There’s No Scientific Basis for Race—It’s a Made-Up Label
It’s been used to define and separate people for millennia. But the concept of race is not grounded in genetics.
The four letters of the genetic code —A, C, G, and T—are projected onto Ryan Lingarmillar, a Ugandan. DNA reveals what skin color obscures: We all have African ancestors.12 MINUTE READBY ELIZABETH KOLBERTPHOTOGRAPHS BY ROBIN HAMMOND
This story is part of The Race Issue, a special issue of National Geographic that explores how race defines, separates, and unites us. Tell us your story with#IDefineMe.
IN THE FIRST half of the 19th century, one of America’s most prominent scientists was a doctor named Samuel Morton. Morton lived in Philadelphia, and he collected skulls.
He wasn’t choosy about his suppliers. He accepted skulls scavenged from battlefields and snatched from catacombs. One of his most famous craniums belonged to an Irishman who’d been sent as a convict to Tasmania (and ultimately hanged for killing and eating other convicts). With each skull Morton performed the same procedure: He stuffed it with pepper seeds—later he switched to lead shot—which he then decanted to ascertain the volume of the braincase.
Morton believed that people could be divided into five races and that these represented separate acts of creation. The races had distinct characters, which corresponded to their place in a divinely determined hierarchy. Morton’s “craniometry” showed, he claimed, that whites, or “Caucasians,” were the most intelligent of the races. East Asians—Morton used the term “Mongolian”—though “ingenious” and “susceptible of cultivation,” were one step down. Next came Southeast Asians, followed by Native Americans. Blacks, or “Ethiopians,” were at the bottom. In the decades before the Civil War, Morton’s ideas were quickly taken up by the defenders of slavery.
This story helps launch a series about racial, ethnic, and religious groups and their changing roles in 21st-century life. The series runs through 2018 and will include coverage of Muslims, Latinos, Asian Americans, and Native Americans.
“He had a lot of influence, particularly in the South,” says Paul Wolff Mitchell, an anthropologist at the University of Pennsylvania who is showing me the skull collection, now housed at the Penn Museum. We’re standing over the braincase of a particularly large-headed Dutchman who helped inflate Morton’s estimate of Caucasian capacities. When Morton died, in 1851, the Charleston Medical Journal in South Carolina praised him for “giving to the negro his true position as an inferior race.”
Today Morton is known as the father of scientific racism. So many of the horrors of the past few centuries can be traced to the idea that one race is inferior to another that a tour of his collection is a haunting experience. To an uncomfortable degree we still live with Morton’s legacy: Racial distinctions continue to shape our politics, our neighborhoods, and our sense of self.
This is the case even though what science actually has to tell us about race is just the opposite of what Morton contended.
Morton thought he’d identified immutable and inherited differences among people, but at the time he was working—shortly before Charles Darwin put forth his theory of evolution and long before the discovery of DNA—scientists had no idea how traits were passed on. Researchers who have since looked at people at the genetic level now say that the whole category of race is misconceived. Indeed, when scientists set out to assemble the first complete human genome, which was a composite of several individuals, they deliberately gathered samples from people who self-identified as members of different races. In June 2000, when the results were announced at a White House ceremony, Craig Venter, a pioneer of DNA sequencing, observed, “The concept of race has no genetic or scientific basis.”
Over the past few decades, genetic research has revealed two deep truths about people. The first is that all humans are closely related—more closely related than all chimps, even though there are many more humans around today. Everyone has the same collection of genes, but with the exception of identical twins, everyone has slightly different versions of some of them. Studies of this genetic diversity have allowed scientists to reconstruct a kind of family tree of human populations. That has revealed the second deep truth: In a very real sense, all people alive today are Africans.
Our species, Homo sapiens, evolved in Africa—no one is sure of the exact time or place. The most recent fossil find, from Morocco, suggests that anatomically modern human features began appearing as long as 300,000 years ago. For the next 200,000 years or so, we remained in Africa, but already during that period, groups began to move to different parts of the continent and become isolated from one another—in effect founding new populations.
ANCIENT FLOWS
OF DARK AND LIGHT
Many genes affect how melanin colors human skin. The genes
predate humanity; some occur in mice and fish. Variations in
four of them—mutations that flip a gene from darkening to
lightening or vice versa—explain much of the skin-color
diversity in Africa. As our ancestors spread across the Earth,
different mutations proved beneficial at different latitudes
and were passed on.
