guidoLamoto

Assuming you guys aren't just experiencing flashbacks to your days as Hippies in Haight-Ashbury, maybe you're experiencing something along the lines of "binocular rivalry" based on our difficulties in simultaneously focusing on red & blue. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3159595/ Or maybe it has something to do with the miraculous ability for the brain to fill in gaps in the data (Gestalt perception). That probably has something to do with Babe Ruth overcoming amblyopia to become arguably the best hitters of all time.

https://emedicine.medscape.com/article/950587-overview#a5 Her's Disease- several possible defects in the enzyme cascade that activates glycogen phosphorylase-- results in impaired production of glucose from glycogen stores.. https://emedicine.medscape.com/article/119318-overview#a5 von Gierke Dis-- defect is in G-6-Phospahatase, so G-6-P builds up in hepatocyte and is metabolized to lactate. Lactate, in turn, competes with uric acid in kidney, so uric acid levels build up.

Even more basic: consider how fortuitous it was that Gregor Mendel chose the sweet pea and paid attention to six traits that each had only a limited number of alleles and followed simple "Mendellian Inheritance" (isn't that amazing? It was called Mendellian and that was his name too!)...Had he chosen traits with more alleles or polygenic inheritance patterns, he may have never noticed the pattern and we would all have been spared the tedious experience of counting all those damn fruit flies in lab, cutting so deeply into our drinking time in college.

A whole lot easier to just utilize fruit walls like they did in The Middle Ages https://www.lowtechmagazine.com/2015/12/fruit-walls-urban-farming.html

"Survival of the Fittest" actually refers to reproductive fitness: the individuals that can produce more offspring that themselves survive to reproduce are the ones that have the best chance for survival (actually, that's trivially deducible.) Darwin's Theory is really a specific case of the more general role of probability in Nature; things exist this way in Nature because they're the most likely to exist. Random mutations are always occurring. Most are neutral; some are deleterious (worse) and occasionally some are immediately successful. More often than not, the neutral ones plod along in low numbers in the population until the environment changes, and then they can become beneficial ones. At that point, they will be selected and increase their numbers in the gene pool. The previously more efficient genes will then become the less efficient ones. Type II Diabetes is an interesting case illustration. Once a pound of time ago, in the jungle where calories were hard to come by, an individual who could maintain body weight on only 800 cal per day would have a decided survival advantage over those who needed 1800 cal/d. Those genes were selected and were represented by a large gene frequency in the pool....Fast forward 40,000 yrs and those descendants with the "easy keeper genes" find themselves in an environment where they can easily smother themselves in YoHos & DingDongs, and we see their BS rise to 250 and they have CAD before you know it. Those easy keepers were the ones who were insulin resistant-- good in the jungle, bad in civilization. If society collapses or Bloomberg is elected president and outlaws BigGulps, they will once again have the advantage in survival. The more varied & diverse the availability of alleles in the gene pool, the more likely a species will survive a change in the environment. It's the generalist species that survive or produce the next evolutionary stock and the specialists are usually doomed to extinction.

"Efficiency" is a relative thing. If you had a race engine and wanted a few more HP, then it's more efficient to slightly modify the existing engine than to completely re-design and build a whole new engine. And when it comes to evolution, given the need for random mutations to effect major changes, it would be almost impossible to count on major revisions to make the recurrent laryngeal nerve follow a shorter course. Not to mention, when it comes to morphology, our DNA complement is more of a general, suggested plan than a rigid prescription. Many of the details are left to physical constraints of the space & stresses involved and physical demands of other genetic determinants...Cf- binding feet or skulls to effect final shape & size (as a poor, contrived analogy).

A few eclectic points: Half the world's population lives within 50 miles of a sea shore. People in Manhattan live 50,000/sq mi and apparently like it that way. Some of us live 5/sq mi and think it's too crowded. Can anyone name a natural resource we are in danger of depleting in the next, say 300 yrs? As the supply of a resource dwindles, it's price goes up, so demand goes down and the resource lasts even longer. We now produce more than enough food to feed our 7.5 B people. It's estimated we waste half of it. People today only starve due to local, politically impaired distribution systems. The agronomists tell us American farmers could increase yields by 25% if they all properly installed good drain tile systems.. Food's not a problem at this point. In the "Survivalists" Forums, they often talk about the " when the SHTF" situations and how they can survive because they've taken all these precautions, put up stores and can produce much of their own food. I always point out that, before they get too full of themselves, the Amish have been living that way for centuries and are much better at it. When the EOTWAWKI (End of the World As We Know It) does occur, all those Third 'World, subsistence living types will live on as if nothing happened. Mankind is safe. Industrialized society/ urban living may come under some challenges. edited to add: It's been the fad lately to talk about "sustainable agriculture." There's a reason The Fertile Crescent ain't so fertile anymore, nor is N.Africa capable any longer of being the bread basket of Rome, or why Daniel Boone & Davy Crockett kept moving west every few yrs: "organic farming" quickly plays out the land. The only sustainable ag is modern ag using inorganic N fixed by the Haber-Bosch Process. Using manure as a soil amendment only shifts fertility from the pasture to the row crops while progressively decreasing fertility of the pasture. It doesn't increase over-all fertility and is limited by the finite efficiency of natural soil microbes.

