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Old 07-17-2015, 03:22 AM   #1
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Default coronary heart disease

while trying to find something about the origin and cause of
the 20th century coronary-heart-disease epidemic
I found this little entertaining story, which I thought I should hare.

It's about how research is done and that it needs a Sherlock Holmes
to find+read+understand the relevant papers and
how they still can't figure out the main things.
[IMO Holmes looks silly here with his unrelated racing horse association,
while Watson does the research]
Where/when arteriosclerosis started, why it declines since the 1980s, what causes it.
Or why the elderly were immune in 1918.
Also, how researchers make up a theory and then collect evidence to support it while trying
to dismiss the challenges and contra-evidence. Rather than curiously investigating the pros
and cons, maybe even switching sides when new evidence comes up.


here is the WHO-data
http://www.who.int/cardiovascular_di...rces/atlas/en/
the global epidemic of heart disease and stroke , 17M deaths yearly

and here is the most striking chart that I could come up with:
http://magictour.free.fr/ANG-CIR1.GIF [this picture may be updated later by adding more charts]
which seems to suggest that it started right after the 1918 pandemic and gained
additional speed in 1930
[some subsequent charts may challenge that ...]

in England it may have started earlier (1904?) [link] but was interrupted by a decline in 1916-1918
maybe due to the war and alcohole prohibition.

The characterics of deaths from angina pectoris / coronary heart disease is a prevalence
in males aged 45-65, and that male/female difference in cardiovascular deaths became first
noticeable in the charts in the mid 1920s.


----------------------

early origins , Heberden link http://www.ncbi.nlm.nih.gov/pmc/articles/PMC459067/

link to 1975 - thread http://thisbluemarble.com/showthread.php?t=62439

In USA there was also an increase of deaths attributed to
"disease of arteries", mostly arteriosclerosis, ecluding coronary-heart arteries.
These deaths had also a strong male preference but it increased to ages
above 65, while male and female coronary deaths approach at higher ages,
so I think it is somehow different and not included in this thread.

======================================

Actually I found this from google scholar since it quoted
Barker DJP, Osmond C. Diet and CHD in England and Wales during and after the second world war
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1052486/

which is another mystery. Cardiovascular deaths declined a lot in England (and some other countries,
Norway,Netherlands,France,) in WW2 and this was attributed to a change in diet.

The above paper challenges that by listing some thousand heart deaths
that were incorrectly attributed
to bronchitis in 1942. But English circulatory deaths continued to be lower in the elderly
in the following _decades_ , you still see a big knick even after Barker/Osmond correction.
[I can't find the 1943,1944,1948,1949 English yearly vital statistics reports]
Apparently noone challenged the challenge according to google-scholar ?!?

chart

---------------edit----------------
it seems that before 1940 under code 97 they included
cerebrovascular disease, but dropped it in ICD5 (1940 and after)
I may have to update my charts in the link accordingly ...
-------------------------------------------
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Old 07-17-2015, 05:16 AM   #2
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how would this sort of research, this phenomenon, be named ?
What would be a suitable keyword, where you can find more about it ?

-----------------------------------------------------------------------------
Researchers commonly start with a theory and then they stay with that theory,
no matter how the evidence goes.
They collect data that support the theory while trying to dismiss the counter-evidence.

As opposed to researchers who are indifferent about a subject and are just curiously
figuring out the pros and cons and are slowly making up an opinion while frequently
switching sites when new evidence comes in.
------------------------------------------------------------------------------
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Old 07-28-2015, 09:20 AM   #3
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Examining the WHO-data (which is now available since 2014 in
computer-readable form)... I was surprised to see the difference
in Chile's and Argentina's+Uruguay's male/female distribution of
circulatory deaths in 40-60 year old people.
This is probably because Argentina is ethnically mostly European, other than Spanish,
while Chile is just American and Spanish.
https://en.wikipedia.org/wiki/Demogr...ic_structur e
https://en.wikipedia.org/wiki/Demogr...#Ethnic_groups
[----added 2015/08/06-------another example seems to be
Mauritius vs. Karibian islands, both sugar producers, tourism, similar
climate, remote islands but big difference in heart-deaths and
different ethnicity ]

Native American and Spanish people had little male middle-age excess coronary deaths
in 1950-1980 while Europeans ("Caucasian") had a lot.
Argentina and Chile are the best example IMO for the genetical dependence
of the Coronary epidemic. In USA this was named the "Hispanic Paradox" ,
that Mexicans had fewer Heart deaths despite weaker social status and other risk factors.