Papua New Guineans, Ethiopians, Hadza, and Tanzanians
Sub-Saharan Africans (except the San), South Asians, and Australo-Melanesians
East Africans, Hadza, San, South Asians, and Australo-Melanesians
Gene variants associated
with dark pigmentation
Africans and East Asians
SLC24A5
DDB1
996,000 years ago
345,000 years ago
Dark-to-light mutation
Dark-to-light mutation
Light-to-dark mutation
Light-to-dark mutation
MFSD12
HERC2
250,000 years ago
Gene variants associated
with light pigmentation
29,000 years ago
Europeans and South Asians
Europeans, East Asians, Indians, and Native Americans
Europeans, San, East Asians, and Africans
Europeans, San, and East Asians
Light skin has many origins
Genetic mutation
Responding to the sun
~300,000 years ago
A key gene mutation promoting lighter skin
(SLC24A5) occurred 29,000 years ago in Asia
and later spread into Europe. But Africa is the
source of other gene variants that contribute
to lighter skin in populations around the
world (DDB1, MFSD12, and HERC2).
Genes randomly mutate
over time. Beneficial
mutations tend to be
passed on to offspring
and to spread through
a population.
Dark skin is favored in the tropics because
it shields tissue from dangerous UV rays.
In regions with less sun, lighter skin allows
the body to absorb enough UV rays to
synthesize vitamin D, which is needed for
healthy bones and immune systems.
Anatomically
modern human
features emerge in
Africa.JASON TREAT AND RYAN T. WILLIAMS, NGM STAFF
SOURCE: SARAH TISHKOFF, UNIVERSITY OF PENNSYLVANIA
In humans, as in all species, genetic changes are the result of random mutations—tiny tweaks to DNA, the code of life. Mutations occur at a more or less constant rate, so the longer a group persists, handing down its genes generation after generation, the more tweaks these genes will accumulate. Meanwhile, the longer two groups are separated, the more distinctive tweaks they will acquire.
By analyzing the genes of present-day Africans, researchers have concluded that the Khoe-San, who now live in southern Africa, represent one of the oldest branches of the human family tree. The Pygmies of central Africa also have a very long history as a distinct group. What this means is that the deepest splits in the human family aren’t between what are usually thought of as different races—whites, say, or blacks or Asians or Native Americans. They’re between African populations such as the Khoe-San and the Pygmies, who spent tens of thousands of years separated from one another even before humans left Africa.TODAY’SPOPULAR STORIES
TRAVEL19 iconic trees around the world
CULTURE & HISTORYDive beneath the pyramids of Egypt’s black pharaohs
ANIMALSWhy shark attacks are more common in the Atlantic than the Pacific
All non-Africans today, the genetics tells us, are descended from a few thousand humans who left Africa maybe 60,000 years ago. These migrants were most closely related to groups that today live in East Africa, including the Hadza of Tanzania. Because they were just a small subset of Africa’s population, the migrants took with them only a fraction of its genetic diversity.
Somewhere along the way, perhaps in the Middle East, the travelers met and had sex with another human species, the Neanderthals; farther east they encountered yet another, the Denisovans. It’s believed that both species evolved in Eurasia from a hominin that had migrated out of Africa much earlier. Some scientists also believe the exodus 60,000 years ago was actually the second wave of modern humans to leave Africa. If so, judging from our genomes today, the second wave swamped the first.
In what was, relatively speaking, a great rush, the offspring of all these migrants dispersed around the world. By 50,000 years ago they had reached Australia. By 45,000 years ago they’d settled in Siberia, and by 15,000 years ago they’d reached South America. As they moved into different parts of the world, they formed new groups that became geographically isolated from one another and, in the process, acquired their own distinctive set of genetic mutations.
Most of these tweaks were neither helpful nor harmful. But occasionally a mutation arose that turned out to be advantageous in a new setting. Under the pressure of natural selection, it spread quickly through the local population. At high altitudes, for instance, oxygen levels are low, so for people moving into the Ethiopian highlands, Tibet, or the Andean Altiplano, there was a premium on mutations that helped them cope with the rarefied air. Similarly, Inuit people, who adopted a marine-based diet high in fatty acids, have genetic tweaks that helped them adapt to it.