A sex linked trait is determined by gene loci on the X or Y chromosomes, whereas a sex influenced trait is one whose basic loci are not on the sex chromosomes but whose penetrance or expressivity is influenced by factors such as estrogenic or androgenic hormone levels. An example of a sex linked trait is color-blindness, while traits like coarseness of body hair, bone density or muscle strength is closely associated with absolute or relative levels of estrogen & androgens....It's been said that embryologically (& figuratively) speaking, we all start out as females, but those that start making enough testosterone at the right time become males.

I agree, it's a poorly conceived question, unless there really are two populations of yeast with identical loci & associated alleles, but loci & chromosome numbers arranged differently. Then it would be a matter illustrating the difficulty of defining "species." If the two populations indeed had all the same loci & alleles, then they would be phenotypically/biochemically the same, although with differing chromosome numbers, they couldn't interbreed without producing some confusing polyploidy. edited to add: Reproductive isolation is the first step on the road to speciation. OTOH- as one who sees the veracity of The Gaia Hypothesis, to me, it doesn't make any difference one way or the other

Mechanism may unclear on the details at the specific biomolecular/genetic level, but in general we can say it has to do with recruitment/inhibition of genes &/or certain enzymes. For example, Cushing's Dis (excess cortisol) pts characteristically show loss of fat stores in the limbs and increase in fat stores in the cheeks and torso (centripetal obesity & moon face). Physiol. stress increase epinephrine levels which in turn influence glucagon & insulin levels which in turn influence glucose & fat metabolism.

You've brought up several good points in your last several posts. Nutritional studies, thanks to those inconvenient ethics rules, won't allow us to do real controlled experiments anymore. (I'm sure this is why our prisons are so overcrowded now-- they can't volunteer as guinea pigs anymore to shorten their sentences.) Most studies rely on questionnaires and the reliability of subjects' memories: "How much smoked meat did you consume everyday from June of1982 - Sept of1996?" as if they could remember and never changed their diets. Other studies with more closely prescribed diets are short term (that's how finding works) and often show any changes occurring over the first few months return to baseline levels after one year-- ?compensatory mechanism as you suggest? You bring up a good point about some studies showing chol levels actually rising on low carb diets--I don't think it's been studied, but could physiological stress cause chlo levels to go up-- like wbc, sed rate, ferritin levels etc?..That would explain the small but definite risk of CAD vs chol levels--- oxidative or mechanical stress on the intima causes "cracks" which then recruit the healing response (fibrinogen-fibrin-WBCs, coagulation cascade and chol incorporated into the "scar?"....Hi chol may be the result, not the cause of arteriosclerosis. After 45 yrs of medical practice, I'm thoroughly convinced the leading cause of HTN is worrying about your chol level.

Exactly. Sugar cane & sugar beets make equal parts of fructose and glucose and combine them to make sucrose ("table sugar"), while corn makes 55% fructose and 45% glucose and doesn't combine them into a disaccharide. It's economically advantageous for may manufacturers to use the corn sugar compared to sucrose. We quickly turn sucrose into 50% glucose/50% fructose. Hexose isomerase facilitates the conversion of fructose to glucose intracellularly. It doesn't even require an energy of activation and can be considered a spontaneous reaction. Where we put on additional fat stores is influenced to a great deal by hormones/genetics. Those who tend to have increased lipogenesis/ increased storage of fat in the pre-abdominal area tend to be the ones with Metabolic Syndrome (elevated chol, decreased insulin sensitivity, abd obesity, increased risk of CAD) so it's difficult to say that specifically fructose contributes to that or merely the total carb load.

