Millennium Strategic Enterprises

PROACTIVE POSITIVE IMAGE PROMOTION
Strategy and Budget Proposal
________________________________________________________________________
Contractual FTE Unit Cost Total Cost
______________________________________________________________________
I. Personnel Cost $0,300,000.00
• Contracts and special projects
II. Operational Cost $1,404,00.00
• 1. Broadcasting Cost
One hour broadcast demands 3 hours’ development hours @ the rate of
$100 per hour (9 x3 x 100=2,700 x52= 1,404,400.00

• 2. Local and regional Transpiration 10,000.00
o @ 41 Cents per mile
41x12x7x52= $1,790.00 x 4 7,163. 52
o Internal Transpiration and accommodation @1,500x4 for 5=24,000

• 3. Communication cost (telephone, internet, web site, etc) $5,000.00
150 x12x4=7,200.00 $7,200.00

• 4. Program Development Cost (Research, interviews, etc) $5,000.00
• Articles, news analysis, panel discussion, etc at the rate of $50.00 per activity
300 products at the rate of 5 pieces per week

5. Mulit-Sectoral Positive Image Promotion Activities

A. Diplomatic and Inter-Governmental Affairs $100,000

B. Business Promotion Conferences and Seminars $100,000

C. Tourism, Cross Cultural Promotion Campaigns $100,000

D. Educational Technology and Development Activities $100,000

E. Talent Search and Skilled Expert Exchange Program $100,000

F. Proactive Media Image Promotion Activities $100,000

G. Search Engine and Cyber Image Promotion $100,000

H. Capacity Building Enterprises (technical Assistance) $200,000
__________________________________________________________________
Total Cost: $1, 300,000.00
• Miscellaneous: at 15% for additional costs $0, 150,000.00
• Grand Total: $1,450,000.00
__________________________________________________________________


EXPECTED OUTCOME

• POSITIVE IMAGE PROMOTION CAMPAIGN for Sustainable Security, Peace and Prosperity

Expected Result: Positive Image for investment, Job creation and business enterprises.

1. Short term: A series of Multi-Sectoral, multi-cultral positive image promotion campaigns

2. Intermediate term: Recruit positive win-win public and private stakeholders and partners

3. Long term: Develop a series of public and private enterprises positively engaged in Ethiopia/Africa

Proactive Strategy: Incremental, continuous interactive engagement of pubic and private sector in positive image development for investment and prosperity.

1. Vision:
• Promoting Individual and Collective Potential towards Millennial Renaissance Transformational Agenda of Peace, Security and Prosperity

2. Value:
•
Promoting individual and collective potential towards transformational Millennium Renaissance Agenda

3. Process:
• Strategic Continuous Strategic Incremental Managed Change

4. Objective:
• Image Change- Promoting Millennial Renaissance Transformation

5. Approach:
• Win-Win Strategic Partnership with local/International Public and Private Stakeholders







Process: From Negative to Positive and Transformational (Win-Win Enterprises)
__________________________________________________________________
Negative Positive Transformational

A. Human Resources Governance: from Poor to Good to Transformational
Via: Transparent, Accountable and Transformational Governance

1. Population Explosion Population Control Thriving Population

2. Unemployment Skill Development Enterprises

2. Corruption Standards/Protocols Excellence

3. Incompetence In-Service Training Best Practice

4. Insecurity Law and order Proactive Vigilance

5. Poor Productivity Performance Enhancing Tools Quality Improvement

6. Famine Food Security Food Export

7. Charity Empowerment Enterprises



Empowerment based strategy: From charity to Development and Enterprises

i. Charities AID agencies accept and expect disempowered populations to continue to exist

ii. Developmental Empowerment expects peace, security and enabling policy environment for investment and productivity.

iii. Enterprises expects an empowered and self sustaining populations with appropriate tools and expertise possible.


Result-based strategies: From Poverty to Wealth Creation to Prosperity

B. Transformation Leadership Development

Immediate Short Term Long Term

1. Paralysis Dynamic Change Proactive/Transformation
Value: Promoting Millennial Renaissance Transformational Agenda 4 P & P

Approach: Ideological/loyalty Goal/Competency Productivity/Result

Strategy: Measurable Progress that is qualitative, quantitative and productive
SMART Objectives: Specific, Measurable, Appropriate, Realistic and Time Sensitive

• Change the current image of consistent insecurity: conflictive, destructive and lose-lose image of the local and Diaspora and friends of Ethiopia/Africa perspective to Positive, interactive, incremental transformational image.
• Use the Millennium Renaissance Transformational Theme effectively!

Specific: Positive Image Promotion: Multi-Media and Multi-Institution based

Promote Ethiopian/African Millennial Renaissance Agenda of Peace & Prosperity

Measurable: Via Qualitative, Quantitative and Productivity Toosl
• Green Economy: Fair and Free Enterprise System of Governance
• Green Energy: Natural Energy: Water, Wind and Non Fossil fuel
• Green Technology: digitized and Wireless Technology
• Green Industrialization: Sustainable Diverse Industries
• Green/Organic Food Production and Marketing: Value Added Marketing
• Productive Education for Development and Enterprises
• Promoting Sustainable Peace and Prosperity
• Managing change via strategic and innovative approaches




C. Transformations Via Re-engineering and Capacity building of all institutions

1. Public Enterprises 2. Private Enterprises 3. Regional/Federal Enterprises

1. Win-Win Partnership for Peace and Prosperity and Sustainable Security

• Encourage win-win Partnership with African, American, Asian and European partners at school, universities, business and cultural and

• Interactive Multi-Media Proactive Web and Cyber Campaign

• Best Practice Protocol and Templates across all enterprises








2. Enhance all Regional Development Association in all regions

Regions: Northern Southern Western Eastern

Africa
• Eastern
• Southern
• Western
• Central
• Northern

Ethiopia
• Afar
• Amhara
• Gambella
• Gurage
• Hadya
• Harari
• Oromo
• Sidama
• Somali
• South
• Tigre
• Wolaita

3. Enhancing Regional and Municipalities Government Capabilities with Leadership Development
• Executive and Strategic Leadership
• Building Learning Institutions
• Participatory Corporate Governance
• Synergizing Public and Private Stakeholder Interests
• Regional Partnerships at Horn and AU/ME level

4. Enhancing Federal Government Capabilities with Leadership Development

• Executive and Strategic Leadership
• Building Learning Institutions
• Participatory Corporate Governance
• Synergizing Federal/Regional -Public and Private Stakeholder Interests
• Regional Partnerships at Horn and AU/ME level


Interactive Multi-Media Campaigns at local and international level with a focus on Patriotic Ethiopians, Diaspora and Friends of Ethiopia/Africa.

5. Aggressive Multi-Media Interactive Image Changing Campaigns

• Audio
• Video
• Radio
• Internet
• Conferences
• Festivals
• Workshops
• Focus Group Meetings
• Interactive educational communications

Remember:
____________________________
1. This is a strategy and needs to be supported with more detailed line item budgeting and time sensitive project management protocols that need to be developed with appropriate consultations with interested groups.

2. The strategy envisions engaging highly skilled and experienced institutions, public an private organizations.

3. The author is Dr Belai Habte-Jesus, and can be contacted at the address below for further discussion and realization of this strategy.
















PROACTIVE POSITIVE IMAGE PROMOTION
Strategy and Budget Proposal
________________________________________________________________________
Contractual FTE Unit Cost Total Cost
______________________________________________________________________
I. Personnel Cost $0,300,000.00
• Contracts and special projects

II. Operational Cost $1,404,00.00
1. Broadcasting Cost
One hour broadcast demands 3 hours’ development hours @ the rate of
$100 per hour (9 x3 x 100=2,700 x52= 1,404,400.00

2. Local and regional Transpiration 10,000.00
o @ 41 Cents per mile
41x12x7x52= $1,790.00 x 4 7,163. 52
oInternal Transpiration and accommodation @1,500x4 for 5=24,000

•3. Communication cost (telephone, internet, web site, etc) $5,000.00
150 x12x4=7,200.00 $7,200.00
•4. Program Development Cost (Research, interviews, etc) $5,000.00
•Articles, news analysis, panel discussion, etc at the rate of $50.00 per activity
300 products at the rate of 5 pieces per week

6. Mulit- Sectoral and Multi-Cultural Positive Image Promotion Activities

A. Diplomatic and Inter-Governmental Affairs $100,000

B. Business Promotion Conferences and Seminars $100,000

C. Tourism, Cross Cultural Promotion Campaigns $100,000

D. Educational Technology and Development Activities $100,000

E. Talent Search and Skilled Expert Exchange Program $100,000

F. Proactive Media Image Promotion Activities $100,000

G. Search Engine and Cyber Image Promotion $100,000

H. Capacity Building Enterprises (technical Assistance) $200,000
___________________________________________________________
Total Cost: $1, 300,000.00
• Miscellaneous: at 15% for additional costs $0, 150,000.00
• Grand Total: $1,450,000.00
__________________________________________________________________





~*~*~*~*~*~*~*~8
Millennium Strategic Enterprises (MSE)
• Strategic Enterprises
• Strategic Planning Session


• The firm specializes in strategic thinking, options, evaluations, re-engineering and reorganization of private and public enterprises, primarily working for profit and nonprofit organizations, associations, government and quasi-government agencies and grant makers.
• Our Competencies:

Strategic Planning for Organizations
Strategic Meeting Facilitation
Strategic Technology Assessment, Planning and Implementation
Strategic Board Development-Board of Directors Development/Training
Strategic Marketing/Fundraising – Defining the Competitive Position
Strategic Communications – media, print materials, Internet
Strategic Multi-Cultural Community Engagement / Collaboration
Strategic Public/Business/Nonprofit Partnership
Strategic Public Presentations/Training
Strategic Trade Associations/Service Organizations
Strategic Writing/Editing Presentations and Multi-Media Broadcasting
Strategic Effective Philanthropy/Grant making

Founded in 1993

• Millennium Strategic Enterprises was founded to empower for profit and nonprofit organizations and business associations achieve their missions with excellence.
• The firm provides services to maximize outcomes, focusing organizations' vision and a strategic use of resources, utilizing the services of professionals in various fields, depending on the assignment.
Consulting Rates
Basic Rates

• Consulting work is based on an hourly fee of $125/hour for work in the Greater Hartford, CT vicinity. Work out of the area is billed at the half-day ($750) or full-day ($1,250) rate, which covers travel time.

• Secretarial, support and administrative work is available and is billed at the rate of $40/hour.

• Miscellaneous Expenses such as long distance calls, faxes, shipping, mileage and out-of-the ordinary costs for postage, materials, or supplies are billed separately with appropriate documentation.

Contract Maximum

• A contract maximum fee or "not to exceed amount" is established and agreed upon by the client and the consultant prior to contract signing.

• The consultant agrees that, assuming the project does not change; total project fees will not exceed this amount without the written consent of the client.

`~*~*~*~*~*~*~*~*~*~*~*~*~*~*~*~*~*~*~*

We are writing to thank you for all your positive contribution to the family of Global Strategic Enterises, Inc. Organizations..

As part of our reorganization to promote success with excellence we are making key strategic changes that encourage transparency, accountability and professionalism across all disciplines in our respective organizations.

Promoting win-win relationship with all stakeholders
• As part of building a strong professional team across all disciplines we believe it is critical to build excellent relationships with all our stakeholders. We appreciate that our employees are the most critical assets and as such you are the engine of our success and excellence. We encourage creating a positive working environment that promotes win-win relationships with all stakeholders, i.e. clients, professionals, providers and regulatory authorities.

Promoting a learning organization with excellent documentation
• Our strategy is to continue to do the good things that you have been doing and provide you with additional tools and supports to provide a highly efficient, effective and high quality service to our client community. We encourage developing a system of communication where you learn every day and have strategies to make changes as you go.

Promoting Success with Excellence via Continuous Quality Improvement Audit
• We believe in success and to achieve it with excellence in satisfaction to the interests of all stakeholders, that is the client community, professional staff and the regulatory authorities both at local, state, federal and our main partners of excellence the Joint Commission for the Accreditation of Health Care.

Focusing on Stability, continuity and productivity with managing time!
• Our focus during the immediate , intermediate and short term future is stability, continuity, productivity and most importantly improving the market share and image of the organization at each site that is based on effective time management (with Calendar and Daily Communication Log and productivity reports)
Promoting a goal and results oriented leadership
• Our key strategy of success is integrating corporate, regional and local team efforts to make our service competitive, professional and highly responsive to the changing needs of our client community. We encourage using the goal and results oriented leadership strategy that was shared at the meeting. Promoting evidence based work environment that enhances performance, results and improvement from day to day.

Promoting Transparency and Accountability
• We believe in horizontal and vertical integration of responsibilities such that we respond to the demands of our internal management and external market and providers with effective communication tools. We encourage every one to maintain a calendar, daily communication logs and productivity reports so that there is seamless communication across the board via evidence based (qualitative, quantitative and productivity led) communication.

Calendar and Productivity driven communication
• We suggest that you maintain a calendar driven weekly agenda, where you have Daily Communication Log for the office and at each individual staff activity level, with clear cut productivity tools that are evidence driven to ensure Continuous Quality Improvement on a daily and weekly basis.

Weekly Meetings and Productivity Reports
• We encourage you to have two or three short meetings every week with appropriate attendance, agenda and talking point minutes as suggested during our meeting with sample minutes to be e-mailed to Dr Belai, Steve and Karen within two hours of the meeting. You will get response within 24 hours from one of us.

Monday Noon: Management Meetings
• Management Meetings with key senior clinical, operational, marketing and accounts representatives. Maintain Managerial Checklist that includes Personnel and Accounting and Operational Management Checklist at each meeting for follow-up.

Wednesday Noon: Clinical Audit Meetings
• Clinical staff that include the DoN, nurses, PT/OT.ST/MSW/HHA as necessary where charts are reviewed for clinical optimum service in line with CMS new guidelines and Joint Commission Standards. Here again, minutes and Clinical Checklists should be maintained. To ensure for follow up.

Friday Noon: Calendar review and preparation for next week

• We encourage all staff to submit their calendars to the Administrator/Director of Nursing by noon every Friday, so that appropriate supervisory prioritization of responsibilities could take place relevant to the needs and challenges of each week. This will feed into the weekly productivity report.

We thank you all for your positive cooperation and making our organization a win-win experience for all. Please do not hesitate to contact us any time via e-mail, phone and fax to ensure transparency and accountability in all our activities as we serve our client communities.

We thank you for all your positive contributions and good luck as we all serve with competence our respective communities!

Managing Hypertension the Exforge factor

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Exforge

Generic Name: amlodipine besylate and valsartan
Dosage Form: tablets



T2007-02/T2007-03

Exforge®

(amlodipine and valsartan)

Tablets

Rx only

Prescribing Information


Use in Pregnancy
When used in pregnancy, drugs that act directly on the renin-angiotensin system can cause injury and even death to the developing fetus. When pregnancy is detected, Exforge® (amlodipine and valsartan) should be discontinued as soon as possible.

See WARNINGS: Fetal/Neonatal Morbidity and Mortality


Exforge Description
Exforge® (amlodipine and valsartan) is a fixed combination of amlodipine and valsartan.

Exforge® contains the besylate salt of amlodipine, a dihydropyridine calcium channel blocker (CCB). Amlodipine besylate is a white to pale yellow crystalline powder, slightly soluble in water and sparingly soluble in ethanol. Amlodipine besylate’s chemical name is 3-Ethyl-5- methyl (4RS)-2-[(2-aminoethoxy)methyl]-4-(2-chlorophenyl)-6-methyl-1,4-dihydropyridine-3,5-dicarboxylate benzenesulphonate; its structural formula is


Its empirical formula is C20H25ClN2O5•C6H6O3S and its molecular weight is 567.1.

Valsartan is a nonpeptide, orally active, and specific angiotensin II antagonist acting on the AT1 receptor subtype. Valsartan is a white to practically white fine powder, soluble in ethanol and methanol and slightly soluble in water. Valsartan’s chemical name is N-(1-oxopentyl)-N-[[2′-(1H-tetrazol-5-yl) [1,1′-biphenyl]-4-yl]methyl]-L-valine; its structural formula is




Its empirical formula is C24H29N5O3 and its molecular weight is 435.5.

Exforge® tablets are formulated in four strengths for oral administration with a combination of amlodipine besylate, equivalent to 5 mg or 10 mg of amlodipine free-base, with 160 mg, or 320 mg of valsartan providing for the following available combinations: 5/160 mg, 10/160 mg, 5/320 mg, and 10/320 mg.

The inactive ingredients for all strengths of the tablets are colloidal silicon dioxide, crospovidone, magnesium stearate and microcrystalline cellulose. Additionally the 5/320 mg and 10/320 mg strengths contain iron oxide yellow and sodium starch glycolate. The film coating contains hypromellose, iron oxides, polyethylene glycol, talc and titanium dioxide.


Exforge - Clinical Pharmacology

Mechanism of Action

Amlodipine
Amlodipine is a dihydropyridine calcium channel blocker that inhibits the transmembrane influx of calcium ions into vascular smooth muscle and cardiac muscle. Experimental data suggest that amlodipine binds to both dihydropyridine and nondihydropyridine binding sites.

The contractile processes of cardiac muscle and vascular smooth muscle are dependent upon the movement of extracellular calcium ions into these cells through specific ion channels. Amlodipine inhibits calcium ion influx across cell membranes selectively, with a greater effect on vascular smooth muscle cells than on cardiac muscle cells.

Negative inotropic effects can be detected in vitro but such effects have not been seen in intact animals at therapeutic doses. Serum calcium concentration is not affected by amlodipine. Within the physiologic pH range, amlodipine is an ionized compound (pKa=8.6), and its kinetic interaction with the calcium channel receptor is characterized by a gradual rate of association and dissociation with the receptor binding site, resulting in a gradual onset of effect.

Amlodipine is a peripheral arterial vasodilator that acts directly on vascular smooth muscle to cause a reduction in peripheral vascular resistance and reduction in blood pressure.


Valsartan
Angiotensin II is formed from angiotensin I in a reaction catalyzed by angiotensin-converting enzyme (ACE, kininase II). Angiotensin II is the principal pressor agent of the renin-angiotensin system, with effects that include vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation, and renal reabsorption of sodium.

Valsartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT1 receptor in many tissues, such as vascular smooth muscle and the adrenal gland. Its action is therefore independent of the pathways for angiotensin II synthesis.

There is also an AT2 receptor found in many tissues, but AT2 is not known to be associated with cardiovascular homeostasis. Valsartan has much greater affinity (about 20,000-fold) for the AT1 receptor than for the AT2 receptor. The increased plasma levels of angiotensin following AT1 receptor blockade with valsartan may stimulate the unblocked AT2 receptor. The primary metabolite of valsartan is essentially inactive with an affinity for the AT1 receptor about one-200th that of valsartan itself.

Blockade of the renin-angiotensin system with ACE inhibitors, which inhibit the biosynthesis of angiotensin II from angiotensin I, is widely used in the treatment of hypertension. ACE inhibitors also inhibit the degradation of bradykinin, a reaction also catalyzed by ACE.

Because valsartan does not inhibit ACE (kininase II), it does not affect the response to bradykinin. Whether this difference has clinical relevance is not yet known. Valsartan does not bind to or block other hormone receptors or ion channels known to be important in cardiovascular regulation.

Blockade of the angiotensin II receptor inhibits the negative regulatory feedback of angiotensin II on renin secretion, but the resulting increased plasma renin activity and angiotensin II circulating levels do not overcome the effect of valsartan on blood pressure.


Pharmacokinetics

Amlodipine
Peak plasma concentrations of amlodipine are reached 6-12 hours after administration of amlodipine alone. Absolute bioavailability has been estimated to be between 64% and 90%. The bioavailability of amlodipine is not altered by the presence of food.

The apparent volume of distribution of amlodipine is 21 L. Approximately 93% of circulating amlodipine is bound to plasma proteins in hypertensive patients.

Amlodipine is extensively (about 90%) converted to inactive metabolites via hepatic metabolism with 10% of the parent compound and 60% of the metabolites excreted in the urine.

Elimination of amlodipine from the plasma is biphasic with a terminal elimination half-life of about 30-50 hours. Steady state plasma levels of amlodipine are reached after 7 to 8 days of consecutive daily dosing.


Valsartan
Following oral administration of valsartan alone peak plasma concentrations of valsartan are reached in 2 to 4 hours. Absolute bioavailability is about 25% (range 10%-35%). Food decreases the exposure (as measured by AUC) to valsartan by about 40% and peak plasma concentration (Cmax) by about 50%.

The steady state volume of distribution of valsartan after intravenous administration is 17 L indicating that valsartan does not distribute into tissues extensively. Valsartan is highly bound to serum proteins (95%), mainly serum albumin.

Valsartan shows bi-exponential decay kinetics following intravenous administration with an average elimination half-life of about 6 hours. The recovery is mainly as unchanged drug, with only about 20% of dose recovered as metabolites. The primary metabolite, accounting for about 9% of dose, is valeryl 4-hydroxy valsartan. The enzyme(s) responsible for valsartan metabolism have not been identified but do not seem to be CYP 450 isoenzymes.

Valsartan, when administered as an oral solution, is primarily recovered in feces (about 83% of dose) and urine (about 13% of dose). Following intravenous administration, plasma clearance of valsartan is about 2 L/h and its renal clearance is 0.62 L/h (about 30% of total clearance).


Exforge
Following oral administration of Exforge® (amlodipine and valsartan) in normal healthy adults, peak plasma concentrations of valsartan and amlodipine are reached in 3 and 6-8 hours, respectively. The rate and extent of absorption of valsartan and amlodipine from Exforge are the same as when administered as individual tablets.


Special Populations

Geriatric
Studies with amlodipine: Elderly patients have decreased clearance of amlodipine with a resulting increase in AUC of approximately 40%-60%; therefore a lower initial dose of amlodipine may be required.

Studies with valsartan: Exposure (measured by AUC) to valsartan is higher by 70% and the half-life is longer by 35% in the elderly than in the young. No dosage adjustment is necessary.


Gender
Studies with valsartan: Pharmacokinetics of valsartan does not differ significantly between males and females.


Renal Insufficiency
Studies with amlodipine: The pharmacokinetics of amlodipine is not significantly influenced by renal impairment. Patients with renal failure may therefore receive the usual initial dose.

Studies with valsartan: There is no apparent correlation between renal function (measured by creatinine clearance) and exposure (measured by AUC) to valsartan in patients with different degrees of renal impairment.

Consequently, dose adjustment is not required in patients with mild-to-moderate renal dysfunction. No studies have been performed in patients with severe impairment of renal function (creatinine clearance <10 mL/min). Valsartan is not removed from the plasma by hemodialysis. In the case of severe renal disease, exercise care with dosing of valsartan.