In Europe we had the "French Paradox", the French drinking wine and eating animal fat
still had fewer Coronary deaths.

In Canada I do see a "Quebec Paradox", Quebec having fewer heart deaths than
neighboring Ontario.

I also suspect a temperature dependence. Colder countries are more suspectable.
One exception is/was Hongkong.

http://magictour.free.fr/SXC21.GIF


http://www.eupedia.com/europe/europe...logroups.shtml
Spain is 69% haplogroup R1b , but, well, England is still 67% although they had much MAMEHD
(middle-aged-male-excess-heart-deaths). The other countries would somehow match the hypothesis
that R1b is inversely associated with MAMEHD.
http://www.eupedia.com/europe/autoso..._dodecad.shtml
MAMTCECHD=middle-aged-male-twentieth-century-excess-coronary-heart-deaths

-------------------------------------------------------------
from recent papers searching haplogroup and coronary:
Mitochondrial haplogroup N9b is protective against myocardial infarction in Japanese males
Haplogroup T, specifically defined by 13368A, was significantly involved in the risk of developing
hypertrophic cardiomyopathy in Spain
Cardiogenics Study
50% higher coronary risk for Y-haplogroup I
mitochondrial haplogroup H was associated with early onset MI in male smokers
Mitochondrial haplogroup A is a genetic risk factor for atherothrombotic cerebral
infarction in Japanese females
Mitochondrial DNA haplogroup T is associated with coronary artery disease .
mtDNA copy number is a strong predictor of all-cause mortality
---------------------------------------------------------
from the WHO-data, I count for the 2nd half of the 20th century for people between 40 and 59 years,
for the available countries (mainly America and Europe, without China,India,Russia) for the
available years for deaths from circulatory causes, except cerebrovascular:

male : ~12 million , female : ~5 million
(USA alone : 3.9M and 1.4M)
(72M and 70M for all ages, since for people >75y female circulatory deaths start to dominate,
females get older than males in average)

-------------------------------------------------------------

now we need a database, which (nonsynonymous) mutations
occur how frequent in which country.
So to identify what mutations cause how much coronary mortality ...
------------------------------------------------
Evidence for contribution of the y chromosome in atherosclerotic plaque occurrence in men.
Y-haplogroup K had a 2.5-fold risk for atherosclerotic plaque
YAP haplogroup had 50% less risk
tRNA(Thr) 15927G>A mutation is associated with CHD.
[genetics however does not yet explain, why coronary heart disease suddenly appeared in the 1920s
while being almost absent before]
------------edit 2015/08/06------------------------------
http://magictour.free.fr/sxg5l4.GIF
constantly low circulatory death rates during 1960-2010 and
good similarity in male and female rates is seen in
Peru,Ecuador,Guatemala,El Salvador,Dominican Republic,
Costa Rica,Nicaragua,Mexico

2015 genealogical DNA testing :
Ecuador : 53.0% Native American, 41.8% European, 5.3% Sub-Saharan African
Peru : 79.1% Native American, 19.8% European, 1.1% Sub-Saharan African
-------------------------------------------------
(Cholesterol-Saturated Fat Index (CSIJ). The CSI was significantly and positively
related to CHD mortality in the 40 countries.

consume more plant foods, including small amounts ofliquid vegetable oils, and more
vegetables (more antioxidants) gave lower rates of CHD mortality.
milk and butterfat were associated with increased CHD mortality, possibly
through their effects on thrombosis as well as on atherosclerosis.


In Finland, risk factor changes explained almost all of the decline in CHD mortality
during the 1970s. However, in the late 1980s and 1990s, mortality declined much
faster than might be expected simply from risk factor reductions. Between 1972
and 1992, altogether 80 percent of the reduction in CHD mortality was explained
by a decline in the major risk factors: smoking, cholesterol, and blood pressure.
The biggest contribution was attributable to a large drop in cholesterol levels (3).