Here's how it actually works: First, there's a difference between pain (simple spinal reflex arc) vs suffering (conscious/subconscious (?) acknowledgement and reaction to a painful stimulus). A pain reflex (stimulus-->reaction) has survival value. Step on a sharp object and quickly be able to withdraw may lead to improved chances of survival. Pretty obvious. The stimulus excites a receptor, which sends a message to the spinal cord, where a synapse relays the message to the appropriate nerve to elicit the appropriate response. Afferent/efferent pathways, if you wanna get technical....Touch a hot stove and you withdraw your hand so fast you may hit yourself in the chest, for example. That's the pain response....A second later, you start hopping around and screaming. That's the suffering response, after the pain stimulus message was sent not only to the spinal cord, but forwarded to the brain...That's for acute pain-- single stimulus/single response. Chronic pain involves the ongoing stimulation of nerves-- chronic arthritis or a broken bone, for example. There's the immediate reflex and then there's the cerebral message/response arc. This elicits the phenomenon of "extinction." The brain sends a message back down to the original receptors "We got the message, You can take a break now." Negative feedback. Compare it to the experience of walking into a musty basement and immediately being hit by the smell of mold. It doesn't take long for you to forget all about it as you continue your work there Just as, say, the immune system works well to help us survive, sometimes the balance between the destructive & constructive forces of the immune response is not perfectly tuned and we get auto-immune diseases, some people have an apparently genetic insufficiency of the extinction portion of the pain system. People with fibromyalgia have unusually sever and prolonged problems with pain. This is somehow related to their metabolism of neurotransmitters such as serotonin. endorphins &/or adrenergics. They often also suffer sleep problems, anxiety &/or depression-- other situations of disordered neurotransmitter levels. Positive feedback at work. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2821819/

I'm saying there's a difference between establishing that the results of a study are scientifically valid vs establishing that they're useful in practical matters. Another example: suppose we test using a regulation baseball bat vs a corked bat. Let's say we find that the corked bat consistently adds 5 feet to the flight of a fly ball...In a game situation, how many flies fall 5 ft short of the fence?..and for a fly ball that would have gone over the fence with a reg bat, anyway, the extra 5 ft from the corked bat is still a home run-- no extra credit for how far into the stands it goes. (For you physics purists, I admit this is a disingenuous argument. -- it has been studied and the ball actually goes farther with the reg bat. Hitting a ball is essentially an elastic impulse and represents conservation of momentum, not addition of force...The increase in bat speed attained by corking is more than offset by the loss of mass. "The Physics of Baseball" is an interesting read.) The cholesterol molecules measured in your blood are not the cholesterol molecules you ate. The cells (mostly in the liver) manufacture cholesterol using the basic building block Ac-CoA derived from the carbs, fats & protein in your diet. Cholesterol itself is essentially a raw material used as the basis for the steroid hormones and is found in the blood en route to the assembly lines that will use it in the various glands.....How much chol the liver dumps into the blood depends mostly on the genetics of chol synthesis, but also, of course, on the availability of raw material--- just like two different auto assembly lines will produce cars at rates determined mostly by the way the lines are set up and manned, but also on how much raw material each has to work with. Union rules and company incentives (enzyme inhibitors & stimulators) may also regulate production rates. The studies done on diet vs chol usually show only small changes in chol levels over the first several weeks to months, with return towards previous levels after 6 months of the continuing diet. ...You'd expect that if it was in fact a self-regulating system. ...It's not nice to mess with MotherNature

I was just making up numbers for the sake of the illustration. If we really applied Student's t-test, I rather doubt the 80/78 result would prove to be significant-- it'd be pretty likely a difference of 2 out of 80 would be random variation. Maybe I should have used as example a study of a drug vs placebo-- and a 70/80 result would mean the drug works but not much better than nothing, while the 80/40 result would mean it was worth taking.....The real point is that sometimes statistically significant results are represented by numbers so small that they don't make any practical difference.

Gladly. Statistical significance is a mathematical treatment of test results that gives us an idea of how much we should trust the results. Eg- we treat 100 pts with drug A and 100 pts with drug B. After the trial, we find that 80 pts taking A survived and, say, 0nly 40 pts on B survived. After the math is done, we find that the difference is "significant at p =0.05 level" Ie- we''d get similar results if we repeated the test in 95% of the trials. I'd certainly want to be given drug A if I had that disease. OTOH- let's say the results were 80 for A and 78 for B, but the statistical analysis still said it's significant at the p = .05 level. We may make the value judgement that that's not clinically significant....If A cost 10x more than B, we'd probably have no reservations about using drug B. In the matter of diet & chol, they may have easily shown that a change of 10mg% is statistically significant, but risk categories are based on changes of 50 -100mg% so 10 is of no consequence-- clinically insignificant, ie - of no practical value. Remember that if statisticians torture the numbers long enough, they can get them to confess to anything.