Hepatic Insufficiency
Studies with amlodipine: Patients with hepatic insufficiency have decreased clearance of amlodipine with resulting increase in AUC of approximately 40%-60%; therefore, a lower initial dose of amlodipine may be required.

Studies with valsartan: On average, patients with mild-to-moderate chronic liver disease have twice the exposure (measured by AUC values) to valsartan of healthy volunteers (matched by age, sex and weight). In general, no dosage adjustment is needed in patients with mild-to-moderate liver disease. Care should be exercised in patients with liver disease.


Pharmacodynamics

Amlodipine
Following administration of therapeutic doses to patients with hypertension, amlodipine produces vasodilation resulting in a reduction of supine and standing blood pressures.

These decreases in blood pressure are not accompanied by a significant change in heart rate or plasma catecholamine levels with chronic dosing. Although the acute intravenous administration of amlodipine decreases arterial blood pressure and increases heart rate in hemodynamic studies of patients with chronic stable angina, chronic oral administration of amlodipine in clinical trials did not lead to clinically significant changes in heart rate or blood pressures in normotensive patients with angina.

With chronic once daily administration, antihypertensive effectiveness is maintained for at least 24 hours. Plasma concentrations correlate with effect in both young and elderly patients. The magnitude of reduction in blood pressure with amlodipine is also correlated with the height of pretreatment elevation; thus, individuals with moderate hypertension (diastolic pressure 105-114 mmHg) had about a 50% greater response than patients with mild hypertension (diastolic pressure 90-104 mmHg). Normotensive subjects experienced no clinically significant change in blood pressure (+1/-2 mmHg).

In hypertensive patients with normal renal function, therapeutic doses of amlodipine resulted in a decrease in renal vascular resistance and an increase in glomerular filtration rate and effective renal plasma flow without change in filtration fraction or proteinuria.

As with other calcium channel blockers, hemodynamic measurements of cardiac function at rest and during exercise (or pacing) in patients with normal ventricular function treated with amlodipine have generally demonstrated a small increase in cardiac index without significant influence on dP/dt or on left ventricular end diastolic pressure or volume.

In hemodynamic studies, amlodipine has not been associated with a negative inotropic effect when administered in the therapeutic dose range to intact animals and man, even when co-administered with beta-blockers to man. Similar findings, however, have been observed in normals or well-compensated patients with heart failure with agents possessing significant negative inotropic effects.

Amlodipine does not change sinoatrial nodal function or atrioventricular conduction in intact animals or man. In patients with chronic stable angina, intravenous administration of 10 mg did not significantly alter A-H and H-V conduction and sinus node recovery time after pacing. Similar results were obtained in patients receiving amlodipine and concomitant beta-blockers.

In clinical studies in which amlodipine was administered in combination with beta-blockers to patients with either hypertension or angina, no adverse effects of electrocardiographic parameters were observed. In clinical trials with angina patients alone, amlodipine therapy did not alter electrocardiographic intervals or produce higher degrees of AV blocks.

Amlodipine has indications other than hypertension which can be found in the Norvasc®* package insert.


Valsartan
Valsartan inhibits the pressor effect of angiotensin II infusions. An oral dose of 80 mg inhibits the pressor effect by about 80% at peak with approximately 30% inhibition persisting for 24 hours. No information on the effect of larger doses is available.

Removal of the negative feedback of angiotensin II causes a 2- to 3-fold rise in plasma renin and consequent rise in angiotensin II plasma concentration in hypertensive patients. Minimal decreases in plasma aldosterone were observed after administration of valsartan; very little effect on serum potassium was observed.

In multiple dose studies in hypertensive patients with stable renal insufficiency and patients with renovascular hypertension, valsartan had no clinically significant effects on glomerular filtration rate, filtration fraction, creatinine clearance, or renal plasma flow.

Administration of valsartan to patients with essential hypertension results in a significant reduction of sitting, supine, and standing systolic blood pressure, usually with little or no orthostatic change.

Valsartan has indications other than hypertension which can be found in the Diovan® package insert.


Exforge
Exforge® (amlodipine and valsartan) has been shown to be effective in lowering blood pressure. Both amlodipine and valsartan lower blood pressure by reducing peripheral resistance, but calcium influx blockade and reduction of angiotensin II vasoconstriction are complementary mechanisms.

Exforge has not been studied in indications other than hypertension.


CLINICAL STUDIES

Exforge was studied in 2 placebo-controlled and 2 active-controlled trials in hypertensive patients. In a double-blind, placebo controlled study, a total of 1018 patients with mild-to-moderate hypertension received treatments of three combinations of amlodipine and valsartan (5/80, 5/160, 5/320 mg), or amlodipine alone (5 mg), valsartan alone (80, 160, or 320 mg) or placebo. At week 8, the combination treatments were statistically significantly superior to their monotherapy components in reduction of diastolic and systolic blood pressures.

Effect of Exforge® on Sitting Diastolic Blood Pressure Amlodipine dosage Valsartan dosage
0 mg 80 mg 160 mg 320 mg
Mean Change* Placebo-subtracted Mean Change* Placebo-subtracted Mean Change* Placebo-subtracted Mean Change* Placebo-subtracted
0 mg -6.4 --- -9.5 -3.1 -10.9 -4.5 -13.2 -6.7
5 mg -11.1 -4.7 -14.2 -7.8 -14.0 -7.6 -15.7 -9.3

*Mean Change and Placebo-Subtracted Mean Change from Baseline (mmHg) at Week 8 in Sitting Diastolic Blood Pressure. Mean baseline diastolic BP was 99.3 mmHg.

Effect of Exforge® on Sitting Systolic Blood Pressure Amlodipine dosage Valsartan dosage
0 mg 80 mg 160 mg 320 mg
Mean Change* Placebo-subtracted Mean Change* Placebo-subtracted Mean Change* Placebo-subtracted Mean Change* Placebo-subtracted
0 mg -6.2 --- -12.9 -6.8 -14.3 -8.2 -16.3 -10.1
5 mg -14.8 -8.6 -20.7 -14.5 -19.4 -13.2 -22.4 -16.2

*Mean Change and Placebo-Subtracted Mean Change from Baseline (mmHg) at Week 8 in Sitting Systolic Blood Pressure. Mean baseline systolic BP was 152.8 mmHg.

In a double-blind, placebo controlled study, a total of 1,250 patients with mild to moderate hypertension received treatments of two combinations of amlodipine and valsartan (10/160, 10/320 mg), or amlodipine alone (10 mg), valsartan alone (160 or 320 mg) or placebo. At week 8, the combination treatments were statistically significantly superior to their monotherapy components in reduction of diastolic and systolic blood pressures.

Effect of Exforge® on Sitting Diastolic Blood Pressure Amlodipine dosage Valsartan dosage
0 mg 160 mg 320 mg
Mean Change* Placebo-subtracted Mean Change* Placebo-subtracted Mean Change* Placebo-subtracted
0 mg -8.2 --- -12.8 - 4.5 -12.8 -4.5
10 mg -15.0 -6.7 - 17.2 - 9.0 -18.1 -9.9

*Mean Change and Placebo-Subtracted Mean Change from Baseline (mmHg) at Week 8 in Sitting Diastolic Blood Pressure. Mean baseline diastolic BP was 99.1 mmHg.

Effect of Exforge® on Sitting Systolic Blood Pressure Amlodipine dosage Valsartan dosage
0 mg 160 mg 320 mg
Mean Change* Placebo-subtracted Mean Change* Placebo-subtracted Mean Change* Placebo-subtracted

0 mg -11.0 --- -18.1 -7.0 -18.5 -7.5
10 mg -22.2 -11.2 -26.6 -15.5 -26.9 -15.9

*Mean Change and Placebo-Subtracted Mean Change from Baseline (mmHg) at Week 8 in Sitting Systolic Blood Pressure. Mean baseline systolic BP was 156.7 mmHg.

In a double-blind, active-controlled study, a total of 947 patients with mild to moderate hypertension who were not adequately controlled on valsartan 160 mg received treatments of two combinations of amlodipine and valsartan (10/160, 5/160 mg), or valsartan alone (160 mg).

At week 8, the combination treatments were statistically significantly superior to the monotherapy component in reduction of diastolic and systolic blood pressures.

Effect of Exforge® on Sitting Diastolic/Systolic Blood Pressure Treatment Group Diastolic BP Systolic BP
Mean change* Treatment Difference** Mean change* Treatment Difference**
Exforge
10/160 mg -11.4 -4.8 -13.9 -5.7
Exforge
5/160 mg -9.6 -3.1 -12.0 -3.9
Valsartan 160 mg -6.6 --- -8.2 ---

*Mean Change from Baseline at Week 8 in Sitting Diastolic/Systolic Blood Pressure. Mean baseline BP was 149.5/ 96.5 (systolic/diastolic) mmHg

**Treatment Difference = difference in mean BP reduction between Exforge and the control group (Valsartan 160 mg)

In a double-blind, active-controlled study, a total of 944 patients with mild to moderate hypertension who were not adequately controlled on amlodipine 10 mg received a combination of amlodipine and valsartan (10/160 mg), or amlodipine alone (10 mg). At week 8, the combination treatment was statistically significantly superior to the monotherapy component in reduction of diastolic and systolic blood pressures.

Effect of Exforge® on Sitting Diastolic/Systolic Blood Pressure Treatment Group Diastolic BP Systolic BP
Mean change* Treatment Difference** Mean change* Treatment Difference**
Exforge
10/160 mg -11.8 -1.8 -12.7 -1.9
Amlodipine 10 mg -10.0 --- -10.8 ---

*Mean Change from Baseline at Week 8 in Sitting Diastolic/Systolic Blood Pressure. Mean baseline BP was 147.0/ 95.1 (systolic/diastolic) mmHg

**Treatment Difference = difference in mean BP reduction between Exforge and the control group (Amlodipine 10 mg)



Exforge was also evaluated for safety in a 6-week, double-blind, active-controlled trial of 130 hypertensive patients with severe hypertension (mean baseline BP of 171/113 mmHg). Adverse events were similar in patients with severe hypertension and mild/moderate hypertension treated with Exforge.

A wide age range of the adult population, including the elderly was studied (range 19-92 years, mean 54.7 years). Women comprised almost half of the studied population (47.3%). Of the patients in the studied Exforge group, 87.6% were Caucasian. Black and Oriental patients each represented approximately 4% of the population in the studied Exforge group.


Indications and Usage for Exforge
Exforge® (amlodipine and valsartan) is indicated for the treatment of hypertension.

This fixed combination drug is not indicated for the initial therapy of hypertension (see DOSAGE AND ADMINISTRATION).


Contraindications
Exforge® (amlodipine and valsartan) is contraindicated in patients who are hypersensitive to any component of this product.


Warnings

Fetal/Neonatal Morbidity and Mortality
Drugs that act directly on the renin-angiotensin system can cause fetal and neonatal morbidity and death when administered to pregnant women. Several dozen cases have been reported in the world literature in patients who were taking angiotensin-converting enzyme inhibitors. There have been reports of spontaneous abortion, oligohydramnios and newborn renal dysfunction when pregnant women have taken valsartan. When pregnancy is detected, valsartan should be discontinued as soon as possible.

The use of drugs that act directly on the renin-angiotensin system during the second and third trimesters of pregnancy has been associated with fetal and neonatal injury, including hypotension, neonatal skull hypoplasia, anuria, reversible or irreversible renal failure, and death. Oligohydramnios has also been reported, presumably resulting from decreased fetal renal function; oligohydramnios in this setting has been associated with fetal limb contractures, craniofacial deformation, and hypoplastic lung development.

Prematurity, intrauterine growth retardation, and patent ductus ateriosus have also been reported, although it is not clear whether these occurrences were due to exposure to the drug.

In addition, first trimester use of ACE inhibitors, a specific class of drugs acting on the renin-angiotensin system, has been associated with a potential risk of birth defects in retrospective data. Healthcare professionals that prescribe drugs acting directly on the renin-angiotensin system should counsel women of childbearing potential about the potential risks of these agents during pregnancy.

Rarely (probably less often than once in every thousand pregnancies), no alternative to a drug acting on the renin-angiotensin system will be found. In these rare cases, the mothers should be apprised of the potential hazards to their fetuses, and serial ultrasound examinations should be performed to assess the intra-amniotic environment.

If oligohydramnios is observed, valsartan should be discontinued unless it is considered life- saving for the mother. Contraction stress testing (CST), a nonstress test (NST), or biophysical profiling (BPP) may be appropriate, depending upon the week of pregnancy. Patients and physicians should be aware, however, that oligohydramnios may not appear until after the fetus has sustained irreversible injury.

Infants with histories of in utero exposure to an angiotensin II receptor antagonist should be closely observed for hypotension, oliguria, and hyperkalemia. If oliguria occurs, attention should be directed toward support of blood pressure and renal perfusion. Exchange transfusion or dialysis may be required as means of reversing hypotension and/or substituting for disordered renal function.


Hypotension

Excessive hypotension was seen in 0.4% of patients with uncomplicated hypertension treated with Exforge® (amlodipine and valsartan) in placebo-controlled studies. In patients with an activated renin-angiotensin system, such as volume-and/or salt-depleted patients receiving high doses of diuretics, symptomatic hypotension may occur in patients receiving angiotensin receptor blockers. This condition should be corrected prior to administration of Exforge, or the treatment should start under close medical supervision.

Caution should be observed when initiating therapy in patients with heart failure or recent myocardial infarction and in patients undergoing surgery or dialysis. Patients with heart failure or post-myocardial infarction patients given valsartan commonly have some reduction in blood pressure, but discontinuation of therapy because of continuing symptomatic hypotension usually is not necessary when dosing instructions are followed.

In controlled trials in heart failure patients, the incidence of hypotension in valsartan-treated patients was 5.5% compared to 1.8% in placebo-treated patients. In the Valsartan in Acute Myocardial Infarction Trial (VALIANT), hypotension in post-myocardial infarction patients led to permanent discontinuation of therapy in 1.4% of valsartan-treated patients and 0.8% of captopril-treated patients.

Since the vasodilation induced by amlodipine is gradual in onset, acute hypotension has rarely been reported after oral administration. Nonetheless, caution, as with any other peripheral vasodilator, should be exercised when administering amlodipine, particularly in patients with severe aortic stenosis.

If excessive hypotension occurs with Exforge, the patient should be placed in a supine position and, if necessary, given an intravenous infusion of normal saline. A transient hypotensive response is not a contraindication to further treatment, which usually can be continued without difficulty once the blood pressure has stabilized.


Increased Angina and/or Myocardial Infarction

Rarely, patients, particularly those with severe obstructive coronary artery disease, have developed documented increased frequency, duration and or/severity of angina or acute myocardial infarction on starting calcium channel blocker therapy or at the time of dosage increase. The mechanism of this effect has not been elucidated.


Precautions

General

Impaired Hepatic Function
Studies with amlodipine: Amlodipine is extensively metabolized by the liver and the plasma elimination half-life (t½) is 56 hours in patients with impaired hepatic function, therefore, caution should be exercised when administering amlodipine to patients with severe hepatic impairment.

Studies with valsartan: As the majority of valsartan is eliminated in the bile, patients with mild-to-moderate hepatic impairment, including patients with biliary obstructive disorders, showed lower valsartan clearance (higher AUCs). Care should be exercised in administering valsartan to these patients.


Impaired Renal Function – Hypertension

In studies of ACE inhibitors in hypertensive patients with unilateral or bilateral renal artery stenosis, increases in serum creatinine or blood urea nitrogen have been reported. In a 4-day trial of valsartan in 12 hypertensive patients with unilateral renal artery stenosis, no significant increases in serum creatinine or blood urea nitrogen were observed. There has been no long-term use of valsartan in patients with unilateral or bilateral renal artery stenosis, but an effect similar to that seen with ACE inhibitors should be anticipated.

As a consequence of inhibiting the renin-angiotensin-aldosterone system, changes in renal function may be anticipated in susceptible individuals. In patients with severe heart failure whose renal function may depend on the activity of the renin-angiotensin-aldosterone system, treatment with angiotensin-converting enzyme inhibitors and angiotensin receptor antagonists has been associated with oliguria and/or progressive azotemia and (rarely) with acute renal failure and/or death. Similar outcomes have been reported with valsartan.


Congestive Heart Failure


Studies with amlodipine: In general, calcium channel blockers should be used with caution in patients with heart failure. Amlodipine (5-10 mg per day) has been studied in a placebo-controlled trial of 1,153 patients with NYHA Class III or IV heart failure on stable doses of ACE inhibitor, digoxin, and diuretics. Follow-up was at least 6 months, with a mean of about 14 months.

There was no overall adverse effect on survival or cardiac morbidity (as defined by life-threatening arrhythmia, acute myocardial infarction, or hospitalization for worsened heart failure). Amlodipine has been compared to placebo in four 8-12 week studies of patients with NYHA class II/III heart failure, involving a total of 697 patients. In these studies, there was no evidence of worsened heart failure based on measures of exercise tolerance, NYHA classification, symptoms, or LVEF.

Studies with valsartan: Some patients with heart failure have developed increases in blood urea nitrogen, serum creatinine, and potassium on valsartan. These effects are usually minor and transient, and they are more likely to occur in patients with pre-existing renal impairment. Dosage reduction and/or discontinuation of the diuretic and/or valsartan may be required.

In the Valsartan Heart Failure Trial, in which 93% of patients were on concomitant ACE inhibitors, treatment was discontinued for elevations in creatinine or potassium (total of 1.0% on valsartan vs. 0.2% on placebo). In the Valsartan in Acute Myocardial Infarction Trial (VALIANT), discontinuation due to various types of renal dysfunction occurred in 1.1% of valsartan-treated patients and 0.8% of captopril-treated patients. Evaluation of patients with heart failure or post-myocardial infarction should always include assessment of renal function.


Beta-Blocker Withdrawal
Amlodipine is not a beta-blocker and therefore gives no protection against the dangers of abrupt beta-blocker withdrawal; any such withdrawal should be by gradual reduction of the dose of beta-blocker.


Information for Patients

Pregnancy
Female patients of childbearing age should be told about the consequences of exposure to drugs that act on the renin-angiotensin system. Discuss other treatment options with female patients planning to become pregnant. Patients should be asked to report pregnancies to their physicians as soon as possible.


Clinical Laboratory Findings

Creatinine
In hypertensive patients, greater than 50% increases in creatinine occurred in 0.4% of patients receiving Exforge and 0.6% receiving placebo. In heart failure patients, greater than 50% increases in creatinine were observed in 3.9% of valsartan-treated patients compared to 0.9% of placebo-treated patients. In post-myocardial infarction patients, doubling of serum creatinine was observed in 4.2% of valsartan-treated patients and 3.4% of captopril-treated patients.


Liver Function Tests
Occasional elevations (greater than 150%) of liver chemistries occurred in Exforge-treated patients.


Serum Potassium
In hypertensive patients, greater than 20% increases in serum potassium were observed in 2.8% of Exforge-treated patients compared to 3.4% of placebo-treated patients. In heart failure patients, greater than 20% increases in serum potassium were observed in 10% of valsartan-treated patients compared to 5.1% of placebo-treated patients.


Blood Urea Nitrogen (BUN)
In hypertensive patients, greater than 50% increases in BUN were observed in 5.5% of Exforge-treated patients compared to 4.7% of placebo-treated patients. In heart failure patients, greater than 50% increases in BUN were observed in 16.6% of valsartan-treated patients compared to 6.3% of placebo-treated patients.


Drug Interactions
No drug interaction studies have been conducted with Exforge and other drugs, although studies have been conducted with the individual amlodipine and valsartan components, as described below:

Studies with Amlodipine:

In clinical trials, amlodipine has been safely administered with thiazide diuretics, beta- blockers, angiotensin-converting enzyme inhibitors, long-acting nitrates, sublingual nitroglycerin, digoxin, warfarin, non-steroidal anti-inflammatory drugs, antibiotics, and oral hypoglycemic drugs.

Cimetidine: Co-administration of amlodipine with cimetidine did not alter the pharmacokinetics of amlodipine.

Grapefruit juice: Co-administration of 240 mL of grapefruit juice with a single oral dose of amlodipine 10 mg in 20 healthy volunteers had no significant effect on the pharmacokinetics of amlodipine.

Maalox® (antacid): Co-administration of the antacid Maalox with a single dose of amlodipine had no significant effect on the pharmacokinetics of amlodipine.

Sildenafil: A single 100 mg dose of sildenafil (Viagra®**) in subjects with essential hypertension had no effect on the pharmacokinetic parameters of amlodipine. When amlodipine and sildenafil were used in combination, each agent independently exerted its own blood pressure lowering effect.

Atorvastatin: Co-administration of multiple 10 mg doses of amlodipine with 80 mg of atorvastatin resulted in no significant change in the steady state pharmacokinetic parameters of atorvastatin.

Digoxin: Co-administration of amlodipine with digoxin did not change serum digoxin levels or digoxin renal clearance in normal volunteers.

Warfarin: Co-administration of amlodipine with warfarin did not change the warfarin prothrombin response time.

Studies with Valsartan:

No clinically significant pharmacokinetic interactions were observed when valsartan was co-administered with amlodipine, atenolol, cimetidine, digoxin, furosemide, glyburide, hydrochlorothiazide, or indomethacin. The valsartan-atenolol combination was more antihypertensive than either component, but it did not lower the heart rate more than atenolol alone.

Warfarin: Co-administration of valsartan and warfarin did not change the pharmacokinetics of valsartan or the time-course of the anticoagulant properties of warfarin.


CYP 450 Interactions
The enzyme(s) responsible for valsartan metabolism have not been identified but do not seem to be CYP 450 isozymes. The inhibitory or induction potential of valsartan on CYP 450 is also unknown.

As with other drugs that block angiotensin II or its effects, concomitant use of potassium sparing diuretics (e.g., spironolactone, triamterene, amiloride), potassium supplements, or salt substitutes containing potassium may lead to increases in serum potassium and in heart failure patients to increases in serum creatinine.


Drug/Food Interactions
Studies with amlodipine: The bioavailability of amlodipine is not altered by the presence of food.

Studies with valsartan: Food decreases the exposure (as measured by AUC) to valsartan by about 40% and peak plasma concentration (Cmax) by about 50%.


Carcinogenesis/Mutagenesis/Impairment of Fertility

Studies with amlodipine: Rats and mice treated with amlodipine maleate in the diet for up to two years, at concentrations calculated to provide daily dosage levels of 0.5, 1.25, and 2.5 mg amlodipine/kg/day, showed no evidence of a carcinogenic effect of the drug.

For the mouse, the highest dose was, on mg/m2 basis, similar to the maximum recommended human dose [MRHD] of 10 mg amlodipine/day. For the rat, the highest dose was, on a mg/m2 basis, about two and a half times the MRHD. (Calculations based on a 60 kg patient.)

Mutagenicity studies conducted with amlodipine maleate revealed no drug-related effects at either the gene or chromosome level.

