The Color of Crime: Race, Crime and Justice in America

The Color of Crime: Race, Crime and Justice in America

Major Findings

  •  There is more black-on-white than black-on-black violent crime.
  •  Of the approximately 1,700,000 interracial crimes of violence involving
    blacks and whites, 90 percent are committed by blacks against whites.
  • Blacks are therefore up to 250 times more likely to do criminal violence to whites than the reverse.
  •  Blacks commit violent crimes at four to eight times the white rate.
  • Hispanics commit violent crimes at approximately three times the white rate,
    and Asians at one half to three quarters the white rate.
  • Blacks are twice as likely as whites to commit hate crimes.
    Hispanics are a hate crime victim category but not a perpetrator category.
  • Hispanic offenders are classified as whites, which inflates the white
    offense rate and gives the impression that Hispanics commit no hate crimes.
  • Blacks are as much more dangerous than whites as men are more
    dangerous than women.

A fairly old publication from 1999, which is based on the FBI crime statistics, and which is technically accurate. It was written in response to earlier use of the information that glossed over the black on white crime rate and focused almost exclusively on the black on black crime rate- amazing how the same set of information can be used to push different agendas. I’ve snipped out a few of the more memorable quotes- remember the numbers are completely correct and verifiable from the FBI crime stats.

Of the approximately 1,700,000 interracial violent crimes involving blacks and whites reported every year, blacks commit 90 percent and whites commit only ten percent. Blacks are therefore more than 50 times more likely than whites to commit interracial crimes of violence. The differences are even greater for multiple-offender interracial crimes, with blacks 100 to 250 times more likely to be involved in gang attacks on whites than the reverse. Some people may argue that blacks attack whites because they expect them to be carrying cash or valuables. However, fewer than 20 percent of black attacks on whites are robberies; rape and assault do not usually have economic motives.

For virtually all crimes, there are consistent and pronounced differences in arrest rates for violent crime by race and ethnicity. Blacks are five to ten times more likely to be arrested than whites, Hispanics are approximately three times more likely, American Indians are about twice as likely, and Asians are only one half to two-thirds as likely to be arrested for violent crimes as whites. The very high rates for blacks means that the single best independent predictor of crime rates for an area is the percentage of the population that is black.

I’m not going to post the whole document, but it roughly matches the trends in the UK race crime stats that I posted earlier. It doesn’t really go into much detail about interracial sex crimes, which are almost entirely white on black, with some years the FBI having less than ten white on black rapes reported. But that’s for another post.

This is also very similar to the Criminal Victimization in the United States, 2005 Statistical Tables (Page 30, chart 42), where the sex offence pattern is near identical but based on surveys rather than reported crimes. No longer available on-line, unfortunately.

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IQ Population Genetics: It’s not as Simple as You Think

IQ Population Genetics: It’s not as Simple as You Think

The question of cognitive differences between human populations is one of the most contentious issues in the study of human diversity. After reviewing the worldwide patterns of cognitive test performance, this article evaluates alternative causal hypotheses and evolutionary mechanisms. Racial affiliation and latitude correlate with IQ test performance, as does economic development. Religion, a history of colonialism, and a history of Communist rule are important in some cases. This article proposes mechanisms of gene-culture co-evolution that can explain the worldwide patterns. The genetic component of these mechanisms is likely to become testable with further advances in molecular genetics.

A long but very interesting publication from 2003. Some of the most interesting snippets from this pdf are..

Also the argument that the 100,000 years or so since the dispersal out of Africa were insufficient for the evolution of genetic differences is invalid. To create an IQ difference of, say, 15 points between two populations in 100,000 years, natural selection would have to drive their IQs apart by only 0.004 points every generation – about 1% of the selective pressure in late 20th-century America.

 

 Genes, like drugs, have many side effects. This is called pleiotropy. For example, the average IQ of nearsighted people is 6 to 8 points higher than the average for normal-sighted people.

 

In the late 20th century United States, unequal reproductive rates favoring the less intelligent would have lowered the IQ of the population by anywhere between 0.35 and 0.8 points per generation had the environment remained unchanged over time (Loehlin, 1997; Retherford and Sewell, 1988; Vining, 1995; Lynn, 1996 – Dysgenics, Praeger).

 

Rushton emphasizes the need for close family ties and high parental investment in harsh climates. While most childhood mortality in the tropics was caused by uncontrollable endemic diseases, most childhood mortality in the arctic was due to the predictable challenges of seasonal food shortages and the rigors of the climate. These challenges demanded intelligent planning in addition to stable families (Rushton, 1995).

Referring to the last quote: smaller head size (easier birthing) and a faster/more prolific reproductive cycle are more important than being smart when the major cause of death in children is unpreventable diseases This could be one reason that Africans have a much higher twinning rate, and why peoples from the tropics have a gestation period about one week shorter than  north east Asians or Northern Europeans. Also nice to find a source for the nearsightedness and IQ relation (I’m blind as a bat without my specs).

