How long does it take for a person to lose all offsprings due to inheritance?

How long does it take for a person to lose all offsprings due to inheritance?

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From this I know we will only inherit some genetic informations from parents, which is about 50 percent. But the problem is, gene has finite size, after some generations a person leaves only $0.5 imes 0.5 imes 0.5$ parts of genes to the offsprings, and it will be casted into zero. My question is, how long does it required for a person to lose all genetic information in the world?

I think your question conveys some misunderstanding.

A child is related to each parent by a factor of ½. Humans have a diploid genome, meaning they have two copies of each chromosome (see: autosome). When two humans reproduce, they each contribute one copy of each chromosome to the offspring, in other words, they contribute a haploid genome to make a diploid child. Genetic information is not "lost" - the genome is not shrinking by a factor of ½ every generation.

However, relatedness does decrease from generation to generation. You are related to each of your parents by a factor of ½, each of your grandparents by a factor of ½ $ imes$ ½, your great-grandparents by a factor of ½ $ imes$ ½ $ imes$ ½… You are also related to your children by a factor of ½, you are related to your grandchildren by a factor of ½ $ imes$ ½… You get the picture, right?

For example, imagine the genome carries just one gene. Your father carries alleles $AA$ at that locus, and your mother $aa$. You would then be $Aa$ and, because half of your alleles came from your father and the other half from your mother, be related to each by a factor of ½, but all three of you have the same number of genes (1) and that gene is the same length (in nucleotides, barring mutations) in all three.

I feel rg255 answered your question very well, however my mind snapped to an exponential relationship, which is part of what I feel your asking and what rg255 has said (but I have a pretty picture to add).

An exponential graph illustrates the relationship you are speaking of where a substance is infinitely divided by itself.

In this way it will never reach zero. It will inevitably and exponentially shrink but not disappear.

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5 Answers 5

Can a person lose their salvation according to 2 Peter 2:20-22?

The short answer is "Yes, most definitely."

The following response may be unpalatable to some. However, it is certainly not my intent to wound those who believe we simply cannot be lost once we receive salvation in Christ. The far greater imperative here is for the truth to be told, that which surpasses any sensitivities of those who may disbelieve it.

It is to the misinterpretation of passages like that of the OP which I speak. I would like to point out several instances where we are told that someone can, indeed, fall away from the faith. And, in doing so, they are in a perilous condition.

1. In the Gospel of John, Jesus proclaimed:

John 15:2, 6: “Every branch in Me that does not bear fruit, He takes away and every branch that bears fruit, He prunes it so that it may bear more fruit." 6 “If anyone does not abide in Me, he is thrown away as a branch and dries up and they gather them, and cast them into the fire and they are burned" (emphasis added).

Is Christ not warning his disciples that anyone who does not abide in Him -- that is, in all His commandments, will be "gathered and cast into the fire where they are burned"? Is that fire not Hell? How else can we read this? Is someone who accepted Christ and was baptized only to later decide to lead the life of an unrepentant criminal still saved? Has this person not, as with the OP's verses, metaphorically returned to "his own vomit" to "wallow in the mire"?

2. In Paul's Letter to the Galatians, the apostle warned that if these Christians continued to abandon their faith in favor of the Law of Moses, the Gospel would be useless:

Galatians 5:2: "Behold I, Paul, say to you that if you receive circumcision, Christ will be of no benefit to you" (emphasis added).

If Christ is "of no benefit" to Christians who looked back to the Old Law, how then can they be spared from eternal separation with God? This is followed by another stern warning from Paul:

Galatians 5:4: "You have been severed from Christ, you who are seeking to be justified by law you have fallen from grace" (emphasis added).

Is it possible to ignore the words "severed from Christ" and "fallen from grace"? How can we be "severed from Christ" if we were never "in Him" in the first place? And, if we are severed or have fallen from Christ, does this not mean we are lost in eternal flames? Is there some "safety net" that will still catch the ex-Christian as they plunge headlong into Hell? If these admonitions are unconvincing, just what will ever convince someone that yes, we can fall away from the faith?

3. Perhaps the "go to" Book of the Bible in the matter of apostasy is the Letter to the Hebrews. There, we read several grave warnings:

Hebrews 2:1-3: For this reason we [Christians] must pay much closer attention to what we have heard, so that we do not drift away from it. For if the word spoken through angels proved unalterable, and every transgression and disobedience received a just penalty [in the O/T], how will we escape if we neglect so great a salvation [in Christ]?"

This passage is asking, if we "drift away" from the faith which we now possess, how will we escape the wrath of God? If I decide to denounce -- for life -- my Christianity, have I not "drifted away" from (indeed, jettisoned) my faith? If not, how so? Are we to actually believe that God will refuse my denunciation?

4. Again, in the Letter to the Hebrews, we are cautioned never to develop faithlessness:

Hebrews 3:12: "Take care, brethren [Christians], that there not be in any one of you an evil, unbelieving heart that falls away from the living God" (emphasis added).

From this verse, the clear implication is that we can develop an evil, unbelieving heart that **falls away from God." And, if we do this, we will never enter into paradise with Him. It seems to me that to believe otherwise constitutes a certain spiritual blindness.

5. Later, in chapter 6 of the same Letter we read:

Hebrews 6:4-6: "For in the case of those who have once been enlightened and have tasted of the heavenly gift and have been made partakers of the Holy Spirit, and have tasted the good word of God and the powers of the age to come, and then have fallen away, it is impossible to renew them again to repentance, since they again crucify to themselves the Son of God and put Him to open shame" (emphasis added).

If the clause of verse 6 above ("then have fallen away") does not mean what it says, how then do words have meaning? Clearly, this passage is speaking of those who received the Gospel. They "were made partakers of the heavenly gift [of Christ]," and have "fallen away" from Him. The writer then warns that it is impossible for someone in this state to be renewed as long as they persist in their present, fallen condition. Obviously, then:

Hebrews 6:8: "[If this person] yields thorns and thistles [produces worthless fruit to God], [they are] worthless and close to being cursed, and end up being burned."

How is someone in such a condition saved? Can we really employ textual contortions to somehow modify the meaning of the text? Or is it not the case that when someone turns to a life of willful disobedience, they are "putting the Son of God to open shame" (6:6)? As chapter 10 of the same Letter explains:

Hebrews 10:26-27: "For if we go on sinning willfully after receiving the knowledge of the truth, there no longer remains a sacrifice for sins, but a terrifying expectation of judgment and THE FURY OF A FIRE WHICH WILL CONSUME THE ADVERSARIES" (cf. Isa. 26:11, 1 Thess. 1:7, emphasis added).

There should be no doubt that if someone falls away from their faith in Christ, there is no longer any sacrifice for their sins unless they return to Him. All that is left is "a terrifying expectation of judgment."

6. Too often, we rely on the advice of those who seem to casually dismiss biblical texts of the clearest import. Everyone should understand the meaning of 2 Peter 2 in the OP:

2 Peter 2:20-22: "For if, after they have escaped the defilements of the world by the knowledge of [Christ], they are again entangled in them and are overcome, the last state has become worse for them than the first… It has happened to them [apostates] according to the true proverb, “A DOG RETURNS TO ITS OWN VOMIT,” and, “A sow, after washing, returns to wallowing in the mire” (emphasis added).

Those who fall away from the faith are in a much more severe state than they were before they received Christ in the first place. I suggest the text of 2 Peter 2 could not be clearer in this regard.

These passages only scratch the surface of the truth that saints can fall away. We should ask ourselves -- not based on someone else's opinion, -- not what we have been told, but rather on our own eyes: How do these passages (and many more) not speak directly to those who have received the gift of grace from God, and have then forsaken it? Is such a person, unrepentant in their denunciation of God, really saved whatsoever? If so, how?

It is truly a wonder that anyone cannot see this obvious "forest" for the trees.

When a crow dies, other crows summon members of their species, and together they gather around the carcass. They'll also typically stop eating for some time after a death. The effects of grief are especially evident in birds that spend their entire life with one partner - like geese or songbirds. Effects sometimes extend to the remaining partner stopping eating, and eventually dying itself.

