What Are Growth Hormone Secretagogues?

Me: It seems the hypothalamic-pituitary pathway system not only releases growth hormones (GH) but also growth hormone secretagogues (GHS). The human body releases growth hormones throughout life, which decreases to a lower rate later in life. At the same time the growth hormone is being released, the growth hormone inhibiting somatostatin is also released at the same time. It would appear that as time moves forward and we grow older, the rate of somatostatin release increase, until it overtakes the rate of GH release. remember that the release of GH by the pituitary is controlled by growth hormone releasing hormone and somatostatin in the hypothalamus.

The synthetic type of GH we could take after reaching physical maturity would have to be in injection form. However, this method is not in the pulsating fashion that GH is supposed to act in the body. Naturally, the hypothalamic-pituitary system releases GH in a pulsation way into the body. The secretagogues are peptides made of 6 amino acids linked together. These GHS can be taken orally without the stomach digesting the peptide and breaking it up effectively destroying it.

It seems that GHS like MK-677 in experiments have mixed results. The link says that the authors think GHS works because it mimics ghrelin towards the body’s GH receptors. If I was asked whether GHS can be used to increase height, I would say it could work for people who are of short stature due to low growth hormones in the system but probably little else. THe IGF-1 level was shown to increase from GHS intake from the first study below. 

From the website Iron Man Magazine, a well written article on GHS.

From the website on The Journal Of Endocrinology & Metabolism

Effects of an Oral Growth Hormone Secretagogue in Older Adults

  1. Heidi K. White, Charles D. Petrie, William Landschulz, David MacLean, Ann Taylor,Kenneth Lyles, Jeanne Y. Wei, Andrew R. Hoffman, Roberto Salvatori, Mark P. Ettinger,Miriam C. Morey, Marc R. Blackman, George R. Merriam and for the Capromorelin Study Group

Author Affiliations


  1. Duke University School of Medicine and Geriatric Research Education and Clinical Center (GRECC), Durham Veterans Affairs (VA) Medical Center (H.K.W., K.L., M.C.M.), Durham, North Carolina 27710; Pfizer Global Research and Development (C.D.P.), Groton, Connecticut 06340; Endocrine Clinical Research (W.L.), Eli Lilly and Co., Indianapolis, Indiana 46285; Brown University Medical School (D.M.), Providence, Rhode Island 02912; Novartis (A.T.), Cambridge, Massachusetts 02139; GRECC, Central Arkansas Veterans Affairs (VA) Healthcare System, and University of Arkansas for Medical Sciences (J.Y.W.), Little Rock, Arkansas 72205; VA Palo Alto Health Care System and Stanford University (A.R.H.), Palo Alto, California 94304; The Johns Hopkins University School of Medicine (R.S.), Baltimore, Maryland 21205; Radiant Research and the Regional Osteoporosis Center (M.P.E.), Stuart, Florida 34996; Washington DC VA Medical Center (M.R.B.), Washington, D.C. 20422; and VA Puget Sound Health Care System and University of Washington School of Medicine (G.R.M.), Seattle and Tacoma, Washington 98493
  1. Address all correspondence and requests for reprints to: Heidi K. White, M.D., M.H.S., Duke University School of Medicine, Box 3003, Durham, North Carolina 27710. E-mail:White031@mc.duke.edu.

Abstract

Context: GH secretion declines with age, possibly contributing to reduced muscle mass, strength, and function. GH secretagogues (GHS) may increase muscle mass and physical performance.

Objectives/Design: We conducted a randomized, double-masked, placebo-controlled, multicenter study to investigate the hormonal, body composition, and physical performance effects and the safety of the orally active GHS capromorelin in older adults with mild functional limitation.

Intervention/Participants: A total of 395 men and women aged 65–84 yr were randomized for an intended 2 yr of treatment to four dosing groups (10 mg three times/week, 3 mg twice a day, 10 mg each night, and 10 mg twice a day) or placebo. Although the study was terminated early according to predetermined treatment effect criteria, 315 subjects completed 6 months of treatment, and 284 completed 12 months.

Results: A sustained dose-related rise in IGF-I concentrations occurred in all active treatment groups. Each capromorelin dose prompted a rise in peak nocturnal GH, which was greatest with the least frequent dosing. At 6 months, body weight increased 1.4 kg in subjects receiving capromorelin and decreased 0.2 kg in those receiving placebo (P = 0.006). Lean body mass increased 1.4 vs. 0.3 kg (P = 0.001), and tandem walk improved by 0.9 sec (P = 0.02) in the pooled treatment vs. placebo groups. By 12 months, stair climb also improved (P = 0.04). Adverse events included fatigue, insomnia, and small increases in fasting glucose, glycosylated hemoglobin, and indices of insulin resistance.

Conclusions: In healthy older adults at risk for functional decline, administration of the oral GHS capromorelin may improve body composition and physical function.

From the Dr. Lam website article on Growth Hormones And Growth Hormone Secretagogues located HERE

B. Amino Acid Secretagogues

A secretagogue (pronounced se-cre’-ta-gog) is a natural polyamino acid chain that is postulated to initiate the pituitary gland to release growth hormone. It is the precursor to hGH. While hGH causes the body to act as if the pituitary has released growth hormone, a secretagogue actually causes the release of it. Hence a secretagogue causes the bodies own natural processes to produce growth hormones. Secretagogues do not act as growth hormones at all as they stimulate the pituitary gland to secrete growth hormone.

Interestingly, the inconvenience of hGH injections first led to the discovery of Secretagogues. For years, it was believed that the pituitary gland, which produces growth hormones, dries up as a natural effect of aging. Science has recently discovered that growth hormones reside in the pituitary gland, which stops the release due to aging. Scientists then discovered that certain combinations of amino acids could actually spur the pituitary gland to release the growth hormones. Experiments soon led to the right combinations.

Natural secretagogue is the most practical approach because there are no side effects. In comparison with hGH, their potency and efficacy are low. Since these are orally taken, they can be a first line approach for those who may not choose hGH injections.

This category of hGH products uses amino acids as “secretagogues,” which stimulate the pituitary gland to produce hGH. Other proprietary agents are usually part of the powder/tablet mix, which provide each product with a presumed marketing advantage. Studies show that certain amino acid combinations such as L-lysine, L-arginine, L-ornithine and L-glutamine can stimulate pituitary hGH. While this is theoretically plausible and positive clinical results have been widely reported, published double blind controlled studies that show evidence that these other proprietary factors provide additional pituitary hGH secretion is still incomplete at best. Most studies reveal at least two grams of amino acids are needed to have any effect on pituitary hGH stimulation.

Glutamine

Glutamine is the most abundant amino acid in the body and causes GH secretion. It is a conditional amino acid as the body may not be able to synthesize it under stressful conditions. Traditionally it has been used to strengthen the immune system. The standard anti-aging intake is 50 mg to 1 gm twice daily.

Glutamine is a neurotransmitter in the brain. It is essential for proper brain functions, immune functions, kidneys, pancreas, bladder, and liver functions.

Glutamine becomes one of our body’s most powerful antioxidants in high quantities. Many people, especially those in weight training, add this amino acid due to its benefit in muscle metabolism. Supplementation of two to three gm/day is quite common. For those who plan to take extra doses, it is best to divide the doses throughout the day with up to four servings daily.

Two grams of glutamine was shown to cause a four fold increase in Growth Hormone levels.

Lysine

Lysine is an essential amino acid, which affects bone formation, height, and genital function. It also boosts the effects of arginine. The recommended dosage is one gram on an empty stomach one hour before bedtime and before exercise.

Ornithine

Ornithine is a non-essential amino acid. It is used to potentate the effect of Arginine. The suggested dosage is one gram at bedtime. Doses of more than two to five grams have been known to cause diarrhea.

C. Oral Peptide Secretagogues

hGH is a hormone made up of a long chain of amino acids. Only a portion of the long chain of amino acids makes up the active ingredient. Researchers have been able to identify and extract these active peptides, which are usually five to ten amino acids linked together in a chain. These are then stabilized and formulated into a power or tablet effervescent form. The oral tablets are dissolved in water to be taken before bedtime on an empty stomach. This is to stimulate the release of hGH from the anterior pituitary, which peaks during the early phase of sleep. The effervescent form is best to draw the peptide away from the gastric juice closer to the mucous for better absorption. Gastric juices are highly acidic. Peptides are proteins that are easily denatured when exposed to an acidic environment. Extraction of the peptide is a tedious process. Peptides are not stable enough to maintain its activity in an aqueous environment. Thus, the peptide is formulated in the oral tablet format. Secretagogues using peptides are abundant in the marketplace. They are sold as a natural nutritional supplement and no FDA approval is required. However, some unscrupulous operators simply use ground bovine pituitary gland and pass them off as secretagogues. The consumer is often faced with the arduous task of identifying which is the real secretagogue.

Secretagogues can also work at multiple sites leading to growth hormone release. For example, a secretagogue targeted towards the hypothalamus would stimulate the hypothalamus to release Growth Hormone Releasing Factor (GHRF) that in turn stimulates the pituitary gland to release growth hormone. An oral peptide pituitary secretagogue, on the other hand, stimulates the pituitary gland directly to effect the release of growth hormone.

An effective secretagogue could easily raise IGF-1 levels, although the result is not as significant as growth hormone injections. Clinically many users have reported better sleep, increased alertness during the day, and less joint pain.

IGF-1 levels may not be the best indicator of how effective a secretagogue is for the GH receptor sites may be damaged. A low IGF-1 level does not mean that the body’s growth hormone level has not increased. It may simply mean that that the level is not accurately measured, or that there is a defective receptor site. If your IGF-1 does not increase, do not be despair. Talk to your health care practitioner. How you feel is just as important and sometimes even more important than laboratory studies alone.

D. Growth Factors

Growth factors (GF) are small protein chains, commonly known as polypeptides, which bind to cell surface receptor sites and exert actions directly on the target cells. This is generally done through cellular proliferation and or differentiation.