Between 2002 and 2011, statin medications apparently explained a large part
of the observed fall in population cholesterol level in Poland

Diets lower in folic acid and carotenoids are associated with the coronary disease
epidemic in Central and Eastern Europe [2004]
no substantial differences between Eastern Europe and democratic countries regarding the
prevalence of traditional risk factors with the significant exception of male smokers
The positive relationship between alcohol and heart disease in eastern Europe: potential
physiological mechanisms
Rapid declines in coronary heart disease mortality in Eastern Europe are associated with
increased consumption of oils rich in alpha-linolenic acid
fruit+vegetable intake significantly linked to CHD in Eastern Europe
Statin use, smoking



================================================
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Old 08-10-2015, 09:35 AM   #4
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the average blood pressure in a country seems to correlate well with
its deaths from circulatory causes

it would be interesting to see the values(estimates) for 1920,1950,1980

Code:
average systolic blood-pressure >18y in 2014 ; both,female,male,country
-----------------------------------------------------------
113.9 ,111.0 ,116.9 ,Republic of Korea
114.8 ,111.4 ,118.2 ,Canada
117.1 ,113.8 ,120.5 ,Peru
118.0 ,114.9 ,121.2 ,Singapore
119.7 ,115.3 ,124.1 ,Australia
119.7 ,116.6 ,122.7 ,Philippines
119.9 ,116.7 ,123.1 ,United States of America
119.9 ,120.9 ,118.9 ,Bangladesh
120.0 ,116.0 ,124.0 ,Greece
120.2 ,116.6 ,123.9 ,Israel
120.3 ,115.2 ,125.7 ,France
120.4 ,115.6 ,125.3 ,Switzerland
120.5 ,117.8 ,123.3 ,Cambodia
120.6 ,116.0 ,125.4 ,Japan
120.7 ,118.8 ,122.7 ,Democratic People's Republic of Korea
120.9 ,121.1 ,120.6 ,Turkey
121.0 ,118.7 ,123.4 ,Thailand
121.3 ,116.0 ,126.6 ,Iceland
121.3 ,116.7 ,126.1 ,Andorra
121.3 ,117.4 ,125.3 ,United Kingdom of Great Britain and Northern Ireland
121.5 ,117.4 ,125.6 ,Brunei Darussalam
121.6 ,117.2 ,126.3 ,New Zealand
121.6 ,118.8 ,124.7 ,El Salvador
121.7 ,116.5 ,127.0 ,Belgium
121.9 ,116.8 ,127.2 ,Spain
122.0 ,116.8 ,127.3 ,Denmark
122.0 ,117.7 ,126.4 ,Argentina
122.1 ,119.1 ,125.1 ,Ecuador
122.1 ,120.9 ,123.3 ,Lao People's Democratic Republic
122.3 ,119.7 ,125.0 ,Bolivia (Plurinational State of)
122.4 ,117.4 ,127.5 ,Netherlands
122.4 ,120.3 ,124.3 ,Jordan
122.5 ,118.0 ,126.8 ,Cyprus
122.5 ,119.2 ,125.8 ,Belize
122.5 ,119.5 ,125.4 ,Venezuela (Bolivarian Republic of)
122.7 ,118.6 ,126.9 ,Germany
122.7 ,118.9 ,126.7 ,Italy
122.8 ,119.9 ,125.6 ,China
122.8 ,120.3 ,125.4 ,Guatemala
122.9 ,119.6 ,126.2 ,Viet Nam
122.9 ,123.9 ,121.9 ,Solomon Islands
123.1 ,119.8 ,126.3 ,Marshall Islands
123.2 ,119.3 ,127.4 ,Austria
123.2 ,120.7 ,125.7 ,Iran (Islamic Republic of)
123.2 ,122.1 ,124.3 ,Papua New Guinea
123.4 ,118.3 ,128.6 ,Ireland
123.6 ,118.1 ,126.0 ,United Arab Emirates
123.6 ,122.4 ,124.9 ,Eritrea
123.7 ,120.1 ,127.4 ,Finland
123.8 ,120.6 ,127.0 ,Panama
123.9 ,119.7 ,128.2 ,Malta
123.9 ,120.2 ,126.3 ,Kuwait
123.9 ,120.5 ,127.5 ,Trinidad and Tobago
124.0 ,119.3 ,128.7 ,Sweden
124.2 ,119.6 ,128.8 ,Norway
124.3 ,120.8 ,128.1 ,Portugal
124.3 ,121.5 ,127.1 ,Cuba
124.3 ,123.2 ,125.4 ,Myanmar
124.4 ,119.5 ,129.4 ,Luxembourg
124.5 ,121.9 ,127.1 ,Honduras
124.6 ,121.5 ,127.9 ,Colombia
124.6 ,122.7 ,126.7 ,Sri Lanka
124.7 ,120.1 ,129.4 ,Chile
124.7 ,120.8 ,128.6 ,Costa Rica
125.1 ,122.7 ,127.4 ,Uzbekistan
125.2 ,120.8 ,129.8 ,Uruguay
125.2 ,124.2 ,126.3 ,Timor-Leste
125.3 ,123.6 ,127.1 ,Jamaica
125.4 ,121.9 ,128.9 ,Antigua and Barbuda
125.5 ,123.1 ,127.7 ,Micronesia (Federated States of)
125.6 ,123.6 ,127.5 ,Dominican Republic
125.6 ,123.6 ,127.6 ,Nicaragua
