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Are there SCIENTIFIC disagreements with evolution theory?

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Showing 126-150 of 860 posts in this discussion
In reply to an earlier post on Oct 7, 2012 1:53:41 AM PDT
Sceptic says:
I meant "men show off more" i.e. risky behaviour, see Alice Robert's video on boys skateboarding with pretty girls present. Point proven!
Men Take More Risks Around Attractive Women - Origins of Us - Series 1 - Episode 2 - BBC Two

In reply to an earlier post on Oct 7, 2012 1:55:07 AM PDT
Sceptic says:
Love it!
Next time make it scan and sing it??!

In reply to an earlier post on Oct 7, 2012 2:01:18 AM PDT
Sceptic says:
I think this is still work in progress medically.
There are lots of theories around menopause and ageing. I am not convinced by them but it is a start.
In female placentals, the number of ovarian oocytes is fixed during embryonic development; possibly as an adaptation to reduce the accumulation of mutations.[2] At birth there are, typically, one million ova; when menopause begins, only 400 eggs would have actually matured.[3] The intriguing question is why somatic cells decline at a slower rate and why humans invest more in somatic longevity than other primates.[4]

More important than the question of why longevity has been extended, however, is why selection has not adjusted female life-history to match. The most frequently cited adaptive causes for the menopause are variations on the `mother', or `grandmother' hypothesis. These theories advocate that the high costs attributed to female reproduction could prevail over the benefits of continuous propagation. It is true that with advancing age and decreasing fertility, there is also a corresponding increase of miscarriages and birth defects, such as Down's syndrome.[5] Age is less significant in the increased foetal abnormalities than is the number of the ova left in the ovarian follicular reserves.[6]

A possible explanation is the rate of oocyte depletion. With ova numbers fixed before birth, it is logical to think extension of fertility would require increased oocyte stocks, which may be a limiting factor, or a slower rate of follicular attrition. In humans, the rate of follicular atresia increases at older ages (around 38-40), for reasons that are not known.

Posted on Oct 7, 2012 2:02:54 AM PDT
Sceptic says:
Why do women cease fertility rather abruptly through menopause at an age well before generalized senescence renders child rearing biologically impossible? The two main evolutionary hypotheses are that menopause serves either (i) to protect mothers from rising age-specific maternal mortality risks, thereby protecting their highly dependent younger children from death if the mother dies or (ii) to provide postreproductive grandmothers who enhance their inclusive fitness by helping to care and provide for their daughters' children. Recent theoretical work indicates that both factors together are necessary if menopause is to provide an evolutionary advantage. However, these ideas need to be tested using detailed data from actual human life histories lived under reasonably `natural' conditions; for obvious reasons, such data are extremely scarce. We here describe a study based on a remarkably complete dataset from The Gambia. The data provided quantitative estimates for key parameters for the theoretical model, which were then used to assess the actual effects on fitness. Empirically based numerical analysis of this nature is essential if the enigma of menopause is to be explained satisfactorily in evolutionary terms. Our results
point to the distinctive (and perhaps unique) role of menopause in human evolution and provide important support for the hypothesized evolutionary significance of grandmothers.

Posted on Oct 7, 2012 2:09:46 AM PDT
Sceptic says:
Here is an interesting paper!

The moulding of senescence by natural selection W.D. Hamilton
Imperial College Field Station, Silwood Park, Sunninghill, Berks., England, How to Cite or Link Using DOI

The consequences to fitness of several types of small age-specific effects on mortality are formulated mathematically. An effect of given form always has a larger consequence, or at least one as large, when it occurs earlier. By reference to a model in which mortality is constant it is shown that this implication cannot be avoided by any conceivable organism. A basis for the theory that senescence is an inevitable outcome of evolution is thus established.

The simple theory cannot explain specially high infant mortalities. Fisher's "reproductive value", the form of which gave rise to an erroneous opinion on this point, is shown to be not directly relevant to the situation. Infant mortality may evolve when the early death of one infant makes more likely the creation or survival of a close relative. Similarly, post-reproductive life-spans may evolve when the old animal still benefits its younger relatives.