Some GFs exert generalized effect, while others are cell and action specific. There are many different classes of GFs. Some common ones include: Insulin-like Growth Factor (IGF-1) that is responsible for much of Growth Hormones (GH) action in the body; Interleukins (IL); Fibroblast Growth Factors (FGF); Transforming Growth Factor (TGF); Tumor Necrosis Factor (TNF); Epidermal Growth Factor (EGF); and Transforming Growth Factors-b (TGFs-b).

GFs come from a wide variety of sources. Epithelial Growth Factors (EGF) comes from sub maxillary gland, and FGF comes from a wide range of cells. A unique family of growth factors that is secreted primarily by leukocytes (white blood cells) is called cytokines. When such cytokines are secreted by lymphocytes, they are called lymphokines. Many of the lymphokines are also known as interleukins (ILs). Not only are interleukins secreted by leukocytes, they are also able to affect the cellular responses of leukocytes.

What Do Growth Factors Do? 

Different GFs have different jobs to do. Generally, all of them work at the cellular level to:

Repair damaged cells

Enhance cellular proliferation

Maintain optimum function of the target organ

Rejuvenate aging tissues

While hormones generally are more specific and sometimes work through other mediations elicited from its simulation of intermediate organs, GFs often act directly on the target tissue and have a wide range of effects. Its action is mostly stimulatory. It can also work synergistically with other GFs or hormones to elicit a biological effect. Growth hormone, for example, exerts its effect in the body via Insulin-like Growth Factor (IGF-1). In other words, it is the IGF-1 that actually carries out the function of growth hormone and not growth hormone itself.

The Connection Between mTOR, Rapamycin, Leucine And Height

Me: Throughout the other boards I have come across on the occasional thread which talks about the possibility of using mTor or Leucine to increase height.

Now as I have shown in previous posts, there is a link between tall stature and increased chance for cancer and faster aging rate. It seems that what makes you taller, makes it more likely that you develop cancer and age faster.

With mTor it has been shown in studies to possibly increase the rate of aging in people and also increase the chance for cancer. So using sort of a reverse causality type of logic, (which is not really logic but correlation) I would guess that Leucine and mTor might have some connection with height and might contribute to growth somehow.

Analysis: From the first article I found, we learn that mTor Stands for mammalian target of rapamycin (didn’t know that) which is a nutrient sensing protein kinase that regulates numerous cellular processes. In an experimental chondrogenic cell line, rapamycin seems to regulate and inhibit proteoglycan accumulation and collagen X exprsesion. This would suggest that the overall affect of Rapamycin is to inhibit the creation of chondrocytes. It decreases the amount of Ihh, which regulates chondrocyte differentiation If you added more ihh into the culture, it reverses the effect of mTor. The researchers concluded that if you can control and manipulate the mTOR signalling, you can control at least part of the mechanism causing chondrocyte differentiation, thus also longitudinal growth. 

In the 2nd article the researchers found that if you inactivate TOR or its substrate s6 kinase you cause cells to be smaller in size and also die. This shows that the TOR pathway controls cell growth. They did a homogolous recombination of the deletion of the C-terminal six amino acids of mTOR, which are essential for kinase activity, resulted in reduced cell size and proliferation arrest in embryonic stem cells. mTOR controls cell size and proliferation at least in mouse stem cells. mTOR can make cells produce chemicals such as cyclins that trigger cell growth.

In the 3rd article, the writer states from the beginning, ” Amino acids, in particular leucine, have been shown to regulate cell growth, proliferation, and differentiation through the mammalian target of rapamycin (mTOR), a nutrient-sensing protein kinase”…plus “we hypothesized that leucine restriction, acting through mTOR, would inhibit growth plate chondrocyte proliferation and differentiation. The effect of leucine restriction was compared with that of the specific mTOR inhibitor, rapamycin. Leucine restriction produced a dose-dependent inhibition of fetal rat metatarsal explant growth. This was accounted by reduced cell proliferation and hypertrophy but not apoptosis. mTOR activity, as reflected by ribosomal protein S6 phosphorylation, was only partially inhibited by leucine restriction, whereas rapamycin abolished S6 phosphorylation. In chondrogenic ATDC5 cells, leucine restriction inhibited cell number, proteoglycan accumulation, and collagen X expression despite minimal inhibition of mTOR

So we can say that leucine can influence mTOR which influences chondrogenesis which influeneces longitudinal growth. Rapamycin also influences mTOR but negatively. increases in leusin increase mTOR which increase chondrogenesis. increase in rapamycin leads to reduced mTOR which reduces chondrogenesis. If you see a decrease in chondrogenesis from leucin restriction you get clumping of proteoglycans and increased production of collagen X. The issues is that leucin and rapamycin both have a small effect on the overall genes.

I did a very quick search on Google for any evidence and this is what i found…

From link HERE

Dev Dyn. 2008 Mar;237(3):702-12.

mTOR signaling contributes to chondrocyte differentiation.

Phornphutkul C, Wu KY, Auyeung V, Chen Q, Gruppuso PA.

Source

Department of Pediatrics, Division of Pediatric Endocrinology and Metabolism, Rhode Island Hospital and Brown University, Providence, Rhode Island 02903, USA. chanika_phornphutkul@brown.edu

Abstract

The mammalian Target Of Rapamycin (mTOR) is a nutrient-sensing protein kinase that regulates numerous cellular processes. Fetal rat metatarsal explants were used as a physiological model to study the effect of mTOR inhibition on chondrogenesis. Insulin significantly enhanced their growth. Rapamycin significantly diminished this response to insulin through a selective effect on the hypertrophic zone. Cell proliferation (bromodeoxyuridine incorporation) was unaffected by rapamycin. Similar observations were made when rapamycin was injected to embryonic day (E) 19 fetal rats in situ. In the ATDC5 chondrogenic cell line, rapamycin inhibited proteoglycan accumulation and collagen X expression. Rapamycin decreased content of Indian Hedgehog (Ihh), a regulator of chondrocyte differentiation. Addition of Ihh to culture medium reversed the effect of rapamycin. We conclude that modulation of mTOR signaling contributes to chondrocyte differentiation, perhaps through its ability to regulate Ihh. Our findings support the hypothesis that nutrients, acting through mTOR, directly influence chondrocyte differentiation and long bone growth.

Me: It seems that mTOR may be one of the things that regulates Ihh.

From link HERE

mTOR Is Essential for Growth and Proliferation in Early Mouse Embryos and Embryonic Stem Cells

  1. Mirei Murakami1,2, Tomoko Ichisaka1,2, Mitsuyo Maeda3, Noriko Oshiro2,4,Kenta Hara2,5, Frank Edenhofer6, Hiroshi Kiyama3, Kazuyoshi Yonezawa2,4,* and Shinya Yamanaka1,2,*

+Author Affiliations

  • 1Research and Education Center for Genetic Information, Nara Institute of Science and Technology
  • 2CREST, Japan Science and Technology Agency, Nara 630-0192
  • 3Department of Anatomy and Neurobiology, Osaka City University Medical School, Osaka 545-8585
  • 4Biosignal Research Institute, Kobe University, Hyogo 657-8501
  • 5Fourth Department of Internal Medicine, Kobe University School of Medicine, Hyogo 650-0017, Japan
  • 6Institute of Reconstructive Neurobiology, University of Bonn Medical Center, D-53105 Bonn, Germany

ABSTRACT

TOR is a serine-threonine kinase that was originally identified as a target of rapamycin in Saccharomyces cerevisiae and then found to be highly conserved among eukaryotes. In Drosophila melanogaster, inactivation of TOR or its substrate, S6 kinase, results in reduced cell size and embryonic lethality, indicating a critical role for the TOR pathway in cell growth control. However, the in vivo functions of mammalian TOR (mTOR) remain unclear. In this study, we disrupted the kinase domain of mouse mTOR by homologous recombination. While heterozygous mutant mice were normal and fertile, homozygous mutant embryos died shortly after implantation due to impaired cell proliferation in both embryonic and extraembryonic compartments. Homozygous blastocysts looked normal, but their inner cell mass and trophoblast failed to proliferate in vitro. Deletion of the C-terminal six amino acids of mTOR, which are essential for kinase activity, resulted in reduced cell size and proliferation arrest in embryonic stem cells. These data show that mTOR controls both cell size and proliferation in early mouse embryos and embryonic stem cells.

Me: So mTOR in general controls cell size and proliferation in stem cells and embryos. That sounds pretty important in longitudinal growth to me.

From link HERE

mTOR inhibitors

mTOR is a kinase protein. It can make cells produce chemicals such as cyclins that trigger cell growth. It may also trigger cells to produce proteins which trigger the development of new blood vessels that cancers need in order to grow. In some types of cancer mTOR is switched on, which makes the cancer cells grow and produce new blood vessels. mTOR inhibitors are a new type of cancer growth blocker being used to try to stop the growth of some cancers. mTOR inhibitors include temsirolimus (Torisel), everolimus (Afinitor) and deforolimus.

As for Leucine, from link HERE

Leucine restriction inhibits chondrocyte proliferation and differentiation through mechanisms both dependent and independent of mTOR signaling

  1. Mimi S. Kim1,*, Ke Ying Wu1,*, Valerie Auyeung2, Qian Chen2,Philip A. Gruppuso2, and Chanika Phornphutkul1

+Author Affiliations

  1. Division of Pediatric Endocrinology and Metabolism, Departments of 1Pediatrics and 2Orthopaedic Surgery, Rhode Island Hospital/Warren Alpert School of Medicine of Brown University, Providence, Rhode Island
  1. Address for reprint requests and other correspondence: C. Phornphutkul, Division of Pediatric Endocrinology and Metabolism, Rhode Island Hospital, 593 Eddy St., Providence, RI 02903 (e-mail: Chanika_Phornphutkul@brown.edu)
  • Submitted 19 December 2008.
  • Accepted in final form15 April 2009.