125.6 ,124.6 ,126.6 ,Pakistan
125.7 ,119.3 ,127.7 ,Qatar
125.7 ,121.7 ,129.8 ,Bahamas
125.7 ,122.3 ,129.1 ,Paraguay
125.7 ,122.7 ,127.9 ,Saudi Arabia
125.7 ,123.3 ,128.1 ,Barbados
125.7 ,123.5 ,128.1 ,Mexico
125.7 ,124.0 ,127.3 ,Guyana
125.8 ,120.6 ,131.2 ,Czech Republic
125.8 ,122.3 ,129.2 ,Kiribati
125.9 ,120.9 ,131.1 ,Slovakia
125.9 ,121.1 ,130.4 ,Lebanon
125.9 ,124.0 ,127.8 ,Syrian Arab Republic
125.9 ,124.3 ,127.6 ,South Africa
126.0 ,123.9 ,128.2 ,Tunisia
126.1 ,123.8 ,128.3 ,Suriname
126.2 ,123.3 ,129.1 ,Saint Vincent and the Grenadines
126.3 ,125.3 ,127.2 ,Maldives
126.4 ,126.0 ,126.7 ,Afghanistan
126.6 ,123.6 ,128.3 ,Oman
126.6 ,123.6 ,128.4 ,Bahrain
126.6 ,125.0 ,128.2 ,Cameroon
126.6 ,125.1 ,128.0 ,Iraq
126.7 ,122.6 ,131.0 ,Brazil
126.7 ,125.1 ,128.2 ,India
126.7 ,125.6 ,127.7 ,Morocco
126.8 ,122.9 ,130.5 ,Nauru
126.9 ,125.9 ,128.0 ,Burkina Faso
127.0 ,124.6 ,129.4 ,Tuvalu
127.1 ,126.2 ,128.0 ,Indonesia
127.2 ,126.1 ,128.1 ,Bhutan
127.3 ,124.4 ,130.0 ,Samoa
127.3 ,124.8 ,130.0 ,Mauritius
127.4 ,125.1 ,129.8 ,Malaysia
127.4 ,126.7 ,128.1 ,Benin
127.4 ,127.6 ,127.1 ,Mali
127.5 ,126.6 ,128.5 ,Haiti
127.6 ,123.1 ,132.2 ,Romania
127.6 ,127.0 ,128.3 ,Ethiopia
127.7 ,125.4 ,130.0 ,Azerbaijan
127.8 ,126.7 ,128.9 ,Algeria
127.8 ,126.7 ,128.9 ,Ghana
127.8 ,127.0 ,128.6 ,Rwanda
127.9 ,123.2 ,133.0 ,Croatia
127.9 ,124.8 ,131.5 ,Russian Federation
128.0 ,127.0 ,129.2 ,Turkmenistan
128.2 ,126.8 ,129.5 ,Tajikistan
128.2 ,127.3 ,129.1 ,Yemen
128.3 ,125.9 ,130.7 ,Saint Lucia
128.3 ,127.4 ,129.3 ,Swaziland
128.4 ,124.9 ,132.0 ,Kazakhstan
128.5 ,126.1 ,131.0 ,Saint Kitts and Nevis
128.5 ,127.4 ,129.5 ,Togo
128.7 ,124.5 ,132.8 ,Cook Islands
128.7 ,126.9 ,130.6 ,Nepal
128.7 ,127.2 ,130.3 ,Egypt
128.7 ,129.9 ,127.4 ,Lesotho
128.8 ,125.5 ,132.1 ,Niue
128.8 ,126.3 ,131.3 ,Kyrgyzstan
129.0 ,126.6 ,131.3 ,Gabon
129.1 ,124.1 ,134.7 ,Hungary
129.2 ,126.2 ,132.1 ,Grenada
129.3 ,127.0 ,131.7 ,Tonga
129.3 ,127.2 ,131.3 ,Fiji
129.3 ,128.3 ,130.3 ,Kenya
129.4 ,126.9 ,131.8 ,Equatorial Guinea
129.6 ,124.5 ,134.8 ,Slovenia
129.6 ,125.1 ,134.3 ,Montenegro
129.6 ,125.3 ,134.1 ,Bulgaria
129.6 ,125.7 ,133.5 ,The former Yugoslav republic of Macedonia
129.6 ,131.3 ,127.9 ,Nigeria
130.0 ,125.7 ,134.1 ,Seychelles
130.0 ,129.4 ,130.6 ,Senegal
130.1 ,129.0 ,131.2 ,Botswana
130.2 ,128.4 ,132.0 ,South Sudan
130.2 ,128.4 ,132.0 ,Sudan
130.2 ,128.6 ,131.7 ,Angola
130.2 ,128.7 ,131.7 ,Djibouti
130.3 ,126.8 ,133.9 ,Mongolia
130.3 ,129.1 ,131.5 ,Congo
130.3 ,129.7 ,130.9 ,Comoros
130.3 ,131.4 ,129.2 ,Zimbabwe
130.5 ,129.1 ,131.9 ,Mauritania
130.5 ,130.0 ,130.9 ,Chad
130.5 ,130.0 ,131.1 ,Guinea-Bissau
130.6 ,128.0 ,133.2 ,Dominica
130.6 ,129.1 ,132.1 ,Uganda
130.6 ,129.7 ,131.5 ,Democratic Republic of the Congo
130.7 ,125.8 ,136.0 ,Poland
130.7 ,127.5 ,134.3 ,Georgia
130.7 ,128.4 ,133.1 ,Bosnia and Herzegovina
130.8 ,126.0 ,136.5 ,Latvia
130.8 ,130.3 ,131.3 ,Central African Republic
130.9 ,126.3 ,136.2 ,Belarus
131.0 ,125.9 ,136.9 ,Lithuania
131.0 ,129.3 ,132.8 ,Namibia
131.0 ,130.4 ,131.6 ,United Republic of Tanzania
131.0 ,130.6 ,131.4 ,Liberia
131.1 ,130.7 ,131.5 ,Madagascar
131.2 ,125.6 ,137.6 ,Estonia
131.2 ,130.4 ,132.0 ,Burundi
131.4 ,130.3 ,132.5 ,Vanuatu
131.6 ,125.8 ,137.6 ,Serbia
131.7 ,128.5 ,135.5 ,Ukraine
131.7 ,129.0 ,134.4 ,Libya
131.8 ,129.6 ,133.9 ,Armenia
131.8 ,130.5 ,133.2 ,Zambia
132.0 ,130.8 ,133.3 ,Somalia
132.1 ,131.3 ,132.8 ,Gambia
132.2 ,130.2 ,134.1 ,Côte d'Ivoire
132.4 ,132.3 ,132.5 ,Sierra Leone
132.6 ,129.9 ,135.5 ,Republic of Moldova
132.8 ,129.6 ,136.0 ,Albania
133.0 ,133.0 ,133.0 ,Guinea
133.2 ,130.2 ,136.2 ,Cabo Verde
133.6 ,130.2 ,136.8 ,Palau
134.2 ,132.8 ,135.7 ,Sao Tome and Principe
134.3 ,132.8 ,135.9 ,Malawi
134.4 ,133.6 ,135.3 ,Mozambique
136.2 ,134.6 ,137.8 ,Niger

