All modern human science suffers from this:
http://www.latimes.com/opinion/op-ed/la-oe-teicholz-wansink-dietary-guidelines-20181009-story.html
Sloppy science bears substantial blame for Americans' bad eating habits
https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(18)32840-X/fulltext?utm_campaign=lancet&utm_content=83224321&utm_medium=social&utm_source=twitter&hss_channel=tw-27013292
Association is not causation: treatment effects cannot be estimated from observational data in heart failure.
Eur Heart J. 2018; 39: 3417-3438a counter is here:
https://www.sciencedirect.com/journal/social-science-and-medicine/vol/210/suppl/C
Genetic Misdiagnoses and the Potential for Health Disparitieshttps://www.nejm.org/doi/full/10.1056/NEJMsa1507092
John P. A. Ioannidis, MD, DSc
The Challenge of Reforming Nutritional Epidemiologic Research
https://jamanetwork.com/journals/jama/article-abstract/2698337
In the Era of Precision Medicine and Big Data, Who Is Normal?https://jamanetwork.com/journals/jama/article-abstract/2679460
Why Most Published Research Findings Are False
https://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.0020124
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https://jamanetwork.com/journals/jama/article-abstract/2498853
Clinical Genomics
From Pathogenicity Claims to Quantitative Risk Estimates
Arjun K. Manrai, PhD1; John P. A. Ioannidis, MD, DSc2,3; Isaac S. Kohane, MD, PhD1
Author Affiliations
JAMA. 2016;315(12):1233-1234. doi:10.1001/jama.2016.1519
Fifteen years after the Human Genome Project, genomic variants have been associated with disease risk and outcomes in thousands of publications. Based largely on this literature, physicians who order genetic testing receive reports that indicate whether “pathogenic” variants have been found. This information aspires to form the basis of precision medicine. Knowledge of pathogenic variants is expected to lead to optimal management of individuals as well as their families through recommendations about further screening, prevention, and tailored treatment. However, in this Viewpoint, we suggest that current information on pathogenic variants is typically impossible to act on. This information is often unreliable and generally does not provide a quantitative measure of risk. The information the physician usually needs is the likelihood of disease among patients with the variant (penetrance), and an assessment of whether the genetic profile requires action or not.
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Stepehen C Myers’s Darwin’s something
Does the math
James Tour has said that he does not understand the molecular mechanism by which micro-evolution could happen....
It also seems that evolution is in contra to Entropy, by nature there is less structure and the random events all follow a downward spiral of energy. From where does the structure and energy come from to create evolutionary biology?
http://www.icr.org/article/does-entropy-contradict-evolution/
http://curious.astro.cornell.edu/about-us/136-physics/general-physics/thermodynamics/816-does-evolution-contradict-the-second-law-of-thermodynamics-intermediate
https://advocatusatheist.wordpress.com/category/the-argument-from-entropy/
The counter argument here:
http://curious.astro.cornell.edu/about-us/136-physics/general-physics/thermodynamics/816-does-evolution-contradict-the-second-law-of-thermodynamics-intermediate
conflates different scales. I think they want to argue that the mutations will be ordered because somewhere outside the organism other mutations will be disordered...weird. Here they say:
"However, evolution does not take place in a closed system, but rather requires the existence of outside forces - i.e., natural selection."
This makes even less sense. The random mutations are not random since after they mutate natural selection limits their ability to reproduce...
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Guy Sella (if I understood correctly) here https://www.youtube.com/watch?v=8IDNDaVcuXU (towards the end) says that it would take 5 million mutations to affect the height and roughly half that to affect the BMI.
Yet the number of mutations seems to be in the neighborhood of 1 per generation....
from:
http://book.bionumbers.org/what-is-the-mutation-rate-during-genome-replication/
Given the existence of these various mechanisms of genome rearrangement, it is interesting to consider the extent to which the space of possible genomic mutations is explored. A recurring class of estimates in various contexts, such as the famed Levinthal paradox, center on how well biological systems “explore” the space of all possible outcomes. In many of these examples (protein folding, space of possible genomes, etc.), the astronomical numbers of possible outcomes are simply staggering. As a result, it is easy to wonder how thoroughly the space of possible mutations is “searched” within the human population. We explore how such an estimate might go in Figure 5. Given that there are about 7 billion people on earth, with on the order of ≈10 mutations per generation, we estimate that the current human occupants of the planet explore roughly 7×109x10 ≈ 1011 new mutations during the turnover from one generation to the next. This means that if we focus our attention on any single site within the 3 billion base pair human genome, dozens of humans harbor a mutation in that particular site. As a result, the space of single base pair mutations is fully explored amongst the entire population of humans on earth. On the other hand, if we consider a specific two base pair mutation we find that by random mutation it would require on the order of 107 generations of the human population to achieve it by chance!
And everyone seems to say that environment and pleiotropy (effects of other non directly associated elements) determine the mutation....
So, really there is very little random mutation, and the environment is the main driver of change....
so when sciam says:
But this does not mean that the mutations themselves occurred nonrandomly. In retrospect, it's as if they occurred where needed. But in fact they just accumulated where needed—first one, then another, and another, over very many generations. Getting two or more helpful mutations together in the same genome may take a while, but if they are not lost from the population, then this will eventually happen in a sexual species.they are hiding behind ignorance, 'may take a while', like 10^7 years/generations?
The dependent probability is ZERO that two people will have significant mutations and those mutations will re-enforce each other and not get cancelled out and that will happen for numerous generations (since to affect change numerous mutations are necessary, 5 million if I understood Guy Sella...)
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Now thinking that the problem with the science of evolution is that there are no experiments to prove or disprove a theory. How do you check if the reason teeth are smaller is because Humans developed a tool to crush food? Get two populations of early humanoids and give one set a tool and the other don’t ?
=-=-= a different example:
=-=- an example might be:
https://www.skepticalscience.com/weather-forecasts-vs-climate-models-predictions.htm
So if we measure a lower level fact, that exists in a high dimensional space it does not help us underside a higher level behavior. Unless we assume causative model.
Also we need to assume a distribution, such as a normal/gaussian distribution. So we know how many observations we need.