Maybe you're confused about the difference between statistical significance and clinical significance. Dietary studies typically show changes of chol of only 10-20 mg%- - that won't change your risk category. ...LDL levels have only a correlation coefficient vs MI of 0.3 --not all that great as a predictor. At least the LDL/HDL ratio has a coeff. of 0.5-- better, but I still wouldn't bet on any given pt's future based on that. BTW- statins have a really miserable success rate in preventing 2nd MIs (no effect at all in preventing 1st MI)- The Need To Treat number is 45-- you gotta treat 45 pts with statins to prevent one additional, 2nd MI. Even that "improvement" is better explained by the anti-inflammatory & anti-coagulant effects of the drug. In the few head to head comparisons of the various statins, outcomes were not correlated at all to chol lowering effects.

a) Better read the article you just quoted. b) https://health.clevelandclinic.org/why-you-should-no-longer-worry-about-cholesterol-in-food/ Plenty of articles in the research literature showing low carb diets lower chol levels better than low fat diets BUT-- neither lowers chol levels enough to move you from a higher risk category to a lower risk category, ie-- no practical benefit. Some diets, like the low fat diets, can lower LDL a little, but also lower HDL levels too-- theoretically increasing your risk profile. BTW- there was a statistical analysis of the chol research lit about 30 y/a-- it found that those with chol level of 200 lived only an average of 4 days longer than those with chol of 300. (!!) BFD.

Actually, physiological studies show that the differences in metabolic rates between those who gain weight easily vs thinner people are minimal. The real differences are in the genetics of the recruitment/inhibition processes. You may find my post on triglycerides interesting. ...Some people are more efficient at burning calories and store them more easily (analogous to "easy keepers" among horses). Tyoe II diabetes (insulin resistance) seems to fall into this category, but that's a complex genetics situation, probably representing a common final pathway of many different genetic factors.

https://en.m.wikipedia.org/wiki/Lipogenesis Probably more than you want to know. In a nutshell: fat metabolism is controlled mainly by insulin interacting with several other hormones and transcription factors to regulate the genes responsible for making or using triglycerides. (The evidence that high triglyceride levels are correlated with arteriosclerosis is pretty flimsy.) Eating fat doesn't make you as fat as eating an equal amount of calories in carbs-- Carbs stimulate more insulin secretion which sets off the enzyme cascade to store more fat and to burn less fat. A simplistic explanation on the evolutionary value of such a system: our ancestors roaming the hot areas of east Africa where we evolved, would do better if they stored less highly insulating fat, so when times were good and game (hi fat source) was plentiful, they could switch off their fat-saving genes. When hunting was bad and they were forced to eat weeds ( hi carb source), they had a better chance of surviving until their next good meal (meat) became available if they would switch on the fat saving genes. It appears insulin is the chemical signal for this. Blood levels of triglycerides are defined only after an 18 hr fast. Triglyds can be high after eating a fatty meal (up to a couple hundred mg%) and are meaningless. For high levels after an 18 hr fast, there is essentially no evidence that it correlates at all with arteriosclerosis in men, and only a very weak pos. corr. for older women...There's also the genetic condition of Familial Hypertriglyceridemia where levels are in excess of a couple thousand mg%. Those people have a slightly elevated risk of heart disease, but a very high risk for pancreatitis. Cholesterol levels are an entirely different matter, controlled almost exclusively by genetics, not diet. Critical analysis of the data shows that, in fact, only those with HDL (the good stuff; H for Happy) levels below 25mg% are at significant risk of early heart disease....and LDL (the bad stuff; L for Lousy) correlate rather poorly with risk. This whole concept of diet and arteriosclerosis is complicated by pharmaceutical profit motives and malpractice risks. It's generally not publicized that the benefits of regular exercise completely offset the negative risks of hi chol levels, or that higher levels of carnitine and CLAs in the diet (only found in meat) are highly correlated with improved risks. Best advice: do what your mother always told you-- eat everything in moderation. Maintain a normal body weight and exercise regularly. The rest is in your genes and you can't change that.