Sometimes it’s clear that natural selection has favored a mutation, but it’s not clear why. Such is the case with a variant of a gene called EDAR (pronounced ee-dar). Most people of East Asian and Native American ancestry possess at least one copy of the variant, known as 370A, and many possess two. But it’s rare among people of African and European descent.
At the University of Pennsylvania’s Perelman School of Medicine, geneticist Yana Kamberov has equipped mice with the East Asian variant of EDAR in hopes of understanding what it does. “They’re cute, aren’t they?” she says, opening the cage to show me. The mice look ordinary, with sleek brown coats and shiny black eyes. But examined under a microscope, they are different from their equally cute cousins in subtle yet significant ways. Their hair strands are thicker; their sweat glands are more numerous; and the fat pads around their mammary glands are smaller.
Kamberov’s mice help explain why some East Asians and Native Americans have thicker hair and more sweat glands. (EDAR’s effect on human breasts is unclear.) But they don’t provide an evolutionary reason. Perhaps, Kamberov speculates, the ancestors of contemporary East Asians at some point encountered climate conditions that made more sweat glands useful. Or maybe thicker hair helped them ward off parasites. Or it could be that 370Aproduced other benefits she’s yet to discover and the changes she has identified were, in effect, just tagalongs. Genetics frequently works like this: A tiny tweak can have many disparate effects. Only one may be useful—and it may outlive the conditions that made it so, the way families hand down old photos long past the point when anyone remembers who’s in them.
“Unless you have a time machine, you’re not going to know,” Kamberov sighs.
THERE’S MORE DIVERSITY IN AFRICA THAN ON ALL THE OTHER CONTINENTS COMBINED.
That’s because modern humans originated in Africa and have lived there the longest. They’ve had time to evolve enormous genetic diversity—which extends to skin color. Researchers who study it sometimes use Africa’s linguistic diversity—it has more than 2,000 languages (see map below)—as a guide. Photographer Robin Hammond followed their lead, visiting five representative language communities. His portraits span the color spectrum from Neilton Vaalbooi (top left in photo grid above), a Khoe-San boy from South Africa, to Akatorot Yelle (bottom right), a Turkana girl from Kenya. “There is no homogeneous African race,” says geneticist Sarah Tishkoff of the University of Pennsylvania. “It doesn’t exist.” The prehistoric humans who left Africa some 60,000 years ago—giving rise over time to the other peoples of the world—reflected only a fraction of Africa’s diversity.1. Neilton Vaalbooi (N), 2. Petrus Vaalbooi (N), 3. Khadar Abdullahi (S), 4. Sadam Abdirisak (S), 5. Askania Saidi (H), 6. Mohamed Ali (S), 7. Helena Hamisi (H), 8. Kooli Naperit (T), 9. David Vaalbooi (N), 10. Sisipho Menze (X), 11. Ayub Abdullahi (S), 12. Bianca Springbok (N), 13. Xolani Mantyi (X), 14. Makaranga Pandisha (H), 15. Erinyok Eyen (T), 16. Isaac Adams (N), 17. Chahida van Neel (N), 18. Griet Seekoei (N), 19. Siphelo Mzondo (X), 20. Piega Mukoa (H), 21. Zacharia Sanga (H), 22. Tulisa Ngxukuma (X), 23. Johanna Koper (N), 24. Abdhllahi Mohamed (S), 25. Monwabisi Makoma (X), 26. Gelmesa Robe (S), 27. Palanjo Kaunda (H), 28. Abdhllahi Said (S), 29. Ejore Elipan Abong (T), 30. Akatorot Yelle (T)
Language diversity of continental Africa
Each dot represents a distinct language.
SAHARA
Somali
(S)
Turkana
(T)
Hadza
(H)
*N u is one of
many Khoe-San
languages.
N u* (N)
Xhosa (X)
NGM MAPS. SOURCES: GLOTTOLOG 3.1, MAX PLANCK
INSTITUTE FOR THE SCIENCE OF HUMAN HISTORY;
SARAH TISHKOFF, UNIVERSITY OF PENNSYLVANIA;
BRENNA HENN, STONY BROOK UNIVERSITY, NEW
YORK; RICHARD E.W. BERL, COLORADO
STATE UNIVERSITY
DNA is often compared to a text, with the letters standing for chemical bases—A for adenine, C for cytosine, G for guanine, and T for thymine. The human genome consists of three billion base pairs—page after page of A’s, C’s, G’s, and T’s—divided into roughly 20,000 genes. The tweak that gives East Asians thicker hair is a single base change in a single gene, from a T to a C.