Abstract

Linear growth in children is sensitive to nutritional status. Amino acids, in particular leucine, have been shown to regulate cell growth, proliferation, and differentiation through the mammalian target of rapamycin (mTOR), a nutrient-sensing protein kinase. Having recently demonstrated a role for mTOR in chondrogenesis, we hypothesized that leucine restriction, acting through mTOR, would inhibit growth plate chondrocyte proliferation and differentiation. The effect of leucine restriction was compared with that of the specific mTOR inhibitor, rapamycin. Leucine restriction produced a dose-dependent inhibition of fetal rat metatarsal explant growth. This was accounted by reduced cell proliferation and hypertrophy but not apoptosis. mTOR activity, as reflected by ribosomal protein S6 phosphorylation, was only partially inhibited by leucine restriction, whereas rapamycin abolished S6 phosphorylation. In chondrogenic ATDC5 cells, leucine restriction inhibited cell number, proteoglycan accumulation, and collagen X expression despite minimal inhibition of mTOR. Microarray analysis demonstrated that the effect of leucine restriction on ATDC5 cell gene expression differed from that of rapamycin. Out of 1,571 genes affected by leucine restriction and 535 genes affected by rapamycin, only 176 genes were affected by both. These findings indicate that the decreased chondrocyte growth and differentiation associated with leucine restriction is only partly attributable to inhibition of mTOR signaling. Thus nutrient restriction appears to directly modulate bone growth through unidentified mTOR-independent mechanisms in addition to the well-characterized mTOR nutrient-sensing pathway.

UNDERNUTRITION IS A WELL-DOCUMENTED cause of poor linear growth, whereas obesity produces accelerated linear growth in children. Primary causes of undernutrition are complex. They can range from inadequate availability of calories to inadequate specific nutrients, such as protein or amino acids. Despite the many causes and forms of undernutrition, one universal outcome is poor long bone growth, which can be presumed to be an effect on endochondral bone elongation (1, 6). Over the last several decades, the mechanisms by which nutritional status affects bone growth have focused on indirect effects via changes in insulin-like growth factor I (IGF-I) biological effect (3, 7). Impaired IGF-I production in undernutrition is in part associated with impaired hepatic growth hormone (GH) sensitivity, which is associated with decreased hepatic GH receptor expression, hepatic IGF-I mRNA, and circulating IGF-I levels (31). Similarly, overnutrition is associated with upregulation of the GH/IGF-I axis (23).

The effect of IGF-I on chondrocyte growth and differentiation within the growth plate has been well documented (14, 24). We and others have demonstrated that IGF-I has an important role in chondrocyte proliferation and differentiation (25, 28). In addition to the effects of IGF-I on chondrocytes, we have demonstrated that insulin at physiological concentration has a direct effect on chondrocyte differentiation (27), thus providing for another mechanism by which nutritional status can modulate bone growth.

In recent years, mechanisms by which nutrients exert a direct effect on cell growth and function have been elucidated (17). Although restriction of essential amino acids has been viewed as limiting because of their requirement as substrates for protein synthesis, essential amino acids also act as signaling factors in several regulatory pathways (15,16). Perhaps the most well-characterized signaling pathway regulated by amino acids has at its center the mammalian target of rapamycin (mTOR) (17). mTOR is a nutrient-sensing kinase that integrates input from amino acids, growth factors, and the energy status of the cell (15). It acts as a central controller of translation, controlling ribosomal biogenesis and global protein synthesis (4). The TOR protein is highly conserved from yeast to mammals (5). Rapamycin, a widely used immunosuppressive agent, directly inhibits mTOR activity and has been key to understanding the role of mTOR in cell regulation (22, 35).

We have recently demonstrated the effect of rapamycin on chondrocyte growth and differentiation in ATDC5 cells (26), fetal rat metatarsal explants (26), and the rabbit growth plate (unpublished observation). mTOR inhibition with rapamycin results in significantly decreased chondrocyte differentiation, a modest decrease in chondrocyte proliferation, and decreased total bone growth in physiological systems.

Leucine is the most potent nutrient regulator of mTOR signaling (29, 30). We therefore hypothesized that leucine availability would have a direct effect on chondrocyte growth and differentiation, resulting in decreased longitudinal bone growth when restricted. We further hypothesized that the effect of leucine restriction would be a direct result of mTOR inhibition, although mTOR-independent pathways have been described. One of these involves the mammalian general control nonderepressible 2 (GCN2) kinase (32). GCN2 is a stress kinase that is activated by amino acid starvation to modulate protein synthesis. GCN2 phosphorylates the α-subunit of the eukaryotic initiation factor (eIF2). The response that allows organisms to tolerate amino acid deprivation in states of malnutrition and starvation involves repression of protein synthesis and upregulation of amino acid biosynthesis and transport (10) with a net effect of decreased cell growth.

Based on our hypothesis and well-defined mechanisms that control chondrocyte growth and differentiation, we have performed studies using embryonic day 19 (E19) fetal rat metatarsal explants. The benefit of this model is the intact bone maintains its cell-cell and cell-matrix interaction. We have also used the ATDC5 chondrogenic cell line to extend our observations to an in vitro model. Last, using microarray analysis, we have explored other potential mechanisms accounting for the effect of leucine restriction on chondrocyte growth and differentiation.

DISCUSSION

The present studies were aimed at characterizing the effect of restricting a key nutrient, leucine, on two models of bone growth: metatarsal explants and growth and a chondrogenic cell line. Amino acids, particularly the branched-chain amino acids, regulate protein synthesis beyond the level of their own availability as the substrate for peptide-chain elongation (15, 17). They do so by functioning as signaling molecules. Leucine appears to be the most potent of the branched-chain amino acids in this regard, having a potent effect on signaling via two important signaling kinases, mTOR and GCN2 (8, 10,32, 33).

The mTOR signaling pathway has been shown to mediate the effects of leucine on mRNA translation initiation. We recently demonstrated the important role of mTOR in the regulation of chondrocyte growth and differentiation (26). Our previous findings provided for a mechanism whereby nutrients, acting through mTOR, can directly modify linear growth. In the present study, we performed analogous experiments comparing the effect of leucine restriction in the fetal metatarsal explant model as well as ATDC5 cells.

The present studies were undertaken to test the hypothesis that leucine restriction would exert its effects on bone growth through its ability to signal via mTOR. Using the more physiological bone explant model, we confirmed that leucine affected growth in a dose-dependent manner. The observed growth inhibition was associated with decreased chondrocyte proliferation as measured by decreased BrdU incorporation. Decreased chondrocyte proliferation presumably results in fewer chondrocytes that are available to differentiate and become hypertrophic cells, consistent with the decreased hypertrophic zone height that we observed.

Chondrocytes that differentiate into prehypertrophic and hypertrophic chondrocytes undergo a 4- to 10-fold increase in cytoplasmic volume, making distal hypertrophic cells a significant component of longitudinal bone growth. In rapidly growing bones, ∼10% of bone length is contributed by proliferating cells, a one-third by matrix synthesis throughout the growth plate, and nearly two-thirds by the contribution of hypertrophic cells (34).

Although leucine restriction appears to have an effect on chondrocyte proliferation and differentiation, we did not observe an increase in apoptosis as assessed by TUNEL staining. Premature cell death can result in reduced bone growth, as observed in humans with skeletal dysplasia (12) and in mice with disruption of genes important to chondrogenesis, including those encoding filamin B, matrilin-3, or components of the β-catenin signaling pathway (11, 21). Our results indicate that the effect of leucine restriction occurs during the early phase of the chondrocyte growth and differentiation process, not as a result of increased apoptosis.

Because mTOR is a signaling target for leucine, we examined the effect of leucine restriction on mTOR signaling in metatarsals by assessing the phosphorylation state of ribosomal protein S6. We observed only a modest decrease in phospho-S6 staining in the explants grown in 0.02 mM leucine. This was in sharp contrast to rapamycin, which abolished phospho-S6 staining. This raised the possibility that leucine response was mediated through a mechanism other than one involving modulation of mTOR activity.

Using the ATDC5 chondrogenic cell line, we extended our observations in an attempt to support or refute conclusions drawn from the metatarsal explant studies. Leucine restriction decreased chondrocyte differentiation as measured by accumulation of proteoglycan and expression of collagen X. Total cell mass measured by Neutral Red accumulation was also decreased. Again, markers of mTOR activity, S6 phosphorylation and the pattern of 4E-BP1 phosphorylation, were modestly inhibited under conditions of leucine restriction relative to the marked effect of rapamycin. The expression of Ihh, a key contributor to chondrocyte proliferation and differentiation (9, 18, 20), was also decreased under conditions of leucine restriction. We previously demonstrated that mTOR inhibition may directly regulate Ihh expression (26).

In an effort to identify an mTOR-independent pathway to account for the effects of leucine restriction, we examined the regulation of GCN2 in the ATDC5 cell line. The GCN2 pathway is activated by the accumulation of uncharged tRNAs during amino acid starvation as shown in myoblasts (10). This leads to the phosphorylation of eIF2α, resulting in inhibition of translation initiation of cellular proteins and a global reduction in protein synthesis (10, 13). We observed only a modest increase in the phosphorylation of eIF2α under conditions of leucine restriction.

Microarray analysis of the effects of leucine restriction vs. rapamycin on gene expression in ATDC5 cells revealed that only a small proportion of genes was affected by both leucine restriction and rapamycin. These genes, which numbered 176, accounted for 11.2% of the genes that were affected in leucine restriction. The large effect of leucine restriction relative to rapamycin (1,571 vs. 535 genes) may indicate that leucine restriction has a broader effect on chondrocyte growth and differentiation than does targeted inhibition of mTOR. Using very stringent criteria for significance, gene ontology and pathway analysis further supported marked differences in the effects of the two conditions.

