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).

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…

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.

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.

 

New drug hope for multiple sclerosis

High hopes for new MS treatment

Published: Thursday, 23 October 2008, 7:40AM
A drug used to treat leukaemia will bring hope to many of the UK’s 100,000 multiple sclerosis sufferers.

A study published in the New England Journal of Medicine led by Cambridge researchers found a drug called alemtuzumab can stop MS advancing in patients in the early stages of the condition.

MS causes the immune system to attack the protective coating around nerve fibres which prevents messages being transmitted between the brain and other parts of the body.

Symptoms of the disease can include loss of physical skills, sensation, vision, bladder control and intellectual abilities.

A three-year trial of alemtuzumab on MS patients showed it can restore lost function, reversing some of the effects of the condition.

Researchers found patients treated with alemtuzumab were 74 per cent less likely to experience relapses than those taking the leading treatment interferon beta-1a.

The risk of disability was reduced by 71 per cent among those given the new drug, suggesting alemtuzumab may allow damaged brain tissue to repair itself and restore lost nerve function.

Dr Alasdair Coles, lecturer at the university’s Department of Clinical Neurosciences, said: “The ability of an MS drug to promote brain repair is unprecedented. We are witnessing a drug which, if given early enough, might effectively stop the advancement of the disease and also restore lost function by promoting repair of the damaged brain tissue.”

More studies are needed before the drug can be approved for the treatment of MS.

During the three-year trial, 20 per cent of people treated with alemtuzumab developed an over- or under-active thyroid gland, while 3 per cent developed a low platelet count – a complication that led to one fatality.

Researchers said these complications can be easily treated if caught early.

Lee Dunster, head of research at the MS Society, said: “We are delighted that it has reported such positive results. This is the first drug that has shown the potential to halt and even reverse the debilitating effects of MS and this news will rightly bring hope to people living with the condition day in, day out.

Nice to know, but not without it’s own problems

The ‘Flynn effect’ is caused by nutrition

Or at least, it is according to Professor Lynn. The Flynn effect is the rise in IQ that was observed over the twentieth century, mostly in developed nations, as the overall standard of living improved. It stabilised in Europe in the eighties, but in places like East Asia it is still rising as the countries modernise.

What has caused the Flynn effect? Secular increases in the Development Quotients of infants

Richard Lynn,

University of Ulster, Coleraine, Northern Ireland, BT52 1SA, UK

Received 23 March 2008;  revised 17 July 2008;  accepted 17 July 2008.  Available online 21 September 2008.

Abstract
Results of five studies show that during the second half of the twentieth century there were increases in the Development Quotients (DQs) of infants in the first two years of life. These gains were obtained for the Bayley Scales in the United States and Australia, and for the Griffiths Test in Britain. The average of 19 data points is a DQ gain of approximately 3.7 DQ points per decade. Similar gains of approximately 3.9 IQ points per decade have been present among preschool children aged 4–6 years. These gains are about the same as the IQ gains of school age students and adults on the Wechsler and Binet tests. This suggests that the same factor has been responsible for all these secular gains. This rules out improvements in education, greater test sophistication, etc. and most of the other factors that have been proposed to explain the Flynn effect. It is proposed that the most probable factor has been improvements in pre-natal and early post-natal nutrition.

Prior to the modern era, Victorians were four inches shorter than the current population, and the IQ was thirty points lower. It would seem reasonable that both increases were proved by a combination of improved nutrition and health care. The greatest IQ rises were seen in the lowest IQ ranges, suggesting that the welfare state, in the UK at least, has contributed to our being geniuses compared to our great grandparents.

The IQ rise has only been observed in our ‘fluid’ intelligence, AKA our reasoning abilities. Our memory seems to have been unaffected by the rise in IQ. I suppose this could mean that as a species learning is a lot more important than reasoning, so our resources are directed towards constructing our memory fully before our problem solving wiring is even begun.

 

Inosine to treat Parkinsons disease?

Using inosine to increase urate  to reduce Parkinson’s disease
American Journal of Epidemiology [2008] 167 (7) : 831-838 (Gao X, Chen H, Choi HK, Curhan G, Schwarzschild MA, Ascherio A.) Complete abstract

End-of-dose wearing off was seen in 13.9% versus 20%, respectively (P=0.09). The Michael J. Fox Foundation announced a $5.6 million award for a Phase 2 clinical trial to investigate the potential of inosine – a naturally occurring chemical that gives rise to urate in the body – to slow or stop the progression of Parkinson’s disease. For more information go to the Complete article. Urate is a natural metabolite and antioxidant in humans. Inosine is widely available to consumers in dietary supplement form. Inosine is able to forum urate, which is why it is being proposed to increase urate levels. For more information go to Urate formation. A recent large study confirmed that higher dietary urate was associated with a lower risk of Parkinson’s Disease Disease. The authors consequently suggest that dietary changes expected to increase plasma urate level may contribute to a lower risk of Parkinson’s Disease. However, no rationale has been provided by the authors that would explain the link. The evidence to date surrounding inosine and Parkinson’s Disease does not prove a cause-effect relationship.  Also, elevated urate levels are known to cause health risks, only some of which have been characterized to date.