A couple thoughts that may help some appreciate the concepts of an expanding universe & Hubble's observations: The Big Bang Theory says that if we could travel back in time towards the origins of the universe, all matter, energy, space & time would be concentrated in a very small area (Can we get back to Time Zero, or only approach it asymptotically?) At the moment of The Big Bang, all matter and energy started flying outward like shrapnel from an exploding grenade, but keep in mind that time & space itself started expanding-- so it's like watching someone on the moving sidewalks at the airport, too. Now take a balloon and draw a couple dots on it and then fill it with more air-- as the balloon gets bigger, the dots move farther and farther apart from each other. Hubble, using the concept of red shift, was able to observe that. ...Now consider an exploding grenade-- all the pieces of shrapnel started moving out from ground zero at the same time, but some fly further than others. Those that land farthest away must have been travelling the fastest....Because space itself is expanding, and the space farthest away, just like the farthest shrapnel is expanding the fastest, so the farthest galaxies, travelling at acceptable speeds in their own piece of local space, like the pedestrians on the moving sidewalk, look like they're moving faster than light to us in our own frame of reference.

I'm a firm believer in the KISS system: Newton's Law states that the total momentum vector of a system remains unchanged in the absence of outside forces.....In the balloon rocket system, the total F vector is 0 as the balloon sits at rest. Release the potential energy of the pressurized air and the balloon of course shoots off in one direction with momentum M(1) = +m(1) v (1), while the air expelled shoots off in the opposite direction with momentum vector M(2) = -m(2)v(2) and M(1) + M(2) = 0 The total force vector is still 0 with +F of the balloon balanced by -F of the expelled gas. Total force & momentum of the system are conserved. Back to the original question about a pump. Let's change the example slightly to better illustrate the workings of the system: let's visualize a nurse filling a syringe from a bottle of medicine-- you know-- how they hold the bottle up and draw back on the plunger of the syringe....The nurse is supplying a new force to the resting syringe/bottle of liquid system. If she held the bottle with syringe stuck in it in only one hand and pulled, the whole thing would move and no liquid would be drawn into the syringe...Instead, she holds the bottle in one hand and the plunger in the other. As she draws back on the plunger (action) she has to push back on the syringe with the other (equal & opposite reaction). ..The fluid pressure, or momentum of the fluid in the bottle, if you prefer, goes down as the momentum/pressure goes up in the syringe. Total system state still conserved...For a mechanical pump and tote system, the reactionary force acts via the pump's anchoring bolts or maybe just friction on its base.

The inspector guy who goes around checking to make sure you didn't tear that tag off your pillow or mattress?

The real question is not "does it have an effect" but rather "if it has an effect, how important is it?" For instance, the question of cell phones causing brain cancer has been brought up and studied. All studies seem to show that there is no statistical difference in disease rates among users of cells vs non-users-- but we're talking about very low rates, so a single case "actually caused" by the radiation" would appear as just a random variation in the data....The risk is so low. it's lost as noise in the data. When confronted with questions about health risks, I always like to point out that about 1 in every 10,000 Americans gets slaughtered in a car accident every year, yet nobody avoids using a car because of that level of risk..How many people die of exposure to glyphosate, GMO foods etc etc or cell phones every year? Should you waste time worrying about those when using a car doesn't warrant concern?