There was no effect on the fertility of rats treated orally with amlodipine maleate (males for 64 days and females for 14 days prior to mating) at doses of up to 10 mg amlodipine/kg/day (about 10 times the MRHD of 10 mg/day on a mg/m2 basis).

Studies with valsartan: There was no evidence of carcinogenicity when valsartan was administered in the diet to mice and rats for up to 2 years at concentrations calculated to provide doses of up to 160 and 200 mg/kg/day, respectively. These doses in mice and rats are about 2.4 and 6 times, respectively, the MRHD of 320 mg/day on a mg/m2 basis. (Calculations based on a 60 kg patient.)

Mutagenicity assays did not reveal any valsartan-related effects at either the gene or chromosome level. These assays included bacterial mutagenicity tests with Salmonella and E. coli, a gene mutation test with Chinese hamster V79 cells, a cytogenetic test with Chinese hamster ovary cells, and a rat micronucleus test.

Valsartan had no adverse effects on the reproductive performance of male or female rats at oral doses of up to 200 mg/kg/day. This dose is about 6 times the maximum recommended human dose on a mg/m2 basis.


Pregnancy

Pregnancy Category C (first trimester) and D (second and third trimesters)
See WARNINGS, Fetal/Neonatal Morbidity and Mortality.

Studies with amlodipine: No evidence of teratogenicity or other embryo/fetal toxicity was found when pregnant rats and rabbits were treated orally with amlodipine maleate at doses of up to 10 mg amlodipine/kg/day (respectively, about 10 and 20 times the maximum recommended human dose [MRHD] of 10 mg amlodipine on a mg/m2 basis) during their respective periods of major organogenesis. (Calculations based on a patient weight of 60 kg.)

However, litter size was significantly decreased (by about 50%) and the number of intrauterine deaths was significantly increased (about 5-fold) for rats receiving amlodipine maleate at a dose equivalent to 10 mg amlodipine/kg/day for 14 days before mating and throughout mating and gestation. Amlodipine maleate has been shown to prolong both the gestation period and the duration of labor in rats at this dose. There are no adequate and well-controlled studies in pregnant women. Amlodipine should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Studies with valsartan: No teratogenic effects were observed when valsartan was administered to pregnant mice and rats at oral doses of up to 600 mg/kg/day and to pregnant rabbits at oral doses of up to 10 mg/kg/day. However, significant decreases in fetal weight, pup birth weight, pup survival rate, and slight delays in developmental milestones were observed in studies in which parental rats were treated with valsartan at oral, maternally toxic (reduction in body weight gain and food consumption) doses of 600 mg/kg/day during organogenesis or late gestation and lactation.

In rabbits, fetotoxicity (i.e., resorptions, litter loss, abortions, and low body weight) associated with maternal toxicity (mortality) was observed at doses of 5 and 10 mg/kg/day. The no observed adverse effect doses of 600, 200 and 2 mg/kg/day in mice, rats and rabbits, respectively, are about 9, 6 and 0.1 times the MRHD of 320 mg/day on a mg/m2 basis. (Calculations based on a patient weight of 60 kg.)

Studies with amlodipine besylate and valsartan: In the oral embryo-fetal development study in rats using amlodipine besylate plus valsartan at doses equivalent to 5 mg/kg/day amlodipine plus 80 mg/kg/day valsartan, 10 mg/kg/day amlodipine plus 160 mg/kg/day valsartan, and 20 mg/kg/day amlodipine plus 320 mg/kg/day valsartan, treatment-related maternal and fetal effects (developmental delays and alterations noted in the presence of significant maternal toxicity) were noted with the high dose combination.

The no-observed-adverse-effect level (NOAEL) for embryo-fetal effects was 10 mg/kg/day amlodipine plus 160 mg/kg/day valsartan. On a systemic exposure [AUC(0-∞)] basis, these doses are, respectively, 4.3 and 2.7 times the systemic exposure [AUC(0-∞)] in humans receiving the MRHD (10/320 mg/60 kg).


Labor and Delivery
The effect of Exforge on labor and delivery has not been studied.


Nursing Mothers
It is not known whether amlodipine is excreted in human milk. In the absence of this information, it is recommended that nursing be discontinued while amlodipine is administered.

It is not known whether valsartan is excreted in human milk, but valsartan was excreted in the milk of lactating rats. Because of the potential for adverse effects on the nursing infant, a decision should be made whether to discontinue nursing or discontinue the drug, taking into account the importance of the drug to the mother.


Pediatric Use
Safety and effectiveness of Exforge in pediatric patients have not been established.


Geriatric Use
In controlled clinical trials, 323 hypertensive patients treated with Exforge were ≥ 65 years and 79 were ≥ 75 years. No overall differences in the efficacy or safety of Exforge was observed in this patient population, but greater sensitivity of some older individuals cannot be ruled out.


Adverse Reactions
Exforge

Exforge® (amlodipine and valsartan) has been evaluated for safety in over 2,600 patients with hypertension; over 1,440 of these patients were treated for at least 6 months and over 540 of these patients were treated for at least one year. Adverse experiences have generally been mild and transient in nature and have only infrequently required discontinuation of therapy.

The overall frequency of adverse experiences was neither dose-related nor related to gender, age, or race. In placebo-controlled clinical trials, discontinuation due to side effects occurred in 1.8% of patients in the Exforge-treated patients and 2.1% in the placebo-treated group. The most common reasons for discontinuation of therapy with Exforge were peripheral edema (0.4%), and vertigo (0.2%).

The adverse experiences that occurred in placebo-controlled clinical trials in at least 2% of patients treated with Exforge but at a higher incidence in amlodipine/valsartan patients (n=1,437) than placebo (n=337) included peripheral edema (5.4% vs. 3.0%), nasopharyngitis (4.3% vs. 1.8%), upper respiratory tract infection (2.9% vs 2.1%) and dizziness (2.1% vs 0.9%).

Orthostatic events (orthostatic hypotension and postural dizziness) were seen in less than 1% of patients.

Other adverse experiences that occurred in placebo-controlled clinical trials with Exforge (≥ 0.2%) are listed below. It cannot be determined whether these events were causally related to Exforge.

Blood and Lymphatic System Disorders: Lymphadenopathy

Cardiac Disorders: Palpitations, tachycardia

Ear and Labyrinth Disorders: Ear pain

Gastrointestinal Disorders: Diarrhea, nausea, constipation, dyspepsia, abdominal pain, abdominal pain upper, gastritis, vomiting, abdominal discomfort, hemorrhoids, abdominal distention, dry mouth, flatulence, toothache, colitis

General Disorders and Administration Site Conditions: Fatigue, chest pain, asthenia, pitting edema, pyrexia, edema, pain

Immune System Disorders: seasonal allergies

Infections and Infestations: Nasopharyngitis, sinusitis, influenza, bronchitis, pharyngitis, urinary tract infection, gastroenteritis, pharyngotonsillitis, bronchitis acute, viral infection, tonsillitis, tooth abscess, cystitis, pneumonia

Injury, Poisoning and Procedural Complications: Contusion, epicondylitis, joint sprain, limb injury, post procedural pain

Investigations: Cardiac murmur

Metabolism and Nutrition Disorders: Gout, non-insulin dependent diabetes mellitus, hypercholesterolemia

Musculoskeletal and Connective Tissue Disorders: Arthralgia, back pain, muscle spasms, pain in extremity, myalgia, osteoarthritis, joint swelling, musculoskeletal chest pain

Nervous System Disorders: Headache, sciatica, parasthesia, cerviocobrachial syndrome, carpal tunnel syndrome, hypoaesthesia, sinus headache, somnolence

Psychiatric Disorders: Insomnia, anxiety, depression

Renal and Urinary Disorders: Hematuria, nephrolithiasis, pollakiuria

Reproductive System and Breast Disorders: Erectile dysfunction

Respiratory, Thoracic and Mediastinal Disorders: Cough, pharyngolaryngeal pain, sinus congestion, dyspnea, epistaxis, productive cough, dysphonia, nasal congestion

Skin and Subcutaneous Tissue Disorders: Pruritus, rash, hyperhidrosis, eczema, erythema

Vascular Disorders: Flushing, hot flush

Isolated cases of the following clinically notable adverse events were also observed in clinical trials: exanthema, syncope, visual disturbance, hypersensitivity, tinnitus, and hypotension.


Amlodipine
Norvasc® has been evaluated for safety in more than 11,000 patients in U.S. and foreign clinical trials. Other adverse events that have been reported <1% but >0.1% of patients in controlled clinical trials or under conditions of open trials or marketing experience where a causal relationship is uncertain were:

Cardiovascular: arrhythmia (including ventricular tachycardia and atrial fibrillation), bradycardia, chest pain, peripheral ischemia, syncope, postural hypotension, vasculitis

Central and Peripheral Nervous System: neuropathy peripheral, tremor

Gastrointestinal: anorexia, dysphagia, pancreatitis, gingival hyperplasia

General: allergic reaction, hot flushes, malaise, rigors, weight gain, weight loss

Musculoskeletal System: arthrosis, muscle cramps

Psychiatric: sexual dysfunction (male and female), nervousness, abnormal dreams, depersonalization

Respiratory System: dyspnea

Skin and Appendages: angioedema, erythema multiforme, rash erythematous, rash maculopapular

Special Senses: abnormal vision, conjunctivitis, diplopia, eye pain, tinnitus

Urinary System: micturation frequency, micturation disorder, nocturia

Autonomic Nervous System: sweating increased

Metabolic and Nutritional: hyperglycemia, thirst

Hemopoietic: leukopenia, purpura, thrombocytopenia

Other events reported with amlodipine at a frequency of ≤ 0.1% of patients include: cardiac failure, pulse irregularity, extrasystoles, skin discoloration, urticaria, skin dryness, alopecia, dermatitis, muscle weakness, twitching, ataxia, hypertonia, migraine, cold and clammy skin, apathy, agitation, amnesia, gastritis, increased appetite, loose stools, rhinitis, dysuria, polyuria, parosmia, taste perversion, abnormal visual accommodation, and xerophthalmia. Other reactions occurred sporadically and cannot be distinguished from medications or concurrent disease states such as myocardial infarction and angina.

Adverse reactions reported for amlodipine for indications other than hypertension may be found in the prescribing information for Norvasc®.


Post-Marketing Experience
Gynecomastia has been reported infrequently and a causal relationship is uncertain. Jaundice and hepatic enzyme elevations (mostly consistent with cholestasis or hepatitis), in some cases severe enough to require hospitalization, have been reported in association with use of amlodipine.


Valsartan
Diovan® has been evaluated for safety in more than 4,000 hypertensive patients in clinical trials. In trials in which valsartan was compared to an ACE inhibitor with or without placebo, the incidence of dry cough was significantly greater in the ACE inhibitor group (7.9%) than in the groups who received valsartan (2.6%) or placebo (1.5%). In a 129 patient trial limited to patients who had had dry cough when they had previously received ACE inhibitors, the incidences of cough in patients who received valsartan, HCTZ, or lisinopril were 20%, 19%, and 69% respectively (p<0.001).

Other adverse events, not listed above, occurring in >0.2% of patients in controlled clinical trials with valsartan are:

Body as a Whole: allergic reaction, asthenia

Musculoskeletal: muscle cramps

Neurologic and Psychiatric: paresthesia

Respiratory: sinusitis, pharyngitis

Urogenital: Impotence

Other reported events seen less frequently in clinical trials were: angioedema.

Adverse reactions reported for valsartan for indications other than hypertension may be found in the prescribing information for Diovan.


Post-Marketing Experience
The following additional adverse events have been reported in post-marketing experience with valsartan:

Blood and Lymphatic: There are very rare reports of thrombocytopenia.

Hypersensitivity: There are rare reports of angioedema.

Digestive: Elevated liver enzymes and very rare reports of hepatitis

Renal: Impaired renal function

Clinical Laboratory Tests: Hyperkalemia

Dermatologic: Alopecia

Rare cases of rhabdomyolysis have been reported in patients receiving angiotensin II receptor blockers.


Overdosage
Information on Amlodipine

Single oral doses of amlodipine maleate equivalent to 40 mg/kg and 100 mg/kg amlodipine in mice and rats, respectively, caused deaths. Single oral doses equivalent to 4 or more mg/kg amlodipine in dogs (11 or more times the maximum recommended human dose on a mg/m2 basis) caused a marked peripheral vasodilation and hypotension.

Overdosage might be expected to cause excessive peripheral vasodilation with marked hypotension. In humans, experience with intentional overdosage of amlodipine is limited. Reports of intentional overdosage include a patient who ingested 250 mg and was asymptomatic and was not hospitalized; another (120 mg) who was hospitalized underwent gastric lavage and remained normotensive; the third (105 mg) was hospitalized and had hypotension (90/50 mmHg) which normalized following plasma expansion. A case of accidental drug overdose has been documented in a 19-month-old male who ingested 30 mg amlodipine (about 2 mg/kg). During the emergency room presentation, vital signs were stable with no evidence of hypotension, but a heart rate of 180 bpm. Ipecac was administered 3.5 hours after ingestion and on subsequent observation (overnight) no sequelae was noted.

If massive overdose should occur, active cardiac and respiratory monitoring should be instituted. Frequent blood pressure measurements are essential. Should hypotension occur, cardiovascular support including elevation of the extremities and the judicious administration of fluids should be initiated. If hypotension remains unresponsive to these conservative measures, administration of vasopressors (such as phenylephrine) should be considered with attention to circulating volume and urine output. Intravenous calcium gluconate may help to reverse the effects of calcium entry blockade. As amlodipine is highly protein bound, hemodialysis is not likely to be of benefit.

Information on Valsartan

Limited data are available related to overdosage in humans. The most likely effect of overdose with valsartan would be peripheral vasodilation, hypotension and tachycardia; bradycardia could occur from parasympathetic (vagal) stimulation. Depressed level of consciousness, circulatory collapse and shock have been reported. If symptomatic hypotension should occur, supportive treatment should be instituted.

Valsartan is not removed from the plasma by hemodialysis.

Valsartan was without grossly observable adverse effects at single oral doses up to 2000 mg/kg in rats and up to 1000 mg/kg in marmosets, except for the salivation and diarrhea in the rat and vomiting in the marmoset at the highest dose (60 and 37 times, respectively, the maximum recommended human dose on a mg/m2 basis). (Calculations assume an oral dose of 320 mg/day and a 60-kg patient.)


Exforge Dosage and Administration
Amlodipine is an effective treatment of hypertension in once daily doses of 2.5 mg-10 mg while valsartan is effective in doses of 80 mg-320 mg. In clinical trials with Exforge® (amlodipine and valsartan) using amlodipine doses of 5 mg-10 mg and valsartan doses of 160 mg-320 mg, the antihypertensive effects increased with increasing doses.

The hazards (see WARNINGS) of valsartan are generally independent of dose; those of amlodipine are a mixture of dose-dependent phenomena (primarily peripheral edema) and dose-independent phenomena, the former much more common than the latter. Therapy with any combination of amlodipine and valsartan will thus be associated with both sets of dose-independent hazards.

A patient who experiences dose-limiting adverse reactions on either component alone may be switched to Exforge containing a lower dose of that component in combination with the other to achieve similar blood pressure reductions. The clinical response to Exforge should be subsequently evaluated and if blood pressure remains uncontrolled after 3-4 weeks of therapy, the dose may be titrated up to a maximum of 10/320 mg.

To minimize dose-independent hazards, it is usually appropriate to begin therapy with Exforge only after a patient has failed to achieve the desired antihypertensive effect with one or the other monotherapy.


Dose Titration Guided by Clinical Effect
A patient whose blood pressure is not adequately controlled with amlodipine (or another DHP CCB) alone or with valsartan (or another ARB) alone may be switched to combination therapy with Exforge.


Replacement Therapy
For convenience, patients receiving amlodipine and valsartan from separate tablets may instead wish to receive tablets of Exforge containing the same component doses.


How is Exforge Supplied
Exforge® (amlodipine and valsartan) is available as tablets containing amlodipine besylate equivalent to 5 mg, or 10 mg of amlodipine free-base with valsartan 160 mg or 320 mg, providing for the following available combinations: 5/160 mg, 10/160 mg, 5/320 mg and 10/320 mg.

All strengths are packaged in bottles of 30 and 90 count, and unit dose blister packages.

5/160 mg Tablets - dark yellow, ovaloid shaped, film coated tablet with beveled edge, debossed with “NVR” on one side and “ECE” on the other side.

Bottles of 30 NDC # 0078-0488-15

Bottles of 90 NDC # 0078-0488-34

Unit Dose 100 tablets (10 X 10 tablets blister cards) NDC # 0078-0488-35

10/160 mg Tablets - light yellow, ovaloid shaped, film coated tablet with beveled edge, debossed with “NVR” on one side and “UIC” on the other side.

Bottles of 30 NDC # 0078-0489-15

Bottles of 90 NDC # 0078-0489-34

Unit Dose 100 tablets (10 X 10 tablets blister cards) NDC # 0078-0489-35

5/320 mg Tablets - very dark yellow, ovaloid shaped, film coated tablet with beveled edge, debossed with “NVR” on one side and “CSF” on the other side.

Bottles of 30 NDC # 0078-0490-15

Bottles of 90 NDC # 0078-0490-34

Unit Dose 100 tablets (10 X 10 tablets blister cards) NDC # 0078-0490-35

10/320 mg Tablets - dark yellow, ovaloid shaped, film coated tablet with beveled edge, debossed with “NVR” on one side and “LUF” on the other side.

Bottles of 30 NDC # 0078-0491-15

Bottles of 90 NDC # 0078-0491-34

Unit Dose 100 tablets (10 X 10 tablets blister cards) NDC # 0078-0491-35


Storage
Store at 25oC (77oF); excursions permitted to 15-30oC (59-86oF). [See USP Controlled Room Temperature.] Protect from moisture.

*Norvasc® is a registered trademark of Pfizer, Inc.

**Viagra® is a registered trademark of Pfizer, Inc.

Distributed by:

Novartis Pharmaceuticals Corporation

East Hanover, New Jersey 07936

©Novartis

April 2007



Patient Information
Exforge®‚ (X-phorj)

(amlodipine and valsartan) Tablets

5/160 mg, 10/160 mg, 5/320 mg, 10/320 mg

Rx only

Read the Patient Information that comes with Exforge before you start taking it and each time you get a refill. There may be new information. This leaflet does not take the place of talking with your doctor about your medical condition or treatment.

What is the most important information I should know about Exforge?
Taking Exforge during pregnancy can cause injury and even death to your unborn baby. If you get pregnant, stop taking Exforge and call your doctor right away. Talk to your doctor about other ways to lower your blood pressure if you plan to become pregnant.


What is Exforge?

Exforge is a prescription medicine used to treat high blood pressure (hypertension). Exforge contains two prescription medicines that work together to lower blood pressure: amlodipine, a calcium channel blocker, and valsartan, an angiotensin receptor blocker. Exforge should not be used before other medicines have been tried first to treat high blood pressure.

Blood pressure is the force of blood in your blood vessels when your heart beats and when your heart rests. You have high blood pressure when the force is too much. Exforge can help your blood vessels relax so your blood pressure is lower. Drugs that lower blood pressure lower your chance of having a stroke or heart attack.

Exforge has not been studied in children under 18 years of age.

Who should NOT take Exforge?

Do not take Exforge if you are allergic to any of the ingredients in Exforge. See the end of this leaflet for a complete list of ingredients in Exforge.

What should I tell my doctor before taking Exforge?

Tell your doctor about all of your medical conditions, including if you:

have heart problems

have liver problems

have kidney problems

are vomiting or having a lot of diarrhea

are pregnant or plan to become pregnant. See “What is the most important information I should know about Exforge?”

are breast-feeding or plan to breast-feed. Exforge may pass into your milk. Do not breast-feed while you are taking Exforge.
Tell your doctor about all the medicines you take, including prescription and nonprescription medicines, vitamins, and herbal supplements. Some of your other medicines and Exforge could affect each other, causing serious side effects.

Especially tell your doctor if you take:

other medicines for high blood pressure or a heart problem

water pills (also called “diuretics”)

potassium supplements

a salt substitute
If you take a beta blocker medicine and your doctor tells you to stop taking it while you are taking Exforge, follow your doctor’s instructions very carefully to slowly and safely stop the beta blocker medicine. Stopping beta blocker medicines too quickly can cause chest pain (angina), heart attack, abnormal heart rhythm or high blood pressure. Taking Exforge does not help to prevent these effects. If you do not know if you take a beta blocker medicine, contact your doctor or pharmacist.

Know the medicines you take. Keep a list of your medicines and show it to your doctor or pharmacist when you get a new medicine.

How do I take Exforge?

Take Exforge exactly as your doctor tells you.

Take Exforge at the same time each day.

If you miss a dose, take it as soon as you remember. If it is close to your next dose, do not take the missed dose. Just take the next dose at the regular time.

If you take too much Exforge, call your doctor or Poison Control Center, or go to the emergency room.

Tell all your doctors or dentist you are taking Exforge if you:
are going to have surgery

go for kidney dialysis
What are the possible side effects of Exforge?

Exforge may cause serious side effects including:

injury or death of unborn babies. See “What is the most important information I should know about Exforge?”

low blood pressure (hypotension). Low blood pressure is most likely to happen if you also take water pills, are on a low salt diet, have heart problems, or get sick with vomiting or diarrhea. Lie down if you feel faint or dizzy. Call your doctor right away.

more chest pain (angina) and heart attacks in people that already have severe heart problems. This may happen when you start Exforge or when there is an increase in your dose of Exforge. Get emergency help if you get worse chest pain or chest pain that does not go away.

kidney problems. Kidney problems may get worse in people that already have kidney disease. Some people will have changes in blood tests for kidney function and need a lower dose of Exforge. Call your doctor if you get swelling in your feet, ankles, or hands or unexplained weight gain.
laboratory blood test changes in patients with congestive heart failure. In studies with valsartan, some patients with congestive heart failure had blood tests that showed increased potassium and decrease in kidney function.

allergic reactions
The most common side effects that occur more frequently with Exforge than placebo (sugar pill) are:

swelling (edema) of the hands, ankles, or feet.

nasal congestion, sore throat and discomfort when swallowing

upper respiratory tract infection (head or chest cold)

dizziness
Tell your doctor if you have any side effect that bothers you or that does not go away.

These are not all the possible side effects of Exforge. For more information, ask your doctor or pharmacist.

How should I store Exforge?

Store Exforge at room temperature between 59°F to 86°F (15°C to 30°C).

Keep Exforge dry (protect it from moisture).
Keep Exforge and all medicines out of the reach of children.

General Information about Exforge

Medicines are sometimes prescribed for conditions that are not mentioned in the patient information leaflet. Do not use Exforge for a condition for which it was not prescribed. Do not give Exforge to other people, even if they have the same symptoms that you have. It may harm them.