In summary, our studies show that leucine restriction affects proliferation and differentiation in the ATDC5 chondrogenic cell line. Results using the fetal metatarsal explant model are consistent with the ATDC5 studies. Our findings support the conclusion that both mTOR and GCN2 signaling may contribute to the effect of leucine restriction on chondrocyte proliferation and differentiation and, therefore, on long bone growth. However, our studies are also consistent with the possibility that the effects of leucine restriction are mediated by pathways that are independent of effects on these two signaling kinases. We are left to conclude that the mechanism by which leucine restriction inhibits chondrogenesis and attenuates linear bone growth is complex, likely involving modulation of multiple pathways that may involve mTOR and GCN2, but that may also be independent of both of these well-characterized pathways.

Who Is The Real Superman? Comparing The Height And Size Of Dwight Howard And Shaquille O’neal

I had stated before once (or a few times before) that I used to really be obsessed with basketball as a teenager. I would practice for 4-5 hours everyday in the Summer heat. I wanted to possibly be a NBA player but I never did gain the size or the skills no matter how much I practiced. I always got my ass handed to me when going up against guys, even ones smaller than me.

I guess I realize now that my fate probably belongs more in the research lab than the court. So for today I wanted to write a rather fun post where I compare the height and size of Dwight Howard and Shaquille O’neal and see what could really claim to be the real “Superman” which they both have been labeled at some point in their professional basketball career. Of course, this will be similar in style and tone as a previous older post I did where I compared the height of Lebron James vs Kevin Durant, who I consider to be the two best basketball players on the planet today.

So let’s first see what the figures seem to say about the Ex-NBA star Shaquille O’neal.

If you have ever been involved in the NBA or know much about Shaq, it is that he has been almost always quoted and listed at a height of 7′ 1″ (2.16 meters) tall.

From a quick search on the internet from WikipediaBasketball ReferenceYahoo, NBA, they have all listed Shaq at 7′ 1″ (2.16 meters) in height.

From the NBA Predraft Measurements Profile on him on DraftExpress.Com (found from this link HERE) we see that Shaq was listed with these numbers….

He was drafted in the 1992 NBA as the #1 pick to the Orlando Magic.

  • Height Without Shoes: 7′ 1″
  • Height With Shoes: N/A
  • Weight: 303 lb
  • Wingspan: 7′ 7″
  • Standing Reach: 9′ 5″
  • Body Fat: 12.2
  • Maximum Vertical: 36 “
  • Maximum Vertical Reach: 12′ 5″
  • Birthday: 03/06/1972 (40 years old by this time in October 2012)
  • NBA time: 18 years with Orlando Magic, Los Angeles Lakers, Phoenix Suns, Miami Heat, Cleveland Cavaliers, Boston Celtics

Shaq’s weight has been far more volatile and has been listed from 325 lb (147 kg) on Wikipedia to claims that he was 360 lbs at one point.

From this source link HERE we find out that Shaq’s biological father named Joseph Toney who worked at a Newark Home Shelter is 6′ 1″ who used to be a local basketball start. Shaq’s mother Lucille has been claimed to have been 6′ 3″ which is extremely tall for any female. I remember years ago reading from a article that both of Shaq’s grandfathers from his mother’s and father’s side were 6′ 9″ in height, which is really insane.

We can see from the picture on the right which is of the 1996 Olympic Basketball Team that Shaq with his abnormally large shoes is standing on a podium with the other basketball All-Stars. It is sort of hard to make out which players are standing where but if you look close enough, you can make out the fact that Shaquille and David Robinson are standing on the same level height, which is three podiums off the ground. I would guess the reason why they took a picture of the team in this way was that they wanted to get a picture of all of the players in the Olympics team and get a good picture of all of the faces. That is not possible if certain people are taller than others which would block the face of some people. If you look closer, you would see that John Stockton and Hakeem Olajuwon are the other two players standing on the same ledge height. Stocken is listed at 6′ 1″ which would put his head at around the shoulder height area of Shaq, which he is. Olajuwon has been listed at 7 feet when he was playing for the Houston Rockets in the 90s but he admitted that his height was lower. I would guess his height was probably 6′ 11″ or maybe even 6′ 10″ (which is a very loweestimate for him). Olajuwon’s height reaches the eyebrow of Shaq and Robinson so his height seems to be right. Robinson was well known for being tall at 7′ 1″ as well. He was a very respected and kind, honest man so his listed height would be honest an accurate. If we look at the height of Robins and Shaq then, their height are almost the same, although Shaq may have slightly thicker shoes than Robinson.

There is a common story told by Shaq that at the age of 13, he was already 6’6″ or 6′ 7″ when he was stationed in Germany because he was what some people called a “military brat”. It was there where he met Coach Brown, who would eventually become his coach at LSU many years later.

His shoe size has also varied throughout his career being either listed at 22 or 23, which seems to be the largest feet of all the NBA players in history. Shaq is a very big guy so the heel and thickness in his sneakers must be large as well. The normal athlete has shoes or sneakers that are about 1-1.5″ thick. I would guess that since Shaq’s feet are so big, he has to get his shoes specifically designed so his shoe’s heel might be ever thicker, up to 2 inches maybe.

What is really strange is that on the CelebHeights.Com website for his profile HERE, there are actually people who claim that Shaq might “only” be 6′ 11″ which I have found really hard to believe. Most people who have ever met Shaq have all stated that he is a very big man, a true giant and almost no one doubts that Shaq is the 7′ 1″ he has been claiming for the last 20 years in basketball. I remember reading from a article post that Chris Kaman who is 7′ 0″ himself had stated that Shaq is probably the biggest man he has ever met, in terms of size, because there are a few guys in the NBA who might have been taller like Yao Ming.

Here is a picture of Shaq with his current girlfriend Nicole “Hoopz” Alexander who was a winner in a reality show (Flavor of Love). Alexander has been claimed to be around 5′ 2″ in height. This pictures gives a person a very good perspective at just how big Shaq is. There is only supposed to be a 2 feet or 24 inch difference in their heights but the picture makes it look like the height difference is far larger. If I was to make a guess, it would be maybe 3 feet difference, not 2. But, one should note that Alexander is not wearing any high heels or thick heeled shoes and shaq seems to be in his shoes, which give 1-2 inches of extra height. Still, the difference in size of the couple is something that I would do a double take on if I ever walked past the couple in the street.

One poster on the celebheights website posts this…

RisingForce says on 18/Jan/12 

RP says on 13/Jul/11 
OK….found out a couple of facts on Shaq. He was measured & weighed twice leading up to the ’92 draft. At one he was 7’0 5/8″ & 301 lbs….at the other he was 7’0 7/8″ & 303 lbs. In 2000-2001 season with the Lakers he weighed in at 327 lbs at training camp. Also, at one point after a injury kept him from practicing & performing any cardio for about 6 weeks in one season with the Lakers, he got as heavy as 368 pounds!!!

Can anyone verify this? Oddly specific figures to make up so that could be accurate, but when I’ve searched, nothing comes up to back this stuff up.

Me: I can only say that the facts might be true. When Shaq was photographed with certain other guys who were profiled at 7′ 1″ like Wilt Chamberlain or Kareem Abdul Jabbar, Chamberlain did look like he was taller than Shaq.

 

Now let’s see what Dwight Howard profile shows.

From sources like

Dwight himself states clearly in this Youtube video HERE (uploaded in 2008) that he is 6′ 11″. He also states that he weighs 270 lbs in the video.

From the NBA Predraft Measurements Profile on him on DraftExpress.Com (found from this link HERE) we see that Dwight was listed with these numbers….

High School:Southwest Atlanta Christian Academy
Hometown:Atlanta
Drafted: Rnd 1, Pick 1 in 2004 by Magic

  • Height Without Shoes: 6′ 9″
  • Height With Shoes: 6′ 10.25″
  • Weight: 240 lb
  • Wingspan: 7′ 4.5″
  • Standing Reach: 9′ 3.5″
  • Body Fat: N/A
  • No Step Vertical: 30.5″
  • Maximum Vertical: 35.5 “
  • Maximum Vertical Reach: N/A
  • Birthday: 12/08/1985 (26 years old by this time on October 2012)
To see whether Dwight is either the 6′ 9″ listed in the predraft measurements page or the 6′ 11″ he claims, let’s look at a few photos I have found around the internet. These two pictures are the photos of the 2008 Olympic Men’s Basketball Team. In the first picture, you can see that Coach K decided to line up all of the players by height, from tallest on the lef to the shortest on the right.
We can now see just how immense the  variability and change in size is of the basketball team. Keep in mind that Chris Paul has been listed at 6 ‘ 0″ which is slightly taller than the average US male citizen. From the picture and maybe the eye perspective it looks like Dwight could be maybe even a 1 foot and a half taller than Paul but he is supposed to be either 9 inches or 11 inches taller than Paul. We can estimate that the height of Dwight Howard is probably the same as Chris Bosh. From the sources and links found, Chris Bosh has been listed at 6′ 11″ on the NBA and basketball sites. I remember seeing a Youtube video once where Jay Leno made the obvious proclamation while talking to Chris Bosh that he is very tall. Leno asked Bosh how tall he is and Bosh said he was 6′ 11″. I seem to remember that earlier in Bosh’s career with the Raptors (I’m not sure about this fact) he was listed at 6′ 10″. The next tallest in the lineup would be Tayshuan Prince who has been listed at 6’ 9″. From the picture, I would easily guess that Prince is at least 2 inches shorter than Howard. It is important to note that Bosh is well known to have a rather long neck, which has been compared to a giraffe by other people. Howard has been talked about on basketball forums for having a rather small head. This shows that in terms of where the shoulder line is and wher ethe neck starts, Howards has a clear higher shoulder level than anyone else. This probably creates the illusion that Howard is taller than what he might actually be.

Here is another picture of Howard with the 2008 Olympic team, in their white uniforms.

I think it is rather clear now that Dwight Howard is probably not the 6′ 9″ that was measured on the predraft. Dwight was a few select players who came to the NBA directly from high school. I think Diwght was only 18 and as I have shown in previous posts, a male does not really stop growing until he is around 19-21. Even the way how NBA players have had growth spurts, it would not be that wild to state that after Howard was in the NBA, he continued to grow another 2 inches.