I’d also like to point out that for the IQ between populations to be the same, evolution of the human brain would have had to effectively stopped cold about 130,000 years ago: before the  African and non-African populations separated. Since it has been shown by Bruce Lahn and others that certain brain affecting mutations have arisen in the last 37,000 years and that they vary wildly in distribution (the MCPH1 gene for example, which affects brain size) this is demonstrably not the case.

The whole paper is worth a read if you have an interest in the subject of race and IQ.

  

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Correlations between estimates of state IQ and FBI crime statistics

Correlations between estimates of state IQ and FBI crime statistics

Previous research suggests that crime is negatively associated with IQ at the individual level and the aggregate state level. The purpose of the present study was to further explore the relationship between state IQ estimates and various categories of violent and property crimes. State demographic information including the gross state product, pupil/teacher ratio, and percent Black, Asian, and Hispanic were included in the correlational analyses. State IQ was significantly and negatively correlated with the violent crimes of murder, aggravated assault and robbery as well as the property crimes of motor vehicle theft, theft and burglary. Additionally, regression analyses were conducted for each crime significantly related to state IQ, controlling for significant state demographic variables. In general, results suggest that the prevalence of both violent and property crimes is associated with lower state IQs.

SO I’m looking for the full text of this, just stored for later reference. One small observation would be that given the racial differences in IQ, this would mean that states with a high percentage of black citizens (IQ about 12-15 points lower) would have a much higher offending rate- not exactly a surprise, as that’s a pattern seen the world over. If I recall, the offending rate for East Asians is about half the white average, which also fits in with the higher East Asian IQ.

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Lies, damn lies and race crime statistsics

After watching the truly execrable Channel 4 series of programs ‘Race, the last taboo…’ I was inspired to do some reading into race and hate crime statistics. I’ll rip Rageh Omar a new one over the show on race and IQ at a later date (it was shamelessly biased and very nearly dishonest in places), but for now I’m studying the myth that ‘racism is something white people do to Asian/black people’, which was pushed on us yet again by the re-hashing of the 70’s brown eye/blue eye experiment. To be truthful I’m fed up with white people being portrayed as the source of all interracial strife by the media.

This involved tracking down a few stats from the race hate crimes ( I found the 2004 figures) and then comparing them to the percentages of which race is living in the UK. At the moment our population is…

91%  white (mainly native).
4.4% Asian (mixed Chinese and South Asian).
2.2% black.

With mixed race and ‘other’ filling up the rest of the space.

Then I checked the offence figures- overall the chance of a minority being victimized is about 1%, and the rate for a white it is less than 1% . The article I got this from pushed this as proof minorities were being victimized by the white British.

However, all is not as it seems.  There were a total of 179,000 race motivated crimes, of which…

87,000 victims were minority.
92,000 victims were white.

And then to consider was that 57% of the offenders where non-white, which meant…

102,000 offences were committed by the 9% minority (5.5million) an offending rate of about 1/53.

76,970 offences were committed by 91% white population   (55.5 million)  an offending rate of about  1/721 .

So in actuality each white British citizen is… 13.6 times less likely to commit a racially motivated crime, at least as an individual.

Breaking this down into violent attacks that involved wounding…

20,000 of the injured were the 91% majority (87% of offences by non white)

4,000 of the injured were the 9% minority. (30% of offences within the minority)

Which means…

The 9% have an offending rate of 1/295

The 91% have an offending rate of 1/19821

So again it looks bad, with the non white community roughly 67 times more likely to commit a violent racially motivated offence  (individually) than the white majority.

One comment I’d like to make that white non-British groups like the Roma, Turkish and people from the near East probably do figure in these statistics (possibly contributing to the white-on-white white crimes against the British and some crimes against the non-white minority) so there’s probably a bit of wiggle room in these stats, but it would be adding to immigrant crime levels, and non detracting from it.

All this is makes me think that its our black and Asian neighbours need racial sensitivity training, not us. And makes me query the wisdom of allowing more of them to immigrate. However.. I’m shy of lumping the Chinese and East Asians in with Indians and Pakistanis, or even Pakistanis with other Southern Asian groups as Islam probably does have a major impact on the rate of offending. I suspect the east Asians have a lower offending rate and the Pakistani rate would be respectively higher (personal experience from living in London).

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Parasitic infections lower multiple sclerosis relapses.

In a small study from Argentinia. There were only 24 patients, but the results were so strong the Dr involved felt it was worth publishing. The control group suffered fifty six relapses, the parasite infested group only three, about 1/18th the number of attacks. I found this article from Medscape:

Parasitic Infection May Benefit MS Patients

January 24, 2007 — Parasitic infection in multiple sclerosis (MS) may benefit patients by modulating the immune response and altering the natural course of the disease, a new study suggests.