Mourning rituals in the animal kingdom


Origins Edit

The inheritance of acquired characteristics was proposed in ancient times, and remained a current idea for many centuries. The historian of science Conway Zirkle wrote in 1935 that: [3]

Lamarck was neither the first nor the most distinguished biologist to believe in the inheritance of acquired characters. He merely endorsed a belief which had been generally accepted for at least 2,200 years before his time and used it to explain how evolution could have taken place. The inheritance of acquired characters had been accepted previously by Hippocrates, Aristotle, Galen, Roger Bacon, Jerome Cardan, Levinus Lemnius, John Ray, Michael Adanson, Jo. Fried. Blumenbach and Erasmus Darwin among others. [3]

Zirkle noted that Hippocrates described pangenesis, the theory that what is inherited derives from the whole body of the parent, whereas Aristotle thought it impossible but that all the same, Aristotle implicitly agreed to the inheritance of acquired characteristics, giving the example of the inheritance of a scar, or of blindness, though noting that children do not always resemble their parents. Zirkle recorded that Pliny the Elder thought much the same. Zirkle also pointed out that stories involving the idea of inheritance of acquired characteristics appear numerous times in ancient mythology and the Bible, and persisted through to Rudyard Kipling's Just So Stories. [4] Erasmus Darwin's Zoonomia (c. 1795) suggested that warm-blooded animals develop from "one living filament. with the power of acquiring new parts" in response to stimuli, with each round of "improvements" being inherited by successive generations. [5]

Darwin's pangenesis Edit

Charles Darwin's On the Origin of Species proposed natural selection as the main mechanism for development of species, but did not rule out a variant of Lamarckism as a supplementary mechanism. [6] Darwin called this pangenesis, and explained it in the final chapter of his book The Variation of Animals and Plants Under Domestication (1868), after describing numerous examples to demonstrate what he considered to be the inheritance of acquired characteristics. Pangenesis, which he emphasised was a hypothesis, was based on the idea that somatic cells would, in response to environmental stimulation (use and disuse), throw off 'gemmules' or 'pangenes' which travelled around the body, though not necessarily in the bloodstream. These pangenes were microscopic particles that supposedly contained information about the characteristics of their parent cell, and Darwin believed that they eventually accumulated in the germ cells where they could pass on to the next generation the newly acquired characteristics of the parents. [7] [8]

Darwin's half-cousin, Francis Galton, carried out experiments on rabbits, with Darwin's cooperation, in which he transfused the blood of one variety of rabbit into another variety in the expectation that its offspring would show some characteristics of the first. They did not, and Galton declared that he had disproved Darwin's hypothesis of pangenesis, but Darwin objected, in a letter to the scientific journal Nature, that he had done nothing of the sort, since he had never mentioned blood in his writings. He pointed out that he regarded pangenesis as occurring in protozoa and plants, which have no blood, as well as in animals. [9]

Lamarck's evolutionary framework Edit

Between 1800 and 1830, Lamarck proposed a systematic theoretical framework for understanding evolution. He saw evolution as comprising four laws: [10] [11]

  1. "Life by its own force, tends to increase the volume of all organs which possess the force of life, and the force of life extends the dimensions of those parts up to an extent that those parts bring to themselves"
  2. "The production of a new organ in an animal body, results from a new requirement arising. and which continues to make itself felt, and a new movement which that requirement gives birth to, and its upkeep/maintenance"
  3. "The development of the organs, and their ability, are constantly a result of the use of those organs."
  4. "All that has been acquired, traced, or changed, in the physiology of individuals, during their life, is conserved through the genesis, reproduction, and transmitted to new individuals who are related to those who have undergone those changes."

Lamarck's discussion of heredity Edit

In 1830, in an aside from his evolutionary framework, Lamarck briefly mentioned two traditional ideas in his discussion of heredity, in his day considered to be generally true. The first was the idea of use versus disuse he theorized that individuals lose characteristics they do not require, or use, and develop characteristics that are useful. The second was to argue that the acquired traits were heritable. He gave as an imagined illustration the idea that when giraffes stretch their necks to reach leaves high in trees, they would strengthen and gradually lengthen their necks. These giraffes would then have offspring with slightly longer necks. In the same way, he argued, a blacksmith, through his work, strengthens the muscles in his arms, and thus his sons would have similar muscular development when they mature. Lamarck stated the following two laws: [12]

  1. Première Loi: Dans tout animal qui n' a point dépassé le terme de ses développemens, l' emploi plus fréquent et soutenu d' un organe quelconque, fortifie peu à peu cet organe, le développe, l' agrandit, et lui donne une puissance proportionnée à la durée de cet emploi tandis que le défaut constant d' usage de tel organe, l'affoiblit insensiblement, le détériore, diminue progressivement ses facultés, et finit par le faire disparoître.[12]
  2. Deuxième Loi: Tout ce que la nature a fait acquérir ou perdre aux individus par l' influence des circonstances où leur race se trouve depuis long-temps exposée, et, par conséquent, par l' influence de l' emploi prédominant de tel organe, ou par celle d' un défaut constant d' usage de telle partie elle le conserve par la génération aux nouveaux individus qui en proviennent, pourvu que les changemens acquis soient communs aux deux sexes, ou à ceux qui ont produit ces nouveaux individus.[12]
  1. First Law [Use and Disuse]: In every animal which has not passed the limit of its development, a more frequent and continuous use of any organ gradually strengthens, develops and enlarges that organ, and gives it a power proportional to the length of time it has been so used while the permanent disuse of any organ imperceptibly weakens and deteriorates it, and progressively diminishes its functional capacity, until it finally disappears.
  2. Second Law [Soft Inheritance]: All the acquisitions or losses wrought by nature on individuals, through the influence of the environment in which their race has long been placed, and hence through the influence of the predominant use or permanent disuse of any organ all these are preserved by reproduction to the new individuals which arise, provided that the acquired modifications are common to both sexes, or at least to the individuals which produce the young. [13]

In essence, a change in the environment brings about change in "needs" (besoins), resulting in change in behaviour, causing change in organ usage and development, bringing change in form over time—and thus the gradual transmutation of the species. The evolutionary biologists and historians of science Conway Zirkle, Michael Ghiselin, and Stephen Jay Gould have pointed out, these ideas were not original to Lamarck. [3] [1] [14]

Weismann's experiment Edit

August Weismann's germ plasm theory held that germline cells in the gonads contain information that passes from one generation to the next, unaffected by experience, and independent of the somatic (body) cells. This implied what came to be known as the Weismann barrier, as it would make Lamarckian inheritance from changes to the body difficult or impossible. [15]

Weismann conducted the experiment of removing the tails of 68 white mice, and those of their offspring over five generations, and reporting that no mice were born in consequence without a tail or even with a shorter tail. In 1889, he stated that "901 young were produced by five generations of artificially mutilated parents, and yet there was not a single example of a rudimentary tail or of any other abnormality in this organ." [16] The experiment, and the theory behind it, were thought at the time to be a refutation of Lamarckism. [15]

The experiment's effectiveness in refuting Lamarck's hypothesis is doubtful, as it did not address the use and disuse of characteristics in response to the environment. The biologist Peter Gauthier noted in 1990 that: [17]

Can Weismann's experiment be considered a case of disuse? Lamarck proposed that when an organ was not used, it slowly, and very gradually atrophied. In time, over the course of many generations, it would gradually disappear as it was inherited in its modified form in each successive generation. Cutting the tails off mice does not seem to meet the qualifications of disuse, but rather falls in a category of accidental misuse. Lamarck's hypothesis has never been proven experimentally and there is no known mechanism to support the idea that somatic change, however acquired, can in some way induce a change in the germplasm. On the other hand it is difficult to disprove Lamarck's idea experimentally, and it seems that Weismann's experiment fails to provide the evidence to deny the Lamarckian hypothesis, since it lacks a key factor, namely the willful exertion of the animal in overcoming environmental obstacles. [17]