Similarly, the mutation that’s most responsible for giving Europeans lighter skin is a single tweak in a gene known as SLC24A5, which consists of roughly 20,000 base pairs. In one position, where most sub-Saharan Africans have a G, Europeans have an A. About a decade ago a pathologist and geneticist named Keith Cheng, at Penn State College of Medicine, discovered the mutation by studying zebrafish that had been bred to have lighter stripes. The fish, it turned out, possessed a mutation in a pigment gene analogous to the one that is mutated in Europeans.
Studying DNA extracted from ancient bones, paleogeneticists have found that the G-to-A substitution was introduced into western Europe relatively recently—about 8,000 years ago—by people migrating from the Middle East, who also brought a newfangled technology: farming. That means the people already in Europe—hunter-gatherers who created the spectacular cave paintings at Lascaux, for example—probably were not white but brown. The ancient DNA suggests that many of those dark-skinned Europeans also had blue eyes, a combination rarely seen today.
A FORMATIVE JOURNEY
As humans migrated out of Africa—in two waves, some
scientists say—they adapted to new environments in many
ways. Skin color is just one; high-altitude populations, for
example, adapted to breathing low-oxygen air.
20,000-15,000
45,000
EUROPE
years ago
years ago
43,000
NORTH
ASIA
years ago
AMERICA
40,000
years ago
AFRICA
70,000
PACIFIC
OCEAN
years ago
200,000
years ago
SOUTH
AMERICA
AUSTRALIA
Jebel Irhoud, Morocco
15,000-12,000
years ago
Site of oldest Homo sapiens remains
(~300,000 years old)
Thousands of years ago
200
60
Present
First wave:
120,000-60,000
years ago
Second wave:
60,000-30,000
years ago
JASON TREAT AND RYAN T. WILLIAMS, NGM STAFF
SOURCE: CHRISTOPHER BAE AND OTHERS, SCIENCE, 2017
“What the genetics shows is that mixture and displacement have happened again and again and that our pictures of past ‘racial structures’ are almost always wrong,” says David Reich, a Harvard University paleogeneticist whose new book on the subject is called Who We Are and How We Got Here. There are no fixed traits associated with specific geographic locations, Reich says, because as often as isolation has created differences among populations, migration and mixing have blurred or erased them.
Across the world today, skin color is highly variable. Much of the difference correlates with latitude. Near the Equator lots of sunlight makes dark skin a useful shield against ultraviolet radiation; toward the poles, where the problem is too little sun, paler skin promotes the production of vitamin D. Several genes work together to determine skin tone, and different groups may possess any number of combinations of different tweaks. Among Africans, some people, such as the Mursi of Ethiopia, have skin that’s almost ebony, while others, such as the Khoe-San, have skin the color of copper. Many dark-skinned East Africans, researchers were surprised to learn, possess the light-skinned variant of SLC24A5. (It seems to have been introduced to Africa, just as it was to Europe, from the Middle East.) East Asians, for their part, generally have light skin but possess the dark-skinned version of the gene. Cheng has been using zebrafish to try to figure out why. “It’s not simple,” he says.
When people speak about race, usually they seem to be referring to skin color and, at the same time, to something more than skin color. This is the legacy of people such as Morton, who developed the “science” of race to suit his own prejudices and got the actual science totally wrong. Science today tells us that the visible differences between peoples are accidents of history. They reflect how our ancestors dealt with sun exposure, and not much else.
“We often have this idea that if I know your skin color, I know X, Y, and Z about you,” says Heather Norton, a molecular anthropologist at the University of Cincinnati who studies pigmentation. “So I think it can be very powerful to explain to people that all these changes we see, it’s just because I have an A in my genome and she has a G.”
YOUR WORDS CREATE YOUR EXPERIENCE OF THE MOMENT====
YOU MUST EXPRESS YOUR FEELINGS AND THE FEELINGS OF ALL THOSE THAT CAME BEFORE US IN A MANNER THAT EMPOWERS +++++
NATURE
———–
NATURE IS SELF CORRECTING
YOUR NATURE WILL SELF CORRECT YOU!!!!!