Investigators from the Raúl Carrea Institute for Neurological Research in Buenos Aires, Argentina, found that MS patients with eosinophilia caused by intestinal parasites had a significantly lower number of relapses, minimal changes in disability scores, and significantly lower activity on magnetic resonance imaging (MRI) compared with uninfected MS patients.

“Parasitic infection has been shown to alter the immune response and confer a protective effect in animal models. However, this is the first time it has been shown in humans with MS,” the study’s principal investigator, Jorge Correale, MD, told Medscape.

The study was published online January 17 in the Annals of Neurology.

Methods

The prospective, double-cohort study, which recruited from a large cohort of 432 regularly followed MS patients, included 12 patients with a diagnosis of clinically definite relapsing-remitting MS and eosiniophilia.

Patients had a mean age of 34 years, a mean extended disability status scale (EDSS) score of 2.8, and mean disease duration of 7.3 years. The study also included 12 patients without eosinophilia and 12 healthy individuals, who served as control subjects.

Patients were subjected to a comprehensive neurological examination every 3 months, including physical assessment of disease activity and EDSS scoring.

Brain MRIs were performed every 6 months, while immunological evaluations were conducted during the last 12 to 18 months of the study, which had an average follow-up of 4.6 years.

Stark Contrast

Over the study period, 3 clinical relapses occurred in the infected MS group, with 9 patients remaining clinically unchanged. In contrast, there were 56 relapses observed in the uninfected group. The median annual relapse rate was 0 in the infected MS group vs 1.09 in the uninfected group.

Furthermore, only 2 infected patients had changes in their EDSS scores, which were characterized as “minimal” and lasted less than 3 months. There was no change in EDSS scores in the remaining 10 infected subjects. In comparison, by the end of the study, 11 of 12 uninfected patients showed an overall increase in baseline EDSS.

In addition, the presence of new or enlarging T2 MRI lesions was evaluated. Among infected MS patients, 14 new or enlarging T2 MRI lesions were detected. In 6 patients, however, scans remained unchanged throughout the study period.

In stark contrast, there were 164 new or enlarging T2 MRI lesions registered in uninfected MS subjects. Furthermore, only 3 relapses were observed among the infected group vs 48 in the uninfected subjects.

Lack of Disease Progression

The lack of disease progression in patients with a parasitic intestinal infection is likely due to the ability of parasites to dampen inflammatory reactions that are characteristic of autoimmune diseases, said Dr. Correale.

Specifically, he said, MS is a Th1-mediated disease. Th1 produces proinflammatory cytokines — specifically, gamma interferon, the main cytokine responsible for MS. When patients acquire a parasitic infection, they develop 3 different cell populations — Tr1, which produces interleukin 10; Th3, which produces TGF-ß; and CD4+CD25+T cells, which modulate Th1 cells and specifically interfere with the production and proliferation of gamma interferon.

In their paper, the authors point out that parasites can inhabit immune-competent hosts for long periods of time. Indeed, said Dr. Correale, these patients were infected for almost 5 years and had few, if any, symptoms. It may be that to ensure its survival, the parasite produces molecules that generate a strong anti-inflammatory response.

Next Steps

Dr. Correale pointed out that the prevalence of MS in Latin American countries is much lower than in Europe or the United States. The higher prevalence of parasitic infections in Latin American countries may be one possible environmental factor that protects MS patients, lowering the prevalence of the disease, he said.

Dr. Correale said his next research steps will be to attempt to replicate these findings in a larger group of patients in a blinded fashion and with longer follow-up.

However, longer-term research goals, he said, will focus on isolating particular molecules produced by the parasite responsible for modulating the immune response and ultimately testing its therapeutic effect.

Upon comparing the results of this study (about a 1,800% improvement) with the results for the new MS treatment undergoing trials (about 70% improvement) I am a little bemused as to why all the time and energy is going into the drug trials, which have a far less impressive outcome (about 20 times less impressive), and more potentially harmful side effects than a controlled parasitic infection. No cash in it for the drug companies I suppose.

So much for Dr Hulda Clarks claims that parasites cause MS…

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Hook worms do work on asthma.

A couple of years ago it was all across the news that Nottingham university was trialling hookworms on asthmatics and hay fever sufferers, but then it all went quite, and I assumed it had been a failure and quietly dropped.

It seems I was wrong. A quote from an article from the project leader, a Dr Pritchard, stated:

Researchers at the University of Nottingham tested this by treating asthma patients with human hookworm. Again, the results were dramatic with nearly 70% of the patients demonstrating improvement.

And also in this publication.