Ghiselin also considered the Weismann tail-chopping experiment to have no bearing on the Lamarckian hypothesis, writing in 1994 that: [1]

The acquired characteristics that figured in Lamarck's thinking were changes that resulted from an individual's own drives and actions, not from the actions of external agents. Lamarck was not concerned with wounds, injuries or mutilations, and nothing that Lamarck had set forth was tested or "disproven" by the Weismann tail-chopping experiment. [1]

The historian of science Rasmus Winther stated that Weismann had nuanced views about the role of the environment on the germ plasm. Indeed, like Darwin, he consistently insisted that a variable environment was necessary to cause variation in the hereditary material. [18]

The identification of Lamarckism with the inheritance of acquired characteristics is regarded by evolutionary biologists including Ghiselin as a falsified artifact of the subsequent history of evolutionary thought, repeated in textbooks without analysis, and wrongly contrasted with a falsified picture of Darwin's thinking. Ghiselin notes that "Darwin accepted the inheritance of acquired characteristics, just as Lamarck did, and Darwin even thought that there was some experimental evidence to support it." [1] Gould wrote that in the late 19th century, evolutionists "re-read Lamarck, cast aside the guts of it . and elevated one aspect of the mechanics—inheritance of acquired characters—to a central focus it never had for Lamarck himself." [19] He argued that "the restriction of 'Lamarckism' to this relatively small and non-distinctive corner of Lamarck's thought must be labelled as more than a misnomer, and truly a discredit to the memory of a man and his much more comprehensive system." [2] [20]

Context Edit

The period of the history of evolutionary thought between Darwin's death in the 1880s, and the foundation of population genetics in the 1920s and the beginnings of the modern evolutionary synthesis in the 1930s, is called the eclipse of Darwinism by some historians of science. During that time many scientists and philosophers accepted the reality of evolution but doubted whether natural selection was the main evolutionary mechanism. [21]

Among the most popular alternatives were theories involving the inheritance of characteristics acquired during an organism's lifetime. Scientists who felt that such Lamarckian mechanisms were the key to evolution were called neo-Lamarckians. They included the British botanist George Henslow (1835–1925), who studied the effects of environmental stress on the growth of plants, in the belief that such environmentally-induced variation might explain much of plant evolution, and the American entomologist Alpheus Spring Packard, Jr., who studied blind animals living in caves and wrote a book in 1901 about Lamarck and his work. [22] [23] Also included were paleontologists like Edward Drinker Cope and Alpheus Hyatt, who observed that the fossil record showed orderly, almost linear, patterns of development that they felt were better explained by Lamarckian mechanisms than by natural selection. Some people, including Cope and the Darwin critic Samuel Butler, felt that inheritance of acquired characteristics would let organisms shape their own evolution, since organisms that acquired new habits would change the use patterns of their organs, which would kick-start Lamarckian evolution. They considered this philosophically superior to Darwin's mechanism of random variation acted on by selective pressures. Lamarckism also appealed to those, like the philosopher Herbert Spencer and the German anatomist Ernst Haeckel, who saw evolution as an inherently progressive process. [22] The German zoologist Theodor Eimer combined Larmarckism with ideas about orthogenesis, the idea that evolution is directed towards a goal. [24]

With the development of the modern synthesis of the theory of evolution, and a lack of evidence for a mechanism for acquiring and passing on new characteristics, or even their heritability, Lamarckism largely fell from favour. Unlike neo-Darwinism, neo-Lamarckism is a loose grouping of largely heterodox theories and mechanisms that emerged after Lamarck's time, rather than a coherent body of theoretical work. [25]

19th century Edit

Neo-Lamarckian versions of evolution were widespread in the late 19th century. The idea that living things could to some degree choose the characteristics that would be inherited allowed them to be in charge of their own destiny as opposed to the Darwinian view, which placed them at the mercy of the environment. Such ideas were more popular than natural selection in the late 19th century as it made it possible for biological evolution to fit into a framework of a divine or naturally willed plan, thus the neo-Lamarckian view of evolution was often advocated by proponents of orthogenesis. [26] According to the historian of science Peter J. Bowler, writing in 2003:

One of the most emotionally compelling arguments used by the neo-Lamarckians of the late nineteenth century was the claim that Darwinism was a mechanistic theory which reduced living things to puppets driven by heredity. The selection theory made life into a game of Russian roulette, where life or death was predetermined by the genes one inherited. The individual could do nothing to mitigate bad heredity. Lamarckism, in contrast, allowed the individual to choose a new habit when faced with an environmental challenge and shape the whole future course of evolution. [27]

Scientists from the 1860s onwards conducted numerous experiments that purported to show Lamarckian inheritance. Some examples are described in the table.

Early 20th century Edit

A century after Lamarck, scientists and philosophers continued to seek mechanisms and evidence for the inheritance of acquired characteristics. Experiments were sometimes reported as successful, but from the beginning these were either criticised on scientific grounds or shown to be fakes. [45] [46] [47] [48] [49] For instance, in 1906, the philosopher Eugenio Rignano argued for a version that he called "centro-epigenesis", [50] [51] [52] [53] [54] [55] but it was rejected by most scientists. [56] Some of the experimental approaches are described in the table.

Early 20th century experiments attempting to demonstrate Lamarckian inheritance
Scientist Date Experiment Claimed result Rebuttal
William Lawrence Tower 1907 to 1910 Colorado potato beetles in extreme humidity, temperature Heritable changes in size, colour Criticised by William Bateson Tower claimed all results lost in fire William E. Castle visited laboratory, found fire suspicious, doubted claim that steam leak had killed all beetles, concluded faked data. [57] [58] [59] [46] [47]
Gustav Tornier 1907 to 1918 Goldfish, embryos of frogs, newts Abnormalities inherited Disputed possibly an osmotic effect [60] [61] [62] [63]
Charles Rupert Stockard 1910 Repeated alcohol intoxication of pregnant guinea pigs Inherited malformations Raymond Pearl unable to reproduce findings in chickens Darwinian explanation [64] [45]
Francis Bertody Sumner 1921 Reared mice at different temperatures, humidities Inherited longer bodies, tails, hind feet Inconsistent results [65] [66]
Michael F. Guyer, Elizabeth A. Smith 1918 to 1924 Injected fowl serum antibodies for rabbit lens-protein into pregnant rabbits Eye defects inherited for 8 generations Disputed, results not replicated [67] [68]
Paul Kammerer 1920s Midwife toad Black foot-pads inherited Fraud, ink injected or, results misinterpreted case celebrated by Arthur Koestler arguing that opposition was political [48] [69]
William McDougall 1920s Rats solving mazes Offspring learnt mazes quicker (20 vs 165 trials) Poor experimental controls [70] [71] [72] [73] [74] [75] [49]
John William Heslop-Harrison 1920s Peppered moths exposed to soot Inherited mutations caused by soot Failure to replicate results implausible mutation rate [76] [77]
Ivan Pavlov 1926 Conditioned reflex in mice to food and bell Offspring easier to condition Pavlov retracted claim results not replicable [78] [79]
Coleman Griffith, John Detlefson 1920 to 1925 Reared rats on rotating table for 3 months Inherited balance disorder Results not replicable likely cause ear infection [80] [81] [82] [83] [84] [85]
Victor Jollos [pl] 1930s Heat treatment in Drosophila melanogaster Directed mutagenesis, a form of orthogenesis Results not replicable [86] [87]

Late 20th century Edit

The British anthropologist Frederic Wood Jones and the South African paleontologist Robert Broom supported a neo-Lamarckian view of human evolution. The German anthropologist Hermann Klaatsch relied on a neo-Lamarckian model of evolution to try and explain the origin of bipedalism. Neo-Lamarckism remained influential in biology until the 1940s when the role of natural selection was reasserted in evolution as part of the modern evolutionary synthesis. [88] Herbert Graham Cannon, a British zoologist, defended Lamarckism in his 1959 book Lamarck and Modern Genetics. [89] In the 1960s, "biochemical Lamarckism" was advocated by the embryologist Paul Wintrebert. [90]