--------edit 2015/08/11----------------
I found this:
http://www.naos.aesan.mspsi.gob.es/v...pre ssure.pdf

blood-pressure charts 1980-2008 by 21 world-regions
so low in North America
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Old 08-11-2015, 08:33 PM   #5
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First time I think I have seen

Code:
code
used here.
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Old 08-12-2015, 02:05 AM   #6
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I've been regularly using it, since at least 2006, in the flu clinic.
I.e. for influenza mutation tables.
IMO it's one of the reasons why a forum is better than a mailing list.
Or a blog. Or twitter, facebook,...
The main reason is, that you can edit posts.
(we just had that discussion on an unrelated mailing list)
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Old 08-13-2015, 08:41 AM   #7
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I had never heard about Trans-fat before !
[-------edit-----, OK, it's usually subsumed under Gehaertete Fette
=hardened fats, which I did hear about. The name "transfett"
is rarely used in Germany]

the usuage history seems to match the history of coronary deaths.
I haven't found anything yet about the usage in Eastern Europe,
where we still have especially many Coronary deaths



my snippets from https://en.wikipedia.org/wiki/Trans_fat


It took only two years until the hardened fat could be successfully produced in
the plant in Warrington, commencing production in the autumn of 1909.
The initial year's production totalled nearly 3,000 tonnes.[25] In 1909,
Procter & Gamble acquired the US rights to the Normann patent;[26] in 1911,
they began marketing the first hydrogenated shortening, Crisco
(composed largely of partially hydrogenated cottonseed oil).