This patient information leaflet summarizes the most important information about Exforge. If you would like more information about Exforge, talk with your doctor. You can ask your doctor or pharmacist for information about Exforge that is written for health professionals. For more information go to www.Exforge.com or call 1-888-8-Exforge (1-888-839-3674).

What are the ingredients in Exforge?

Active ingredients: amlodipine besylate and valsartan

The inactive ingredients of all strengths of the tablets are colloidal silicon dioxide, crospovidone, magnesium stearate and microcrystalline cellulose. Additionally, the 5/320 mg and 10/320 mg strengths contain iron oxide yellow and sodium starch glycolate. The film coating contains hypromellose, iron oxides, polyethylene glycol, talc and titanium dioxide.

April 2007 Printed in U.S.A.

© Novartis

Distributed by:

Novartis Pharmaceuticals Corp.

East Hanover, New Jersey 07936


Exforge (amlodipine besylate and valsartan)
PRODUCT INFO
Product Code 0078-0488 Dosage Form TABLET, FILM COATED
Route Of Administration ORAL DEA Schedule

INGREDIENTS
Name (Active Moiety) Type Strength
amlodipine besylate (amlodipine) Active 5 MILLIGRAM In 1 TABLET
valsartan (valsartan) Active 160 MILLIGRAM In 1 TABLET
colloidal silicone dioxide Inactive
crospovidone Inactive
hypromellose Inactive
iron oxides Inactive
magnesium stearate Inactive
microcrystalline cellulose Inactive
polyethylene glycol Inactive
talc Inactive
titanium dioxide Inactive

IMPRINT INFORMATION
Characteristic Appearance Characteristic Appearance
Color YELLOW (dark yellow) Score 1
Shape OVAL (ovaloid shaped) Symbol false
Imprint Code NVR;ECE Coating true
Size 14mm

PACKAGING
# NDC Package Description Multilevel Packaging
1 0078-0488-35 10 BLISTER PACK In 1 BOX contains a BLISTER PACK
1 10 TABLET In 1 BLISTER PACK This package is contained within the BOX (0078-0488-35)
2 0078-0488-15 30 TABLET In 1 BOTTLE None
3 0078-0488-34 90 TABLET In 1 BOTTLE None


Exforge (amlodipine besylate and valsartan)
PRODUCT INFO
Product Code 0078-0489 Dosage Form TABLET, FILM COATED
Route Of Administration ORAL DEA Schedule

INGREDIENTS
Name (Active Moiety) Type Strength
amlodipine besylate (amlodipine) Active 10 MILLIGRAM In 1 TABLET
valsartan (valsartan) Active 160 MILLIGRAM In 1 TABLET
colloidal silicone dioxide Inactive
crospovidone Inactive
hypromellose Inactive
iron oxides Inactive
magnesium stearate Inactive
microcrystalline cellulose Inactive
polyethylene glycol Inactive
talc Inactive
titanium dioxide Inactive

IMPRINT INFORMATION
Characteristic Appearance Characteristic Appearance
Color YELLOW (light yellow) Score 1
Shape OVAL (ovaloid shaped) Symbol false
Imprint Code NVR;UIC Coating true
Size 14mm

PACKAGING
# NDC Package Description Multilevel Packaging
1 0078-0489-35 10 BLISTER PACK In 1 BOX contains a BLISTER PACK
1 10 TABLET In 1 BLISTER PACK This package is contained within the BOX (0078-0489-35)
2 0078-0489-15 30 TABLET In 1 BOTTLE None
3 0078-0489-34 90 TABLET In 1 BOTTLE None


Exforge (amlodipine besylate and valsartan)
PRODUCT INFO
Product Code 0078-0490 Dosage Form TABLET, FILM COATED
Route Of Administration ORAL DEA Schedule

INGREDIENTS
Name (Active Moiety) Type Strength
amlodipine besylate (amlodipine) Active 5 MILLIGRAM In 1 TABLET
valsartan (valsartan) Active 320 MILLIGRAM In 1 TABLET
colloidal silicone dioxide Inactive
crospovidone Inactive
hypromellose Inactive
iron oxide yellow Inactive
iron oxides Inactive
magnesium stearate Inactive
microcrystalline cellulose Inactive
polyethylene glycol Inactive
sodium starch glycolate Inactive
talc Inactive
titanium dioxide Inactive

IMPRINT INFORMATION
Characteristic Appearance Characteristic Appearance
Color YELLOW (very dark yellow) Score 1
Shape OVAL (ovaloid shaped) Symbol false
Imprint Code NVR;CSF Coating true
Size 19mm

PACKAGING
# NDC Package Description Multilevel Packaging
1 0078-0490-35 10 BLISTER PACK In 1 BOX contains a BLISTER PACK
1 10 TABLET In 1 BLISTER PACK This package is contained within the BOX (0078-0490-35)
2 0078-0490-15 30 TABLET In 1 BOTTLE None
3 0078-0490-34 90 TABLET In 1 BOTTLE None


Exforge (amlodipine besylate and valsartan)
PRODUCT INFO
Product Code 0078-0491 Dosage Form TABLET, FILM COATED
Route Of Administration ORAL DEA Schedule

INGREDIENTS
Name (Active Moiety) Type Strength
amlodipine besylate (amlodipine) Active 10 MILLIGRAM In 1 TABLET
valsartan (valsartan) Active 320 MILLIGRAM In 1 TABLET
colloidal silicone dioxide Inactive
crospovidone Inactive
hypromellose Inactive
iron oxide yellow Inactive
iron oxides Inactive
magnesium stearate Inactive
microcrystalline cellulose Inactive
polyethylene glycol Inactive
sodium starch glycolate Inactive
talc Inactive
titanium dioxide Inactive

IMPRINT INFORMATION
Characteristic Appearance Characteristic Appearance
Color YELLOW (dark yellow) Score 1
Shape OVAL (ovaloid shaped) Symbol false
Imprint Code NVR;LUF Coating true
Size 19mm

PACKAGING
# NDC Package Description Multilevel Packaging
1 0078-0491-35 10 BLISTER PACK In 1 BOX contains a BLISTER PACK
1 10 TABLET In 1 BLISTER PACK This package is contained within the BOX (0078-0491-35)
2 0078-0491-15 30 TABLET In 1 BOTTLE None
3 0078-0491-34 90 TABLET In 1 BOTTLE None



Revised: 07/2007

Ethiopian Glory of Kings translated into Hebrew by a Jewish Author Dr Ran Hakohin

ክብረ ነገሥት በእሥራኤላዊው ምሁር ዓይን
Wednesday, 09 April 2008

ዶ/ር ራን ሐኮኸን “ክብረ ነገሥት” በኢትዮጵያ ለ700 ዓመታት ያህል ብሔራዊ መተዳደሪያ ሆኖ ሲያገለግል የኖረ መጽሐፍ ነው፡፡ የኢትዮጵያ ንጉሠ ነገሥት መንግሥት የቤተ ሰለሞን ሥርወ መንግሥት (ሰሎሞናይክ ዳይናስቲ) ምንጭ ለመጀመሪያ ጊዜም የተገኘው በክብረ ነገሥት ውስጥ ነው፡፡ ንግሥተ ሳባ ኢየሩሳሌምን ጎብኝታ ከንጉሥ ሰሎሞን ጋር ስለመገናኘቷና ቀዳማዊ ምኒሊክ ስለመወለዱ ታቦተ ጽዮን ወደ አክሱም ስለመምጣቷ ይተርካል፡፡


ከ16ኛው ምእት ዓመት ወዲህ ስለ ኢትዮጵያ ነገሥታት ስለ ሥርወ መንግሥቱ የሚተረኩትን በተለያዩ የአውሮጳ አገሮች መጻፉ አልቀረም፡፡ በቅርቡ አንድ እሥራኤላዊ ምሁር ክብረ ነገሥትን ወደ እብራይስጥ ተርጉመውታል፡፡ የቀደሙትን እትሞች ስንቃኝ ፍራንሲስኮ አልቫሬዝ የፖርቱጋል ንጉሥ ማኑኤል ቀዳማዊ ልዩ መልዕክተኛ ሆኖ ወደ ዳግማዊ አፄ ዳዊት በመጣ ጊዜ በ1525 ዓ.ም ያየውንና የሰማውን የኢትዮጵያን ልዩ ልዩ ባህላዊ ገጽታዎች በተነተነበት “ዘ ፕሬስተር ጆን” በተሰኘው መጽሐፉ ስለ ኢትዮጵያ ነገሥታት መነሻ ጽፏል፡፡ ስለ ክብረ ነገሥት ተጨማሪ መረጃ የሰጠው የኢየሱሳውያን ካህን የሆነው ማኖኤል ዶ አልሜዳ “ሒስቶሪያ ደ ኢትዮጵያ” በሚባለው መጽሐፉ ነው፡፡

በ16ኛው ምእት የመጀመሪያ ሩብ ዓመታት ስለ ንጉሥ ሰሎሞንና ስለ ልጁ ምኒልክ ከክብረ ነገሥት ያገኘውን ትውፊት ፒ.ኤን ጎዲንሆ ያሳተመ ሲሆን፣ ስኮትላንዳዊው ጀምስ ብሩስ በ18ኛው ምእት ዓመት የዓባይን ምንጭ ለማሰስ በመጣ ጊዜ የአፄ ተክለሃይማኖት ዳግማዊ እንደራሴና ባለሙሉ ሥልጣን የነበሩት ራስ ሚካኤል ሥሁል ከሰጡት የብራና መጻሕፍት መካከል አንዱ ክብረ ነገሥት ነበር፡፡

ኦገስት ዲልማን የክብረ ነገሥትን ምጥን (ሰመሪ) ሲያዘጋጅ ኤፍ. ፕሬቶሪየስ 12 ምዕራፎችን (ከ19-32) ወደ ላቲን ተርጉሞ አሳትሟል፡፡ የግእዙን ክብረ ነገሥት ከትንተና ጋር ጀርመን ውስጥ በ1897 ዓ.ም(1905) ከጀርመንኛ ምጥን ትርጉም ጋር ያሳተመው ካርል ቤዞልድ ነው፡፡ የመጀመሪያው የእንግሊዝኛ ትርጉም የተከናወነው በዋሊስ በጅ አማካይነት ሲሆን ሁለት እትሞች በ1922 እና በ1932 አውጥቷል፡፡ መጽሐፉ በሩሲያኛ፣ በፈረንሣይኛም ተተርጉሟል፡፡ አሁን ደግሞ እሥራኤላዊው ዶክተር ራን ሐኮኸን ወደ እብራይስጥ ቋንቋ ሲተረጉሙት በቅርቡ ይታተማል ተብሎ ይጠበቃል፡፡

ከእርሳቸው ጋር ባደረግነው ቃለ ምልልስ፣ “ኢትዮጵያ ከእሥራኤል ጋር ስላላት ተዛምዶ የሚያስረዳውን ክብረ ነገሥት በእሥራኤል ኅብረተሰብ ዘንድ እምብዛም አይታወቅም፡፡ ይሁን እንጂ የእብራይስጥ ትርጉም ከሌሎች ይልቅ አስፈላጊ ነው፡፡ በዐውደ ንባቡ ኢትዮጵያውያን ፣እኛ ቤተ እሥራኤላውያን ነን፣ ይላሉና” ያሉት ዶክተር ሐኮኸን፣ ክብረ ነገሥትን ወደ እብራይስጥ ቋንቋ መተርጐም በእሥራኤል ለሚኖሩት ከ100,000 በላይ ቤተ እሥራኤላውያን ጠቀሜታ ይኖረዋል ብለዋል፡፡

“የእሥራኤል መገናኛ ብዙኀን ስለ ኢትዮጵያውያን አይሁዶች ሲጽፉ የሚጠቅሱት ድህነታቸውና ባህላዊ ችግሮቻቸውን ነው፡፡ ከገጠር አካባቢ መምጣታቸውና ያልተማሩ መሆናቸው ከእስራኤል ማኅበረሰብ ጋር ለመዋሐድ ችግር እንደፈጠረባቸው ይጠቁማሉ”

በጥቁሮቹ አይሁዶች (ኢትዮጵያውያኑ) ላይ በተለይ በአክራሪ አይሁዶች የዘረኝነት ጥቃት ይደርስባቸዋል፡፡ አጥባቂ ሃይማኖተኞቹ ከለዘብተኞቹ ይልቅ ዘረኞች ናቸው፡፡

ቀደም ሲል በኢትዮጵያ ክርስትና ውስጥ የአይሁድ ልማዶች መኖራቸው እንደማያውቁ የጠቀሱት እስራኤላዊው ምሁር፣ የጣና ሐይቅ በጎበኙበት ጊዜ በሐይቁ ካሉት የአሣ ዝርያዎች መካከል እንደ አይሁዶች የማይበሉ መኖራቸውን መረዳታቸውን ገልጸዋል፡፡ እንደ ምሁሩ አገላለጽ እሥራኤላውያን ለበርካታ ሺሕ ዓመታት የዘለቀውን ልዩና የበለጸገ ባህል ያላትን፣ ለየት ያለውን አፍሪካዊ ክርስትና የመሠረተችውን ኢትዮጵያን አለማወቃቸው የሚገርም ነው፡፡

ይህን ክፍተት ለመሙላት ኢትዮጵያ ከባህሏና ከአይሁዳዊነት ጋር ካላት ልዩ ተዛምዶ አንፃር ክብረ ነገሥትን ለመተርጐም ካነሳቸው ዐበይት ጉዳዮች አንዱ መሆኑን ዶ/ር ሐኮኸን አስረድተዋል፡፡ ንግሥተ ሳባ በክብረ ነገሥቱ አጠራር ንግሥት ማክዳ ወደ ጠቢቡ ሰሎሞን ስላደረገችው ጉዞና በብልሃቱ እንዴት እንደተገናኛትና እንደፀነሰች አገሯ ተመልሳ ልጅዋን እንደወለደች ይተርካል፡፡

በኢትዮጵያ የንግሥና ትውፊት ውስጥ የልጁ ስም ቀዳማዊ ምኒልክ ቢሆንም በክብረ ነገሥት ውስጥ ስሙ “በይነል ሐኪም” (ኢብነ እል ሐኪም) ተብሎ ተጽፏል፡፡ ወልደ ጥበብ ማለት ነው፡፡

በይነል ሐኪም ወደ ኢየሩሳሌም ሄዶ ከአባቱ ጋር መገናኘቱን፣ በኢትዮጵያም እንደነገሠ ቤተ ሰለሞን ሥርወ መንግሥትም መጀመሩን ያወሳል፡፡

ክብረ ነገሥት እውነተኛ ታሪክ ነው ወይስ ሌጀንድ (አፈ ታሪክ) ተብለው ለተጠየቁት ምሁሩ ሲመልሱ፣ “በቴል አቪቭ ዩኒቨርሲቲ ሥነ ጽሑፍ አስተምራለሁ፡፡ በሥነ ጽሑፍ ዘርፍ ውስጥ ታሪክ ትክክለኛ ይሁን አይሁን መሠረታዊ ነገር አይደለም፤ በክብረ ነገሥትም ቢሆን እንዲሁ ነው፡፡ ይሁን እንጂ የኢትዮጵያን ባህላዊ ማንነትን ለበርካታ መቶ ዓመታት ቀርፆታል፡፡ ይህም ከጥያቄው በላይ በጣም ጠቃሚ የሆነ ክንውን ነው” ብለዋል፡፡

ለእሥራኤላውያን ክብረ ነገሥቱንና ታሪኩን በቋንቋቸው ማቅረብ ጠቀሜታው ከፍ ያለ ነው፤ ኢትዮጵያውያን ቤተ እሥራኤሎችን በቅጡ ለመረዳትና አይሁዳዊ መሠረት ያለውን ክርስትና ለመገንዘብም ይረዳቸዋል፡፡

ዶ/ር ራን ሐኮኸን ያዘጋጁት የክብረ ነገሥት እብራይስጥ ትርጉም “አኖቴሽን” (መግለጫ) ያለው በመኾኑ፣ የቀደሙት ቋንቋዎች ትርጉሞች ካሏቸው የመጽሐፍ ቅዱስ ጥቅሶች ግርጌ ማስታወሻ ይለያል፡፡ በክብረ ነገሥት ውስጥ የሚገኙትን የአይሁድ ምልክቶች ከመጽሐፍ ቅዱስ ብቻ ሳይሆን፣ ታልሙድን ከመሳሰሉ የአይሁድ ሥነ ጽሑፎች እንደመረመሯቸው ምሁሩ ገልጸዋል፡፡

በክብረ ነገሥት የመጨረሻ ገጾች ላይ መጽሐፉ መጀመሪያ የተጻፈው በኮፕት (የግብጽ ኦርቶዶክስ ቤተክርስቲያን ቋንቋ) መሆኑን ወደ ዐረብኛ ከተተረጐመው እትም በ14ኛው ምእት መጀመሪያ ወደ ግእዝ መተርጐሙ ተጽፏል፡፡ አብዛኞቹ ምሁራን መጽሐፉ የተደረሰው በ14ኛው ምእት እንደሆነ ይናገራሉ፡፡

ትርጉም አይደለም፤ የአክሱም ንቡረ እድ ይስሐቅ ከስድስት ሊቃውንት ካህናት ጋር በመሆኑ ከውጭና ከሀገር ውስጥ ልዩ ልዩ መጻሕፍት በመመሥረት በግእዝ ደርሰውታል የሚል የሌሎች ወገኖች አስተያየት አለ፡፡

ዘመኑን በተመለከተ ትውልደ ዐረብ የሆኑ አሜሪካዊ በስድስተኛው ምእት መጻፉን ሲጠቅሱ፣ እንግሊዛዊው አርኪዮሎጂስትም ስለታቦተ ጽዮን ከ16ኛው ምእት በፊት የተጠቀሰበት የለም ይላሉ፡፡

ዶክተር ሐኮኸን ክብረ ነገሥት ከኢትዮጵያ ጋር ጥብቅ ቁርኝት እንዳለው በተለይ ኤድዋርዶ ዑልንዶርፍ የገለጹበትን መንገድ ይሁንታ ይሰጡበታል፡፡

“ብሉይ ኪዳን (ኦሪት) ለእሥራኤሎች፣ ወይም ቁርዓን ለዐረቦች እንዳላቸው ልዩ ስፍራ ሁሉ ክብረ ነገሥትም ኢትዮጵያ ከሥነ ጽሑፋዊው እሴት ባሻገር የኢትዮጵያ ብሔራዊ መለዮና ሃይማኖታዊ መሠረት አመልካች ነው”

የክብረ ነገሥት እብራይስጥ እትም ከሁለት ወር በኋላ እሥራኤል ውስጥ ለአደባባይ እንደሚበቃ ተርጓሚው ገልጸዋል፡፡

በሔኖክ ያሬድ

The Ethiopian Economic Disparity in 2008

Fake gold, depreciating Birr, unofficial foreign exchange transactions, escalating prices of cement, prices of almost everything going mad . . . these are hot issues of interest to gossip corridors across the city. People seem to be at a loss of what to make of all the rumours, unable to determine the truth from the baseless.

That was of course up until last Tuesday, when the Prime Minister appeared before Parliament where it was highly anticipated that he would make sense out of the utter confusion spread around the capital and aggravated by the follow up raids by law enforcement agencies on about twelve currency black market shops.

Gossip corridors were not impressed with the Prime Minister’s explanation on any of these issues.

Why the government has acted unaware of the existence of overtly operating exchange shops across town and the clamp down on them still remains a mystery to many at the gossip corridor.

The threat that these currency dealers posed to the national economy, as claimed by the Prime Minister, was far from being taken seriously. Neither will the action taken against these dealers bring about the kind of result the government hopes to achieve; it will only drive these operators further underground, according to the general opinion at the gossip corridor.

The government was forewarned when it decided to grant permission for companies to import cement, using Franco valuta; a form of import that does not require the treasury commit foreign currency.

It was meant to allow construction firms to bring in cement for their requirement, while traders would import to distribute the cement to the local market. Government had hoped that it would identify and control such imports. Not many of Addis Abeba’s high-flying businessmen, however, were excited with the idea.

In fact, they proved reluctant to take advantage of the new policy, as they were worried that involvement in this would expose them to uncalled for attention by the government on how much they have in their foreign accounts, gossip claimed.

Thus, the field was left largely to foreigners; a year on, these people had to choose between investing whatever they have brought here in to the country, or taking the money out.

According to gossip, there emerged a new development in the region where demand for sugar in Somalia suddenly surged. Suppliers needed to be liquid to buy sugar from the international market in order to export sugar there.

Some at the gossip corridors attribute these factors as reasons for the sudden fallout of the Birr against the dollar - from 9.2 Br in December 2007 to 9.6 Br in mid-March 2008 - yet the dollar itself is fallingalarmingly against the basket of other currencies.

Such was also the case with the “parallel” market, which jumped from 9.3 Br against a dollar three months ago to 10.65 Br to the same just before the crackdown.

Others at the gossip corridors, however, relate this development to the emergence of a scandal at the central bank, where the national treasury is said to have paid hundreds of millions of Birr to buy fake gold.

They felt that Ethiopia’s reserve in gold has been compromised and this has shattered public confidence.

The apprehension of black market shop owners and the subsequent government bashing of businessmen and women does little to restore this, all according to gossip. The subject of interest at gossip corridors will remain the same for weeks as the Birr continues to fall.

The link-Intelligence, Health and Wealth

Intelligent Quotient- Health and Wealth-
Are they connected?


Abstract:
Wilkinson contends that economic inequality reduces the health and life expectancy of the whole population but his argument does not make sense within its own evolutionary framework.

Recent evolutionary psychological theory suggests that the human brain, adapted to the ancestral environment, has difficulty comprehending and dealing with entities and situations that did not exist in the ancestral environment and that general intelligence evolved as a domain-specific adaptation to solve evolutionarily novel problems.

Since most dangers to health in the contemporary society are evolutionarily novel, it follows that more intelligent individuals are better able to recognize and deal with such dangers and live longer.

Consistent with the theory, the macro-level analyses show that income inequality and economic development have no effect on life expectancy at birth, infant mortality and age-specific mortality net of average intelligence quotient (IQ) in 126 countries.

They also show that an average IQ has a very large and significant effect on population health but not in the evolutionarily familiar sub-Saharan Africa. At the micro level, the General Social Survey data show that, while both income and intelligence have independent positive effects on self-reported health, intelligence has a stronger effect than income.

The data collectively suggest that individuals in wealthier and more egalitarian societies live longer and stay healthier, not because they are wealthier or more egalitarian but because they are more intelligent. No way!

Document Type: Research article
DOI: 10.1348/135910705X69842
Affiliations: 1: Interdisciplinary Institute of Management, London School of Economics and Political Science, UK


Dear Ms Gibson of London School of Economics:
Re: It is not IQ It is the biological and physical environment Stupid! That impacts the health of nations.