Neo-Lamarckism was dominant in French biology for more than a century. French scientists who supported neo-Lamarckism included Edmond Perrier (1844–1921), Alfred Giard (1846–1908), Gaston Bonnier (1853–1922) and Pierre-Paul Grassé (1895–1985). They followed two traditions, one mechanistic, one vitalistic after Henri Bergson's philosophy of evolution. [91]

In 1987, Ryuichi Matsuda coined the term "pan-environmentalism" for his evolutionary theory which he saw as a fusion of Darwinism with neo-Lamarckism. He held that heterochrony is a main mechanism for evolutionary change and that novelty in evolution can be generated by genetic assimilation. [92] [93] His views were criticized by Arthur M. Shapiro for providing no solid evidence for his theory. Shapiro noted that "Matsuda himself accepts too much at face value and is prone to wish-fulfilling interpretation." [93]

Ideological neo-Lamarckism Edit

A form of Lamarckism was revived in the Soviet Union of the 1930s when Trofim Lysenko promoted the ideologically-driven research programme, Lysenkoism this suited the ideological opposition of Joseph Stalin to genetics. Lysenkoism influenced Soviet agricultural policy which in turn was later blamed for crop failures. [94]

Critique Edit

George Gaylord Simpson in his book Tempo and Mode in Evolution (1944) claimed that experiments in heredity have failed to corroborate any Lamarckian process. [95] Simpson noted that neo-Lamarckism "stresses a factor that Lamarck rejected: inheritance of direct effects of the environment" and neo-Lamarckism is closer to Darwin's pangenesis than Lamarck's views. [96] Simpson wrote, "the inheritance of acquired characters, failed to meet the tests of observation and has been almost universally discarded by biologists." [97]

Botanist Conway Zirkle pointed out that Lamarck did not originate the hypothesis that acquired characteristics could be inherited, so it is incorrect to refer to it as Lamarckism:

What Lamarck really did was to accept the hypothesis that acquired characters were heritable, a notion which had been held almost universally for well over two thousand years and which his contemporaries accepted as a matter of course, and to assume that the results of such inheritance were cumulative from generation to generation, thus producing, in time, new species. His individual contribution to biological theory consisted in his application to the problem of the origin of species of the view that acquired characters were inherited and in showing that evolution could be inferred logically from the accepted biological hypotheses. He would doubtless have been greatly astonished to learn that a belief in the inheritance of acquired characters is now labeled "Lamarckian," although he would almost certainly have felt flattered if evolution itself had been so designated. [4]

Peter Medawar wrote regarding Lamarckism, "very few professional biologists believe that anything of the kind occurs—or can occur—but the notion persists for a variety of nonscientific reasons." Medawar stated there is no known mechanism by which an adaptation acquired in an individual's lifetime can be imprinted on the genome and Lamarckian inheritance is not valid unless it excludes the possibility of natural selection but this has not been demonstrated in any experiment. [98]

A host of experiments have been designed to test Lamarckianism. All that have been verified have proved negative. On the other hand, tens of thousands of experiments— reported in the journals and carefully checked and rechecked by geneticists throughout the world— have established the correctness of the gene-mutation theory beyond all reasonable doubt. In spite of the rapidly increasing evidence for natural selection, Lamarck has never ceased to have loyal followers. There is indeed a strong emotional appeal in the thought that every little effort an animal puts forth is somehow transmitted to his progeny. [99]

According to Ernst Mayr, any Lamarckian theory involving the inheritance of acquired characters has been refuted as "DNA does not directly participate in the making of the phenotype and that the phenotype, in turn, does not control the composition of the DNA." [100] Peter J. Bowler has written that although many early scientists took Lamarckism seriously, it was discredited by genetics in the early twentieth century. [101]

Studies in the field of epigenetics, genetics and somatic hypermutation [102] [103] have highlighted the possible inheritance of traits acquired by the previous generation. [104] [105] [106] [107] [108] However, the characterization of these findings as Lamarckism has been disputed. [109] [110] [111] [112]

Transgenerational epigenetic inheritance Edit

Epigenetic inheritance has been argued by scientists including Eva Jablonka and Marion J. Lamb to be Lamarckian. [113] Epigenetics is based on hereditary elements other than genes that pass into the germ cells. These include methylation patterns in DNA and chromatin marks on histone proteins, both involved in gene regulation. These marks are responsive to environmental stimuli, differentially affect gene expression, and are adaptive, with phenotypic effects that persist for some generations. The mechanism may also enable the inheritance of behavioral traits, for example in chickens [114] [115] [116] rats [117] [118] and human populations that have experienced starvation, DNA methylation resulting in altered gene function in both the starved population and their offspring. [119] Methylation similarly mediates epigenetic inheritance in plants such as rice. [120] [121] Small RNA molecules, too, may mediate inherited resistance to infection. [122] [123] [124] Handel and Romagopalan commented that "epigenetics allows the peaceful co-existence of Darwinian and Lamarckian evolution." [125]

Joseph Springer and Dennis Holley commented in 2013 that: [126]

Lamarck and his ideas were ridiculed and discredited. In a strange twist of fate, Lamarck may have the last laugh. Epigenetics, an emerging field of genetics, has shown that Lamarck may have been at least partially correct all along. It seems that reversible and heritable changes can occur without a change in DNA sequence (genotype) and that such changes may be induced spontaneously or in response to environmental factors—Lamarck's "acquired traits." Determining which observed phenotypes are genetically inherited and which are environmentally induced remains an important and ongoing part of the study of genetics, developmental biology, and medicine. [126]

The prokaryotic CRISPR system and Piwi-interacting RNA could be classified as Lamarckian, within a Darwinian framework. [127] [128] However, the significance of epigenetics in evolution is uncertain. Critics such as the evolutionary biologist Jerry Coyne point out that epigenetic inheritance lasts for only a few generations, so it is not a stable basis for evolutionary change. [129] [130] [131] [132]

The evolutionary biologist T. Ryan Gregory contends that epigenetic inheritance should not be considered Lamarckian. According to Gregory, Lamarck did not claim that the environment directly affected living things. Instead, Lamarck "argued that the environment created needs to which organisms responded by using some features more and others less, that this resulted in those features being accentuated or attenuated, and that this difference was then inherited by offspring." Gregory has stated that Lamarckian evolution in epigenetics is more like Darwin's point of view than Lamarck's. [109]

In 2007, David Haig wrote that research into epigenetic processes does allow a Lamarckian element in evolution but the processes do not challenge the main tenets of the modern evolutionary synthesis as modern Lamarckians have claimed. Haig argued for the primacy of DNA and evolution of epigenetic switches by natural selection. [133] Haig has written that there is a "visceral attraction" to Lamarckian evolution from the public and some scientists, as it posits the world with a meaning, in which organisms can shape their own evolutionary destiny. [134]

Thomas Dickens and Qazi Rahman (2012) have argued that epigenetic mechanisms such as DNA methylation and histone modification are genetically inherited under the control of natural selection and do not challenge the modern synthesis. They dispute the claims of Jablonka and Lamb on Lamarckian epigenetic processes. [135]

In 2015, Khursheed Iqbal and colleagues discovered that although "endocrine disruptors exert direct epigenetic effects in the exposed fetal germ cells, these are corrected by reprogramming events in the next generation." [137] Also in 2015, Adam Weiss argued that bringing back Lamarck in the context of epigenetics is misleading, commenting, "We should remember [Lamarck] for the good he contributed to science, not for things that resemble his theory only superficially. Indeed, thinking of CRISPR and other phenomena as Lamarckian only obscures the simple and elegant way evolution really works." [138]

Somatic hypermutation and reverse transcription to germline Edit

In the 1970s, the Australian immunologist Edward J. Steele developed a neo-Lamarckian theory of somatic hypermutation within the immune system and coupled it to the reverse transcription of RNA derived from body cells to the DNA of germline cells. This reverse transcription process supposedly enabled characteristics or bodily changes acquired during a lifetime to be written back into the DNA and passed on to subsequent generations. [139] [140]