Hydrogenated fat such as Crisco and Spry, sold in England, began to replace
butter and lard in the baking of bread, pies, cookies, and cakes in 1920.[27]

In 1994, it was estimated that trans fats caused 20,000 deaths annually
in the US from heart disease.[31]

Animal-based fats were once the only trans fats consumed, but by far the largest
amount of trans fat consumed today is created by the processed food industry as
a side effect of partially hydrogenating unsaturated plant fats (generally vegetable oils).
These partially hydrogenated fats have displaced natural solid fats and liquid oils in
many areas, the most notable ones being in the fast food, snack food, fried food,
and baked goods industries. [48]

Baking shortenings, in general, contain 30% trans fats compared to their total fats,
whereas animal fats from ruminants such as butter contain up to 4%.
Margarines not reformulated to reduce trans fats may contain up
to 15% trans fat by weight.[49]

Denmark (where trans fats are restricted).

In 2004, the European Food Safety Authority produced a scientific opinion on
trans fatty acids, surmising that "higher intakes of TFA may increase risk for
coronary heart disease".[131]

Before 2006, consumers in the United States could not directly determine the
presence (or quantity) of trans fats in food products.

In 2013, the FDA planned to phase out the use of trans fats in all foods,
considering that there is no safe amount of trans fats that should be consumed.[171]
June 17, 2015, the FDA issued a final determination that there is no consensus that
industrially-produced trans fatty acids are generally recognized as safe for any use
in human food. Trans fat must be removed from prepared foods within three years
by June 2018.[172]
----------------------------------------------
-----------------------------------------------------
"Transfette" in Deutsch.
https://de.wikipedia.org/wiki/Trans-..._Lebensmitteln
v. a. in Frittierfetten
Blätterteig, Frittieröl und Instantsuppen
In Deutschland müssen nach der Lebensmittel-Kennzeichnungsverordnung (LMKV) gehärtete
Fette mit dem Hinweis „gehärtet“ deklariert werden. Eine Kennzeichnung von trans-Fettsäuren
wird nach Angaben des Bundesverbraucherschutzministeriums zurzeit in den entsprechenden
EU-Gremien diskutiert.
Seit Mitte 2012 existiert in Deutschland eine gemeinsame Initiative des
Verbraucherschutzministeriums und der Lebensmittelwirtschaft zur Minimierung
von trans-Fettsäuren in Lebensmitteln.[26][27][28]
----------------------------------------------------

A recent report [2008] has shown that rapid declines in the rate of mortality from
coronary heart disease in Eastern Europe are associated with increased
consumption of α-linolenic acid (31).
Zatonski W, Campos H, Willett W. Rapid declines in coronary heart disease
mortality in Eastern Europe are associated with increased consumption of
oils rich in alpha-linolenic acid. Eur J Epidemiol 2008;23:3–10.
wikipedia seems to have doubts
https://en.wikipedia.org/wiki/Alpha-Linolenic_acid


There are two major vegetable oils consumed in Eastern Europe (rapeseed and sunflower)
that differ greatly in their content of n-3 fatty acids, specifically alpha-linolenic acid (ALA). [rapeseed has more : 10%]
Low ALA intake has been associated with risk of fatal CHD and sudden cardiac death. [but ALA capsules have no effect]
Eastern European countries which experienced an increase in ALA consumption also
experienced a substantial decline in CHD mortality. [since 1990]

In 2005, a high-trans menu provided above 30 g of I-TFA in five EU countries
in Eastern Europe and 20–30 g in eight EU countries in Western Europe.
In 2009 the values in Hungary, Poland and the Czech Republic remained high
between 10 and 20 g, whereas they were less than 2 g in Germany, France and the UK.
----------------------------------------------------------------

seems that they finally figured it out :-)
After 70 years and >100M deaths.
Somehow reminds me to smoking and lung cancer,
although that was obvious much earlier and the warnings
were widespread, but often ignored.
While here they thought it was animal fat, sugar, obesity,
inactivity, fruit and vegetables, wine, ....