The model shows that higher fertility will be a primary factor leading to the evolution of higher rates of senescence unless the resulting extra mortality is confined to the immature period. Some more general analytical notes on the consequences of modifications to the reproductive schedule are given.

Applications to species with populations in continual fluctuation are briefly discussed. Such species apart, it is argued that general stationarity of population can be assumed, in which case the measurement of consequences to fitness in terms of consequences to numerical expectation of offspring is justified.

All the age-functions discussed are illustrated by graphs derived from the life-table of the Taiwanese about 1906, and the method of computation is shown.

In reply to an earlier post on Oct 7, 2012 4:53:04 AM PDT
Re Frango, 10-6 2:12 PM: "If cell types differ, ..." Which, of course, they do...
"then there must be an overriding supervisory function determining when to supply telomerase or otherwise control the deteriorative process." Which there may well be; the genes which describe the various cell types may specify this as well as the other properties of cells of a particular organ. But I am not an expert in this field.

"Would an older animal somehow need more resources than a younger one?" Off point. The mechanisms to ENABLE long life require more resources -- such as the extra bases at the end of a DNA strand.

"The "suicide mechanism" concept ..." Technically called "apoptosis". This is a key facility for getting rid of unnecessary cells. An example which I particularly like has to do with the human visual cortex, where the images from the two eyes are combined. This structure is basically a PROM, not unlike the one containing the BIOS in your computer, but instead of blowing fuses to instill bits, nature does it by killing off neurons that "don't contribute to the discussion." Which is why infants need to see a variety of visual effects during their first few months of life, so that this programming can happen.

In reply to an earlier post on Oct 7, 2012 11:23:10 AM PDT
Dr. Paul S. J. Smith:
The summary mentioned in the initial post describes a scientific disagreement that has existed for 50 years and concerns the relationship between the ability of individual organisms to survive and reproduce to the ability of populations of the same species to survive. It is obvious that in most cases a trait that increased survival/reproductive fitness of individuals would also increase the probability that a population of those individuals would survive. The questions are therefore: 1) Do there hypothetically exist organism traits that decrease the probability of population extinction but are simultaneously adverse to individual survival and reproduction? 2) Would the evolution process support evolution of such a trait? That is, can population survival trade off against individual fitness? There are now multiple aging theories that are based on the idea that both 1, and 2 are true, and that specifically a limited life span creates an evolutionary benefit that causes the evolution of suicide mechanisms that limit life (or mechanisms that limit reproduction such as menopause) without having a benefit to individual reproduction. They present arguments in support of both 1 and 2 and claim that various observations fit. These developments postdate Hamilton's 1966 paper and much similar earlier thinking and seem to fit recent discoveries like genes that cause aging.
It seems to me that the current situation is that the scientific community needs to either provide logical arguments as to why 1 or 2 are false, OR, in each case of an observation such as infant mortality, fertility, etc. provide arguments as to how the observation fits or does not fit both evolutionary concepts. It seems to me scientifically ideological to merely pretend that the newer theories do not exist but I am interested in any logical arguments as to why they are invalid.

Posted on Oct 7, 2012 11:25:05 AM PDT
Robert A. Saunders:
Yes, organisms have the ability to kill off their own cells (apoptosis) but do they also (generally, including humans) have the ability to kill the entire organism, technically called "phenoptosis," that is, organism suicide or "programmed death" as opposed to cell suicide? Google "programmed aging."
I agree that in order to live longer, an organism has to have a different design. But is the difference in that it has a different setting in the biological clock that activates the programmed death mechanism or is it merely that longer lived organisms evolved more bases in their telomeres? (See arguments against simple telomere theories posted earlier).

In reply to an earlier post on Oct 7, 2012 8:04:27 PM PDT
Re Frango, above: "do they also ... have the ability to kill the entire organism,..." No. Individual cells will kill themselves when the organism ceases essential functions, such as respiration, and the CO2 level increases unsustainably. Such an ability would provide no evolutionary advantage.