The mechanism was meant to explain why homologous DNA sequences from the VDJ gene regions of parent mice were found in their germ cells and seemed to persist in the offspring for a few generations. The mechanism involved the somatic selection and clonal amplification of newly acquired antibody gene sequences generated via somatic hypermutation in B-cells. The messenger RNA products of these somatically novel genes were captured by retroviruses endogenous to the B-cells and were then transported through the bloodstream where they could breach the Weismann or soma-germ barrier and reverse transcribe the newly acquired genes into the cells of the germ line, in the manner of Darwin's pangenes. [103] [102] [141]

The historian of biology Peter J. Bowler noted in 1989 that other scientists had been unable to reproduce his results, and described the scientific consensus at the time: [136]

There is no feedback of information from the proteins to the DNA, and hence no route by which characteristics acquired in the body can be passed on through the genes. The work of Ted Steele (1979) provoked a flurry of interest in the possibility that there might, after all, be ways in which this reverse flow of information could take place. . [His] mechanism did not, in fact, violate the principles of molecular biology, but most biologists were suspicious of Steele's claims, and attempts to reproduce his results have failed. [136]

Bowler commented that "[Steele's] work was bitterly criticized at the time by biologists who doubted his experimental results and rejected his hypothetical mechanism as implausible." [136]

Hologenome theory of evolution Edit

The hologenome theory of evolution, while Darwinian, has Lamarckian aspects. An individual animal or plant lives in symbiosis with many microorganisms, and together they have a "hologenome" consisting of all their genomes. The hologenome can vary like any other genome by mutation, sexual recombination, and chromosome rearrangement, but in addition it can vary when populations of microorganisms increase or decrease (resembling Lamarckian use and disuse), and when it gains new kinds of microorganism (resembling Lamarckian inheritance of acquired characteristics). These changes are then passed on to offspring. [143] The mechanism is largely uncontroversial, and natural selection does sometimes occur at whole system (hologenome) level, but it is not clear that this is always the case. [142]

Baldwin effect Edit

The Baldwin effect, named after the psychologist James Mark Baldwin by George Gaylord Simpson in 1953, proposes that the ability to learn new behaviours can improve an animal's reproductive success, and hence the course of natural selection on its genetic makeup. Simpson stated that the mechanism was "not inconsistent with the modern synthesis" of evolutionary theory, [144] though he doubted that it occurred very often, or could be proven to occur. He noted that the Baldwin effect provide a reconciliation between the neo-Darwinian and neo-Lamarckian approaches, something that the modern synthesis had seemed to render unnecessary. In particular, the effect allows animals to adapt to a new stress in the environment through behavioural changes, followed by genetic change. This somewhat resembles Lamarckism but without requiring animals to inherit characteristics acquired by their parents. [145] The Baldwin effect is broadly accepted by Darwinists. [146]

Within the field of cultural evolution, Lamarckism has been applied as a mechanism for dual inheritance theory. [147] Gould viewed culture as a Lamarckian process whereby older generations transmitted adaptive information to offspring via the concept of learning. In the history of technology, components of Lamarckism have been used to link cultural development to human evolution by considering technology as extensions of human anatomy. [148]

What to know about calcification

Calcium is one of the most abundant minerals in the body. It is present in the bones, teeth, and bloodstream. Sometimes, a health professional may find calcium deposits in different organs throughout a person’s body. They call this condition “calcification.”

Calcification can occur with age, but it can also be related to infections, injuries, and cancer. Having too much calcium accumulate in the arteries, kidneys, or pericardium (the membrane that encloses the heart) can be dangerous.

Most often, breast calcifications are benign. Sometimes, however, they can be a sign of cancer.

Read on to learn about the different types of calcification, including their symptoms, causes, and treatments.

Share on Pinterest A doctor may order an imaging scan to detect calcium deposits in the body.

Bones and teeth store the greatest amount of calcium in the body. People also have calcium in their bloodstream, but this accounts for only 1% of the body’s total calcium content.

Over time, calcium deposits can form in different parts of the body, including in the:

  • arteries
  • pericardium
  • kidneys
  • tendons
  • joints
  • brain
  • breasts

Small calcium deposits are not likely to alter bodily functions. However, if the deposits become very large, they may begin to interfere with organ function or cause other health issues.

Depending on the location, calcification can be a sign of:

Each type of calcification has its own characteristics, management, and treatment, depending on where in the body it occurs and what the cause is.

The sections below will discuss these types in more detail.

Artery calcification can start at a young age, but a doctor may only notice it once the deposit is large enough to appear in an imaging scan. Artery calcification at a detectable level typically occurs in adults over 40 years of age .

People with coronary artery disease will have calcification of the blood vessels.

Also, artery calcification can worsen with age. Researchers suggest that 90% of men and 67% of women over 70 years of age have coronary artery calcification.


Artery calcification has no typical symptoms. However, locating it can help a doctor predict the person’s risk of cardiovascular complications.


The following factors may increase a person’s risk of developing coronary artery calcification:

  • metabolic syndrome
  • high cholesterol
  • tobacco use
  • high blood pressure
  • chronic kidney disease
  • high baseline C-reactive protein levels


Treatment tends to include addressing the risk factors that can worsen the artery calcification.

When a person has calcium deposits along the coronary arteries, doctors will recommend risk factor reduction. This is because people with artery calcification have a higher risk of cardiovascular diseases.

Calcification in the arteries that supply blood to the heart increases the risk of cardiovascular disease. It can affect:

  • how well the blood flows through the heart
  • how the arteries contract and dilate to alter the flow of blood
  • how well the arteries react to changes in blood flow

In constrictive pericarditis, a thick calcified lining replaces the normal lining around the heart, or the pericardium. The thicker lining makes it difficult for the lower chambers of the heart to fill with blood.


The symptoms of pericardial calcification can be similar to those of heart failure. They tend to occur once constrictive pericarditis is present.

  • fatigue
  • shortness of breath during physical exertion
  • shortness of breath when lying down
  • shortness of breath when leaning forward

That being said, in some people, pericardial calcification may not cause any symptoms at all.


One of the main causes of pericardial calcification is pericarditis. This refers to inflammation within the pericardium, of which the cause is often unknown.

Major heart surgery may give rise to subsequent constrictive pericarditis, and sometimes it occurs following a viral infection in the pericardium.

Some other causes of pericardial calcification include:


If there are no symptoms of pericardial calcification, the person is not likely to require treatment.

Some people experiencing pericardial calcification also have underlying inflammation. If this is the case, anti-inflammatories such as colchicine, corticosteroids, or nonsteroidal anti-inflammatory drug (NSAID) therapy may help.

A surgical procedure called a pericardiectomy has the potential to cure pericardial calcification. It involves the removal of a portion of the pericardium.

Calcium deposits can also form in the kidneys. This is called nephrocalcinosis.

People with nephrocalcinosis may also have high levels of calcium or phosphate in their blood or urine.

Doctors classify nephrocalcinosis as molecular, microscopic, or macroscopic. The classification depends on the size of the calcium deposit and whether it is visible on an X-ray or microscope.

A doctor will typically find calcium deposits in the renal medulla of the kidney, which is the inner part.


With kidney calcification, many people experience no symptoms at all.

Once a doctor notices calcium buildup on an X-ray image, they will check the person’s blood and urine for:


The following factors could be potential causes of nephrocalcinosis:

  • high levels of calcium in the blood
  • high levels of calcium in the urine
  • high levels of phosphate in the blood
  • high levels of phosphate in the urine
  • high levels of oxalate in the urine

These conditions can develop due to:

  • primary hyperparathyroidism
  • vitamin D therapy
  • sarcoidosis
  • chronically low potassium levels in the blood


When a doctor diagnoses kidney calcification, they will need to determine the cause.

Kidney calcification can develop due to vitamin D therapy, primary hyperparathyroidism, or sarcoidosis, among other things. Treatment will depend and focus on the cause.