Asthma and Current Intestinal Parasite Infection

Systematic Review and Meta-Analysis
Jo Leonardi-Bee, David Pritchard, John Britton and the Parasites in Asthma Collaboration
Division of Epidemiology and Public Health and School of Pharmacy, University of Nottingham, Nottingham, United Kingdom

Methods: We searched MEDLINE, EMBASE, and CINAHL (up to January 2006); reviews; and reference lists from publications, with no language restrictions. We included studies that reported asthma or wheeze as an outcome measure and ascertained parasite infection by fecal examination. We estimated pooled odds ratios (OR) and 95% confidence intervals (CI) using data extracted from published papers, or where available, original data provided by authors, using random effect models.

Measurements and Main Results: Thirty-three studies met the inclusion criteria. Infection with any parasite was associated with a small, nonsignificant increase in asthma risk (OR, 1.24; 95% CI, 0.98–1.57; 29 studies). In species-specific analysis, Ascaris lumbricoides was associated with significantly increased odds of asthma (OR, 1.34; 95% CI, 1.05–1.71; 20 studies), while hookworm infection was associated with a significantly strong reduction(OR, 0.50; 95% CI, 0.28–0.90; 9 studies) that was directly and significantly related to infection intensity (p < 0.001; OR for highest tertile of infection, 0.34; 95% CI, 0.19–0.62). Other species had no significant effects on asthma. Infection effects on wheeze were derived from smaller numbers, but revealed a broadly similar pattern of results.

Conclusions: Parasite infections do not in general protect against asthma, but infection with hookworm may reduce the risk of this disease.

Which ties in nicely with all the research about some parasites having a soothing effect on other autoimmune conditions like Crohn’s disease and multiple sclerosis. See link.

The medical community is quietly enthusiastic about the chance of acquiring new drug therapies from the study of these parasites, but seem to generally disapprove of the idea of deliberately infesting patients. This isn’t a sentiment a lot of the patients share, as several refused to eliminate the hookworms when the Nottingham study concluded. I myself have no issues with having a dozen hookworm if I’ll still be able walk and see in ten years time. It’s not the ideal situation, but it beats a catheter and motorized wheelchair any day.

Some patients are so desperate to get their hands on hookworms that a private clinic  has opened to infest them. It costs $3,900 dollars, and a return ticket to Mexico. There’s even a Yahoo group called the ‘helminthic therapy group’ that’s interested in whipworms to treat Crohn’s.

I have hay fever too. Would it be dishonest of me to enrol in the Nottingham study just to treat my MS? What it really need is a UK study of MS and parasites to enter. The Argentinian study (small scale) had teh control group having fifty six relapses, but the parasite infested only having three. Quite honestly, reducing my MS by a factor of 18 is very appealing.

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Is a universal flu jab possible?

Universal flu jab works in people  
 
A single jab that could give lifelong protection against all types of flu has produced promising results in human trials.  The vaccine, made by Acambis, should protect against all strains of influenza A – the cause of pandemics.

Currently, winter flu jabs have to be regularly redesigned because the flu virus keeps changing.

The new vaccine would overcome this and could be stockpiled in advance of a bird flu outbreak, say experts.

Each year winter flu kills around 4,000 people in the UK.

Globally, between 500,000 and one million people die each year from influenza.

But a pandemic of the human form of bird flu, which experts believe is inevitable, could kill as many as 50m people worldwide.

The US trials show that the jab is safe and it works fast to make the body immune against flu.    It could be stockpiled in advance of a pandemic

Nine out of 10 of those who had two doses of the jab ACAM-FLU-A developed antibodies against flu virus.

Scientists at Acambis are now working alongside Professor Walter Fiers and his team from the University of Ghent in Belgium and the Flemish Institute of Biotechnology to perfect the formulation before doing larger human trials.

Dr Michael Watson of Acambis said: “As a universal vaccine, ACAM-FLU-A can potentially overcome many of the drawbacks of existing influenza vaccines.

“It can be manufactured at any time of the year, and could be stockpiled in advance of a pandemic or potentially used routinely to ensure population protection against future pandemics.”

Current flu vaccines work by giving immunity to two proteins called haemagglutinin and neuraminidase, which are found on the surface of flu viruses.

However, these proteins keep mutating which means doctors have to keep making new vaccines to keep up.

The Acambis vaccine homes in on a different protein, called M2, which is found on the surface of all A-strains of flu and does not appear to mutate so readily.

Professor Ian Jones, a University of Reading virologist, said the jab could end the scramble to produce a new winter jab each year.

But he said it would still be some years before it was widely available for patients.

“Larger trials and tests on a wider range of viruses will be needed before the full potential for pandemic protection can be assured,” he said.

This could save everyone a world a grief, and the NHS a lot of money every winter. I for one look forward to only having one flu jab every five years, as my current vaccination is swollen and tender as hell.

 

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