Most people have stated that the athleticism of Dwight is extremely high, and people like 4 time NBA champion Tim Duncan at 6′ 11″ has admitted that Dwight is far more talented than he was during his development.

Dwight is know around the NBA for his chiseled muscular build, his shoulders which are very big which has had many people wonder whether he has been using steroids to gain that big, and and his amazing jumping ability. In the  2008 Sprite Slam Dunk Competition which happens usually during the Halftime break for the annual All-Star game, Dwight jumped up to a reach of 12′ 6″ which is 1 inch higher than Shaq’s old record of 12′ 5″. That event can be validated from this Youtube Video of the event HERE.

As for the real question “Who is the real superman?” I would have to look into more than just the physical attributes that make up a person. Superman was not only big and strong, he also had strong character and cared about other people. When the character of Superman was first created in the 30s around the Great Depression, his listed height was 6′ 2″ and I think around 220 lbs. Back then 6′ 2″ was considered very big, but these days, there are many people who are taller than that. Some of the actors who played Superman in the movies like Christopher Reeves at 6′ 4″ and Brandon Routh at 6′ 3″ are taller than the original superman. When it comes to size, Shaq would be the clear choice. In terms of size, Shaq may have been the heaviest, and strongest NBA player in history, although Wilt Chamberlain has been shown to be super strong as well. For Wilt and Shaq, the very rules of how the game of basketball had to be changed because they were so dominant at one point.

For Dwight, most NBA greats have talked about ihs insane athleticism and jumping ability. It is very rare to find a man who is almost 7 feet be able to jump that high in the air. At his best, he is around 270 lbs of almost pure muscle, chiseled features, and can jump higher than shaq.

When you give the title or nickname of “Superman” to a person in any profession, they have to be great at almost everything when you combine and analysis all of the elements of the game. Offensively Dwight has been rather lacking in his career. Because of his jumping ability, he is a great shot blocker.

Personality wise, Shaq and Dwight both have a very friendly, outgoing, cheerful persona. Towards the media, Shaq has ventured into more venues than Dwight at this time. Shaq has been a musician producing a few records, had his own reality television show (even if Dwight was on it once), Has been in a few movies that he starred in, had been shown to be able to break dance on TV, has a Ph.D, has had his own statue unveiled at his alma mater, has being buying and investing in a diversified portfolio of companies, been a big social media star with twitter, and many other projects. Dwight has been on many commercials, TV appearances, has a youtube profile.

In terms of professional accomplishments, Shaq has won 4 NBA championships with a few MVPs while Dwight has been Defensive player of the year a few times ans is still chasing after his first championships.

When it comes to be the question of  title of superman to either Shaq or Dwight, I would have to give it to Shaq at this point because of his professional accomplishments and also his many projects and ventures out of his basketball life. He has been accomplished in academics, athletics, music, and television.

Determining Skeletal Maturity And Bone Age Using The Greulich Pyle Method Or Tanner Whitehouse Method

From this source link HERE

How does your endocrinologist determine whether you have stopped growing? Let’s find out.

There seems to be two main ways to determine skeletal maturity and bone age, using either the Greulich Pyle Method or the Tanner and Whitehouse Method. You get an X-ray or a radiograph done on your left hand. The reason it is your left hand has raised some questions and so far I have not found a reasonable answer for it. It seems the Greulich Pyle method is only used in the Netherlands from the source and it is far faster but not as reproducible and accurate as the Tanner and Whitehouse method.

For the Greulich Pyle Method…

There is a description for each of the development stages seen in the growth of the hand radiograph. The description is a guideline on how the physician should examine and diagnose the state of development of the bone.

Quoted from the source link…

The first step in an analysis is to compare the given radiograph with the image in the atlas that corresponds closest with the chronological age of the patient. Next one should compare it with adjacent images representing both younger and older children. When comparing the radiograph against an image in the atlas there are certain features a physician should use as maturity indicators. These features vary with the age of the child. In younger children the presence or absence of certain carpal or epiphyseal ossification centers are often pointers for the physician about the skeletal age of a child. In older children the shape of the epiphyses and the amount of fusion with the metaphysis is a good indicator of skeletal age. Once the atlas image that most resembles the radiograph is found the physician should conduct a more detailed examination of the individual bones and epiphyses. When the physician is sure that the matching radiograph has been found, she can find the skeletal age printed at the top of the page.

Me: When I read how this Method for determining bone age was done I couldn’t but felt slightly let down on how it is performed. I sort of expected the procedure to be more complex with some calculations. It seems to show that endocrinologists today might not even have a real way of calculating growth plate maturity, but sort of guess at it with an eyeball estimate which is not very accurate. 

For the Tanner and Whitehouse Method…

The tanner whitehouse method seems to be based on the bone standard maturity of certain areas in the hand instead of age. The method uses 20 regions of interest. Each region of interest is broken up into 3 parts, the epiphysis, diaphysis, and metaphysis, and the sections can be determined in the phalanx promixity.

Quoted from the source link…

The development of each ROI is divided into discrete stages and each stage is given a letter (A,B,C,D, . . ., I). A numerical score is associated with each stage of each bone. By adding the scores of all ROIs, an overall maturity score is obtained. This score is correlated with the bone age differently for males and females. The method has a modular structure which makes it suitable for automation. For the tanner whitehouse method, three score systems have been developed.

  • TW2 20 Bones: characterized by twenty bones including the bones of the first, third and fifth finger and the
  • carpal bones.
  • RUS: considers the same bones of the TW2 method except the carpal bones;
  • CARPAL: considers only the carpal bones.

For the finer details on the method, please refer to the source link above. I hope I gave you an idea on how pediatricians and endocrinologists try to evaluate whether you can still grow or not.

Graphical Outline Of The Endocrine System For Growth Development , For the Visual Learner

I was doing more research and I found this rather lovely graphical representation of the basic theoretical model on how the general growth hormones like GH and IGF are linked to accelerate and deccelerate the growth process. The source of the picture where it was taken from was from BCM on their website HERE

As you can see there appears to be two main negative feedback mechanisms causing and telling the hypothalamus to decrease the release of the growth hormone releasing hormone and increase somatotropin release inhibiting hormone. Ordinarily the hypothalamus would be releasing more GHRH and using less SRIF when the person is growing.

Overall there is actually 4 negative feedback mechanisms (but two mains ones). As you can see from the smaller graph, the GH release rate is far higher during sleep than waking periods. So kids, sleep more if you want to increase the growth rate.

What is surprising for me is that the GH seems to get to the IGFBP-3 as well as IGF-1 . Somehow I forgot that you need a binding protein to work on the actual protein.

The other odd thing from the diagram is that it suggests that there may be actually something else controlling the hypothalamus, which the graph termed “higher brain centers” which seems to be releasing neurotransmitters to the hypothalamus. What type of neurotransmitters is not stated in the document.

From the article…

Recently, a new class of orally active GH-secreting compounds (peptidyl and nonpeptidyl GH secretagogues) have been developed. GH secretagogue receptors are located in the hypothalamus
and pituitary. Their endogenous ligand, although not yet identified, may be part of a novel neuroendocrine system in the regulation of GH secretion.

Me: so there are more than just the old GHRH and SRIF controlling the release the release of GH, but now there is discovered the GH secretagogues

From the article…

IGFs influence fetal growth independently of GH. IGFBP-3 is highly GH dependent, and its circulating concentrations correlate closely with GH secretory status. Circulating concentrations of both IGF-1 and
IGFBP-3 are low during the first 5 years of life; they slowly increase to peak concentrations during ado-lescence. Both circulating concentrations and the biologic actions of IGF-1 are regulated closely by GH, but they also are influenced by malnutrition, chronic renal and liver disease, and hypothyroidism

Me: I know that IGF indeed influence fetal growth independent of GH. I did not know that IGFBP-3 is dependent on release rate of GH. It does seem that postnatally, the IGF influence on growth does become affected by GH. In addition, the GH can skip the liver production of IGF-1 stage and go directly to the growth plates and just start producing IGF-1 in the local zone.

I hope this visual diagram helped some people get a better overall picture of the basic endocrinology steps going on the growth development.

Mind Hack IX: Being Self Aware Of One’s Subjective Bias And Inferiority By Learning About The Dunning- Kruger Effect, The Downing Effect, And Illusory Superiority

Me: This is a continuation of the mind hack series, and I wanted to stress that for one to function as optimally and effectively as possible in the modern world today, it is critical that the person must learn about three extremely problematic subjective cognitive biases that can most often lead to ruin and spectacular failure. 

1. The Dunning- Kruger Effect – unskilled individuals suffer from illusory superiority, mistakenly rating their ability much higher than average. This bias is attributed to a metacognitive inability of the unskilled to recognize their mistakes (from Wikipedia)

2. The Downing Effect – the tendency of people with a below average IQ to overestimate their IQ, and of people with an above average IQ to underestimate their IQ (from wikipedia) This problem effects males at a far higher degree than females. 

3.  Illusory Superiority – people overestimate their positive qualities and abilities and to underestimate their negative qualities, relative to others. (Wiki) Again, men are far more likely to be affected by this issue than women.

These subjective biases can cause the most painful eventual problems if they are not corrected or at least made self aware in time. This type of problem is most prevalently seen in countries in the west, specifically the USA where individualism is stressed.

There is no doubt that in a culture that stresses the importance of the individual, each individual starts to think that they are special, great, and better than average. No one want sot feel depressed or bad about themselves in believing that they are not as good as others. Most psychologists have said that for the “average healthy” mind of a regular person, they tend to be more optimistic and positive about themselves and their fate than of other people. This means that most people are designed to make inaccurate judgements of their skills and ability.