I read with interest and some level of disgust by the assumption of IQ as defined by Western Culture to define the competence of Africans and especially Ethiopians as mentioned in this article.

I would like to challenge the Cultural and Competency IQ of the author of this rather ridiculous and racist author. We should question the integrity and implication of such rather depressing and outmoded research and generalizations.

Imagine an Ethiopian High School Student administering a literature IQ test to all the Nobel Literature laureates on Quine and Semina Work in Amharic and in Geez even better and assessing their Quine IQ status.

I am sure all of them will score 00.00 let alone this rather racist and demented Eco-psychologist of the LSE will surface on the Quine IQ square. Just imagine the class discussion on a paper presented by such Ethiopian High School student on the performance of Western Noble laureates of literature. This is the analogy of this rather disturbing paper presented to us.

If you then gave the same Geez or Amharic Quine IQ test to the rest of the world and mapped the Quine IQ you will be shocked to realize that world IQ may not even reach 1% and that will be a tragedy. In effect, this is the tragedy of this paper.

I am a physician and public health scientist who have studied child development (physical and cognitive development) and evaluated research material on child survival across developing an developed countries for the past 25 years. My MPH thesis was on "Evaluating Mother and Child Health Services in Developing and Developed countries with a focus on Perinatal Survival of children in developing and developed countries.

My research indicates that child survival is dependent on two key determinants, both relevant to the situation of the mother. Biological marker of maternal birth weight that is also dependent on the pool of matriarchal birth weights for generations. This in effect defines the genetic pool reserve as well as the weight and gestation of the pregnancy at birth.

The second critical issue is environmental and behavioral and that is the educational status of the mother. This education could be cultural, environmental and empirical as it relates to the survival of the child.

This in effect means a well adjusted and educated mother will ensure the survival of her offspring by either ensuring her own socio-economic and cultural environment by either producing the appropriate environments or by organizing the environment around her for the child to succeed and survive.

Where cultural or empirical IQ will really matters is on the social and economic paradigm more than the biological environment.

That is why it is commonly said that: “If you educate a man, you educate one person; but if you educate a woman, you educate a family, the home, the community and the nation at large. If you educate both then hey can educate the world!

It is clear that a child born in Africa has more opportunities for challenging immunological experiences than a child born in Europe or North America. Talk to Madonna who is not a scientist but has definitely a much higher IQ than your author about the chances of the survival of her newly adopted Malawian son.

The African environment is hostile as it is very conducive to the survival of micro-organisms that are pathogenic to humans than it is in the temperate climate. We now know in current medical research almost all diseases are associated with the competence of our immune system' s ability to differentiate between self and non self.

Infections manifest themselves in many forms and most of the Cardiovascular and chronic diseases including cancers are closely associated with our body's response to viral and other microbial infections.

This is true of Cancer of the Stomach, Peptic Acid Disease, Cardio-vascular accidents and even degenerative disorders. Science is giving us the opportunity to identify the inter-relatedness of most chronic conditions and our immune system's competency.

Our immune system is challenged by more infectious conditions in Developing and temperate climates that makes us all susceptible for continuous challenges to our immune system's response to infections and stressors in life.

In short, it is the biological and physical environment that is more critical than the IQ as suggested by your author. After all, if the Massai in Africa were to define IQ in the sense of their ability to survive in the wilds of Africa, most so called geniuses of the West and noble laureates will not last for long.

So, does that mean the noble scientists have a diminishing Massai defined IQ and as such will have a short survival and quality of life in the Massai world?

Surely, this is a highly erroneous and rather racist research and you should allow alternative perspectives to be explored before you sensationalize such highly controversial research findings.

Remember! Health is not the mere absence of disease, disability and injury, but, the comprehensive wellbeing of the spiritual, emotional, psychological and physical wellbeing of an individual and the community at large. Within this larger construct, the IQ has little to do with health as much as the environment and how our system adopts to it.

All the same, I believe all human beings given the opportunity have the capacity to adopt to new skills, new challenges and opportunities, may be some faster than others but with diverse context and depth and competency.

The question is not IQ, it is rather the hostile environment at home, school, work and leisure that stresses our immune system to such an extent that our whole system collapses in the end. Even geriatric changes are now been associated to our immune system's capacity to adjust with changing age, gender, emotional and physical stressful life events we all face in our life time.

This is not yet complete science and we need to observe and expand research to understand our own body and how we adopt to changing life events.

I request your department which I believe is an Economics center to look at how education and IQ impacts wealth creation rather than delving in highly unscientific association of IQ and health.

It is the environment stupid, more than the IQ that determines our health outcome!

Having said that, nurture or nature is part of the same universe, why bother!

I trust you will consider this contribution as you make future research and line of enquiry to follow us the recent publication in your department.

Please do not hesitate to contact me if I can be helpful. Thanking you for your attention to this matter, I remain;

Yours sincerely

Belai Habte-Jesus, MD, MPH
Global Strategic Enterprises, Inc;03.933.8737; globalbelai@hotmail.com

Intelligence quotient
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"IQ" redirects here. For other uses, see IQ (disambiguation).


IQ tests are designed to give approximately this Gaussian distribution. Colors delineate one standard deviation.

An intelligence quotient or IQ is a score derived from a set of standardized tests of intelligence. Intelligence tests come in many forms, and some tests use a single type of item or question. Most tests yield both an overall score and individual subtest scores. Regardless of design, all IQ tests attempt to measure the same general intelligence.[1] Component tests are generally designed and selected because they are found to be predictive of later intellectual development, such as educational achievement.

IQ also correlates with job performance, socioeconomic advancement, and "social pathologies". Recent work has demonstrated links between IQ and health, longevity, and functional literacy. [2] [3] However, IQ tests do not measure all meanings of "intelligence", such as creativity. IQ scores are relative (like placement in a race), not absolute (like the measurement of a ruler).


For people living in the prevailing conditions of the developed world, IQ is highly heritable, and by adulthood the influence of family environment on IQ is undetectable. That is, significant variation in IQ between adults can be attributed to genetic variation, with the remaining variation attributable to environmental sources that are not shared within families. In the United States, marked variation in IQ occurs within families, with siblings differing on average by almost one standard deviation.


The average IQ scores for many populations were rising during the 20th century: a phenomenon called the Flynn effect. It is not known whether these changes in scores reflect real changes in intellectual abilities. On average, IQ scores are stable over a person's lifetime, but some individuals undergo large changes. For example, scores can be affected by the presence of learning disabilities.

Contents
[hide]
• 1 The definition of the IQ
• 2 Components of intelligence
• 3 History
• 4 IQ and general intelligence factor
• 5 Genetics versus environment
o 5.1 Environment
o 5.2 Development
o 5.3 Mental retardation
o 5.4 IQ, education, and income
o 5.5 Regression
• 6 IQ and the brain
o 6.1 Brain size and IQ
o 6.2 Brain areas associated with IQ
o 6.3 Brain structure and IQ
• 7 The Flynn effect
• 8 Group differences
o 8.1 Sex and intelligence
o 8.2 Race and IQ
o 8.3 Health and IQ
o 8.4 Wealth and IQ
• 9 Practical validity
• 10 Public policy
o 10.1 Use of IQ in the United States legal system
• 11 Validity and g-loading of specific tests
• 12 Controversy
o 12.1 Social construct
o 12.2 The Mismeasure of Man
o 12.3 The view of the American Psychological Association
o 12.4 IQ test
• 13 Notes
• 14 See also
• 15 References
• 16 External links
o 16.1 Collective statements
o 16.2 Review papers
o 16.3 Professional Intelligence Testing

[edit] The definition of the IQ

Originally, IQ was calculated with the formula
A 10-year-old who scored as high as the average 13-year-old, for example, would have an IQ of 130 (100*13/10).

Because this formula only worked for children, it was replaced by a projection of the measured rank on the Gaussian bell curve with a center value (average IQ) of 100, and a standard deviation of 15 or occasionally 16.

[edit] Components of intelligence

Component tests are generally designed and selected because they are found to be predictive of later intellectual development, such as educational achievement. IQ also correlates with job performance, socioeconomic advancement, and, usually negatively, with "social pathologies".

Recent work has demonstrated links between IQ and health, longevity, and functional literacy. [4] [5] However, IQ tests do not measure all meanings of "intelligence", such as creativity. IQ scores are relative (like placement in a race), not absolute (like the measurement of a ruler).


For people living in the prevailing conditions of the developed world, IQ is highly heritable, and by adulthood the influence of family environment on IQ is undetectable. That is, significant variation in IQ between adults can be attributed to genetic variation, with the remaining variation attributable to environmental sources that are not shared within families. In the United States, marked variation in IQ occurs within families, with siblings differing on average by almost one standard deviation.

The average IQ scores for many populations were rising during the 20th century: a phenomenon called the Flynn effect. It is not known whether these changes in scores reflect real changes in intellectual abilities. On average, IQ scores are stable over a person's lifetime, but some individuals undergo large changes. For example, scores can be affected by the presence of learning disabilities.

[edit] History
In 1905, the French psychologist Alfred Binet published the first modern intelligence test, the Binet-Simon intelligence scale.

His principal goal was to identify students who needed special help in coping with the school curriculum. Along with his collaborator Theodore Simon, Binet published revisions of his intelligence scale in 1908 and 1911, the last appearing just before his untimely death. In 1912, the abbreviation of "intelligence quotient" or I.Q., a translation of the German Intelligenz-Quotient, was coined by the German psychologist William Stern.

A further refinement of the Binet-Simon scale was published in 1916 by Lewis M. Terman, from Stanford University, who incorporated Stern's proposal that an individual's intelligence level be measured as an intelligence quotient (I.Q.). Terman's test, which he named the Stanford-Binet Intelligence Scale formed the basis for one of the modern intelligence tests still commonly used today. They are all colloquially known as IQ tests.

[edit] IQ and general intelligence factor

Main article: General intelligence factor

Modern IQ tests produce scores for different areas (e.g., language fluency, three-dimensional thinking, etc.), with the summary score calculated from subtest scores. The average score, according to the bell curve, is 100. Individual subtest scores tend to correlate with one another, even when seemingly disparate in content.

Analysis of individuals' scores on the subtests of a single IQ test or the scores from a variety of different IQ tests (e.g., Stanford-Binet, WISC-R, Raven's Progressive Matrices, Cattell Culture Fair III, Universal Nonverbal Intelligence Test, and others) reveal that they all measure a single common factor and various factors that are specific to each test. This kind of factor analysis has led to the theory that underlying these disparate cognitive tasks is a single factor, termed the general intelligence factor (or g), that corresponds with the common-sense concept of intelligence. In the normal population, g and IQ are roughly 90% correlated and are often used interchangeably.

Various IQ tests measure a standard deviation with different number of points. Thus, when an IQ score is stated, the standard deviation used should also be stated. A result of 124 in a test with a 24-point standard deviation corresponds to a score of 115 in a test with a 15-point deviation. [6]

Where an individual has scores that do not correlate with each other, there is a good reason to look for a learning disability or other cause for the lack of correlation. Tests have been chosen for inclusion because they display the ability to use this method to predict later difficulties in learning.

[edit] Genetics versus environment

Main article: Inheritance of intelligence

The role of genes and environment (nature vs. nurture) in determining IQ is reviewed in Plomin et al. (2001, 2003). The degree to which genetic variation contributes to observed variation in a trait is measured by a statistic called heritability.

Heritability scores range from 0 to 1, and can be interpreted as the percentage of variation (e.g. in IQ) that is due to variation in genes. Twins studies and adoption studies are commonly used to determine the heritability of a trait. Until recently heritability was mostly studied in children. Some studies find the heritability of IQ around 0.5 but the studies show ranges from 0.4 to 0.8;[7] that is, depending on the study, a little less than half to substantially more than half of the variation in IQ among the children studied was due to variation in their genes. The remainder was thus due to environmental variation and measurement error.

A heritability in the range of 0.4 to 0.8 implies that IQ is "substantially" heritable. Studies with adults show that they have a higher heritability of IQ than children do and that heritability could be as high as 0.8.

The American Psychological Association's 1995 task force on "Intelligence: Knowns and Unknowns" concluded that within the white population the heritability of IQ is "around .75" (p. 85). [8] The Minnesota Study of Twins Reared Apart, a multiyear study of 100 sets of reared apart twins which was started in 1979, concluded that about 70% of the variance in IQ was found to be associated with genetic variation. [9]

The heritability of IQ has been tested on large numbers of twins, siblings, parent-child relationships, and adoptees. Evidence from family studies provides the main supporting evidence from which arguments about the relative roles of genetics and environment are constructed. Put all these studies together, which include the IQ tests of tens of thousands of individuals, and the table looks like this[citation needed]:

Percent Correlation of IQ Tests
Relationship Correlation
The same person tested twice 87%
Identical twins reared together 86%
Identical twins reared apart 76%
Fraternal twins reared together 55%
Biological siblings 47%
Parents and children living together 40%
Parents and children living apart 31%
Adopted children living together 0%
Unrelated people living apart 0%

[edit] Environment

Environmental factors play a major role in determining IQ in extreme situations. Proper childhood nutrition appears critical for cognitive development; malnutrition can lower IQ. Other research indicates environmental factors such as prenatal exposure to toxins, duration of breastfeeding [citation needed], and micronutrient deficiency can affect IQ. In the developed world, there are some family effects on the IQ of children, accounting for up to a quarter of the variance. However, by adulthood, this correlation disappears, so that the IQ of adults living in the prevailing conditions of the developed world may be more heritable.

Nearly all personality traits show that, contrary to expectations, environmental effects actually cause adoptive siblings raised in the same family to be as different as children raised in different families (Harris, 1998; Plomin & Daniels, 1987). Put another way, shared environmental variation for personality is zero, and all environmental effects would be nonshared.

Conversely, IQ is actually an exception to this, at least among children. The IQs of adoptive siblings, who share no genetic relation but do share a common family environment, are correlated at .32. Despite attempts to isolate them, the factors that cause adoptive siblings to be similar have not been identified. However, as explained below, shared family effects on IQ disappear after adolescence.

Active genotype-environment correlation, also called the "nature of nurture", is observed for IQ. This phenomenon is measured similarly to heritability; but instead of measuring variation in IQ due to genes, variation in environment due to genes is determined. One study found that 40% of variation in measures of home environment are accounted for by genetic variation. This suggests that the way human beings craft their environment is due in part to genetic influences.


A study of French children adopted between the ages of 4 and 6 shows the continuing interplay of nature and nurture. The children came from poor backgrounds with I.Q.’s that initially averaged 77, putting them near retardation. Nine years later after adoption, they retook the I.Q. tests, and all of them did better. The amount they improved was directly related to the adopting family’s status. "Children adopted by farmers and laborers had average I.Q. scores of 85.5; those placed with middle-class families had average scores of 92.

The average I.Q. scores of youngsters placed in well-to-do homes climbed more than 20 points, to 98." [10] This study suggests that IQ is not stable over the course of ones lifetime and that, even in later childhood, a change in environment can have a significant effect on IQ.


It is well known that it is possible to increase ones IQ score by training, for example by regulary playing puzzle games. Recent studies have shown that training ones working memory may increase IQ. (Klingberg et al., 2002)

[edit] Development

It is reasonable to expect that genetic influences on traits like IQ should become less important as one gains experiences with age. Surprisingly, the opposite occurs. Heritability measures in infancy are as low as 20%, around 40% in middle childhood, and as high as 80% in adulthood.[11]

Shared family effects also seem to disappear by adulthood. Adoption studies show that, after adolescence, adopted siblings are no more similar in IQ than strangers (IQ correlation near zero), while full siblings show an IQ correlation of 0.6. Twin studies reinforce this pattern: monozygotic (identical) twins raised separately are highly similar in IQ (0.86), more so than dizygotic (fraternal) twins raised together (0.6) and much more than adopted siblings (~0.0).[12]

Most of the IQ studies described above were conducted in developed countries, such as the United States, Japan, and Western Europe. Also, a few studies have been conducted in Moscow, East Germany, and India, and those studies have produced similar results.

Any such investigation is limited to describing the genetic and environmental variation found within the populations studied. This is a caveat of any heritability study.[citation needed]. Another caveat is that people with chromosomal abnormalities - such as klinefelter's syndrome and Triple X syndrome, will score considerably higher than the normal population without the chromosomal abnormalities, when scored against visual IQ tests, not IQ tests that have been tailored to measure IQ against the normal population.[13]


[edit] Mental retardation

About 75–80 percent of mental retardation is familial (runs in the family), and 20–25 percent is due to biological problems, such as chromosomal abnormalities or brain damage. [14] Mild to severe mental retardation is a symptom of several hundred single-gene disorders and many chromosomal abnormalities, including small deletions. Based on twin studies, moderate to severe mental retardation does not appear to be familial, but mild mental retardation does. That is, the relatives of the moderate to severely mentally retarded have normal ranges of IQs, whereas the families of the mildly mentally retarded have lower IQs.

IQ score ranges (from DSM-IV):

• mild mental retardation: IQ 50–55 to 70; children require mild support; formally called "Educable Mentally Retarded".

• moderate retardation: IQ 35–40 to 50–55; children require moderate supervision and assistance; formally called "Trainable Mentally Retarded".
• severe mental retardation: IQ 20–25 to 35–40; can be taught basic life skills and simple tasks with supervision.

• profound mental retardation: IQ below 20–25; usually caused by a neurological condition; require constant care.

The rate of mental retardation is higher among males than females, according to a 1991 U.S. Centers for Disease Control and Prevention (CDC) study. [15] This is aggravated by the fact that males, unlike females, do not have a spare X chromosome to offset chromosomal defects.

Individuals with IQs below 70 have been essentially exempted from the death penalty in the U.S. since 2002. [16]

[edit] IQ, education, and income

Tambs et al. (1989) found that occupational status, educational attainment, and IQ are individually heritable; and further found that "genetic variance influencing educational attainment … contributed approximately one-fourth of the genetic variance for occupational status and nearly half the genetic variance for IQ". In a sample of U.S. siblings, Rowe et al. (1997) report that the inequality in education and income was predominantly due to genes, with shared environmental factors playing a subordinate role.

[edit] Regression

The heritability of IQ measures the extent to which the IQ of children appears to be influenced by the IQ of parents. Because the heritability of IQ is less than 100%, the IQ of children tends to "regress" towards the mean IQ of the population. That is, high IQ parents tend to have children who are less bright than their parents, whereas low IQ parents tend to have children who are brighter than their parents. The effect can be quantified by the equation where

• is the predicted average IQ of the children;
• is the mean IQ of the population to which the parents belong;
• h2 is the heritability of IQ;

• m and f are the IQs of the mother and father, respectively. [17]
Thus, if the heritability of IQ is 50%, a couple averaging an IQ of 120 may have children that average around an IQ of 110, assuming that both parents come from a population with a median IQ of 100.

A caveat to this reasoning are those children who have chromosomal abnormalities, such as Klinefelter's syndrome and Triple X syndrome whose "normal" IQ is only one indicator; their visual IQ is another indicator. And so forth.
[edit] IQ and the brain


Main article: Neuroscience and intelligence
[edit] Brain size and IQ

Modern studies using MRI imaging have shown that brain size correlates with IQ (r = 0.35) among adults (McDaniel, 2005). The correlation between brain size and IQ seems to hold for comparisons between and within families (Gignac et al. 2003; Jensen 1994; Jensen & Johnson 1994). However, one study found no familial correlation (Schoenemann et al. 2000).

A study on twins (Thompson et al., 2001) showed that frontal gray matter volume was correlated with g and highly heritable. A related study has reported that the correlation between brain size (reported to have a heritability of 0.85) and g is 0.4, and that correlation is mediated entirely by genetic factors (Posthuma et al 2002).

In a study of the head growth of 633 term-born children from the Avon Longitudinal Study of Parents and Children cohort, it was shown that prenatal growth and growth during infancy were associated with subsequent IQ. The study’s conclusion was that the brain volume a child achieves by the age of 1 year helps determine later intelligence. Growth in brain volume after infancy may not compensate for poorer earlier growth. [18]

[edit] Brain areas associated with IQ

Many different sources of information have converged on the view that the frontal lobes are critical for fluid intelligence. Patients with damage to the frontal lobe are impaired on fluid intelligence tests (Duncan et al 1995). The volume of frontal grey (Thompson et al 2001) and white matter (Schoenemann et al 2005) have also been associated with general intelligence.

In addition, recent neuroimaging studies have limited this association to the lateral prefrontal cortex. Duncan and colleagues (2000) showed using Positron Emission Tomography that problem-solving tasks that correlated more highly with IQ also activate the lateral prefrontal cortex. More recently, Gray and colleagues (2003) used functional magnetic resonance imaging (fMRI) to show that those individuals that were more adept at resisting distraction on a demanding working memory task had both a higher IQ and increased prefrontal activity. For an extensive review of this topic, see Gray and Thompson (2004). [19]


In 2004, Richard Haier, professor of psychology in the Department of Pediatrics and colleagues at University of California, Irvine and the University of New Mexico used MRI to obtain structural images of the brain in 47 normal adults who also took standard IQ tests. The study demonstrated that general human intelligence appears to be based on the volume and location of gray matter tissue in the brain. Regional distribution of gray matter in humans is highly heritable. The study also demonstrated that, of the brain's gray matter, only about 6 percent appeared to be related to IQ. [20]

[edit] Brain structure and IQ

A study involving 307 children (age between six to nineteen) measuring the size of brain structures using magnetic resonance imaging (MRI) and measuring verbal and non-verbal abilities has been conducted (Shaw et al 2006). The study has indicated that there is a relationship between IQ and the structure of the cortex—the characteristic change being the group with the superior IQ scores starts with thinner cortex in the early age then becomes thicker than average by the late teens. [21]

[edit] The Flynn effect

Main article: Flynn effect

The Flynn effect is named after James R. Flynn, a New Zealand based political scientist. He discovered that IQ scores worldwide appear to be slowly rising at a rate of around three IQ points per decade (Flynn, 1999). Attempted explanations have included improved nutrition, a trend towards smaller families, better education, greater environmental complexity, and heterosis (Mingroni, 2004). However, tests are renormalized occasionally to obtain mean scores of 100, for example WISC-R (1974), WISC-III (1991) and WISC-IV (2003). Hence it is difficult to compare IQ scores measured years apart.

There is recent evidence that the tendency for intelligence scores to rise has ended in some first world countries. In 2004, Jon Martin Sundet of the University of Oslo and colleagues published an article documenting scores on intelligence tests given to Norwegian conscripts between the 1950s and 2002, showing that the increase in scores of general intelligence stopped after the mid-1990s and in numerical reasoning subtests, declined. [22]

Thomas W. Teasdale of the University of Copenhagen and David R. Owen of Brooklyn College, City University of New York, discovered similar results in Denmark, where intelligence test results showed no rise across the 1990s. [23]
Indications that scores on intelligence tests are not universally climbing have also come from the United Kingdom. Michael Shayer, a psychologist at King's College, University of London, and two colleagues report that performance on tests of physical reasoning given to children entering British secondary schools declined markedly between 1976 and 2003. [24]

[edit] Group differences

Among the most controversial issues related to the study of intelligence is the observation that intelligence measures such as IQ scores vary between populations. While there is little scholarly debate about the existence of some of these differences, the reasons remain highly controversial both within academia and in the public sphere.