In reply to an earlier post on Oct 8, 2012 3:01:59 AM PDT
You mean like the way prairie dogs or many birds will sound an alarm to the rest of the group, even though it attracts a predator's attention to the individual doing the signalling?

In reply to an earlier post on Oct 8, 2012 8:31:51 AM PDT
Robert A. Saunders: There seem to be many examples of organisms that kill themselves. Multiple modern theories suggest evolutionary advantages to a limited life as justification for biological suicide. Do you have specific objections to these theories?

Posted on Oct 8, 2012 8:46:32 AM PDT
Jason: Yes. If the behavior benefits mainly mate or direct descendants of the animal taking the risk, then the behavior fits with traditional evolution theory as described by Darwin. It is risking its own survival in a trade with survival of its descendants, which could increase the chance it will produce descendants. However, there are all sorts of behaviors and other characteristics of animals that do not appear to benefit it or its immediate family but do appear to benefit a larger group. This is the basis of "group selection" theories that appeared about 1960. There are multiple theories that suicide of older animals can benefit the chance that a population will survive.

Posted on Oct 8, 2012 8:52:40 AM PDT
Sceptic says:
What traits are advantageous to survival and or longevity and which aid reproducton differs in context. In the palaeolithic times up until modern aseptic conditions for birth, giving birth was a significant danger to the mother. Do you see what I mean? The woman personally takes a risk becoming pregnant for the ??species or for her own genes' (50% ) propagation . Mind you I am not sure there was much choice. However birth is still a risk to survival of the mother.

In reply to an earlier post on Oct 8, 2012 9:43:25 AM PDT
Paul quoted from Wiki: In female placentals, the number of ovarian oocytes is fixed during embryonic development; possibly as an adaptation to reduce the accumulation of mutations.[2] At birth there are, typically, one million ova; when menopause begins, only 400 eggs would have actually matured.[3] The intriguing question is why somatic cells decline at a slower rate and why humans invest more in somatic longevity than other primates.[4]

Doesn't the way this is worded, Paul, rather suggest that the writers feel that there is purpose or intention behind these mutations? Am I taking it too literally, in which case it must surely be possible to explain it without the *purpose* inferences.

For example, your quote said: possibly as an adaptation to reduce the accumulation of mutations.[2]

In my elementary understanding of all this, an adaptation is in response to outside influences, not to *look ahead and anticipate*.

Sorry if this is a very basic question. I'm sure you won't hesitate to tell me if it is too basic.

In reply to an earlier post on Oct 8, 2012 9:54:45 AM PDT
Philip--"In my elementary understanding of all this, an adaptation is in response to outside influences, not to *look ahead and anticipate*."

>>JGC: I do not mean to speak for Dr. Smith, but this is a trap that biologists often fall into--speaking teleologically. We say things like, "The giraffe has a long neck so it can browse the leaves of acacia trees," when what we mean is, "The giraffe has a long neck because the ability to browse the leaves of taller plants conferred a selective advantage." My Masters advisor summarized this succinctly: "It is OK to *talk* teleologically, as long as we do not *think* teleologically."

In reply to an earlier post on Oct 8, 2012 11:16:20 AM PDT
Sceptic says:
No, I think you are sort of on to something. We as doctors of medicine, go into the teleological ( Purpose of ...) too easily. There is no a priori purpose, just a better success or survival rate with some trait or another.

In reply to an earlier post on Oct 8, 2012 11:17:40 AM PDT
Sceptic says:
YES,I agree with you.

Posted on Nov 13, 2012 6:09:43 AM PST
Philip: Do you believe in the "grandmother hypothesis?" Humans have a longer post-reproductive life span because grandparents provide nurturing and training to their own direct descendents thus increasing their survival potential. If not, why not?

In reply to an earlier post on Nov 13, 2012 9:54:13 PM PST
Re Frango, above: This may be true -- but to claim that it is deducible is an example of the "post hoc, ergo proper hoc" fallacy.

In reply to an earlier post on Nov 14, 2012 7:02:58 AM PST
Grandmother hypothesis? No, I don't think so. Why wouldn't any kind of meaningful work for *grandma* help her keep active?