I personally have met some very , very, VERY smart people in my life, people who I would guess are either have insane raw intelligence, or insanely great work ethic. I have a cousin who has a Ph.D in engineering, has a MD from Stanford Medical school, and is about to be a neurosurgeon making more than 7 figures each year. Another counsin has a MS in Electrical engineering. Another cousin has a Ph. D in Computer science. I have 3 friends who all got full scholarships to study engineering in school and graduated with perfect GPAs and made the top students in the entire university.  I know people who have beaten out over a million other hard working high schools students to become #1 in an entire county (within China no less). One of my college friends has a uncle who is a Nobel Prize winner in Physics currently teaching at Stanford. I know people who got accepted into MIT at the age of 16 and was working for IMB when they were 15. I know people my age who went into investment banking making almost 7 figures each year in bonuses alone. I know people who got a near complete 2400 SAT score without studying at all. Nearly everyone I know has some form of graduate degree.

If you can just go to almost any of the asian countries today, like South Korea, China, Singapore, India, Japan, Russia, Malaysia, etc. you would see that the entire rest of the world is coming after the jobs of the average american worker. Every year millions and million of college graduates come out of university of these asian nations, most of them having degrees in the sciences or engineering. They are hungry , they want to achieve, and they are harder working people than probably 99% of the people you will meet in your lifetime. If you want to compete and have some form of wealth in the coming years ahead, I strongly suggest that you take a trip for half a year in any of these asian countries, go see how the students behave and study, and hopefully find the drive and will inside of yourself to be better and be smarter than the competition.

I have been humbled again and again in life and have come to realize my own ignorance, stupidity, and lack of intelligence when compared to my contemporaries

Here is a 5 basic axiom I have gone on since I was 22:

1. Most people are a lot smarter than you think. No one is stupid. Everyone knows what is going on.

2. Every time you meet someone, assume they are smarter than you so shut up, listen, and try to learn as much as possible from them. At least get 1 take away from the conversation or interaction.

3. If you think you are better than someone else, think again. They are more likely to be better than you in the areas that you think you are good in.

4. Hard work, strong integrity, discipline, and persistence will always result in at least some substantial form of success in the long term.

5. Being physically lazy is dangerous to your health. Being mentality lazy is deadly to your life. 


Me: This next section is basically just me copy and pasting the Wikipedia article/ section on the topic of the Illusory superiority, Downing Effect, and the Dunning- Kruger Effect. READ IT.

Illusory superiority is a cognitive bias that causes people to overestimate their positive qualities and abilities and to underestimate their negative qualities, relative to others. This is evident in a variety of areas including intelligence, performance on tasks or tests, and the possession of desirable characteristics or personality traits. It is one of many positive illusions relating to the self, and is a phenomenon studied insocial psychology.

Illusory superiority is often referred to as the above average effect. Other terms include superiority biasleniency errorsense of relative superiority, the primus inter pares effect,[1] and the Lake Wobegon effect (named after Garrison Keillor’s fictional town where “all the children are above average”). The phrase “illusory superiority” was first used by Van Yperen and Buunk in 1991.[1]

Illusory superiority has been found in individuals’ comparisons of themselves with others in a wide variety of different aspects of life, including performance in academic circumstances (such as class performance, exams and overall intelligence), in working environments (for example in job performance), and in social settings (for example in estimating one’s popularity, or the extent to which one possesses desirable personality traits, such as honesty or confidence), as well as everyday abilities requiring particular skill.[1]

Effects in different situations

For illusory superiority to be demonstrated by social comparison, two logical hurdles have to be overcome. One is the ambiguity of the word “average”. It is logically possible for nearly all of the set to be above the mean if the distribution of abilities is highly skewed. For example, the mean number of human legs is slightly lower than two, because of a small number of people have only one or no legs. Hence experiments usually compare subjects to the median of the peer group, since by definition it is impossible for a majority to exceed the median.

A further problem in inferring inconsistency is that subjects might interpret the question in different ways, so it is logically possible that a majority of them are, for example, more generous than the rest of the group each on their own understanding of generosity.[2] This interpretation is confirmed by experiments which varied the amount of interpretive freedom subjects were given. As subjects evaluate themselves on a specific, well-defined attribute, illusory superiority remains.[3]

Cognitive ability

IQ

One of the main effects of illusory superiority in IQ is the Downing effect. This describes the tendency of people with a below average IQ to overestimate their IQ, and of people with an above average IQ to underestimate their IQ.[citation needed] The propensity to predictably misjudge one’s own IQ was first noted by C. L. Downing who conducted the first cross-cultural studies on perceived ‘intelligence’. His studies also evidenced that the ability to accurately estimate others’ IQ was proportional to one’s own IQ.[citation needed] This means that the lower the IQ of an individual, the less capable they are of appreciating and accurately appraising others’ IQ. Therefore individuals with a lower IQ are more likely to rate themselves as having a higher IQ than those around them.[citation needed] Conversely, people with a higher IQ, while better at appraising others’ IQ overall, are still likely to rate people of similar IQ as themselves as having higher IQs.[citation needed]

The disparity between actual IQ and perceived IQ has also been noted between genders by British psychologist Adrian Furnham, in whose work there was a suggestion that, on average, men are more likely to overestimate their intelligence by 5 points, while women are more likely to underestimate their IQ by a similar margin.[4][5]

Memory

Illusory superiority has been found in studies comparing memory self-report, such as Schmidt, Berg & Deelman’s research in older adults. This study involved participants aged between 46 and 89 years of age comparing their own memory to that of peers of the same age group, 25-year-olds and their own memory at age 25. This research showed that participants exhibited illusory superiority when comparing themselves to both peers and younger adults, however the researchers asserted that these judgements were only slightly related to age.[6]

Cognitive tasks

In Kruger and Dunning’s experiments participants were given specific tasks (such as solving logic problems, analyzing grammar questions, and determining whether or not jokes were funny), and were asked to evaluate their performance on these tasks relative to the rest of the group, enabling a direct comparison of their actual and perceived performance.[7]

Results were divided into four groups depending on actual performance and it was found that all four groups evaluated their performance as above average, meaning that the lowest-scoring group (the bottom 25%) showed a very large illusory superiority bias. The researchers attributed this to the fact that the individuals who were worst at performing the tasks were also worst at recognizing skill in those tasks. This was supported by the fact that, given training, the worst subjects improved their estimate of their rank as well as getting better at the tasks.[7]

The paper, titled “Unskilled and Unaware of It: How Difficulties in Recognizing One’s Own Incompetence Lead to Inflated Self-Assessments,” won a 2000 Ig Nobel Prize.[8]

In 2003 Dunning and Joyce Ehrlinger, also of Cornell University, published a study that detailed a shift in people’s views of themselves influenced by external cues. Participants in the study (Cornell Universityundergraduates) were given tests of their knowledge of geography, some intended to positively affect their self-views, some intended to affect them negatively. They were then asked to rate their performance, and those given the positive tests reported significantly better performance than those given the negative.[9]

Daniel Ames and Lara Kammrath extended this work to sensitivity to others, and the subjects’ perception of how sensitive they were.[10] Work by Burson Larrick and Joshua Klayman has suggested that the effect is not so obvious and may be due to noise and bias levels.[11]

Dunning, Kruger, and coauthors’ latest paper on this subject comes to qualitatively similar conclusions after making some attempt to test alternative explanations.[12]

Academic ability and job performance

In a survey of faculty at the University of Nebraska, 68% rated themselves in the top 25% for teaching ability.[13]

In a similar survey, 87% of MBA students at Stanford University rated their academic performance as above the median.[14]

Findings of illusory superiority in research have also explained phenomena such as the large amount of stock market trading (as each trader thinks they are the best, and most likely to succeed),[15] and the number of lawsuits that go to trial (because, due to illusory superiority, many lawyers have an inflated belief that they will win a case).[16]

Self, friends and peers

One of the first studies that found the effect of illusory superiority was carried out in 1976 by the College Board in the USA.[17] A survey was attached to the SAT exams (taken by approximately one million students per year), asking the students to rate themselves relative to the median of the sample (rather than the average peer) on a number of vague positive characteristics. In ratings of leadership ability, 70% of the students put themselves above the median. In ability to get on well with others, 85% put themselves above the median, and 25% rated themselves in the top 1%.

More recent research [18] has found illusory superiority in a social context, with participants comparing themselves to friends and other peers on positive characteristics (such as punctuality and sensitivity) and negative characteristics (such as naivety or inconsistency). This study found that participants rated themselves more favorably than their friends, but rated their friends more favorably than other peers. These findings were, however, affected by several moderating factors.

Research by Perloff and Fetzer,[19] Brown,[20] and Tajfel and Turner[21] also found similar effects of participants rating friends higher than other peers. Tajfel and Turner attributed this to an “ingroup bias” and suggested that this was motivated by the individual’s desire for a “positive social identity”.

Popularity

In Zuckerman and Jost’s study, participants were given detailed questionnaires about their friendships and asked to assess their own popularity. By using social network analysis, they were able to show that the participants generally had exaggerated perceptions of their own popularity, particularly in comparison to their own friends.[22]

Relationship happiness

Researchers have also found the effects of illusory superiority in studies into relationship satisfaction. For example, one study found that participants perceived their own relationships as better than others’ relationships on average, but thought that the majority of people were happy with their relationships. Also, this study found evidence that the higher the participants rated their own relationship happiness, the more superior they believed their relationship was. The illusory superiority exhibited by the participants in this study also served to increase their own relationship satisfaction, as it was found that – in men especially – satisfaction was particularly related to the perception that one’s own relationship was superior as well as to the assumption that few others were unhappy with their relationship, whereas women’s satisfaction was particularly related to the assumption that most others were happy with their relationship.[23]

Health

Illusory superiority effects have been found in a self-report study of health behaviors (Hoorens & Harris, 1998). The study involved asking participants to estimate how often they, and their peers, carried out healthy and unhealthy behaviors. Participants reported that they carried out healthy behaviors more often than the average peer, and unhealthy behaviors less often, as would be expected given the effect of illusory superiority. These findings were for both past self-report of behaviors and expected future behaviors.[24]

Driving ability

Svenson (1981) surveyed 161 students in Sweden and the United States, asking them to compare their driving safety and skill to the other people in the experiment. For driving skill, 93% of the US sample and 69% of the Swedish sample put themselves in the top 50% (above the median). For safety, 88% of the US group and 77% of the Swedish sample put themselves in the top 50%.[25]

McCormick, Walkey and Green (1986) found similar results in their study, asking 178 participants to evaluate their position on eight different dimensions relating to driving skill (examples include the “dangerous-safe” dimension and the “considerate-inconsiderate” dimension). Only a small minority rated themselves as below average (the midpoint of the dimension scale) at any point, and when all eight dimensions were considered together it was found that almost 80% of participants had evaluated themselves as being above the average driver.[26]

Immunity to bias

Subjects describe themselves in positive terms compared to other people, and this includes describing themselves as less susceptible to bias than other people. This effect is called the bias blind spot and has been demonstrated independently.