--------------------------------------------------------

where is the chart : estimated consumption of transfats per capita
per country per year ? i.e. USA,England, 1900-1970

----------------------------------------------------------
[2010]

A 2% absolute increase in energy intake from trans fat has been associated
with a 23% increase in cardiovascular risk.

In 1993 the Nurses Health Study reported that escalating intake of trans fats
was associated with increased cardiovascular risk (1).

As summarized by Eckel and colleagues (2), a number
of companies have now taken innovative steps to reduce
trans fats in their food products. These companies must
consider not only the fat composition of their products,
but also taste, texture, cost, and availability of materials
when reformulating their comestibles. These companies
currently include
Campbell Soup Co (Camden, NJ), Con-
Agra Foods (Omaha, NE), General Mills (Golden Valley,
MN), The Hershey Company (Hershey, PA), The J.M.
Smucker Co (Orrville, OH), Johnson & Johnson (New
Brunswick, NJ), Kellogg Co (Battle Creek, MI), Kraft
Foods (Northfield, IL), Nestle SA (Vevey, Switzerland),
PepsiCo (Purchase, NY), Procter & Gamble (Cincinnati,
OH), Sara Lee Corp (Downers Grove, IL), The Schwan
Food Co (Marshall, MN), and Unilever (London, UK) (2),
as well as GFA Brands, Inc (Boulder, CO), which formu-
lates products based on the fat blend described above
(33).

2. Eckel RH, Borra S, Lichtenstein AH, Yin-Piazza SY. Understanding
the complexity of trans fatty acid reduction in the American diet:
American Heart Association trans Fat Conference 2006: Report of the
trans Fat Conference Planning Group. Circulation. 2007;115:2231-
2246.

the total trans fat intake in the United States is currently
unknown [so, how much was produced ? That should be known]

However, we now know that
trans fats have greater adverse health implications than
the saturated fats they sought to replace. Eliminating
trans fats by returning to a high-saturated-fat diet is
inappropriate.

----------------------------------------------------------

ahh, back to square 1.
Now I looked at these numbers:
http://www.bmj.com/content/348/bmj.g2272.full.pdf

and there seems to be no correlation with high trans fat
intake and cardiovascular mortality.
I.e. North America vs. Eastern Europe.
-------------------------------------------
started with the 1993 Nurses Health Study
Dutch Zutphen study, transfat reduction 1960-->2000
from 19g/d(=7% of engergy) to 4g/d
3.5% less coronary deaths per g/d
USA 2012: 1.3g/d , 2003: 4.6g/d
2007 NY-ban on trans-fats
[doesn't seem to be enough to explain the rise of CHD 1920-1970
nor does it exlain the rise in Eastern Europe -
there should be another male-specific factor ]

I used to eat that chocolate with 23g saturated fat per 100g :-(
[ok, hardened fats in it should have been declared]

worst seems to be t/t-18:2 linoleic acid, although unsaturated,
contained in bakery goods
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Old 10-12-2015, 12:51 PM   #8
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I found this:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2538034/
with a graphics of deathcauses by country in 1940

1930-1940 is the time when CHD deaths first increased a lot in USA
and some other countries (Canada,England,Australia,...)
but not (yet) in others.
You see a correlation between circulatory deaths and cancer deaths.
A better marker of the process of CHD would have been the male/female
ratio of circulatory deaths at age ~40-60. Unfortunately this was rarely
examined.
In Korea there was quite some CHD by 1990, when they first submitted
to the WHO-database and a big male/female ratio. Since then it is declining.


The WHO data starts at 1950
http://magictour.free.fr/cau1940.GIF


http://magictour.free.fr/sxh3-al.GIF
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Old 11-15-2015, 06:30 AM   #9
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what's so typical about coronary heart disease (CHD) is,
how it suddenly rose in English speaking countries in the 1920s-1940s
(others somehow later) and how it preferrently killed middle-aged males.
Females also got it, but died from it later, at old age.
The reason is apparently not understood.

So, I wondered whether there were other diseases with this characteristics.
And yes, duodenal ulcer. And to lesser degree also stomach ulcer,
although it existed before 1900 but the male-deaths increased
also in the first half of the 20th century.
But for duodenal ulcer even more.
And again there was a "push" after the 1918 pandemic
and the peak was already reached in USA in ~1940.