[edit] Sex and intelligence

Main article: Sex and intelligence

Most studies show that despite sometimes significant differences in subtest scores, men and women have the same average IQ. Women perform better on tests of memory and verbal proficiency for example, while men perform better on tests of mathematical and spatial ability. Although gender-related differences in average IQ are insignificant, male scores display a higher variance: there are more men than women with both very high and very low IQs (for more details, see main article Sex and intelligence).

[edit] Race and IQ

Main article: Race and intelligence

While IQ scores of individual members of different racial or ethnic groups are distributed across the IQ scale, groups may vary in where their members cluster along the IQ scale. East Asians cluster higher than Europeans, while Hispanics and Sub-Saharan Africans cluster lower in the USA.[25] Much research has been devoted to the extent and potential causes of racial-ethnic group differences in IQ, and the underlying purposes and validity of the tests has been examined. Most experts conclude that examination of many types of test bias and simple differences in socioeconomic status have failed to explain the IQ clustering differences. [26] For a summary of expert opinions, see Race and Intelligence.

The findings in this field are often thought to conflict with fundamental social philosophies, and have resulted in controversy.[27]

[edit] Health and IQ

Persons with a higher IQ have generally lower adult morbidity and mortality. This may be because they better avoid injury and take better care of their own health, or alternatively may be due to a slight increased propensity for material wealth (see above). Post-Traumatic Stress Disorder, severe depression, and schizophrenia are less prevalent in higher IQ bands.

The Archive of General Psychiatry published a longitudinal study of a randomly selected sample of 713 study participants (336 boys and 377 girls), from both urban and suburban settings. Of that group, nearly 76 percent had suffered through at least one traumatic event. Those participants were assessed at age 6 years and followed up to age 17 years.

In that group of children, those with an IQ above 115 were significantly less likely to have Post-Traumatic Stress Disorder as a result of the trauma, less likely to display behavioral problems, and less likely to experience a trauma. The low incidence of Post-Traumatic Stress Disorder among children with higher IQs was true even if the child grew up in an urban environment (where trauma averaged three times the rate of the suburb), or had behavioral problems. [28] On the other hand, higher IQ shows a higher prevalence of those conditioned with Obsessive Compulsive Disorder. [29]

Research in Scotland has shown that a 15-point lower IQ meant people had a fifth less chance of seeing their 76th birthday, while those with a 30-point disadvantage were 37% less likely than those with a higher IQ to live that long. [30]
A decrease in IQ has also been shown as an early predictor of late-onset Alzheimer's Disease and other forms of dementia. In a 2004 study, Cervilla and colleagues showed that tests of cognitive ability provide useful predictive information up to a decade before the onset of dementia.[31]

However, when diagnosing individuals with a higher level of cognitive ability, in this study those with IQ's of 120 or more, [32] patients should not be diagnosed from the standard norm but from an adjusted high-IQ norm that measured changes against the individual's higher ability level.

In 2000, Whalley and colleagues published a paper in the journal Neurology, which examined links between childhood mental ability and late-onset dementia. The study showed that mental ability scores were significantly lower in children who eventually developed late-onset dementia when compared with other children tested. [33]

The longstanding belief that breast feeding correlates with an increase in the IQ of offspring has been challenged in a 2006 paper published in the British Medical Journal. The study used data from 5,475 children, the offspring of 3,161 mothers, in a longitudinal survey.

The results indicated that mother's IQ, not breast feeding, explained the differences in the IQ scores of offspring. The results of this study indicated that prior studies had not allowed for the mother's IQ. Since mother's IQ was predictive of whether a child was breast fed, the study concluded that "breast feeding [itself] has little or no effect on intelligence in children." Instead, it was the mother's IQ that had a significant correlation with the IQ of her offspring, whether the offspring was breast fed or was not breast fed. [34]
[edit] Wealth and IQ

A book IQ and the Wealth of Nations, claims to show that the wealth of a nation can in large part be explained by the average IQ score. This claim has been both disputed and supported in peer-reviewed papers. The data used has also been questioned.

In addition, IQ and its correlates to health, violent crime, gross state product, and government effectiveness are the subject of a 2006 paper in the publication Intelligence. The paper breaks down IQ averages by U.S. states using the federal government's National Assessment of Educational Progress math and reading test scores as a source. [35]

[edit] Practical validity


Linear correlations between 1000 pairs of numbers. The data are graphed on the lower left and their correlation coefficients listed on the upper right. Each set of points correlates maximally with itself, as shown on the diagonal (all correlations = +1).
Evidence for the practical validity of IQ comes from examining the correlation between IQ scores and life outcomes.
Economic and social correlates of IQ
Factors Correlation
School grades and IQ 0.5
Total years of education and IQ 0.55
IQ and parental socioeconomic status 0.33
Job performance and IQ 0.54
Negative social outcomes and IQ −0.2
IQs of identical twins 0.86
IQs of husband and wife 0.4
Heights of parent and child 0.47
Economic and social correlates of IQ in the USA

IQ <75 75–90 90–110 110–125 >125
U.S. population distribution 5 20 50 20 5
Married by age 30 72 81 81 72 67
Out of labor force more than 1 month out of year (men) 22 19 15 14 10
Unemployed more than 1 month out of year (men) 12 10 7 7 2
Divorced in 5 years 21 22 23 15 9
% of children w/ IQ in bottom decile (mothers) 39 17 6 7 < 1
Had an illegitimate baby (mothers)
32 17 8 4 2
Lives in poverty 30 16 6 3 2
Ever incarcerated (men) 7 7 3 1 < 1
Chronic welfare recipient (mothers) 31 17 8 2 < 1
High school dropout 55 35 6 0.4 < 0.4
Values are the percentage of each IQ sub-population, among non-Hispanic whites only, fitting each descriptor. Compiled by Gottfredson (1997) from a U.S. study by Herrnstein & Murray (1994) pp. 171, 158, 163, 174, 230, 180, 132, 194, 247–248, 194, 146 respectively.

Research shows that general intelligence plays an important role in many valued life outcomes. In addition to academic success, IQ correlates with job performance (see below), socioeconomic advancement (e.g., level of education, occupation, and income), and "social pathology" (e.g., adult criminality, poverty, unemployment, dependence on welfare, children outside of marriage). Recent work has demonstrated links between general intelligence and health, longevity, and functional literacy. Correlations between g and life outcomes are pervasive, though IQ and happiness do not correlate. IQ and g correlate highly with school performance and job performance, less so with occupational prestige, moderately with income, and to a small degree with law-abidingness.

General intelligence (in the literature typically called "cognitive ability") is the best predictor of job performance by the standard measure, validity. Validity is the correlation between score (in this case cognitive ability, as measured, typically, by a paper-and-pencil test) and outcome (in this case job performance, as measured by a range of factors including supervisor ratings, promotions, training success, and tenure), and ranges between −1.0 (the score is perfectly wrong in predicting outcome) and 1.0 (the score perfectly predicts the outcome). See validity (psychometric). The validity of cognitive ability for job performance tends to increase with job complexity and varies across different studies, ranging from 0.2 for unskilled jobs to 0.8 for the most complex jobs.

A meta-analysis (Hunter and Hunter, 1984) which pooled validity results across many studies encompassing thousands of workers (32,124 for cognitive ability), reports that the validity of cognitive ability for entry-level jobs is 0.54, larger than any other measure including job tryout (0.44), experience (0.18), interview (0.14), age (−0.01), education (0.10), and biographical inventory (0.37).

Because higher test validity allows more accurate prediction of job performance, companies have a strong incentive to use cognitive ability tests to select and promote employees. IQ thus has high practical validity in economic terms.


The utility of using one measure over another is proportional to the difference in their validities, all else equal. This is one economic reason why companies use job interviews (validity 0.14) rather than randomly selecting employees (validity 0.0).
However, legal barriers, most prominently the U.S. Civil Rights Act, as interpreted in the 1971 United States Supreme Court decision Griggs v. Duke Power Co., have prevented American employers from using cognitive ability tests as a controlling factor in selecting employees where (1) the use of the test would have a disparate impact on hiring by race and (2) where the test is not shown to be directly relevant to the job or class of jobs at issue.

Instead, where there is not direct relevance to the job or class of jobs at issue, tests have only been legally permitted to be used in conjunction with a subjective appraisal process. The U.S. military uses the Armed Forces Qualifying Test (AFQT), as higher scores correlate with significant increases in effectiveness of both individual soldiers and units, [36] and Microsoft is known for using non-illegal tests that correlate with IQ tests as part of the interview process, weighing the results even more than experience in many cases. [37]

Some researchers have echoed the popular claim that "in economic terms it appears that the IQ score measures something with decreasing marginal value. It is important to have enough of it, but having lots and lots does not buy you that much." [38] [39]
However, some studies suggest IQ continues to confer significant benefits even at very high levels. [40] Ability and performance for jobs are linearly related, such that at all IQ levels, an increase in IQ translates into a concomitant increase in performance (Coward and Sackett, 1990). In an analysis of hundreds of siblings, it was found that IQ has a substantial effect on income independently of family background (Murray, 1998).

Other studies question the real-world importance of whatever is measured with IQ tests, especially for differences in accumulated wealth and general economic inequality in a nation. IQ correlates highly with school performance but the correlations decrease the closer one gets to real-world outcomes, like with job performance, and still lower with income. It explains less than one sixth of the income variance. [41] Even for school grades, other factors explain most the variance. One study found that, controlling for IQ across the entire population, 90 to 95 percent of economic inequality would continue to exist. [42]


Another recent study (2002) found that wealth, race, and schooling are important to the inheritance of economic status, but IQ is not a major contributor and the genetic transmission of IQ is even less important. [43] Some argue that IQ scores are used as an excuse for not trying to reduce poverty or otherwise improve living standards for all. Claimed low intelligence has historically been used to justify the feudal system and unequal treatment of women (but note that many studies find identical average IQs among men and women; see sex and intelligence). In contrast, others claim that the refusal of "high-IQ elites" to take IQ seriously as a cause of inequality is itself immoral. [44]

[edit] Public policy

Main article: Intelligence and public policy

Because public policy is often intended to influence the same outcomes (for example to improve education, fight poverty and crime, promote fairness in employment, and counter racial discrimination), policy decisions frequently interact with intelligence measures. In some cases, modern public policy references intelligence measures or even aims to alter cognitive development directly.


While broad consensus exists that intelligence measures neither dictate nor preclude any particular social policy, controversy surrounds many other aspects of this interaction. Central issues concern whether intelligence measures should be considered in policy decisions, the role of policy in influencing or accounting for group differences in measured intelligence, and the success of policies in light of individual and group intelligence differences. The importance and sensitivity of the policies at issue have produced an often-emotional ongoing debate spanning scholarly inquiry and the popular media from the national to the local level.

[edit] Use of IQ in the United States legal system

Title VII of the Civil Rights Act generally prohibits employment practices that are unfair or discriminatory. One provision of Title VII, codified at 42 USC 2000e-2(h), specifically provides that it is not an "unlawful employment practice for an employer to give and to act upon the results of any professionally developed ability test provided that such test, its administration or action upon the results is not designed, intended or used to discriminate because of race, color, religion, sex or national origin." This statute was interpreted by the Supreme Court in Griggs v. Duke Power Co., 401 US 424 (1971).

In Griggs, the Court ruled that the reliance solely on a general IQ test that was not found to be specifically relevant to the job at issue was a discriminatory practice where it had a "disparate impact" on hiring. The Court gave considerable weight in its ruling to an Equal Employment Opportunity Commission regulation interpreting Section 2002e-2(h)'s reference to a "professionally developed ability test" to mean "a test which fairly measures the knowledge or skills required by the particular job or class of jobs which the applicant seeks, or which fairly affords the employer a chance to measure the applicant's ability to perform a particular job or class of jobs." In other words, the use of any particular test would need to be shown to be relevant to the particular job or class of jobs at issue.


In the educational context, the 9th Circuit Court of Appeals interpreted similar state and federal statutes to require that IQ Tests not be used in a manner that was determinative of tracking students into classes designed for the mentally retarded. Larry P. v. Riles, 793 F.2d 969 (9th Cir. 1984).

The court specifically found that the tests involved were designed and standardized based on an all-white population, and had not undergone a legislatively mandated validation process. In addition, the court ruled that predictive validity for a general population is not sufficient, since the rights of an individual student were at issue, and emphasized that had the tests not been treated as controlling but instead used as part of a thorough and individualized assessment by a school psychologist a different result would have been obtained.

In September 1982, the judge in the Larry P. case, Federal District Judge Robert F. Peckham, relented in part in response to a lawsuit brought by black parents who wanted their children tested. The parents' attorney, Mark Bredemeier, said his clients viewed the modern special education offered by California schools today as helpful to children with learning disabilities, not a dead-end track, as parents contended in the original 1979 Larry P. case.


The Supreme Court of the United States has utilized IQ test results during the sentencing phase of some criminal proceedings. The Supreme Court case of Atkins v. Virginia, decided June 20, 2002, [45] held that executions of mentally retarded criminals are "cruel and unusual punishments" prohibited by the Eighth Amendment. In Atkins the court stated that

"…[I]t appears that even among those States that regularly execute offenders and that have no prohibition with regard to the mentally retarded, only five have executed offenders possessing a known IQ less than 70 since we decided Penry. The practice, therefore, has become truly unusual, and it is fair to say that a national consensus has developed against it."

In overturning the Virginia Supreme Court's holding, the Atkins opinion stated that petitioner's IQ result of 59 was a factor making the imposition of capital punishment a violation of his eighth amendment rights. In the opinion's notes the court provided some of the facts relied upon when reaching their decision


At the sentencing phase, Dr. Nelson testified: "Atkins' full scale IQ is 59. Compared to the population at large, that means less than one percentile…. Mental retardation is a relatively rare thing. It's about one percent of the population." App. 274. According to Dr. Nelson, Atkins' IQ score "would automatically qualify for Social Security disability income." Id., at 280. Dr. Nelson also indicated that of the over 40 capital defendants that he had evaluated, Atkins was only the second individual who met the criteria for mental retardation. Id., at 310. He testified that, in his opinion, Atkins' limited intellect had been a consistent feature throughout his life, and that his IQ score of 59 is not an "aberration, malingered result, or invalid test score." Id., at 308.


.
The Social Security Administration also uses IQ results when deciding disability claims. In certain cases, IQ results alone are used (in those cases where the result shows a "full scale IQ of 59 or less") and in other cases IQ results are used along with other factors (for a "full scale IQ of 60 through 70") when deciding whether a claimant qualifies for Social Security Disability benefits.[46]
In addition, because people with IQs below 80 (the 10th percentile, Department of Defense "Category V") are difficult to train, federal law bars their induction into the military. As of 2005, only 4 percent of the recruits were allowed to score as low as in the 16th to 30th percentile, a grouping known as "Category IV" on the U.S. Armed Forces' mental-aptitude exam. [47]
[edit] Validity and g-loading of specific tests
While IQ is sometimes treated as an end unto itself, scholarly work on IQ focuses to a large extent on IQ's validity, that is, the degree to which IQ predicts outcomes such as job performance, social pathologies, or academic achievement. Different IQ tests differ in their validity for various outcomes.
Tests also differ in their g-loading, which is the degree to which the test score reflects general mental ability rather than a specific skill or "group factor" such as verbal ability, spatial visualization, or mathematical reasoning). g-loading and validity have been observed to be related in the sense that most IQ tests derive their validity mostly or entirely from the degree to which they measure g (Jensen 1998).
[edit] Controversy
[edit] Social construct
This section does not cite its references or sources.
You can help Wikipedia by introducing appropriate citations.
Some maintain that IQ is a social construct invented by the privileged classes [citation needed], used to maintain their privilege.[citation needed] Others maintain that intelligence, measured by IQ or g, reflects a real ability, is a useful tool in performing life tasks and has a biological reality.
The social-construct and real-ability interpretations for IQ differences can be distinguished because they make opposite predictions about what would happen if people were given equal opportunities. The social explanation predicts that equal treatment will eliminate differences, while the real-ability explanation predicts that equal treatment will accentuate differences. Evidence for both outcomes exists. Achievement gaps persist in socioeconomically advantaged, integrated, liberal, suburban school districts in the United States (see Noguera, 2001). Test-score gaps tend to be larger at higher socioeconomic levels (Gottfredson, 2003). Some studies have reported a narrowing of score gaps over time.
The reduction of intelligence to a single score seems extreme and unrealistic to many people. Opponents argue that it is much more useful to know a person's strengths and weaknesses than to know a person's IQ score. Such opponents often cite the example of two people with the same overall IQ score but very different ability profiles.[citation needed] As measured by IQ tests, most people have highly balanced ability profiles, with differences in subscores being greater among the more intelligent.[citation needed] However, this assumes the ability of IQ tests to comprehensively gauge the wide variety of human intellectual abilities.
There are different types of IQ tests. Certainly the information described on this topic relates to a generic IQ test—against a general population, and therefore the results obtained are consistent across the population. However the results do not tell a full story, and are slanted towards 46,XX, and 46,XY candidates.[citation needed]
Candidates with Klinefelter's Syndrome, have a decreased frontal lobe, so for the most part have a reduced IQ when measured against the normal population (46,XX, and 46,XY candidates), but have an enhanced parietal lobe. If measured against IQ tests that are based on matching (patterns, shapes, colors, mathematical series, puzzles), some klinefelters measure into the genius level.[citation needed]
The creators of IQ testing did not intend for the tests to gauge a person's worth, and in many (or in all) situations, IQ may have little relevance. [citation needed]
[edit] The Mismeasure of Man
Some scientists dispute psychometrics entirely. In The Mismeasure of Man, a controversial book, professor Stephen Jay Gould argued that intelligence tests were based on faulty assumptions and showed their history of being used as the basis for scientific racism. He wrote:
…the abstraction of intelligence as a single entity, its location within the brain, its quantification as one number for each individual, and the use of these numbers to rank people in a single series of worthiness, invariably to find that oppressed and disadvantaged groups—races, classes, or sexes—are innately inferior and deserve their status. (pp. 24–25)
He spent much of the book criticizing the concept of IQ, including a historical discussion of how the IQ tests were created and a technical discussion of why g is simply a mathematical artifact. Later editions of the book included criticism of The Bell Curve, also a controversial book. Despite the many updates Gould made to his book, he did not discuss the modern usage of Magnetic Resonance Imaging (MRI) and other modern brain imaging techniques used in psychometrics.
Arthur Jensen, Professor of Educational Psychology, University of California, Berkeley, responded to Gould's criticisms in a paper titled The Debunking of Scientific Fossils and Straw Persons. [48]


[edit] The view of the American Psychological Association
In response to the controversy surrounding The Bell Curve, the American Psychological Association's Board of Scientific Affairs established a task force to write a consensus statement on the state of intelligence research which could be used by all sides as a basis for discussion. The full text of the report is available at a third-party website. [49]
The findings of the task force state that IQ scores do have high predictive validity for individual differences in school achievement. They confirm the predictive validity of IQ for adult occupational status, even when variables such as education and family background have been statistically controlled. They agree that individual (but specifically not population) differences in intelligence are substantially influenced by genetics.
They state there is little evidence to show that childhood diet influences intelligence except in cases of severe malnutrition. They agree that there are no significant differences between the average IQ scores of males and females. The task force agrees that large differences do exist between the average IQ scores of blacks and whites, and that these differences cannot be attributed to biases in test construction. While they admit there is no empirical evidence supporting it, the APA task force suggests that explanations based on social status and cultural differences may be possible. Regarding genetic causes, they noted that there is not much direct evidence on this point, but what little there is fails to support the genetic hypothesis.
The APA journal that published the statement, American Psychologist, subsequently published eleven critical responses in January 1997, most arguing that the report failed to examine adequately the evidence for partly-genetic explanations.
The report was published in 1995 and thus does not include a decade of recent research.
[edit] IQ test
This section does not cite its references or sources.
You can help Wikipedia by introducing appropriate citations.
The controversy over IQ tests (also called cognitive ability tests [citation needed]), what they measure, and what this means for society has not abated since their initial development by Alfred Binet.
IQ tests rely largely upon Symbolic Logic [citation needed] as a means to scoring, and as Symbolic Logic is not inherently synonymous with intelligence [citation needed], the question remains as to exactly what is being measured via such tests. For instance, it is feasible that someone could possess a prodigious wealth of emotional intelligence while being simultaneously unable to comprehend the significance of sequentially arranged shapes [citation needed]. Additionally, someone who cannot read would be at a significant disadvantage on an IQ test [citation needed], though illiteracy is not indicative of being unintelligent. Measurements of other forms of "intelligence" have been proposed to augment the current IQ Testing Methodology, though such alternative measurements may also be a subject of debate.
Some key issues in the debate include defining intelligence itself (see general intelligence factor) and the political ramification of findings.
Some proponents of IQ testing argue that lower scores by certain groups justify cutting back on welfare and programs like Head Start and New Deal. Many proponents believe different IQ scores demonstrate that power and wealth will always be distributed unequally. Critics claim that IQ tests do not measure intelligence, but rather a specific skill set valued by those who create IQ tests.
Various statistical studies have reported that income level, education level, nutrition level, race, and sex all correlate with IQ scores, but what this means is debated.
Some researchers have concluded from twin studies and adoption studies that IQ has high heritability, and this is often interpreted by the general public as meaning that there is an immutable genetic factor affecting or determining intelligence [citation needed]. This hereditarian interpretation fuels much of the controversy over books such as The Bell Curve, which claimed that various racial groups have lower or higher group intelligence than other racial and ethnic groups (East Asians and Ashkenazi Jews, according to The Bell Curve, are slightly more intelligent on the average than generic whites, whereas blacks on the average have slightly lower IQs) and suggested changing public policy as a result of these findings.
The degree to which nature versus nurture influences the development of human traits (especially intelligence) is one of the most intractable scholarly controversies of modern times.