Some causes of nephrocalcinosis can lead to chronic kidney disease if a person does not receive proper treatment. Like coronary artery calcification, kidney calcification requires treating the underlying cause and addressing the risk factors.

Radiologists frequently find calcification in joints and tendons. However, they may find it difficult to tell calcification from ossification or a foreign body.

Joint and tendon calcification are both relatively common. For example, about 3–15% of people have calcification of a tendon, called calcific tendonitis.


People with calcific tendonitis may sometimes feel a “pinching” of the calcified tendon. However, the condition may also cause significant pain or no symptoms at all.

Calcification most often affects tendons in the shoulder, but tendons in the wrist, hip, and elbow are also susceptible to this condition.


Calcium pyrophosphate dihydrate crystal disease is often the cause of joint calcification. In fact, research suggests that around 45% of people aged 85 and over have calcium deposits in the cartilage of their joints.


People with painless joint or tendon calcification typically do not require treatment. They may require treatment if they start to experience pain, however.

No treatments can remove calcium deposits from the cartilage of the joints, so doctors tend to rely on glucocorticoid injections, oral colchicine, and NSAIDs, which can help relieve pain and underlying inflammation.

Surgery may be necessary for some people with this condition.

Primary familial brain calcification occurs when abnormal calcium deposits form in the blood vessels in the brain. These deposits typically form in the basal ganglia, which initiate and control bodily movement.

Like many other types of calcification, these calcium deposits will only be visible using imaging scans.


Symptoms usually start to manifest in mid-adulthood, worsening over time. Symptoms involve movement dysfunction and can include:

  • dystonia, or involuntary tensing of the muscles
  • uncontrollable movements
  • an unsteady walk
  • slowness of movement
  • tremor

Around 20–30% of people with primary familial brain calcification may also experience psychiatric and behavioral symptoms, including:

  • dementia
  • psychosis
  • memory loss
  • personality changes
  • difficulty concentrating
  • seizures
  • impaired speech


The cause of primary familial brain calcification is the genetic mutation of certain genes. It is an inherited condition. In about 50% of cases, however, the exact genetic cause is unknown.

Due to mutations of certain genes, calcium deposits form in the affected blood vessels of the brain and brain cells. These calcium deposits then disrupt nerve signal connections between different areas of the brain.


The treatment options for brain calcification focus on addressing and relieving the symptoms, as the calcification itself is irreversible.

One common symptom of brain calcification is dystonia. Some treatment options for dystonia include:

  • physical therapy
  • speech and voice therapy
  • relaxation and stress management
  • deep brain stimulation using an implanted device
  • oral medication, such as benzodiazepines or anticholinergics
  • injected medication
  • surgery, if the symptoms do not respond to other therapies

Only a mammogram can detect breast calcification.

Doctors classify breast calcifications based on the size of the calcium deposit.

Macrocalcifications are large, well-defined deposits. These are not usually a sign of cancer.

Microcalcifications, on the other hand, will appear as small specks on X-rays from mammograms. These are not usually a cause for concern either, but having deposits of varying shapes and sizes clumped together in an area of rapidly multiplying cells may be a sign of cancer.


Most breast calcifications have no symptoms.


Breast calcification has no link to dietary calcium. It is a marker of an underlying process within the tissue.

As people age, their bodies have more chances to develop noncancerous breast cell changes that can leave behind calcium deposits.

Some benign processes that can lead to breast calcification are:

  • secretion of calcium into the milk ducts
  • injuries or infections within the breast
  • noncancerous growths in the breast
  • breast cysts
  • past radiation therapy to the breast
  • atherosclerosis of the blood vessels in the breast


Although most breast calcifications are noncancerous, doctors must investigate the tissue further to confirm this. This is because calcium deposits may be the result of ductal carcinoma in situ, which is an early stage and type of cancer that develops inside the milk duct.

People with invasive ductal carcinoma may also have breast calcification. This type of cancer spreads from the milk duct to invade the surrounding breast tissue.

If a radiologist finds breast calcifications when reading a person’s mammogram, their course of action will be to compare this imaging with any prior mammogram(s). If necessary, they may perform additional testing to determine the origins and cause of the calcification. This could involve magnification mammography, ultrasound imaging, an MRI scan, or a biopsy.

Treatment for breast calcifications will depend on the type. If it indicates cancer, some people may require surgery, radiation therapy, or chemotherapy.

Calcification refers to the formation of calcium deposits in different parts of the body, such as the arteries, kidneys, or breasts.

Some types of calcification can be dangerous, and others may simply be a sign of tissue repair.

People may not know they have calcification because it does not always cause any symptoms.

Some types of calcification are irreversible, but depending on the type, there may be ways to reduce pain and lower the risk of complications.

Effects on offspring of epigenetic inheritance via sperm

As an organism grows and responds to its environment, genes in its cells are constantly turning on and off, with different patterns of gene expression in different cells. But can changes in gene expression be passed on from parents to their children and subsequent generations? Although indirect evidence for this phenomenon, called "transgenerational epigenetic inheritance," is growing, it remains controversial because the mechanisms behind it are so mysterious.

Now researchers at UC Santa Cruz have demonstrated that epigenetic information carried by parental sperm chromosomes can cause changes in gene expression and development in the offspring. Their study, published March 20 in Nature Communications, involved a series of clever experiments using the nematode worm Caenorhabditis elegans.

Epigenetic changes do not alter the DNA sequences of genes, but instead involve chemical modifications to either the DNA itself or to the histone proteins with which DNA is packaged in the chromosomes. These modifications or "marks" change gene expression, turning genes on or off.

In their experiments with C. elegans, researchers in Susan Strome's lab at UC Santa Cruz have focused on histone marks, modifications to specific amino acids in the tails of histone proteins. Strome, a professor of molecular, cell and developmental biology, said the new study addressed a central question in the field of epigenetics.

"It's a very direct question: Does inheriting sperm chromosomes with altered histone packaging of the DNA affect gene expression in the offspring? And the answer is yes," she said.

First author Kiyomi Kaneshiro, a graduate student in Strome's lab who led the study, said C. elegans is a good model for studying this question because histone packaging is fully retained in the worm's sperm chromosomes. In humans and other mammals, histone packaging is only partially retained in sperm.

"There is debate over how much histone packaging is retained in humans, but we know it is retained in some developmentally important regions of the genome," Kaneshiro said.

Researchers have focused on epigenetic inheritance in the paternal line because the sperm contributes little more than its chromosomes to the embryo. The egg contains many other components that may influence the development of the embryo, making it harder to tease out epigenetic effects in the maternal line.

In her experiments, Kaneshiro selectively removed a specific histone mark from sperm chromosomes, then fertilized eggs with the modified sperm and studied the resulting offspring. A crucial innovation was to use sperm and eggs from two different strains of C. elegans, which enabled Kaneshiro to distinguish between the chromosomes inherited from the sperm and those inherited from the egg. She chose worm strains from Britain and Hawaii that had evolved separately long enough to accumulate many small genetic differences (called single nucleotide polymorphisms).

"The dads were British and the moms were Hawaiian, and there are enough differences between them that we could distinguish between the two parental genomes in the cells of their offspring," Kaneshiro said. "Through this hybrid system, we were able to see differences in gene expression that were a direct result of the changes in histone marks on the sperm chromosomes."

Furthermore, those changes in gene expression had developmental consequences. With removal of the histone marks, the sperm chromosomes lost a repressive signal that normally keeps certain genes from being active in the offspring's germline (the cells that give rise to eggs and sperm). Kaneshiro observed that the offspring's germline cells turned on neuronal genes and began developing into neurons.

The particular histone mark removed in these experiments is a widely studied epigenetic mark found in animals ranging from worms to fruit flies to humans. "This mark is found on the histones that are retained on sperm chromosomes in humans," Kaneshiro said.

The new findings show that inherited epigenetic marks affect gene expression and development. But the study involved artificially changing the marks on the sperm chromosomes. What remains to be understood is how environmental effects on an adult organism could alter epigenetic marks in its germline cells, making it possible for those environmental effects to be transmitted to subsequent generations.

