          The fairly distinct types of cancer you’re talking about are not genetically identical. Common mechanisms. Like for example retinoblastoma, caused by mutations of a particular tumor suppressor gene.

          Then again, it couldn’t hurt to look.

          Reply
          • Martin L. says:
            November 21, 2016 at 1:09 pm

            “The fairly distinct types of cancer you’re talking about are not genetically identical. Common mechanisms.”

            In the three or so cases where we know of direct person-to-person transmission of non-HPV, non-transplant cancers (the needlesticks/scalpelsticks), the neoplasm growing in the medical worker’s wound site consisted of their own DNA, not the patient’s. (I will try to find the link that says that.) That means that the cancer was able to not only evade the new host’s immune system, but also to successfully induce their DNA to begin misfolding on its own and keep on replicating that indefinitely with those errors, like when a prion is transmitted.

            Certainly, I think we can all agree that cancer has extraordinary properties compared to all other known microbes. I seem to recall an algorithm that was devised that demonstrated that small-cell lung cancer cells were capable of creating an infinite number of pathways of resistance to drugs–meaning, of course, that eventually they would have immunity to all imaginable cancer drugs that we could ever throw at them. Compared to that, doesn’t our own foreign-protein recognition system seem like a cakewalk to beat?

            Reply
          • Martin L. says:
            November 21, 2016 at 1:13 pm

            Here, Greg, I found one of the links that talks about person-to-person cancers being able to change the new host’s genetic material and not just propagate themselves in them. Of course, the author of the article is a “don’t panic and trust us” establishmentarian type:

            http://www.abc.net.au/science/articles/2012/10/23/3616950.htm

            “In the case of the surgeon, it turned out that the cancer itself had performed a genetic miracle and incorporated some of the surgeon’s genes into itself.”

            Yeah, and very few Muslims ever dream of terrorism…

            Reply
  6. Tocharo-Lusitanian says:
    November 22, 2016 at 4:45 pm

    I would even claim that it is quite likely that the original bearers of the Lapita culture did not speak CEMP but another kind of Austronesian. If the original Lapitans would have been, let´s say 10% Melanesian, I would have favored the “established” model of the Lapita culture being the vector of Oceanic languages.

    Reply

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