[edit] Notes
Linda S. Gottfredson (November 1998). The General Intelligence Factor. Scientific American. Retrieved on August 6, 2006.
Cervilla et al (2004). Premorbid cognitive testing predicts the onset of dementia and Alzheimer's disease better than and independently of APOE genotype. Psychiatry 2004;75:1100-1106.. Retrieved on August 6, 2006.
^ Whalley and Deary (2001). Longitudinal cohort study of childhood IQ and survival up to age 76. British Medical Journal 2001, 322:819-819. Retrieved on August 6, 2006.
^ Cervilla et al (2004). Premorbid cognitive testing predicts the onset of dementia and Alzheimer's disease better than and independently of APOE genotype. Psychiatry 2004;75:1100-1106.. Retrieved on August 6, 2006.
^ Whalley and Deary (2001). Longitudinal cohort study of childhood IQ and survival up to age 76. British Medical Journal 2001, 322:819-819. Retrieved on August 6, 2006.
^ Jensen, A.R. (1979)
^ R. Plomin, N. L. Pedersen, P. Lichtenstein and G. E. McClearn (Volume 24, Number 3 / May, 1994). Variability and stability in cognitive abilities are largely genetic later in life. Behavior Genetics. Retrieved on August 6, 2006.
^ Neisser et al. (August 7, 1995). Intelligence: Knowns and Unknowns. Board of Scientific Affairs of the American Psychological Association. Retrieved on August 6, 2006.
^ Thomas J. Bouchard Jr.; David T. Lykken; Matthew McGue; Nancy L. Segal; Auke Tellegen (October 12, 1990). Minnesota Study of Twins Reared Apart. National Institutes of Health / Science, Oct 12, 1990 v250 n4978 p223(6). Retrieved on August 6, 2006.
^ David L. Kirp (July 23, 2006). After the Bell Curve. New York Times Magazine. Retrieved on August 6, 2006.
^ Plomin et al. (2001, 2003)
^ Plomin et al. (2001, 2003)
^ Shannon, RWJ (2003, 2004, 2005)
^ June 24, 2002 (Steve Sailer). IQ Defenders Feel Vindicated by Supreme Court. UPI. Retrieved on August 6, 2006.
^ Coleen A. Boyle, et.al. (April 19, 1996). Prevalence of Selected Developmental Disabilities in Children 3-10 Years of Age: the Metropolitan Atlanta Developmental Disabilities Surveillance Program, 1991. National Center for Environmental Health, Division of Birth Defects and Developmental Disabilities. Retrieved on August 6, 2006.
^ June 24, 2002 (Steve Sailer). IQ Defenders Feel Vindicated by Supreme Court. UPI. Retrieved on August 6, 2006.
^ Phillip McClean (1997,1999). Estimating the Offspring Phenotype. Quantitative Genetics. Retrieved on August 6, 2006.
^ Catharine R. Gale, PhD, Finbar J. O'Callaghan, PhD, Maria Bredow, MBChB, Christopher N. Martyn, DPhil and the Avon Longitudinal Study of Parents and Children Study Team (October 4, 2006). The Influence of Head Growth in Fetal Life, Infancy, and Childhood on Intelligence at the Ages of 4 and 8 Years. PEDIATRICS Vol. 118 No. 4 October 2006, pp. 1486-1492. Retrieved on August 6, 2006.
^ Jeremy R. Gray, Psychology Department, Yale University, and Paul M. Thompson, Laboratory of Nero Imaging, Department of Neurology, University of California, Los Angeles School of Medicine (June 2004). Neurobiology of Intelligence: Science and Ethics. Nature Publishing Group, Volume 5. Retrieved on August 6, 2006.
^ Richard Haier (July 19, 2004). Human Intelligence Determined by Volume and Location of Gray Matter Tissue in Brain. Brain Research Institute, UC Irvine College of Medicine. Retrieved on August 6, 2006.
^ Nicholas Wade (March 30, 2006). Scans Show Different Growth for Intelligent Brains. Brain Research Institute, UCLA. Retrieved on August 6, 2006.
^ The end of the Flynn Effect. A study of secular trends in mean intelligence scores of Norwegian conscripts during half a century.. Retrieved on August 6, 2006.
^ A long-term rise and recent decline in intelligence test performance: The Flynn Effect in reverse.. Retrieved on August 6, 2006.
^ Children are less able than they used to be. Retrieved on August 6, 2006.
^ Gottfredson et al. 1994 (ctrl+f "groups")
^ Neisser et al. (August 7, 1995). Intelligence: Knowns and Unknowns. Board of Scientific Affairs of the American Psychological Association. Retrieved on August 6, 2006.
^ The controversy itself has caused some scientists to debate whether such fields of inquiry are not scientific, or whether group differences in traits are just another area of the science of human nature, as Steven Pinker and others argue. (See Race and intelligence#Utility of research and racism.)
^ Naomi Breslau, PhD; Victoria C. Lucia, PhD; German F. Alvarado, MD, MPH (11, November 2006). Intelligence and Other Predisposing Factors in Exposure to Trauma and Posttraumatic Stress Disorder. A Follow-up Study at Age 17 Years. Arch Gen Psychiatry. 2006;63:1238-1245. Retrieved on August 6, 2006.
^ GT_DM_5b.pdf (PDF).
^ Whalley and Deary (2001). Longitudinal cohort study of childhood IQ and survival up to age 76. British Medical Journal 2001, 322:819-819. Retrieved on August 6, 2006.
^ Cervilla et al (2004). Premorbid cognitive testing predicts the onset of dementia and Alzheimer's disease better than and independently of APOE genotype. Psychiatry 2004;75:1100-1106.. Retrieved on August 6, 2006.
^ Dorene Rentz, Brigham and Women's Hospital's Department of Neurology and Harvard Medical School. More Sensitive Test Norms Better Predict Who Might Develop Alzheimer's Disease. Neuropsychology, published by the American Psychological Association. Retrieved on August 6, 2006.
\^ Whalley et al. (2000). Childhood mental ability and dementia. Neurology 2000;55:1455-1459.. Retrieved on August 6, 2006.
^ Geoff Der, G David Batty, Ian J. Deary (2006). Effect of breast feeding on intelligence in children: prospective study, sibling pairs analysis, and meta-analysis (Abstract). British Medical Journal.
^ Michael A. McDaniel, Virginia Commonwealth University (accepted for publication August 2006). Estimating state IQ: Measurement challenges and preliminary correlates (PDF). Intelligence.
^ RAND_TR193.pdf (PDF)., MR818.ch2.pdf (PDF).
^ Rich Karlgaard (October 31, 2005). Talent Wars. Forbes. Retrieved on August 6, 2006.
^ Detterman and Daniel, 1989.
^ Earl Hunt. The Role of Intelligence in Modern Society pp. 4 (Nonlinearities in Intelligence). American Scientist. Retrieved on August 6, 2006.
^ Top1in10000.pdf (PDF). Retrieved on August 6, 2006.
^ Neisser et al. (August 7, 1995). Intelligence: Knowns and Unknowns. Board of Scientific Affairs of the American Psychological Association. Retrieved on August 6, 2006.
^ IQ best predicts if you will succeed or fail in life. Retrieved on August 6, 2006.
^ intergen.pdf (PDF). Retrieved on August 6, 2006.
^ Steve Sailer. How to Help the Left Half of the Bell Curve. VDARE.com. Retrieved on August 6, 2006.
^ DARYL RENARD ATKINS, PETITIONER v. VIRGINIA (June 20, 2002). Retrieved on August 6, 2006.
^ SOCIAL SECURITY ADMINISTRATION.
^ DoD (September 20, 2005). Department of Defense INSTRUCTION, Number 1145.01. Retrieved on August 6, 2006.
^ Jensen, Arthur (1982). "The Debunking of Scientific Fossils and Straw Persons". Contemporary Education Review 1 (2): 121-135. Retrieved on 2006-08-06.
^ Neisser et al. (August 7, 19). Intelligence: Knowns and Unknowns. Board of Scientific Affairs of the American Psychological Association. Retrieved on August 6, 2006.
[edit] See also
• High IQ Societies
• Nature versus nurture
• Emotional intelligence
• Theory of multiple intelligences
• Gifted
• SAT
• Graduate Record Examination
[edit] References
• Carroll, J.B. (1993). Human cognitive abilities: A survey of factor-analytical studies. New York: Cambridge University Press.
• Coward, W.M. and Sackett, P.R. (1990). Linearity of ability-performance relationships: A reconfirmation. Journal of Applied Psychology, 75:297–300.
• Duncan, J., P. Burgess, and H. Emslie (1995) Fluid intelligence after frontal lobe lesions. Neuropsychologia, 33(3): p. 261-8.
• Duncan, J., et al., A neural basis for general intelligence. Science, 2000. 289(5478): p. 457-60.
• Flynn, J.R. (1999). Searching for Justice: The discovery of IQ gains over time. American Psychologist, v. 54, p. 5-20
• Frey, M.C. and Detterman, D.K. (2003) Scholastic Assessment or g? The Relationship Between the Scholastic Assessment Test and General Cognitive Ability. Psychological Science, 15(6):373–378. PDF
• Gottfredson, L. S. (1997). "Why g matters: The complexity of everyday life." Intelligence, 24(1), 79–132. PDF
• Gottfredson, L.S. (1998). The general intelligence factor. Scientific American Presents, 9(4):24–29. PDF
• Gottfredson, L. S. (2005). Suppressing intelligence research: Hurting those we intend to help. In R. H. Wright & N. A. Cummings (Eds.), Destructive trends in mental health: The well-intentioned path to harm (pp. 155–186). New York: Taylor and Francis. Pre-print PDF PDF
• Gottfredson, L. S. (in press). "Social consequences of group differences in cognitive ability (Consequencias sociais das diferencas de grupo em habilidade cognitiva)". In C. E. Flores-Mendoza & R. Colom (Eds.), Introdução à psicologia das diferenças individuais. Porto Alegre, Brazil: ArtMed Publishers. PDF
• Gray, J.R., C.F. Chabris, and T.S. Braver, Neural mechanisms of general fluid intelligence. Nat Neurosci, 2003. 6(3): p. 316-22.
• Gray, J.R. and P.M. Thompson, Neurobiology of intelligence: science and ethics. Nat Rev Neurosci, 2004. 5(6): p. 471-82.
• Haier RJ, Jung RE, Yeo RA, et al. (2005). "The neuroanatomy of general intelligence: sex matters". NeuroImage 25: 320–327.
• Harris, J. R. (1998). The nurture assumption : why children turn out the way they do. New York, Free Press.
• Hunt, E. (2001). Multiple views of multiple intelligence. [Review of Intelligence Reframed: Multiple Intelligences for the 21st Century.]
• Jensen, A.R. (1979). Bias in mental testing. New York: Free Press.
• Jensen, A.R. (1998). The g Factor. Praeger, Connecticut, USA.
• Jensen, A.R. (2006). "Clocking the Mind: Mental Chronometry and Individual Differences." Elsevier Science. --->New release scheduled for early June, 2006.
• Klingberg, T., Forssberg, H., & Westerberg, H. (2002). Training of working memory in children with ADHD. Journal of Clinical & Experimental Neuropsychology, 24, 781-791.
• McClearn, G. E., Johansson, B., Berg, S., Pedersen, N. L., Ahern, F., Petrill, S. A., & Plomin, R. (1997). Substantial genetic influence on cognitive abilities in twins 80 or more years old. Science, 276, 1560–1563.
• McDaniel, M.A. (2005) Big-brained people are smarter: A meta-analysis of the relationship between in vivo brain volume and intelligence. Intelligence, 33, 337-346.
• Mingroni, M.A. (2004). "The secular rise in IQ: Giving heterosis a closer look". Intelligence 32: 65–83.
• Murray, Charles (1998). Income Inequality and IQ, AEI Press PDF
• Noguera, P.A. (2001). Racial politics and the elusive quest for excellence and equity in education. In Motion Magazine article
• Plomin, R., DeFries, J. C., Craig, I. W., & McGuffin, P. (2003). Behavioral genetics in the postgenomic era. Washington, DC: American Psychological Association.
• Plomin, R., DeFries, J. C., McClearn, G. E., & McGuffin, P. (2001). Behavioral genetics (4th ed.). New York: Worth Publishers.
• Rowe, D. C., W. J. Vesterdal, and J. L. Rodgers, "The Bell Curve Revisited: How Genes and Shared Environment Mediate IQ-SES Associations," University of Arizona, 1997
• Schoenemann, P.T., M.J. Sheehan, and L.D. Glotzer, Prefrontal white matter volume is disproportionately larger in humans than in other primates. Nat Neurosci, 2005.
• Shaw P, Greenstein D, Lerch J, Clasen L, Lenroot R, Gogtay N, Evans A, Rapoport J, and Giedd J (2006), "Intellectual ability and cortical development in children and adolescents". Nature 440, 676-679.
• Tambs K, Sundet JM, Magnus P, Berg K. "Genetic and environmental contributions to the covariance between occupational status, educational attainment, and IQ: a study of twins." Behav Genet. 1989 Mar;19(2):209–22. PMID 2719624.
• Thompson, P.M., Cannon, T.D., Narr, K.L., Van Erp, T., Poutanen, V.-P., Huttunen, M., Lönnqvist, J., Standertskjöld-Nordenstam, C.-G., Kaprio, J., Khaledy, M., Dail, R., Zoumalan, C.I., Toga, A.W. (2001). "Genetic influences on brain structure." Nature Neuroscience 4, 1253-1258.
[edit] External links
[edit] Collective statements
• The Wall Street Journal: Mainstream Science on Intelligence
• PDF Reprint - Mainstream science on intelligence: An editorial with 52 signatories, history, and bibliography.
• APA: Intelligence: Knowns and Unknowns
• APA Committee on Online Psychological Tests and Assessment report
[edit] Review papers
• Scientific American: The General Intelligence Factor
• Scientific American: Intelligence Considered
• Neurobiology of Intelligence: Science and Ethics PDF
[edit] Professional Intelligence Testing
• "Scans Show Different Growth for Intelligent Brains", New York Times, March 30, 2006
Retrieved from "http://en.wikipedia.org/wiki/Intelligence_quotient"
Categories: Articles with unsourced stateme





Low IQs are Africa's curse, says lecturer


Researcher accused of promoting racist stereotype wins backing from LSE

Denis Campbell
Sunday November 5, 2006
The Observer
The London School of Economics is embroiled in a row over academic freedom after one of its lecturers published a paper alleging that African states were poor and suffered chronic ill-health because their populations were less intelligent than people in richer countries.

Satoshi Kanazawa, an evolutionary psychologist, is now accused of reviving the politics of eugenics by publishing the research which concludes that low IQ levels, rather than poverty and disease, are the reason why life expectancy is low and infant mortality high. His paper, published in the British Journal of Health Psychology, compares IQ scores with indicators of ill health in 126 countries and claims that nations at the top of the ill health league also have the lowest intelligence ratings.

Paul Collins, a spokesman for War On Want, the international development charity, said the research 'runs the risk of resurrecting the racist stereotype that Africans are responsible for their own plight, and may reinforce prejudices that Africans are less intelligent'.
Collins added: 'The notion that people in poor countries have inferior intelligence has been disproved by much research in the past. This is another example, which other academics will shoot down.'

Philippa Atkinson, who chairs the LSE student union's 85-strong Africa Forum and teaches in the school's Department of Government, said the paper 'reflects the now discredited theories of eugenics, which should have been left behind'.

'Eugenics was a very influential discourse for centuries,' she said. 'It's the discourse that colonialism and racism in America until the Sixties were based on, and was part of the basis of apartheid too. Nobody could prove that there are racial or national differences in IQ. It's very, very controversial to say that national IQ levels are low in Africa, and completely unproven. It's a surprise that the odd person would try to bring it back,' she said.

However, she said the research contained some interesting ideas and merited serious consideration, and stressed that academics such as Kanazawa should not be deterred from exploring controversial subjects.

The reaction to Kanazawa's paper will reopen the simmering debate about whether academics are entitled to express opinions that many people may find offensive.
The Observer revealed last March that Frank Ellis, a lecturer in Russian and Slavonic studies at Leeds University, supported the Bell Curve theory, which holds that black people are less intelligent than whites. He also believed that women did not have the same intellectual capacity as men and backed the 'humane' repatriation of ethnic minorities. Initially, the university backed Ellis, despite protests by students and teaching staff, but he took early retirement in July.

Kanazawa declined to comment on either War on Want or Atkinson's allegations about reviving eugenics because, he said, other academics had come up with the national IQ scores that underpinned his analysis of 126 countries. In the paper he cites Ethiopia's national IQ of 63, the world's lowest, and the fact that men and women are only expected to live until their mid-40s as an example of his finding that intelligence is the main determinant of someone's health.

Having examined the effects of economic development and income inequality on health, he was 'surprised' to find that IQ had a much more important impact, he said. 'Poverty, lack of sanitation, clean water, education and healthcare do not increase health and longevity, and nor does economic development.'

The LSE declined to offer any opinion on Kanazawa's conclusions but defended his right to publish controversial research. A spokeswoman said: 'This is academic research by Dr Kanazawa based on empirical data and published in a peer-reviewed journal. People may agree or disagree with his findings and are at liberty to voice their opinions to him. The school does not take any institutional view on the work of individual academics.'
Kate Raworth, a senior researcher with Oxfam, said it was 'ridiculous' for Kanazawa to blame ill health on low IQ and 'very irresponsible' to reach such conclusions using questionable and 'fragile' international data on national IQ levels.

Rumit Shah, chairman of the LSE student union's 52-member Kenyan Society, said lack of education was probably one reason why many Kenyans die young. Aids, tuberculosis and malaria were key factors too.

Kanazawa's article was a 'misrepresentation' of the true causes of ill health in Kenya, added Shah. 'It portrays a bad picture of Kenya, because not everyone in Kenya has an IQ of 72. If there was more education, Kenyans would be wiser about their health.'






Belai Habte-Jesus, MD, MPH
Global Strategic Enterprises, Inc;e-mail:globalbelai@yahoo.com; Telephone: 703 933 8737

CONFIDENTIALITY NOTICE: This electronic message, including any attachment(s), is intended only for the person or entity to which it is addressed and may contain confidential and/or privileged material. .


Dorina Asmanio wrote:

Low IQs are Africa's curse, says lecturer
Researcher accused of promoting racist stereotype wins backing from LSE
Denis Campbell
Sunday November 5, 2006
The Observer
Photo Credit The London School of Economics (LSE)


The London School of Economics is embroiled in a row over academic freedom after one of its lecturers published a paper alleging that African states were poor and suffered chronic ill-health because their populations were less intelligent than people in richer countries.
Satoshi Kanazawa, an evolutionary psychologist, is now accused of reviving the politics of eugenics by publishing the research which concludes that low IQ levels, rather than poverty and disease, are the reason why life expectancy is low and infant mortality high. His paper, published in the British Journal of Health Psychology, compares IQ scores with indicators of ill health in 126 countries and claims that nations at the top of the ill health league also have the lowest intelligence ratings.
In the paper he cites Ethiopia's national IQ of 63
Paul Collins, a spokesman for War On Want, the international development charity, said the research 'runs the risk of resurrecting the racist stereotype that Africans are responsible for their own plight, and may reinforce prejudices that Africans are less intelligent'.

Collins added: 'The notion that people in poor countries have inferior intelligence has been disproved by much research in the past. This is another example, which other academics will shoot down.'

Philippa Atkinson, who chairs the LSE student union's 85-strong Africa Forum and teaches in the school's Department of Government, said the paper 'reflects the now discredited theories of eugenics, which should have been left behind'.
'Eugenics was a very influential discourse for centuries,' she said. 'It's the discourse that colonialism and racism in America until the Sixties were based on, and was part of the basis of apartheid too. Nobody could prove that there are racial or national differences in IQ. It's very, very controversial to say that national IQ levels are low in Africa , and completely unproven. It's a surprise that the odd person would try to bring it back,' she said.

However, she said the research contained some interesting ideas and merited serious consideration, and stressed that academics such as Kanazawa should not be deterred from exploring controversial subjects.

The reaction to Kanazawa 's paper will reopen the simmering debate about whether academics are entitled to express opinions that many people may find offensive.
The Observer revealed last March that Frank Ellis, a lecturer in Russian and Slavonic studies at Leeds University , supported the Bell Curve theory, which holds that black people are less intelligent than whites. He also believed that women did not have the same intellectual capacity as men and backed the 'humane' repatriation of ethnic minorities. Initially, the university backed Ellis, despite protests by students and teaching staff, but he took early retirement in July.

Kanazawa declined to comment on either War on Want or Atkinson's allegations about reviving eugenics because, he said, other academics had come up with the national IQ scores that underpinned his analysis of 126 countries. In the paper he cites Ethiopia 's national IQ of 63, the world's lowest, and the fact that men and women are only expected to live until their mid-40s as an example of his finding that intelligence is the main determinant of someone's health.

Having examined the effects of economic development and income inequality on health, he was 'surprised' to find that IQ had a much more important impact, he said. 'Poverty, lack of sanitation, clean water, education and healthcare do not increase health and longevity, and nor does economic development.'

The LSE declined to offer any opinion on Kanazawa 's conclusions but defended his right to publish controversial research. A spokeswoman said: 'This is academic research by Dr Kanazawa based on empirical data and published in a peer-reviewed journal. People may agree or disagree with his findings and are at liberty to voice their opinions to him. The school does not take any institutional view on the work of individual academics.'

Kate Raworth, a senior researcher with Oxfam, said it was 'ridiculous' for Kanazawa to blame ill health on low IQ and 'very irresponsible' to reach such conclusions using questionable and 'fragile' international data on national IQ levels.

Rumit Shah, chairman of the LSE student union's 52-member Kenyan Society, said lack of education was probably one reason why many Kenyans die young. Aids, tuberculosis and malaria were key factors too.

Kanazawa 's article was a 'misrepresentation' of the true causes of ill health in Kenya , added Shah. 'It portrays a bad picture of Kenya , because not everyone in Kenya has an IQ of 72. If there was more education, Kenyans would be wiser about their health.'
---------------
Contact info for Dr. Satoshi Kanazawa
s.kanazawa@lse.ac.uk
LSE phone number: 020 7955 7297
WebSite
---------------
Related Links

Average person in Ethiopia retarded? What?!
Mild mental retardation: IQ 50–55 to 70
Moderate retardation: IQ 35–40 to 50–55;
Severe mental retardation: IQ 20–25 to 35–40
Profound mental retardation: IQ below 20–25
Source: Wikipedia
-----------------------------
The British Journal of Health Psychology
Mind the gap…in intelligence: Re-examining the relationship between inequality and health
Author: Kanazawa , Satoshi1
Source: British Journal of Health Psychology, Volume 11, Number 4, November 2006, pp. 623-642(20)


Belai Habte-Jesus, MD, MPH
Global Strategic Enterprises, Inc; e-mail:globalbelai@yahoo.com; Telephone: 703 933 8737

CONFIDENTIALITY NOTICE: This electronic message, including any attachment(s), is intended only for the person or entity to which it is addressed and may contain confidential and/or privileged material. .