In fact, listening to our *grandmother* neighbour *looking after* the grandchildren while the parents are away at work, and the shouting and the tears that result, I would have thought the opposite was the case.

In reply to an earlier post on Nov 15, 2012 5:11:00 PM PST
Frango--It's a hypothesis all right and a reasonable one at that. But I'm not aware of any actual data to support it.

In reply to an earlier post on Nov 15, 2012 5:13:36 PM PST
Philip--I think the point is that having the grandmother nurture the kids is a survival advantage for *the kids* and thereby helps to promote her "nurturing gramma genes" and incidentally her longevity genes.

In reply to an earlier post on Nov 15, 2012 6:44:57 PM PST
Last edited by the author on Nov 15, 2012 6:46:58 PM PST
noman says:
Grandmother hypothesis and primate life histories
Helen Perich Alvarez*

Article first published online: 17 OCT 2000

DOI: 10.1002/1096-8644(200011)113:3<435::AID-AJPA11>3.0.CO;2-O

Copyright © 2000 Wiley-Liss, Inc.

American Journal of Physical Anthropology

Volume 113, Issue 3, pages 435-450, November 20

midlife menopause;postcycling longevity;human evolution;life history theory;senescence

The adaptive significance of midlife menopause in human females has long engaged the attention of evolutionary anthropologists. In spite of extensive debate, the problem has only recently been examined in the context of primate life histories. Here I extend those investigations by comparing life history traits in 16 primate species to test predictions generated from life history theory. In humans, late ages of maturity and higher than expected birth rates are systematically associated with extended postmenopausal longevity. Links among these adjustments on the primate pattern can explain how selection could slow somatic senescence without favoring extension of the fertile span. This conclusion is consistent with the observation that our fertile spans are similar to those of other pongids. The shape of the argument herein demonstrates the utility of life history theory for solving problems of adaptive evolution in female life history traits, with consequences for broader arguments regarding human evolution. Am J Phys Anthropol 113:435-450, 2000. © 2000 Wiley-Liss, Inc.;2-O/abstract

An evolutionary perspective on the origin
and ontogeny of menopause
Barry X. Kuhle ∗
Department of Psychology, Dickinson College, P.O. Box 1773, Carlisle, PA 17013, USA
Received 3 August 2006; received in revised form 30 January 2007; accepted 11 April 2007
The "grandmother hypothesis" proposes that menopause evolved because ancestral middle-aged women gained greater reproductive
success from investing in extant genetic relatives than from continuing to reproduce [Williams GC. Pleiotropy, natural selection, and the evolution of senescence. Evolution 1957;11:398-411]. Because middle-aged women faced greater risks of maternal death during pregnancy and their offspring's infancy than did younger women, offspring of middle-aged women may not have received the needed level of prolonged maternal investment to survive to reproductive age. I put forward the "absent father hypothesis" proposing that reduced paternal investment linked with increasing maternal age was an additional impetus for the evolution of menopause. Reduced paternal investment was linked with increasing maternal age because men died at a younger age than their mates and because some men were increasingly likely to defect from their mateships as their mates aged. The absent father hypothesis is not an alternative to the grandmother hypothesis but rather a complement. It outlines an additional cost-reduced paternal investment-associated with continued reproduction by ancestral middle-aged women that could have been an additional impetus for the evolution of menopause. After reviewing additional explanations for the origin of menopause
("patriarch hypothesis," "lifespan-artifact" hypotheses), I close by proposing a novel hypothesis for the ontogeny of menopause. According to the "adaptive onset hypothesis," the developmental timing of menopause is a conditional reproductive strategy in
which a woman's age at onset is influenced by the likelihood that any children she could produce would survive to reproductive age. Twelve variables predicted to be associated with age at onset and evidence that bears upon the predictions is discussed.

In reply to an earlier post on Nov 15, 2012 6:47:56 PM PST
jpl says:
The war is in your head. There is no war; only ignorance and fear of death.

In reply to an earlier post on Nov 20, 2012 11:34:52 AM PST
Charlie T. says:
Are there SCIENTIFIC disagreements with evolution theory?

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