"Our findings raise the possibility that histone marks are carriers for transgenerational epigenetic inheritance," Kaneshiro said. "We know that the environment an organism experiences can change gene expression patterns in somatic cells [non-germline body cells]. If it changes gene expression patterns in the germline, we expect that those changes can be inherited, but we haven't shown that yet."

In addition to Kaneshiro and Strome, the coauthors of the study include Andreas Rechtsteiner, a bioinformaticist in Strome's lab. This work was supported by the National Institutes of Health.


John V. Forrester MB ChB MD FRCS(Ed) FRCP(Glasg) (Hon) FRCOphth(Hon) FMedSci FRSE FARVO , . Eric Pearlman BSc PhD , in The Eye (Fourth Edition) , 2016

Structural chromosomal abnormalities

Structural chromosomal abnormalities result from chromosomal breakage. Normally single breaks are repaired quickly, but if more than one break occurs repair mechanisms may cause random rejoining of the wrong ends. Spontaneous breakage increases with exposure to mutagenic chemicals and ionizing radiation. The following structural abnormalities may occur:

translocation – chromosomes break and exchange segments

inversion – segment of chromosome is inverted in sequence

deletion – section of chromosome is lost

mutation – point mutation occurs with a change in a single base of a triplet code of a gene.

Translocation usually results in no loss of DNA so that individuals may appear clinically normal. Translocation may be reciprocal if exchange of chromosomal segments distal to the breaks occurs. Robertsonian translocation arises from breaks at or near the centromere in two acrocentric chromosomes (where centromere is located nearer one end of the chromosome). For example translocation of segments on chromosomes 14 and 21 may occur and, during meiosis, a trivalent is formed which will then lead to a mosaic of normal and abnormal karyotype during anaphase. Insertional translocation requires the occurrence of three breaks in one or two chromosomes, resulting in deletion of one segment and insertion of another into the gap in the first chromosome. Inversions arise from two chromosomal breaks and the segment being inverted through 180° between the breaks. Inversions interfere with the pairing of chromosomes during meoisis and crossovers are suppressed, generating unbalanced gametes. Deletion may also occur when only part of the chromosome is lost. This can occur between two breakpoints or as a result of breaks and loss of segments in both arms of the chromosome. Point mutations, on the other hand, occur when a single nucleotide base is replaced by another, which may in turn alter the amino acid coding for that protein.

5 Tips Before You Leave Your Kids an Inheritance

If you are a parent who worries about what your wealth will do to your children, you are not alone. Many clients want to leave money to their kids, but they are concerned that their children are ill-equipped to handle sudden wealth. Some worry that by providing too much money that it will rob their children of the ambition and hard work that it took for them to amass the wealth. And it’s not just parents who worry. At least one beneficiary has reservations.

CNN news-show host Anderson Cooper is the son of Gloria Vanderbilt — a successful fashion and interior designer and daughter to the Vanderbilt railroad and shipping empire who is believed to be worth $200 million. Is Anderson chomping at the bit for an inheritance? No. Here is what Anderson said recently in an interview with Howard Stern:

“I don’t believe in inheriting money,” he said. “I think it’s an initiative sucker. I think it’s a curse, ” Cooper went on to say. “Who has inherited a lot of money that has gone on to do things in their own life?” When Stern reminded him that his mother did this Anderson responded, “I think that’s an anomaly.”

What is your view of inherited money? Is it an “initiative sucker” or can it be used to create a better and more fulfilled life? In my sudden wealth management firm I’ve found that the answer is a resounding YES to both! Yes it can cause some to lose their drive and ambition, but with the proper work and structure, those who inherit can use the money as a tool to create meaningful lives of their own. But for many parents who are not convinced their children are ready to handle wealth, they are not idly sitting by hoping their children have a sudden flash of financial acumen. No, these parents are taking matters into their own hands.

1. Give your kids a financial test. Each person can gift up to $14,000 (in 2014) per year to as many people as they wish without any gift tax consequence. If you are married, both you and your spouse can give $28,000 per person. Parents are gifting their children money without any restrictions or rules and then sitting back and watching what happens. How will your children handle a $5 million inheritance? Why don’t you see what they do with $20,000 first? Do they save it? Do they ask for help? Do they pay off debt? Do they blow it in Vegas?

2. Use incentive trusts. The fear of many parents (and apparently Anderson Cooper) is that too much money can squash ambition and drive. The image that keeps many affluent up at night is the idea that their kids will be robbed of zeal to make an impact – this same zeal and inner drive that pushed them to make their own mark on the world. The solution for many parents is to use incentives within a trust rather than leaving a large inheritance outright. The incentives can be as creative as you can imagine. For example, a common incentive – euphemistically called an “investment banker clause” – calls for trust distributions that match the child’s income. If Suzie makes $75,000 from her job, the trust will distribute to her $75,000 each year. If her younger brother Johnny spends too much time playing Xbox and only makes $22,000 a year, the trust will distribute just $22,000 to him. The built-in incentive with this clause is, of course, to make money. But what if Suzie wants to join the Peace Corps? You can add language that will ensure distributions if your child is involved in a non-profit. Again, the sky is the limit when it comes to drafting who gets what and when. Newport Beach estate planning attorney Cheryl Barrett, says “I often build educational incentives in parents’ and grandparents' trusts that are designed to reward the beneficiaries' educational accomplishments.” For example, the trustee might be directed to disburse $10,000 upon attainment of a Bachelor's degree and $20,000 upon attainment of a Master's or Doctorate degree. While Barrett acknowledges that a degree is not a guarantee of a beneficiary's personal success, she states, “The pursuit of it requires vision, goal setting, and engagement with other motivated individuals, all of which enhance a beneficiary's likelihood of success."

3. Tie distributions to ages and events. Think back to when you were 20 years old. Would you have been emotionally and intellectually mature enough to handle a large inheritance? Many parents create their trust so that their kids get a small amount of money each year and larger amounts when they reach certain ages (e.g., 30, 35, 40). They will also allow for trust distributions to pay for college expenses, weddings, or house down payments. A popular strategy is to distribute income from the trust assets when the kids are young and then to distribute principal when they are older and, ideally, have a career and greater financial sophistication.

4. Get your kids involved in a personal foundation. If you have children still living with you, creating a personal foundation can be a wonderful opportunity to support causes you believe in, get a nice tax deduction, and more importantly to our point, teach kids about money. One of my clients sold his business and overnight was worth more than $25 million. He and his wife had three young kids and they were worried that the dad’s strong work ethic would be lost on the kids now that they could have anything they wanted. We created a personal foundation, and because it was required to disburse 5% of the foundation’s balance each year, we gave each family member the responsibility of researching a cause and donating 1%. This got each of the kids excited about their own cause and seeing how their money could have an impact. It was a great learning experience for the whole family.

5. Give without giving cash. There is another win-win alternative to outright gifting. Jeff Lewis, an estate planning attorney in Los Angeles likes this approach. Lewis says, "Many of my clients have started using their annual federal gift exclusion ($14,000 as of this writing) to directly pay down either an adult child's mortgage principal or school loans. This will make a significant difference to the child's future financial position, while not putting that amount of cash in their hands today.” Many parents realize that mortgages and school loans are substantially larger now than in their time, so helping to reduce that huge burden is a rewarding proposition for both generations. Lewis continues, “Be sure to check there are no pre-payment penalties or other negative loan consequences."

As a parent, you want what is best for your kids. It’s natural and reasonable to worry how a large inheritance will affect their drive and choices for life. With some planning, money can be a tool that enriches their lives rather than an anchor that drags them down. Consider the strategies above and talk to your financial advisor and estate attorney for more ideas.

Connect with me on Twitter @rpagliarini, my financial planning blog, or email me. This discussion is not intended as financial, legal or tax advice, and cannot be relied upon for any purpose without the services of a qualified professional.