Very impressive experiment-- the problem is, it demonstrates the concept of heat capacity (specific heat) and not the GH Effect. Heat capacity of pure co2 is about 85% that of ambient air (look it up yourself) so a given amount of energy will cause about a 15% higher temp rise in a volume of co2 than an equal volume of air. Now in the demonstration above, we don't know the actual [co2] in the exp bottle, but it's less than 100% and more than that in ambient air Let's say it's 1/3rd -- so we should expect a rise in temps around 5% more in the exp vs control--That's just what we see 306 degK vs 317deg K....306/317 = 95.6%. …. ….We won't get into details about most of the energy transferred from the light source is in the visible range (our hands are sensitive to IR and I doubt you'd feel much heat coming off the bulb at the distance of the bottles) and that co2's GH Effect is mediated thru IR. ..Actually, virtually all the heating done on the bottles' contents is via conduction, not radiation-- the bottle is heated by the lite and then conducts it by direct contact to the internal gas. The GHG Theory is predicated on the concept that monoatomic molecules can absorb energy only by conduction and that increases their translational (kinetic) energy. They move faster. Diatomic molecules can capture energy to cause them to increase translational &/or rotational energy, and tri (or more) atomic molecules can also vibrate and absorb a photon at its resonant frequency....Keep in mind that temperature is a measure of the average KINETIC energy of the gas-- PV = nRT --> T = V x P/nR. That means only increased translational energy produces rising temps.... …. This implies that the additional energy absorbed by GHGs (for co2 that's IR only at ~ 5u) does not actually make the air temp rise. What it does do is re-direct the IR that's on its way from the surface off into space, delaying its exit to space. Once absorbed by the gas, it is immediately re- radiated at the incident wavelength, but at random angles-- just as likely to be sent off towards space as it is to be sent back down towards its sourse (This brings up an objection on the quantum mech level-- we have a deterministic mechanical model acting on a QM system. But I digress...) ...GHG Theory calls for no significant warming during the day, but slower cooling at nite. A better experiment would be to take the exp hi co2 bottle and heat it to the same temp as the control bottle, then see which one cools off faster. I would point out that, with IR travelling at the speed of light and an apparatus only a few cm big, we wouldn't be able to measure the difference. That doesn't deny the theory, it just doesn't offer the proof we need. This is why I stated previously that there is not good exp evidence to support GHG Theory, only correlations & computer art work. Now you can check the UAH or Roy Spencer's (director if the UAH satellite program) blog to find that over the 40 yrs of the satellite record, the average planet temp has risen ~0.6deg (0.13 deg C /decade)...The tropics have warmed only minimally (a few 1/100ths of a deg), while the temperate zones have warmed only at nite (0.5deg), but the polar regions have warmed 4+degC. Regardless of the source of warming, we'd expect this-- energy flows from hi to low...So what is the significance to the biosphere? Nothing. ..Down here where most of us Earthlings ( I'm including all life forms) live, no species or biome can sense a difference between today's average temp of X deg vs next decade's temp of x + 0.13 deg with almost all of the excess in the polar regions. In an earlier post I compared rain forests vs deserts/ co2 vs h2o and was criticized that that represented local conditions, not "average." Reminds me of the story about the two statisticians who went deer hunting. After hrs of waiting patiently in their cold, damp blind, a big buck finally presented itself. The first guy took a shot but missed four ft to the right. The second guy took a shot but missed four ft to the left. Jubilantly they jumped up, high-fived each other and triumphantly shouted "We got him!"...What exactly does "average world temp mean? Someone also objected earlier to my method of estimating SD. It's a well accepted method, based on the definition & geometry of the normal distribution: https://www.thoughtco.com/range-rule-for-standard-deviation-3126231 SD ~ range/ 4 edited to add: I didn't bring up the matter of statistical analysis in order to deny that's there's warming, but to point out the difficulties in proving it's not just random variations..... If it were random, then we should see random alternations of hotter and colder yrs, but we don't . We do see what appears to be (pseudo) cyclic variations over time. We would expect this because climate is certainly related to many cyclic phenomena that are quite obvious: rotation of planet about its axis, orbit of planet about the sun, precession of planetary axis and precession of elliptical orbit, orbit of solar system about galaxy, solar cycles, various oceanic cycles etc Fourier Analysis could come up with a formula that could accurately reproduce a graph mimicking the historical temp record.-- even "explaining" the apparent step function jumps we see so prominently and can't explain deterministically. ...and then there's the non-cyclic factors that have major influences-- randomness of volcanic eruptions and other influences of plate tectonics....It's a system governed by mathematical chaos and complexity. No single factor, like [co2] can explain it simplistically. In fact, it looks like [co2], while technically applicable to the problem, is insignificantly influential (at current and predicted future levels) and can be ignored in our calculations, just like we can safely ignore air resistance and relativistic factors in predicting the trajectory of a bowling ball dropped from the Leaning Tower. The 100+ computer models predicting dire consequences of rising co2 have all selected co2 sensitivity factors of 4-6 deg C/ co2 doubling. That would appear to be much too high. Note the poor predictive values of their models over the last 10-20 yrs. Several physisists have calculated the value to be 1.6 -7 deg C based on energy budget considerations-- IF all the warming seen is due to co2. For instance-- many others if you care to search it. https://wattsupwiththat.com/2020/01/13/climate-sensitivity-in-light-of-the-latest-energy-imbalance-evidence/ It's ironic that The True Believers always accuse the skeptics of ignoring the science. Almost all of the retorts to my posts have been of the form "Oh, Yea?" I don't like talking anybody out of their religion. It serves a useful purpose for them, I guess. I won't post any more on this topic.