Cultural differences

Self-esteem

A vast majority of the literature on self-esteem originates from studies on participants in the United States. However, research that only investigates the effects in one specific population is severely limited as this may not be a true representation of human psychology as a whole. As a result, more recent research has focused on investigating quantities and qualities of self-esteem around the globe. The findings of such studies suggest that illusory superiority varies between cultures.

While a great deal of evidence suggests that we compare ourselves favorably to others on a wide variety of traits, the links to self-esteem are uncertain. The theory that those with high self-esteem maintain this high level by rating themselves over and above others does carry some evidence behind it; it has been reported that non-depressed subjects rate their control over positive outcomes higher than that of a peer; despite an identical level in performance between the two individuals.[27]

Furthermore, it has been found that non-depressed students will also actively rate peers below themselves, as opposed to rating themselves higher; students were able to recall a great deal more negative personality traits about others than about themselves.[28]

The data suggests those with a positive self view are more likely to display the above-average effect, as opposed to those with a negative self appraisal. Similarly, those with low self-esteem appear to engage in far less illusory superiority, showing more realism in their self-rating.

These results go against a basic humanistic principle within psychology. In particular, Carl Rogers, a pioneer of humanistic psychology, claims that those with low self-esteem will be far more likely to attempt to belittle others, with the aim of strengthening their fragile self view. On the other hand, Rogers hypothesizes that those with high self-esteem will have no need to put others down or below themselves; and therefore, would be unlikely to exhibit illusory superiority.

It should be noted though, that in these studies there was no distinction made between people with legitimate and illegitimate high self-esteem, as other studies have found that absence of positive illusions may coexist with high self-esteem[29] and that self-determined individuals with personality oriented towards growth and learning are less prone to these illusions.[30] Thus it may be likely that while illusory superiority is associated with illegitimate high self-esteem, people with legitimate high self-esteem don’t exhibit it.

Relation to mental health

Psychology has traditionally assumed that generally accurate self-perceptions are essential to good mental health.[2] This was challenged by a 1988 paper by Taylor and Brown, who argued that mentally healthy individuals typically manifest three cognitive illusions, namely illusory superiority, illusion of control and optimism bias.[2] This idea rapidly became very influential, with some authorities concluding that it would be therapeutic to deliberately induce these biases.[31] Since then, further research has both undermined that conclusion and offered new evidence associating illusory superiority with negative effects on the individual.[2]

One line of argument was that in the Taylor and Brown paper, the classification of people as mentally healthy or unhealthy was based on self-reports rather than objective criteria.[31] Hence it was not surprising that people prone to self-enhancement would exaggerate how well-adjusted they are. One study claimed that “mentally normal” groups were contaminated by defensive deniers who are the most subject to positive illusions.[31] A longitudinal study found that self-enhancement biases were associated with poor social skills and psychological maladjustment.[2] In a separate experiment where videotaped conversations between men and women were rated by independent observers, self-enhancing individuals were more likely to show socially problematic behaviors such as hostility or irritability.[2] A 2007 study found that self-enhancement biases were associated with psychological benefits (such as subjective well-being) but also inter- and intra-personal costs (such as anti-social behavior).[32]

Neuroimaging

The degree to which people view themselves as more desirable than the average person links to reduced activation in their orbitofrontal cortex and dorsal anterior cingulate cortex. This is suggested to link to the role of these areas in processing “cognitive control”.[33]

Explanations

Noisy mental information processing

A recent Psychological Bulletin suggests that illusory superiority (as well as other biases) can be explained by a simple information-theoretic generative mechanism that assumes a noisy conversion of objective evidence (observation) into subjective estimates (judgment).[34] The study suggests that the underlying cognitive mechanism is essentially similar to the noisy mixing of memories that can cause theconservatism bias or overconfidence: after our own performance, we readjust our estimates of our own performance more than we readjust our estimates of others’ performances. This implies that our estimates of the scores of others are even more conservative (more influenced by the previous expectation) than our estimates of our own performance (more influenced by the new evidence received after giving the test). The difference in the conservative bias of both estimates (conservative estimate of our own performance, and even more conservative estimate of the performance of others) is enough to create illusory superiority. Since mental noise is a sufficient explanation that is much simpler and straightforward than any other explanation involving heuristics, behavior, or social interaction,[17] Occam’s razor would argue in its favor as the underlying generative mechanism (it is the hypotheses which makes the fewest assumptions).

Selective recruitment

This is the idea that when making a comparison with a peer an individual will select their own strengths and the other’s weaknesses in order that they appear better on the whole. This theory was first tested by Weinstein (1980); however, this was in an experiment relating to optimistic bias, rather than the better-than-average effect. The study involved participants rating certain behaviors as likely to increase or decrease the chance of a series of life events happening to them. It was found that individuals showed less optimistic bias when they were allowed to see others’ answers.[35]

Perloff and Fetzer (1986) suggested that when comparing themselves to an average peer on a particular ability or characteristic an individual would choose a comparison target (the peer being compared) that scored less well on that ability or characteristic, in order that the individual would appear to be better than average. To test this theory Perloff and Fetzer asked participants to compare themselves to specific comparison targets (a close friend), and found that illusory superiority decreased when specific targets were given, rather than vague constructs such as the “average peer”. However these results are not completely reliable and could be affected by the fact that individuals like their close friends more than an “average peer” and may as a result rate their friend as being higher than average, therefore the friend would not be an objective comparison target.[19]

Egocentrism

The second explanation for how the better-than-average effect works is egocentrism. This is the idea that an individual places greater importance and significance on their own abilities, characteristics and behaviors than those of others. Egocentrism is therefore a less overtly self-serving bias. According to egocentrism, individuals will overestimate themselves in relation to others because they believe that they have an advantage that others do not have, as an individual considering their own performance and another’s performance will consider their performance to be better, even when they are in fact equal. Kruger (1999) found support for the egocentrism explanation in his research involving participant ratings of their ability on easy and difficult tasks. It was found that individuals were consistent in their ratings of themselves as above the median in the tasks classified as “easy” and below the median in the tasks classified as “difficult”, regardless of their actual ability. In this experiment the better-than-average effect was observed when it was suggested to participants that they would be successful, but also a worse-than-average effect was found when it was suggested that participants would be unsuccessful.[36]

Focalism

The third explanation for the better-than-average effect is focalism, the idea that greater significance is placed on the object that is the focus of attention. Most studies of the better-than-average effect place greater focus on the self when asking participants to make comparisons (the question will often be phrased with the self being presented before the comparison target – e.g. “compare yourself to the average person…”). According to focalism this means that the individual will place greater significance on their own ability or characteristic than that of the comparison target. This also means that in theory if, in an experiment on the better-than-average effect, the questions were phrased so that the self and other were switched (e.g. “compare the average peer to yourself”) the better-than-average effect should be lessened.[37]

Research into focalism has focused primarily on optimistic bias rather than the better-than-average effect. However, two studies found a decreased effect of optimistic bias when participants were asked to compare an average peer to themselves, rather than themselves to an average peer.[38][39]

Windschitl, Kruger & Simms (2003) have conducted research into focalism, focusing specifically on the better-than-average effect, and found that asking participants to estimate their ability and likelihood of success in a task produced results of decreased estimations when they were asked about others’ chances of success rather than their own.[40]

“Self versus aggregate” comparisons

This idea, put forward by Giladi and Klar, suggests that when making comparisons any single member of a group will be evaluated[by whom?] to rank above that group’s statistical mean performance level or the median performance level of its members. Research has found this effect in many different areas of human performance and has even generalized it beyond individuals’ attempts to draw comparisons involving themselves. Findings of this research therefore suggest that rather than individuals evaluating themselves as above average in a self-serving manner, the better-than-average effect is actually due to a general tendency to evaluate any single person or object as better than average.

Better-than-average heuristic

Alicke and Govorun proposed the idea that, rather than individuals consciously reviewing and thinking about their own abilities, behaviors and characteristics and comparing them to those of others, it is likely that people instead have what they describe as an “automatic tendency to assimilate positively-evaluated social objects toward ideal trait conceptions”. For example, if an individual evaluated themselves as honest, they would be likely to then exaggerate their characteristic towards their perceived ideal position on a scale of honesty. Importantly, Alicke has noted that this ideal position is not always the top of the scale, for example, in the case of honesty, someone who is always brutally honest may be regarded as rude. Instead, the ideal is a balance perceived differently by different individuals.