Language Patterns Discriminate Mild Depression From Normal Sadness and Euthymic State
Daria Smirnova,1,2,*Paul Cumming,3Elena Sloeva,4Natalia Kuvshinova,4Dmitry Romanov,1 andGennadii Nosachev1Author informationArticle notesCopyright and License informationDisclaimer
Associated Data
Abstract
Objectives
Deviations from typical word use have been previously reported in clinical depression, but language patterns of mild depression (MD), as distinct from normal sadness (NS) and euthymic state, are unknown. In this study, we aimed to apply the linguistic approach as an additional diagnostic key for understanding clinical variability along the continuum of affective states.
Methods
We studied 402 written reports from 124 Russian-speaking patients and 77 healthy controls (HC), including 35 cases of NS, using hand-coding procedures. The focus of our psycholinguistic methods was on lexico-semantic [e.g., rhetorical figures (metaphors, similes)], syntactic [e.g., predominant sentence type (single-clause and multi-clause)], and lexico-grammatical [e.g., pronouns (indefinite, personal)] variables. Statistical evaluations included Cohen’s kappa for inter-rater reliability measures, a non-parametric approach (Mann–Whitney U-test and Pearson chi-square test), one-way ANOVA for between-group differences, Spearman’s and point-biserial correlations to analyze relationships between linguistic and gender variables, discriminant analysis (Wilks’ ?) of linguistic variables in relation to the affective diagnostic types, all using SPSS-22 (significant, p?<?0.05).
Results
In MD, as compared with healthy individuals, written responses were longer, demonstrated descriptive rather than analytic style, showed signs of spoken and figurative language, single-clause sentences domination over multi-clause, atypical word order, increased use of personal and indefinite pronouns, and verb use in continuous/imperfective and past tenses. In NS, as compared with HC, we found greater use of lexical repetitions, omission of words, and verbs in continuous and present tenses. MD was significantly differentiated from NS and euthymic state by linguistic variables [98.6%; Wilks’ ?(40)?=?0.009; p?<?0.001; r?=?0.992]. The highest predictors in discrimination between MD, NS, and euthymic state groups were the variables of word order (typical/atypical) (r?=??0.405), ellipses (omission of words) (r?=?0.583), colloquialisms (informal words/phrases) (r?=?0.534), verb tense (past/present/future) (r?=??0.460), verbs form (continuous/perfect) (r?=?0.345), amount of reflexive (e.g., myself)/personal (r?=?0.344), and negative (e.g., nobody)/indefinite (r?=?0.451) pronouns. The most significant between-group differences were observed in MD as compared with both NS and euthymic state.
Conclusion
MD is characterized by patterns of atypical language use distinguishing depression from NS and euthymic state, which points to a potential role of linguistic indicators in diagnosing affective states.Keywords: euthymic state, language patterns, mild depression, negative pronouns, normal sadness, past tense verbs, personal pronouns, word useGo to:
Introduction
Mild depression (MD) is a common mental state (1), observed in 15% of the adult population (2), with only 23% receiving any treatment (3). MD is mostly related to life stresses (4) and [unlike moderate and severe major depressive disorder (MDD)] is poorly responsive to antidepressant medication (1, 5, 6). Nonetheless, MD [as distinct from subthreshold, minor depression (7) or normal sadness (NS) (8, 9)] is a serious medical condition causing professional and personal disabilities (10–12). Indeed, MD is associated with unemployment in 16% of cases (13). The chronic course of mild depressive symptoms within dysthymia brings an elevated suicidality risk, compared with MDD (14). MD is often prodromal to MDD (7, 15, 16). NS in the absence of clinical depression is also frequent (29.8%) in the general population (17).
The ICD-10 (18) diagnosis of MD requires four symptoms, whereas the DSM-V (19) criteria are based on seven main symptoms, and the Hamilton Depression Rating Scale (HDRS) gives an MD diagnosis threshold for scores ranging from 7 to 17 as widely accepted by clinicians or cutoff scores from 8 to 16 as suggested by the recent severity classification of HDRS (20–23). However, depression is heterogeneous and presents with highly variable clinical symptoms, so its diagnosis cannot be made merely by the number of symptoms, but should include their detailed analysis and causal relations (24–26). Diagnosis of MD was reported to be less stable compared with diagnosis of severe depression using ICD-10 criteria and was characterized by a fair level of agreement (kappa?=?0.25) between clinicians compared with the moderate reliability in severe depression cases (kappa?=?0.53) (8, 27). The claimed high prevalence of MD is sometimes viewed with skepticism, given the questionable reliability of psychiatric diagnoses in general (28), and especially with respect to the differentiation of MD from NS (8, 29). Correct recognition of subthreshold forms of NS is based upon the number, duration, and quality of presented symptoms (30). Despite the elaboration of criteria cited above, psychiatry still lacks objective clinical tests of symptoms comparable with those routinely used in other medical disciplines (31). Affective (e.g., decreased mood) and cognitive (e.g., negative content of thoughts) components of MD and NS are mostly expressed through language, while more severe forms of depression are also recognized by a motor component (e.g., slow bodily movements). The search for objective indicators of MD vs. NS might help to increase the reliability of MD diagnosis. Andreasen and Pfohl (32) first showed that language is a specific marker of depression, and currently active study groups have concluded that an analysis of natural language processing could afford the foundation for developing objective diagnostic tests “based on dimensions of observable behavior” (33) (p. 904).