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Dear All

in relation to the recent controversy of this guy from LSE. I'd like to proudly bring to your attention a forthcoming review of Dr. Girma Berhanu from Goteborg University for the controversial book "IQ and the Wealth of Nations" by Lynn and Vanhanen from which Kanazawa from LSE copied the alleged national IQ's. As recalled, Lynn and Vanhanen calculated 63 as the national IQ of Ethiopia (the lowest in the world) and it turns out that they did so on the basis of test results from Ethiopian-Jewish young students in Israel (a fact that was brought to my attention by Dr. Girma) which in itself is outrageous!


you can read the abstract for his review and also a letter he sent to the journal's editor.
I really thank Dr. Girma Berhanu for taking the initiative to challenge these racist views that unfortunately many find still to be appropriate to entertain in higher educational and academic institutions.

here is what i wrote on Kanazawa's article: http://www.ethrev.com/articles/Nov2006/DanielAlemu_11082006.html
Thanks,
Daniel Alemu,
London


Black Intellectual genocide: When does all this ‘?abstract atrocities’ end?
A Response to “IQ and the Wealth of Nations” by Richard Lynn & Tatu Vanhanen
Girma Berhanu Department of Education
Göteborg University
> > Box 300, SE 405 30
> > Göteborg, Sweden
> > Tel. +46 (0) 31-7732325
> > Fax +46 (0) 31-7732315
> > E-mail: Girma.Berhanu@ped.gu.se



Intelligent Quotient and the Wealth of Nations

Abstract

This paper is a response to the book ”IQ and the wealth of nations” written by Richard Lynn & Tatu Vanhanen. It is a critique of the authors’ major assertion that a significant part of the gap between rich and poor countries is due to differences in national intelligence. (The authors claim that they have evidence that differences in national IQ account for the substantial variation in national per capita income and growth).

This paper debunks their assumptions that intellectual and income differences between nations stems from genetic differences. This critique provides an extended review of the research literature that tells different stories (from what the authors postulate) about the concept of intelligence, what IQ measures and does not measure. The paper exposes the racist, sexist and antihuman nature of the research tradition in which the authors anchored their studies and the deep methodological flaw, and theoretical assumptions used in their book.

The low standards of scholarship evident in the book render it largely irrelevant for modern science. This paper has specifically dealt with the IQ value of Ethiopian immigrants that came from Israel, used by the authors as representing the National Average IQ of Ethiopia. Most of these immigrants hade rudimentary knowledge of literacy, and experienced abrupt transition from rural Ethiopia to Israel with all the accompanying effects that it entails such as trauma, dislocation and cultural shock. The test was conducted a few months after their arrival. That specific study (conducted by two Israelis) that assigns low IQ for the immigrants is also replete with technical/statistical errors to say the least. The paper concludes that this is tantamount to intellectual genocide deserving a legal treatment by the International Court of Justice.
Keywords: Scientific racism, Mental (IQ) testing, Intelligence, Economic development, Intellectual Genocide the request for the review of the book:

(1)The book I want to comment on is entitled”IQ and the wealth of
nations”. It is written by Richard Lynn (prof. emeritus of psychology at the
University of Ulster, North Ireland) and Tatu Vanhanen (prof. emeritus of
political science at the University of Tampere in Finland). I came to
notice the debate surrounding the book this past summer during my holiday
in Finland. The second author, Prof. Vanhanen, was interviewed by a Finnish
journalist (s) about the book and he expressed his view that IQ and the
wealth of nations are strongly correlated and the reason why some countries
are poor has to do with their IQ. He further indicated that IQ is
substantially heritable and racial differences in intelligence are not a myth
but a fact of life. His statement also carried the message that poor
countries should blame themselves for their poverty. His outrageous
statements were widely criticized by Finnish media and have been the subject
of hot debate during this past summer.

I presume the issue became interesting not really because the governing elite is genuinely concerned about the cultural / political message that he conveyed but because the man is the father of the current prime minister of Finland. And it was the opposition party that instigated the debate which in many ways embarrassed the prime minister. The prime minister commented “my father is a bit confused because of age”. This is just to tell you how I came to read the book.
The authors argue that a significant part of the gap between rich and poor
countries is due to differences in national intelligence. Their hypothesis
is that the intelligence of the populations has been a major factor responsible
for the national differences in economic growth and the gap in per capita
income between rich and poor nations The argument is line with Arthur R. Jensen’s controversial article in Harvard Educational Review (1969) through to Richard Herrnstein and
Charles Murray’s (1994) book, The Bell curve and J. Philippe Ruston’s book
Race, evolution and behavior (?). The difference is that these studies
attempt to document the relationship between IQ and individual achievement
and racial differences in intelligence where as Lynn and Vanhanen have
scaled this connection up to a national level. The authors ridicule
enrichment programmes and cognitive education aimed at raising school
performance among disadvantaged children.

To get to my point, the IQ figure which stood to represent Ethiopia came
from Israel, not directly from Ethiopia[1]. It is very likely that a few of
them (I mean ‘the people whose apparent IQ levels were used’) were my friends. Most of these students (250) who are described in Lynn’s and Vanhanen’s book as having IQs of 63 are presently having a satisfying life and are occupationally competent and socially adequate. (They
are in their late 20s or early 30s.) I am confident that some of them have
done their first (and second) degrees, if not in Israel in the USA. As many of
us know, these young immigrants were new arrivals, malnourished, unfamiliar
with “western school based skills”; they had lived as refugees in the Sudan under
hard poverty, while in Ethiopia they lived most of their life in isolation
from and suffering discrimination from the dominant Christian neighbors, and many lost their parents during the mysterious journey to Israel; they were “saved”
through a dramatic life-saving operation by Mossad. Most of these young people had rudimentary knowledge of formal education and the Hebrew language, and had followed a very traditional way of life while in Ethiopia, so the dramatic and abrupt transition from village life in Ethiopia to Israel which occurred en masse was accompanied by adjustment crises which in turn immensely affected their learning and integration in to Israeli society. The authors
tested these young people and concluded that the average Ethiopian IQ is 63.
What is outrageous about the book is its emphasis on one direction of
causation ie a high IQ is the cause of a high income and intellectual and
income differences between nations stems from genetic differences. “… we
believe that national differences in intelligence have a substantial
genetic basis…” (p.193 ) Do they have the data to substantiate this claim? None, except for a fragmented, undocumented and extremely over-simplified assertion about the effects of trans-racial adoption and a few twin studies. The distorted data allows them to talk only about the strength of relationships not cause and effect relationships.
With kindest regards!
Girma Berhanu
[1] (see Kaniel, Shlomo; Fisherman, Shraga.
Title Level of performance and distribution of errors in the Progressive Matrices test: A comparison of Ethiopian immigrant and native Israeli adolescents.

Source
International Journal of Psychology. Vol 26(1) 1991, 25-33


IQ and the Wealth of Nations
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IQ and the Wealth of Nations
IQ and the Wealth of Nations is a controversial 2002 book by Dr. Richard Lynn, Professor Emeritus of Psychology at the University of Ulster, Northern Ireland, and Dr. Tatu Vanhanen, Professor Emeritus of Political Science at the University of Tampere, Tampere, Finland. The book demonstrates that differences in national income (in the form of per capita gross domestic product) correlate with, and arguably attributes it to, differences in average national IQ.
The book was followed by Lynn's 2006 Race Differences in Intelligence, which expands the data by nearly four times and concludes the average human IQ is presently 90 when compared to a norm of 100 based on UK data, or two thirds of a standard deviation below the UK norm.
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[edit] Outline


The central thesis of IQ and the Wealth of Nations is that the average IQ of a nation correlates with its GDP. Above is a scatterplot with Lynn and Vanhanen's IQ figures and estimates² (explained below) plotted against 2004 per capita GDP (PPP), as reported by the IMF.³ Similar diagrams appear in the book.
The book includes the authors' estimates of average IQ scores for each country, based on their analysis of published reports; their observation that national gross domestic product per capita is correlated with IQ; and their conclusion that the IQ differences correlated with income differences by a factor of about 0.7, meaning that IQ explains more than half of the variation in per capita GDP.
The authors stated that they believe IQ is due to both genetic and environmental factors. They also stated that low GDP can cause low IQ, just as low IQ can cause low GDP. (See: Positive feedback)
The authors argued that it is the ethical responsibility of rich, high-IQ nations to financially assist poor, low-IQ nations, as it is the responsibility of rich citizens to assist the poor.
The book was cited several times in the popular press, notably the British conservative newspaper The Times. Because Tatu Vanhanen is the father of Matti Vanhanen, the Finnish Prime minister, his work has received wide publicity in Finland.
[edit] National IQ estimates
Central to the book's thesis is a tabulation of what Lynn and Vanhanen believe to be the average IQs of the world's nations. Rather than do their own IQ studies (a potentially massive project), the authors average and adjust existing studies.
For most of the 185 nations, no reliable studies are available. In those cases, the authors have used an estimated value by taking averages of the IQs of surrounding nations. For example, the authors arrived at a figure of 84 for El Salvador by averaging their calculations of 79 for Guatemala and 88 for Colombia. Those estimates are not included in the calculations of income differences and do not appear in the table below.
Several cases merit specific attention. To obtain a figure for South Africa, the authors averaged IQ studies done on different ethnic groups, resulting in a figure of 72. The figures for Colombia, Peru and Singapore were arrived at in a similar manner. For People's Republic of China, the authors used a figure of 109.4 for Shanghai and adjusted it down by an arbitrary 6 points because they believed the average across China's rural areas was probably less than that in Shanghai. Another figure from a study done in Beijing was not adjusted downwards. Those two studies formed the resultant score for China (PRC).
In many cases, the IQ of a country is estimated by averaging the IQs of "neighboring countries" that are not actually neighbors of the country in question. For example, Kyrgyzstan's IQ is estimated by averaging the IQs of Iran and Turkey, neither of which is close to Kyrgyzstan – China, which is a neighbor, is not counted as such by Lynn and Vanhanen. Such arbitrary selections of "neighbors" raise additional questions as to the objectivity of the IQ estimates.[citation needed]
To account for the Flynn effect (an increase in IQ scores over time), the authors sometimes adjusted the results of older studies upward by an arbitrary number of points. Because of these arbitrary adjustments and the fact that only limited data were available for most nations, the figures should be considered rough estimates.[citation needed]
Country IQ estimate Country IQ estimate Country IQ estimate
Hong Kong (PRC)
107 Russia
96 Fiji
84
South Korea
106 Slovakia
96 Iran
84
Japan
105 Uruguay
96 Marshall Islands
84
Taiwan (ROC)
104 Portugal
95 Puerto Rico (US)
84
Singapore
103 Slovenia
95 Egypt
83
Austria
102 Israel
94 India
81
Germany
102 Romania
94 Ecuador
80
Italy
102 Bulgaria
93 Guatemala
79
Netherlands
102 Ireland
93 Barbados
78
Sweden
101 Greece
92 Nepal
78
Switzerland
101 Malaysia
92 Qatar
78
Belgium
100 Thailand
91 Zambia
77
China (PRC)
100 Croatia
90 Congo-Brazzaville
73
New Zealand
100 Peru
90 Uganda
73
United Kingdom
100 Turkey
90 Jamaica
72
Hungary
99 Indonesia
89 Kenya
72
Poland
99 Suriname
89 South Africa
72
Australia
98 Colombia
89 Sudan
72
Denmark
98 Brazil
87 Tanzania
72
France
98 Iraq
87 Ghana
71
Norway
98 Mexico
87 Nigeria
67
United States
98 Samoa
87 Guinea
66
Canada
97 Tonga
87 Zimbabwe
66
Czech Republic
97 Lebanon
86 Congo-Kinshasa
65
Finland
97 Philippines
86 Sierra Leone
64
Spain
97 Cuba
85 Ethiopia
63
Argentina
96 Morocco
85 Equatorial Guinea
59
[edit] Special cases
In several cases, actual GDP did not correspond with that predicted by IQ. In these cases, the authors argued that differences in GDP were caused by differences in natural resources and whether the nation used a "planned" or "market" economy.
One example of this was Qatar, whose IQ was estimated by Lynn and Vanhanen to be about 78, yet had a disproportionately high per capita GDP of roughly USD $17,000. The authors explain Qatar's disproportionately high GDP by its high petroleum resources. Similarly, the authors think that large resources of diamonds explain the economic growth of the African nation Botswana, the fastest in the world for several decades.
The authors argued that the People's Republic of China's per capita GDP of roughly USD $4,500 could be explained by its use of a communist economic system for much of its recent history. The authors also predicted that communist nations who they believe have comparatively higher IQs, including the PRC, Vietnam, and North Korea, can be expected to gain GDP by moving from centrally-planned to market economic systems, while predicting continued poverty for African nations. Recent trends in the economy of the People's Republic of China seem to confirm this prediction, as China's GDP has quadrupled since market reforms in 1978.
[edit] Peer-reviewed papers using IQ scores from the book
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Like many books, IQatWoN's results were not peer-reviewed, but peer review has occurred in subsequent articles.
A review of the book in Contemporary Psychology (49 (4). pp389-395. Barnett, Susan M.; Williams, Wendy) stated: "In sum, we see an edifice built on layer upon layer of arbitrary assumptions and selective data manipulation. The data on which the entire book is based are of questionably validity and are used in ways that cannot be justified."
The book is sharply criticized in a peer-reviewed paper The Impact of National IQ on Income and Growth [1]. Although critical of the IQ data, for the sake of argument the paper assumes that the data is correct but then criticizes the statistical methods used, finding no effect on growth or income.
Another peer-reviewed paper with the same assumption, Intelligence, Human Capital, and Economic Growth: An Extreme-Bounds Analysis [2], finds a strong connection between intelligence and economic growth, although the paper makes no explicit claim that IQ explains most of the difference in growth between nations.
In a reanalysis of the Lynn and Vanhanen's hypothesis, Dickerson (in press) finds that IQ and GDP data is best fitted by an exponential function, with IQ explaining approximately 70% of the variation in GDP. Dickerson concludes that as a rough approximation "an increase of 10 points in mean IQ results in a doubling of the per capita GDP."
Whetzel and McDaniel (2006) conclude that the book's "results regarding the relationship between IQ, democracy and economic freedom are robust". Moreover, they address "criticisms concerning the measurement of IQ in purportedly low IQ countries", finding that by setting "all IQ scores below 90 to equal 90, the relationship between IQ and wealth of nations remained strong and actually increased in magnitude." On this question they conclude that their findings "argue against claims made by some that inaccuracies in IQ estimation of low IQ countries invalidate conclusions about the relationship between IQ and national wealth."
Voracek (2004) used the national IQ data to examine the relationship between intelligence and suicide, finding national IQ was positively correlated with national male and female suicide rates. The effect was not attenuated by controlling for GDP.
Barber (2005) found that national IQ was associated with rates of secondary education enrollment, illiteracy, and agricultural employment. The effect on illiteracy and agricultural employment remained with national wealth, infant mortality, and geographic continent controlled.
Both Lynn and Rushton have suggested that high IQ is associated with colder climates. To test this hypothesis, Templer and Arikawa 2006 compare the national IQ data from Lynn and Vanhanen with data sets that describe national average skin color and average winter and summer temperatures (see also discussion [3]). They find that the strongest correlations to national IQ were −0.92 for skin color and −0.76 for average high winter temperature. They interpret this finding as strong support for IQ-climate association. Templer and Arikawa 2006 is currently listed as the most downloaded article in Intelligence at ScienceDirect (Jan. - March 2006).[4] Other studies using different data sets find no correlation [5][6].
Kanazawa (2006), "IQ and the wealth of states" (in press in Intelligence), replicates across U.S. states Lynn and Vanhanen's demonstration that national IQs strongly correlate with macroeconomic performance. Kanazawa finds that state cognitive ability scores, based on the SAT data, correlate moderately with state economic performance, explaining about a quarter of the variance in gross state product per capita.[7]
[edit] Critique

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Please see the discussion on the talk page.

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The figures were obtained by taking unweighted averages of different IQ tests. The number of studies is very limited; the IQ figure is based on one study in 34 nations, two studies in 30 nations. There were actual tests for IQ in 81 nations. In 104 of the world's nations there were no IQ studies at all and IQ was estimated based on IQ in surrounding nations.[8] The number of participants in each study was usually limited, often numbering under a few hundred. The exceptions to this were the United States and Japan, for which studies using more than several thousand participants are available.
Studies that were averaged together often used different methods of IQ testing, different scales for IQ values and/or were done decades apart. IQ in children is different although correlated with IQ later in life and many of the studies tested only young children.
Many nations are very heterogeneous ethnically. This is true for many developing countries. It is very doubtful that an often limited number of participants from one or a few areas are representative for the population as whole.
There are also errors in the raw data presented by authors. The results from Vinko Buj's 1981 study of 21 European cities and the Ghanaian capital Accra used different scaling from Lynn and Vanhanen's. A comparison of the reported to actual data from only a single study found 5 errors in 19 reported IQ scores [9][10].
As noted earlier, in many cases arbitrary adjustments were made by authors to account for the Flynn effect or when the authors thought that the studies were not representative of the ethnic or social composition of the nation.
There is controversy about whether IQ is a valid measurement of intelligence, especially among third-world populations. (See the article at IQ for details, as well as the article race and intelligence.) It is generally agreed many factors, including environment, culture, demographics, wealth, pollution, and educational opportunities, affect measured IQ. However, the origin of differences in IQ is disputed; according to those positing a partly genetic origin, non-hereditary factors account for anywher from 20-60% of the disparity [11]. Others posit an exclusively non-hereditary origin.
One common criticism is that many of the countries with the best average scores are those where testing (e.g. American SATs, baccalaureate examinations) is a crucial aspect of the educational process, and that many of these tests (esp. the SATs) have been shown to be very similar to IQ tests. In these nations, because students study extensively for the high-stakes examinations, it is quite possible that IQ scores are higher because people are subjected to frequent examinations for which they prepare extensively.
There are many difficulties when one is measuring IQ scores across cultures, and in multiple languages. First of all, use of the same set of exams requires translation, with all its attendant difficulties. To adapt to this, many IQ testers rely on both verbal tests, involving word analogies and the like, and non-verbal tests, which involve pictures, diagrams, and conceptual relationships (such as in-out, big-small, and so on). Roughly the same results tend to be gained with either approach.
The book reports a correlation between IQ and GDP. The book does not explicitly point out other factors which may directly cause the correlation. The Copenhagen Consensus points out that "iodine-deficient individuals score an average of 13.5 points lower in IQ tests." Countries with individuals plagued by iodine deficiency may have other factors depressing IQ, so this finding in isolation does not suggest that such a deficiency alone accounts for 13.5 IQ points. In this case, barring intervention, a nation's poverty may be self-sustaining in cases where successive generations cannot meet basic nutrition requirements.
Other factors may serve to heighten poverty while simultaneously decreasing IQ. For example, it is common for teenage children in sub-Saharan Africa to be the primary earners for their family. This is due to AIDS-related deaths of older caregivers. As children leave school to begin subsistence farming, their education ends and IQs will be markedly lower. The book does not adequately address the casual relationship of these outside factors to both poverty and intelligence.
Finally, the Flynn effect may well reduce or eliminate differences in IQ between nations in the future. One estimate is that the average IQ of the US was below 75 before factors like improved nutrition started to increase IQ scores. Some predict that considering that the Flynn effect started first in more affluent nations, it will also disappear first in these nations. Then the IQ gap between nations will diminish. However, to take a reductio ad absurdum, that the IQ difference will disappear among the babies born today, the differences will remain for decades simply because of the composition of the current workforce. Steve Sailer noted as much when discussing the workforce in both India and China (see second diagram) [12].
[edit] U.S. states and political party hoax
Some sources, such as The Economist, 15th-21st May 2004 (p.44 in the UK edition), have reported a list of average IQs of U.S. states, supposedly from IQ and the Wealth of Nations. In fact, such data do not appear in the book. At about the same time, conservative American commentator Steve Sailer exposed the table as a hoax that had already circulated among hundreds of liberal-leaning blogs and other Internet sites [13]. In the following week's edition of The Economist, the editors admitted their error and stated in the column On the trail that they "were the victim of a hoax." The hoax recurred after the 2004 U.S. election, and it was again falsely attributed to IQ and the Wealth of Nations [14], but the incident prompted yet another hoax—a claim that a computer scientist had compiled a genuine state-by-state chart using SAT and ACT scores [15]. This was allegedly compiled by Psychology "Professor Mark Jones, from Virginia Tech," who does not exist. While there is a faculty member by that name, he is an Assistant Professor in the computer science department [16]. Furthermore, no link to such a study, or evidence that he did such a study, has ever been provided.
Sailer and anthropologist Henry Harpending provide a list of mean IQs of U.S. states from 1960, arguing that the scores correlate reasonably with public school 8th graders' achievement test scores on the 2003 National Assessment of Education, and thus may be one of the closest data sets to a national sample of IQ scores (table here; discussion here, also see [17]).
[edit] End material
[edit] References
1. IQ and the Wealth of Nations Richard Lynn, Tatu Vanhanen Praeger, ISBN 0-275-97510-X
2. See [18]
3. International Monetary Fund reported 2004 per capita GDP (PPP). [19]
• Barber, N. (2005). "Educational and ecological correlates of IQ: A cross-national investigation". Intelligence 33 (3): 273-284.
• Dickerson, R. E.. "Exponential correlation of IQ and the wealth of nations". Intelligence In Press, Corrected Proof.
• Hunt, E. & Wittmann, W. (in press) Relations Between National Intelligence and Indicators of National Prosperity. Sixth Annual Conference of International Society for Intelligence Research, Albuquerque, NM. [20]
• Templer, D. I. and Arikawa, H. (2006). "Temperature, skin color, per capita income, and IQ: An international perspective". Intelligence 34 (2): 121-139.
• Voracek, M. (2004). "National intelligence and suicide rate: an ecological study of 85 countries". Personality and Individual Differences 37 (3): 543-553.
• McDaniel, M.A. & Whetzel, D.L. (2005). IQ and the Wealth of Nations: Prediction of National Wealth. Sixth Annual Conference of International Society for Intelligence Research, Albuquerque, NM. [21]
• Whetzel, D. L. & McDaniel, M. A.. "Prediction of national wealth". Intelligence 34: 449-458.
[edit] See also
• The Bell Curve
• Race and intelligence
• Economic inequality
[edit] External links
• "Intelligence and the Wealth and Poverty of Nations" - article by Lynn and Vanhanen
• PISA scores transformed into IQ values in comparison with IQ estimated by Lynn and Vanhanen
• Smart Fraction Theory of IQ and the Wealth of Nations
• Exponential correlation of IQ and the wealth of nations - Peer reviewed article to be published in an upcoming edition of Intelligence (journal)
• "The Bigger Bell Curve: Intelligence, National Achievement, and The Global Economy", review by J. Philippe Rushton
• "A Reader's statistical update of IQ & The Wealth of Nations"
• A Few Thoughts on IQ and the Wealth of Nations, Steve Sailer, VDARE, April 2002.
Retrieved from "http://en.wikipedia.org/wiki/IQ_and_the_Wealth_of_Nations"