Non-social explanations

The better-than-average effect may not have wholly social origins: judgements about inanimate objects suffer similar distortions.[41]

Moderating factors

While illusory superiority has been found to be somewhat self-serving, this does not mean that it will predictably occur: it is not constant. Instead the strength of the effect is moderated by many factors, the main examples of which have been summarized by Alicke and Govorun (2005).[17]

Interpretability/ambiguity of trait

This is a phenomenon that Alicke and Govorun have described as “the nature of the judgement dimension” and refers to how subjective (abstract) or objective (concrete) the ability or characteristic being evaluated is.[17] Research by Sedikides & Strube (1997) has found that people are more self-serving (the effect of illusory superiority is stronger) when the event in question is more open to interpretation,[42] for example social constructs such as popularity and attractiveness are more interpretable than characteristics such as intelligence and physical ability.[43] This has been partly attributed also to the need for a believable self-view.[44]

The idea that ambiguity moderates illusory superiority has empirical research support from a study involving two conditions: in one, participants were given criteria for assessing a trait as ambiguous or unambiguous, and in the other participants were free to assess the traits according to their own criteria. It was found that the effect of illusory superiority was greater in the condition where participants were free to assess the traits.[45]

The effects of illusory superiority have also been found to be strongest when people rate themselves on abilities at which they are totally incompetent. These subjects have the greatest disparity between their actual performance (at the low end of the distribution) and their self-rating (placing themselves above average). This Dunning–Kruger effect is interpreted as a lack of metacognitive ability to recognize their own incompetence.[7]

Method of comparison

The method used in research into illusory superiority has been found to have an implication on the strength of the effect found. Most studies into illusory superiority involve a comparison between an individual and an average peer, of which there are two methods: direct comparison and indirect comparison. A direct comparison – which is more commonly used – involves the participant rating themselves and the average peer on the same scale, from “below average” to “above average”[46] and results in participants being far more self-serving.[47] Researchers have suggested that this occurs due to the closer comparison between the individual and the average peer, however use of this method means that it is impossible to know whether a participant has overestimated themselves, underestimated the average peer, or both.

The indirect method of comparison involves participants rating themselves and the average peer on separate scales and the illusory superiority effect is found by taking the average peer score away from the individual’s score (with a higher score indicating a greater effect). While the indirect comparison method is used less often it is more informative in terms of whether participants have overestimated themselves or underestimated the average peer, and can therefore provide more information about the nature of illusory superiority.[46]

Comparison target

The nature of the comparison target is one of the most fundamental moderating factors of the effect of illusory superiority, and there are two main issues relating to the comparison target that need to be considered.

First, research into illusory superiority is distinct in terms of the comparison target because an individual compares themselves with a hypothetical average peer rather than a tangible person. Alicke et al. (1995) found that the effect of illusory superiority was still present but was significantly reduced when participants compared themselves with real people (also participants in the experiment, who were seated in the same room), as opposed to when participants compared themselves with an average peer. This suggests that research into illusory superiority may itself be biasing results and finding a greater effect than would actually occur in real life.[46]

Further research into the differences between comparison targets involved four conditions where participants were at varying proximity to an interview with the comparison target: watching live in the same room; watching on tape; reading a written transcript; or making self-other comparisons with an average peer. It was found that when the participant was further removed from the interview situation (in the tape observation and transcript conditions) the effect of illusory superiority was found to be greater. Researchers asserted that these findings suggest that the effect of illusory superiority is reduced by two main factors, individuation of the target and live contact with the target.

Second, Alicke et al.’s (1995) studies investigated whether the negative connotations to the word “average” may have an effect on the extent to which individuals exhibit illusory superiority, namely whether the use of the word “average” increases illusory superiority. Participants were asked to evaluate themselves, the average peer and a person whom they had sat next to in the previous experiment, on various dimensions. It was found that they placed themselves highest, followed by the real person, followed by the average peer, however the average peer was consistently placed above the mean point on the scale, suggesting that the word “average” did not have a negative effect on the participant’s view of the average peer.[46]

Controllability

An important moderating factor of the effect of illusory superiority is the extent to which an individual believes they are able to control and change their position on the dimension concerned. According to Alicke & Govorun positive characteristics that an individual believes are within their control are more self-serving, and negative characteristics that are seen as uncontrollable are less detrimental to self-enhancement.[17] This theory was supported by Alicke’s (1985) research, which found that individuals rated themselves as higher than an average peer on positive controllable traits and lower than an average peer on negative uncontrollable traits. The idea, suggested by these findings, that individuals believe that they are responsible for their success and some other factor is responsible for their failure is known as the self-serving bias.

Individual differences of judge

Personality characteristics vary widely between people and have been found to moderate the effects of illusory superiority, one of the main examples of this is self-esteem. Brown (1986) found that in self-evaluations of positive characteristics participants with higher self-esteem showed greater illusory superiority bias than participants with lower self-esteem. Similar findings come from a study by Suls, Lemos & Stewart (2002), but in addition they found that participants pre-classified as having high self-esteem interpreted ambiguous traits in a self-serving way, whereas participants who were pre-classified as having low self-esteem did not do this.

Worse-than-average effect

In contrast to what is commonly believed, research has found that better-than-average effects are not universal. In fact, much recent research has found the opposite effect in many, especially more difficult, tasks.

IQ

One of the main effects of illusory superiority in IQ is the Downing effect. This describes the tendency of people with a below average IQ to overestimate their IQ, and of people with an above average IQ to underestimate their IQ. The propensity to predictably misjudge one’s own IQ was first noted by C. L. Downing who conducted the first cross-cultural studies on perceived ‘intelligence’. His studies also evidenced that the ability to accurately estimate others’ IQ was proportional to one’s own IQ. This means that the lower the IQ of an individual, the less capable they are of appreciating and accurately appraising others’ IQ. Therefore individuals with a lower IQ are more likely to rate themselves as having a higher IQ than those around them. Conversely, people with a higher IQ, while better at appraising others’ IQ overall, are still likely to rate people of similar IQ as themselves as having higher IQs.

The disparity between actual IQ and perceived IQ has also been noted between genders by British psychologist Adrian Furnham, in whose work there was a suggestion that, on average, men are more likely to overestimate their intelligence by 5 points, while women are more likely to underestimate their IQ by a similar margin.

Dunning–Kruger effect

From Wikipedia, the free encyclopedia

The Dunning–Kruger effect is a cognitive bias in which unskilled individuals suffer from illusory superiority, mistakenly rating their ability much higher than average. This bias is attributed to a metacognitive inability of the unskilled to recognize their mistakes.[1]

Actual competence may weaken self-confidence, as competent individuals may falsely assume that others have an equivalent understanding. As Kruger and Dunning conclude, “the miscalibration of the incompetent stems from an error about the self, whereas the miscalibration of the highly competent stems from an error about others” (p. 1127).[2]

Historical references

Although the Dunning–Kruger effect was put forward in 1999, David Dunning and Justin Kruger have quoted Charles Darwin (“Ignorance more frequently begets confidence than does knowledge”)[3] and Bertrand Russell (“One of the painful things about our time is that those who feel certainty are stupid, and those with any imagination and understanding are filled with doubt and indecision”)[4] as authors who have recognised the phenomenon. Geraint Fuller, commenting on the paper, notes that Shakespeare expresses similar sentiment in As You Like It (“The fool doth think he is wise, but the wise man knows himself to be a fool.” (V.i)) [5].

Hypothesis

The hypothesized phenomenon was tested in a series of experiments performed by Justin Kruger and David Dunning, both then of Cornell University.[2][6] Kruger and Dunning noted earlier studies suggesting that ignorance of standards of performance is behind a great deal of incompetence. This pattern was seen in studies of skills as diverse as reading comprehension, operating a motor vehicle, and playing chess or tennis.

Kruger and Dunning proposed that, for a given skill, incompetent people will:

  1. tend to overestimate their own level of skill;
  2. fail to recognize genuine skill in others;
  3. fail to recognize the extremity of their inadequacy;
  4. recognize and acknowledge their own previous lack of skill, if they are exposed to training for that skill

Dunning has since drawn an analogy (“the anosognosia of everyday life”)[1][7] to a condition in which a person who suffers a physical disability because of brain injury seems unaware of or denies the existence of the disability, even for dramatic impairments such as blindness or paralysis.

Supporting studies

Kruger and Dunning set out to test these hypotheses on Cornell undergraduates in various psychology courses. In a series of studies, they examined the subjects’ self-assessment of logical reasoning skills,grammatical skills, and humor. After being shown their test scores, the subjects were again asked to estimate their own rank, whereupon the competent group accurately estimated their rank, while the incompetent group still overestimated their own rank. As Dunning and Kruger noted,

Across four studies, the authors found that participants scoring in the bottom quartile on tests of humor, grammar, and logic grossly overestimated their test performance and ability. Although test scores put them in the 12th percentile, they estimated themselves to be in the 62nd.

Meanwhile, people with true ability tended to underestimate their relative competence. Roughly, participants who found tasks to be relatively easy erroneously assumed, to some extent, that the tasks must also be easy for others.

A follow-up study, reported in the same paper, suggests that grossly incompetent students improved their ability to estimate their rank after minimal tutoring in the skills they had previously lacked—regardless of the negligible improvement in actual skills.

In 2003, Dunning and Joyce Ehrlinger, also of Cornell University, published a study that detailed a shift in people’s views of themselves when influenced by external cues. Participants in the study (Cornell University undergraduates) were given tests of their knowledge of geography, some intended to positively affect their self-views, some intended to affect them negatively. They were then asked to rate their performance, and those given the positive tests reported significantly better performance than those given the negative.[8]

Daniel Ames and Lara Kammrath extended this work to sensitivity to others, and the subjects’ perception of how sensitive they were.[9] Other research has suggested that the effect is not so obvious and may be due to noise and bias levels[vague].[10]

Dunning, Kruger, and coauthors’ 2008 paper on this subject comes to qualitatively similar conclusions to their original work, after making some attempt to test alternative explanations. They conclude that the root cause is that, in contrast to high performers, “poor performers do not learn from feedback suggesting a need to improve.”[4]

Studies on the Dunning–Kruger effect tend to focus on American test subjects. A study on some East Asian subjects suggested that something like the opposite of the Dunning–Kruger effect may operate on self-assessment and motivation to improve.[11]

Awards

Dunning and Kruger were awarded the 2000 Ig Nobel Prize in Psychology for their report, “Unskilled and Unaware of It: How Difficulties in Recognizing One’s Own Incompetence Lead to Inflated Self-Assessments”.[12]