It seems they are trying it on everything these days. Apparently the Michael J. Fox foundation has dropped a few  million dollars into this trial.

One treatment won’t fit all for Multiple Sclerosis.

Animal studies by University of Michigan scientists suggest that people who experience the same clinical signs of multiple sclerosis (MS) may have different forms of the disease that require different kinds of treatment.

The results, if borne out in further studies, point to a time when doctors will be able to target specific inflammatory processes in the body and more effectively help MS patients, using available drugs and new ones in the pipeline.

Since the 1990s, the treatment picture has brightened for people with multiple sclerosis in its most common form, relapsing-remitting MS. Beta interferon drugs and glatiramer acetate (marketed as Copaxone) have proved effective at decreasing the attack rate and suppressing inflammatory plaque development in many patients with MS. Yet why the drugs help some patients, but not others, has remained a mystery.

The U-M research team conducted the studies in mice that have a disease similar to MS: experimental autoimmune encephalomyelitis or EAE. The team found that different inflammatory chemicals, whose activity is linked to two different types of immune system T cells, could bring on the same paralysis and other MS-like signs. They also showed that drugs that block one of the inflammation pathways were not effective at blocking the other. The results, published online ahead of print, will appear in the July 7 issue of the Journal of Experimental Medicine.

“These two forms of disease differ in the specific anti-inflammatory agents that they are responsive to,” says Benjamin Segal, M.D., the study’s senior author and the director of the Multiple Sclerosis Center at the U-M Health System.

“We already know that some people respond better to the drugs beta interferon or Copaxone than others. Now we’ve shown proof that you can cause MS-like syndrome in mice due to qualitatively different types of inflammatory damage. As a result, these two kinds of inflammation likely require different approaches to treatment,” says Segal. He directs the Holtom-Garrett Program in Neuroimmunology and is the Holtom-Garrett Family Professor of Neurology at the U-M Medical School.

Context:

MS is an inflammatory disease of the central nervous system believed to be autoimmune in nature. Certain cells in the body’s immune system mount an inappropriate response against proteins in the nervous system, in particular myelin, the fatty substance that covers nerve axons. MS affects an estimated 2.5 million people worldwide. Symptoms, which vary widely, include numbness and weakness, incontinence, double vision, tremor, imbalance and pain.

In 85 percent of MS cases, patients begin with what is called a relapsing-remitting form of the disease. Initially, they have attacks in which they experience symptoms for a time, return to normal, then have attacks again. In the last 15 years, several beta interferon drugs and Copaxone have been effective in many patients at limiting the number of attacks. These drugs also can also decrease damage in the brain as visualized on MRI scans.

Research details:

Segal’s research team injected one group of mice with an immune system T helper cell, Th1, long believed to play a role in MS, and another group with a T helper cell, Th17, whose potential role in MS has recently come to light. They measured the activity of specific inflammatory agents that are induced by each type of T cell as the immune system mounts its misguided attack on the myelin sheaths of nerve cells.

Both groups of mice developed similarly severe and rapid paralysis. But the researchers found clear differences in the inflammatory agents involved, called cytokines and chemokines, and in the resulting damage to the central nervous system.

Mice injected with Th1 cells showed a pattern of central nervous system inflammation that resembled that of common MS, with lesions filled with macrophages, a type of immune system defender cell. Mice injected with Th17 cells, however, had lesions filled with another immune cell type, neutrophils. In these mice, inflammation reached deep in central nervous system tissues and in the optic nerve.

In both groups of mice, the scientists tested the effects of neutralizing antibody drugs similar to drugs being developed against autoimmune diseases in humans. Some of the drugs inhibited disease in the Th17 mice, but not in the mice receiving Th1 cells. Other drugs were effective against both types of disease.

“That’s our proof that these really are different mechanisms of disease,” says Mark Kroenke, the study’s first author and a Ph.D. student in immunology at U-M.

Implications:

It’s not yet known whether the same differences will prove true in people with MS. But the study suggests the need to develop drugs tailored to affect distinct inflammation pathways that might drive different forms of relapsing-remitting MS.

“We speculate at some point being able to identify and measure active inflammatory agents in patients, and to develop customized profiles that would help predict what treatments will be effective,” Segal says.

In addition, Segal says, the findings may aid the search for effective drugs for two difficult-to-treat diseases closely related to MS: neuromyelitis optica, which affects the optic nerve and spinal cord, and opticospinal MS, most common in Asia. The pattern of inflammation the team saw in the Th17-injected mice resembled the pattern in these variants of MS.