While a clinical interview remains the basic tool for diagnosing depression (34), linguistic research has demonstrated that systematic analysis of language content reliably classifies patients into appropriate diagnostic groups (35, 36). Nguyen et al. (37) report that computerized word counting techniques (38, 39) discriminate depression communities from other subgroups and also reveal strong online-language predictors of depression (40) and suicide (41). Aberrant written and spoken languages are frequently reported in patients with depression (42–46). Being a chronic affective disorder presenting either within mild depressive symptoms or with marked absence of pleasure in daily activities, dysthymia is characterized by increased speech flow, in contrast to the slowed speech typical of MDD (14). The excessive use of first-person singular pronouns (I) correlated with depression in many (22, 23, 38, 46, 47), but not all studies (48). Objective (me) and possessive (my) first-person pronouns were more frequent in speech of a group with depression, and predicted depression better than did subjective (I) pronouns (47). Elevated usage of first-person pronouns was attributed to self-focused attention or self-preoccupation (44, 47, 49). Among various measures of depressive self-focusing style, rumination (repetitions of the same, usually negative, information) has been mentioned in many studies (50–52). Other features of depression included elevated use of mental state verbs (think), words denoting causal relations (because) (53), greater use of generalizing terms (everything, always), negation (nothing, never), and words referring to ambivalent emotional states (54, 55). The increased use of discrepancy words (should), possibly reflecting enhanced aspirations for the future (56), has been discussed as a marker of improvement with therapy for depression. Together, these promising results denote that “the styles in which people use words” represent no less meaningful information than “the content of what they say” about their symptoms (38) (p. 548). Nonetheless, language phenomena are still not widely considered for psychiatric diagnosis of affective states.
In-timid-ate
You can see “timid” in the middle of intimidate, and to be timid is to be frightened or to pull back from something. When you intimidate, you frighten or make someone afraid. A pet rat might intimidate your sister’s friends, keeping them out of your fort.
THERE ARE GENETICS TO YOUR FEELINGS THAT LOCK UP YOUR SUPER POWERS!
YOUR SUPER POWERS ARE IN YOUR ENERGY FIELD!!!
MEEK MEANS – DEFENCELESS!!!
“To frighten” or “make fearful” is at the root of the verb intimidate. An animal might intimidate a smaller animal by bearing its teeth, and a person can intimidate another by threatening to do something harmful. You can be intimidated with mental or emotional bullying, as well as with something physical: “they were all good spellers, but some of them knew how to intimidate the competition into thinking they didn’t have a chance at winning the spelling bee.”Start learning this word
Think you know intimidate? Quiz yourself:
ASSESSMENT: 100 POINTSWhich of the following would most likely intimidate someone?cleaning a dirty bathroomtaking a canoe trip across a lakerunning into a bear in the woodsbuying a new pair of shoesAdd to List…Thesaurus Share It
Definitions ofintimidate1
vcompel or deter by or as if by threats
Synonyms:restrainTypes:dash, daunt, frighten away, frighten off, pall, scare, scare away, scare offcause to lose courageType of:discouragedeprive of courage or hope; take away hope from; cause to feel discouraged
vmake timid or fearful
“Her boss intimidates her”Types:hold overintimidate somebody (with a threat)ballyrag, boss around, browbeat, bully, bullyrag, hector, push around, strong-armbe bossy towardsdomineer, tyrannise, tyrannizerule or exercise power over (somebody) in a cruel and autocratic mannerType of:affright, fright, frighten, scarecause fear in