Achondroplasia is a genetic (inherited) condition that results in abnormally short stature and is the most common cause of short stature with disproportionately short limbs. The average height of an adult with achondroplasia is 131 cm (52 inches, or 4 foot 4 inches) in males and 124 cm (49 inches, or 4 foot 1 inch) in females.

Although achondroplasia literally means "without cartilage formation," the defect in achondroplasia is not in forming cartilage but in converting it to bone, particularly in the long bones.

Achondroplasia is one of the oldest known birth defects. The frequency of achondroplasia is estimated to range from about 1 in 10,000 births in Latin America to about 12 in 77,000 in Denmark. An average figure worldwide is approximately 1 in 25,000 births.

What are the characteristics of achondroplasia?

Achondroplasia is a distinctive condition that usually can be noted at birth.

  • The baby with achondroplasia has a relatively long, narrow torso (trunk) with short extremities (arms and legs) and a disproportionate shortening of the proximal (near the torso) segments of the limbs (the upper arms and thighs).
  • There is a typically large head with prominence of the forehead (frontal bossing), underdevelopment (hypoplasia) of the midface with cheekbones that lack prominence, and a low nasal bridge with narrow nasal passages.
  • The baby's fingers appear short and the ring and middle fingers may diverge, giving the hand a trident (three-pronged) appearance. Most joints can extend more than normal. For example, the knees can hyperextend beyond the normal stopping point. Not all joints are lax in this way. To the contrary, extension and rotation of the elbow are abnormally limited. Hip extension also tends to be limited.
  • At birth there is often prominence of the mid-to-lower back with a small gibbus (a hump). With walking, the hump goes away and a pronounced sway (lordosis) of the lumbar region (the lower back) becomes apparent. The lumbar lordosis is persistent into adulthood. The legs are bowed (genu varum).
  • The baby exhibits some decrease in muscle tone (hypotonia). Because of the large head, especially compared to rest of the body, and the decreased muscle tone, the child with achondroplasia will run "behind schedule" in reaching the usual motor developmental milestones. The schedule to which an achondroplastic child's development should be compared is not that for all children in the general population, but rather the growth charts and timetable followed by children with achondroplasia.
  • Intelligence is generally normal in patients with achondroplasia. Enlargement of the brain (megalencephaly) is common and normal with achondroplasia.

Achondroplasia Symptoms & Signs

Signs and symptoms of achondroplasia include short stature with disproportionately short limbs. Other signs include a

  • large head with prominence of the forehead (frontal bossing),
  • underdevelopment (hypoplasia) of the midface with cheekbones that lack prominence,
  • narrow nasal passages with a low nasal bridge,
  • short fingers,
  • the ability of many joints to extend beyond the normal range, and
  • an excessive inward curvature (lordosis) of the low back.

How is achondroplasia diagnosed?

The diagnosis of achondroplasia can be based on the typical physical features, the hallmarks of achondroplasia, evident at birth. Characteristic features are also seen by X-rays, ultrasound, and other imaging techniques. With ultrasound imaging, the diagnosis can sometimes be strongly suspected before birth.

The molecular diagnosis of achondroplasia before birth is possible if there is suspicion of the diagnosis or an increased risk (such as when a parent is affected by achondroplasia). In families in which both parents have achondroplasia, prenatal diagnosis may be particularly useful, the aim being to distinguish fatal homozygous achondroplasia (with two copies of the defective gene) from heterozygous achondroplasia (with one copy of the achondroplasia gene) from normal. Diagnosis before birth is accomplished by examining cells obtained by chorionic villus sampling (CVS) or amniocentesis.

What can be done for patients with achondroplasia?

Children and adults with achondroplasia can lead normal lives provided they receive attentive, informed care by their physicians and parents. Considerations in monitoring children with achondroplasia include careful measurements of growth (length/height and weight) and head circumference using curves specially standardized for those with achondroplasia. Knowledgeable pediatric care and periodic orthopedic and neurologic examinations are critical.

When special problems complicate achondroplasia, prompt and expert intervention is important. For example:

  • The foramen magnum (the large opening under the skull) may need to be surgically enlarged in cases of severe narrowing (stenosis) and compression of the spinal cord. When this opening is too narrow, the blood vessels and nerves are compressed, which can lead to central apnea (loss of breathing control). This is responsible for the risk of sudden death in infants (SIDS) with achondroplasia. The risk of sudden death for infants with achondroplasia is 2% to 5%.
  • The back of individuals with achondroplasia can develop a marked sway (lordosis) to the lower back while abnormalities in the mid-back may cause a small hump (kyphosis) in infancy and compression of the spinal cord in adolescence. The spinal cord compression can require surgery to decompress it. Spinal stenosis is the most common medical complication of achondroplasia seen in adulthood.
  • Orthopedic procedures may be performed for lengthening of the limb bones and correction of bowed legs (usually after full growth has been achieved).
  • Surgery (lumbar laminectomy) is also indicated when spinal stenosis (narrowing) causes symptoms, which tends to be evident in young adults.
  • Disproportion between the brain and the base of the skull can sometimes result in hydrocephalus ("water on the brain") which needs to be promptly detected and treated by placement of a shunt to drain the excess fluid.
  • The large head with achondroplasia increases the chance of bleeding within the baby's head during vaginal delivery. This should be taken into account in planning the birth and postnatal care, and Cesarean delivery (C-section) may be recommended for a fetus with achondroplasia. The brainstem (which contains a center for controlling respiration) may be compressed in achondroplasia and contribute to abnormal breathing. women with achondroplasia should have their babies delivered by cesarean section, due to their characteristically small pelvis, and high risk of birth related trauma.
  • Middle ear infections (otitis media) are frequent and can lead to mild to moderate hearing loss. Therefore, ear infections should be readily suspected and promptly and fully treated with antibiotics and/or ear tubes.
  • Dental crowding is also common. Teeth should be straightened and, if necessary, removed to alleviate this problem.
  • Control of obesity is essential, and obesity can be a significant problem in people with achondroplasia. The excessive weight gain usually occurs during childhood. When obesity is present, the back and joint problems that are characteristic of this condition worsen in severity. The child with achondroplasia must not be allowed to become overweight. Adults with achondroplasia should also monitor and control their weight.
  • Treatment with human growth hormone, which is still considered experimental, has been preliminarily reported to increase the growth rate after treatment, but studies have not yet demonstrated that adult height is increased by this treatment.


How is achondroplasia inherited?

Achondroplasia is inherited as an autosomal dominant trait whereby only a single copy of the abnormal gene (mutation) is required to cause achondroplasia. The gene for achondroplasia is fully penetrant, meaning that everyone who possesses it has achondroplasia. No one with the gene escapes achondroplasia. However, there is some variation in the expression of the gene, meaning that children with achondroplasia are not carbon copies of each other, although they may look alike to the untutored eye.

In only about an eighth of cases is the gene inherited from a parent who has achondroplasia. Rather, about seven-eighths of cases are due to a new mutation (a new change in the gene). This means that most cases of achondroplasia occur sporadically (out of the blue) and are the result of a new mutation in a sperm or ovum of one of the normal- appearing parents. The chance of a new mutation rises with the age of the father. As early as 1912 it was noted that sporadic (new) cases were more often last-born than first-born children. This fits with the fact that the chance of an achondroplastic birth has been shown to increase with paternal age (age of the father).

What if someone with achondroplasia has children?

Although most children with achondroplasia do not have an achondroplastic parent but have a new mutant gene for achondroplasia, they can still transmit the gene to their children, and the risk for passing that gene down to a child is 50% in each pregnancy.

What if two people with achondroplasia have children?

People with achondroplasia sometimes have children together. If so, each parent has a 50:50 chance of passing on the gene. Thus, with each conception, there is a 25% chance for an average-size child, a 50% chance for a child (like them) with achondroplasia and a 25% chance for a conception with two achondroplasia genes. The combined presence of two genes for achondroplasia (called homozygous achondroplasia) causes a grievous skeletal disorder that leads to early death from breathing failure due to constriction by a tiny chest cage and neurologic problems from hydrocephalus.