This doesn’t surprise me at all It’s been believed for a while that MS is a collection of different causes with a similar end. I’d love to know how the uric acid levels feature into all of this.

Global IQ’s

What you do have to remember when looking at this map is that living conditions, particularly medical care and nutrition, have a major effect and IQ. About 100 years ago the average IQ of Britain was 70, so comparing developing countries with places like Japan and Germany is massively unfair. However, comparing countries in South Asia with  better developed African countries is fair. They both have equally poor standards of living.

A few of the IQ tests that this map is based on were quite suspect. The Ethiopian one in particular, which was done on half-starved, war traumatised Jewish refugees, freshly resettled in Israel.

1 Hong Kong 107             28  Argentina 96           55  Fiji 84
2  South Korea 106           29  Slovakia 96            56  Iran 84
3  Japan 105                      30  Uruguay 96            57  Marshall Islands 84
4  Taiwan 104                    31  Portugal 95           58  Puerto Rico 84
5  Singapore 103               32  Slovenia 95            59  Egypt 83
6  Austria 102                   33  Israel 95                 60  India 82
7  Germany 102                 34  Romania 95           61  Ecuador 80
8  Italy 102                        35   Bulgaria 94           62  Guatemala 79
9  Netherlands 102            36  Ireland 94              63  Barbados 78
10  Sweden 101                 37  Greece 94               64  Nepal 78
11  Switzerland 101           38  Malaysia 94            65  Qatar 78
12  Belgium 100                 39  Thailand 93            66  Zambia 77
13  China (PRC) 100            40  Croatia 92              67  Republic of the Congo 73
14  New Zealand 100           41  Peru 91                 68  Uganda 73
15  United Kingdom 100     42  Turkey 90               69  Jamaica 72
16  Hungary 99                   43  Indonesia 90          70  Kenya 72
17  Poland 99                      44  Mexico 89              71  South Africa 72
18  Spain 99                        45  Suriname 89          72  Sudan 72
19  Australia 98                  46  Brazil 87                 73  Tanzania 72
20  Denmark 98                  47  Iraq 87                   74  Ghana 71
21  France 98                      48  Colombia 87           75  Nigeria 69
22  Norway 98                    49  Samoa 87               76  Guinea 69
23  Finland 98                    50  Tonga 87                77  Zimbabwe 68
24  Canada 97                    51  Lebanon 86             78  Dem Rep Congo 67
25  Czech Republic 97        52  Philippines 86         79  Sierra Leone 67
26  United States 97           53  Cuba 85                   80  Ethiopia 66
27  Russia 96                     54  Morocco 85              81  Equatorial Guinea 66

Part of my argument that a fair part of racial IQ differences are genetic. The average black American IQ is 15 points lower than the white, this would put them lower than places like Suriname, Indonesia and Lebanon. I don’t think the living conditions of the average black American are anything like that bad.

It’s also apparent that the highest scorers are in the far East,  and while Taiwan is doing reasonably well, it’s living standards aren’t as high as those in America and Northern Europe, yet it’s population performs better.

IQ, race and assortive mating.

I’ve had an idea to do with race and IQ that’s to do with assortive mating.

The average IQ of people with one black and one white parent in the USA is in between the averages for both groups. I keep seeing this put down to white parent IQ 100+black parent IQ 85=185/2= IQ of 92.5 for the mixed race child.

But that’s not how people work

There’s something called ‘assortive mating’, where someone will seek out a like individual to pair up with, and the most matched trait in couples (more so than political views, education or physical attractiveness) is IQ. Generally it will be put down as similar interests/same sense of humour/educational level. But really, to understand your life-mate properly you have to think on the same level as them. It’s uncommon to see a couple with an IQ more than six points apart.

This brings us to racial diffences in IQ.

This bell curve, that I have shamelessly swiped from Wikipedia, is a good visual aid for this. The orange pointed are in the middle is where most of the overlap in IQ occurs, and the IQ range of 90 to 95 seems to be where the most overlap between the two groups occurs. So black people on the higher end of their groups IQ range, will actually have more chance of meeting a European with a similar IQ: the higher the black genius’s IQ, the more likely it will that any prospective equals he meets will be white. Particularly as white strongly outnumber black Americans. There is a trend for degree educated black Americans to marry inter-racially.

Add this together with a tendency for successful black American men to marry white women, and you’ve got a trend where the most intelligent black people are distancing their offspring from their parent group. I really don’t think intermarriage has made any positive impact on the IQ of black Americans at all, I think it has had a mildly negative impact if anything.

What this means is that European ancestry doesn’t mean a higher IQ for the mixed kid, it’s black parent was probably roughly that smart; they were just more likely to meet a white mate with a matching IQ than their black friends were.  What thoes does mean is that intermarriage won’t solve the problem very fast, you’ll just end up with the middle and upper IQ ranges  getting more European DNA in them, and the lower range being marked out by their African appearance. Not a thought to induce racial harmony in the future.