Now, ulcer-deaths are mainly caused by the bacterium
helicobacter pylory which was not discovered before the 1970s.

CHD shows also the typical rise and fall of an epidemic,
with a recent "new wave" in Eastern Europe.


heart(CHD),stomach(ulcer), and lung (influenza) are close together ...
but why the middle-aged-males ?
Smoking doesn't fully explain it.

Also prostate cancer, which was very rare before 1920,
and maybe some other diseases as well.


Here is a file with male and female deaths per decade, (1900s - 1950s)
sorted by disease.
USA is available from the old yearly mortality statistics files,
but not in computer-readable form. So I took England.


timing is roughly the first 7 decades of the 20th century

one file per decade
male deaths,female deaths, disease-name
England, only deaths in the agegroup 50-54 (45-54 for icd1) are considered
sorted by quotient male/female
diseases with less than 10 deaths per decade are omitted



England,icd1:1901-1910
icd2:1911-1920
icd3:1921-1930
icd4:1931-1939
icd5:1940-1948
icd6:1950-1957
icd7:1958-1967

Italy:1887-1955

(if google don't grasp those keywords inside the files,
then I'll post the whole text here in [code]-tables)


one surprise for me were the many male deaths from bronchitis,
pneumonia,tuberculosis (phthisis)

About 68% of diseases had more male deaths in that agegroup
than female deaths
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Old 11-15-2015, 08:57 AM   #10
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gsgs ... your link to the file is missing .

..
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Old 11-15-2015, 09:10 AM   #11
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Old 11-15-2015, 10:05 AM   #12
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Ross, the links come soon ... I changed it a bit
-----------... done ... ------------

Can you make the picture smaller, please ?
Because of Sidescroll.

Note, that CHD had decreased a lot in most industrialized
countries in the last decades.
It could also become bad in India with 1B population.
Eastern Asia and Latin America is somehow different.

WHO should have these maps since 1980 (for Europe, at least;
worldwide only the charts/graphs), and they have the data
since 1950 , but I can't easily make world-maps since I don't
have a world map with the country-coordinates in it.

http://apps.who.int/healthinfo/stati...ality/whodpms/

http://data.euro.who.int/hfamdb/maps...d=3086 &qnt=0
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I doubt there are many ulcer deaths in the U.S. Or Western Europe now.

You present with stomach pains, vomiting blood, dark stool,or have a positive fecal occult blood test and culture for h. Pylori is almost de reguer.
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Old 11-17-2015, 01:01 PM   #14
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JMHO, but...........

We all have to die from something.

Less folks die from old scourges like infectious diseases, so something has to take their place.
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Old 11-22-2015, 12:59 PM   #15
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http://www.ptolemy.ca/members/archiv...cs/lam2000.pdf (2000)
In the West, the incidence of
peptic ulcer, particularly duodenal ulcer, rose sharply at the turn of the century and has
shown a rapid decline in the past three decades. In the East, the rise was equally impressive,
but the decline appears to have been delayed, only starting in the past decade. Asians present
their ulcer symptoms a decade earlier than Caucasians
the male-to-female ratio is much higher in the East

five environmental factors
Aspirin was marketed in 1902
cigarettes - Bonsack machine ~1905
Industrialization, stress ~1905
NSAIDs

The fall - decrease cigarette
change to vegetable oil

The regional di?erences in ulcer rate in India and China have been ascribed
to the use of the staple diet: stored, milled rice has been shown to be ulcerogenic in
Shay rats, and wheat to be gastroprotective. But similar H-pylori rates

The sex ratio for duodenal ulcer has been reported as 18:1 in India19, 9:1 in
Africa44and Bangladesh19, 4:1 in Hong Kong46, 3:1 in Scotland47, 2:1 in Denmark, and
England and Wales15,48, 1.4:1 in Sweden49and 1:1 in the USA.

The sex ratio patterns cannot be explainedonthe basis of H. pylori infection


[IMO the rise and fall , the appearance out of nothing, is not well
explained by these arguments.
And why does it prefer men
- same for CHD]

--------------------------------------------------
http://www.researchgate.net/profile/...1a96000000.pdf

2009

In an analysis of PUD mortality data from 1921 to 2004 from 6 European countries,
there was a high correlation of data on PUD.
[but e.g. Italy does show a clear delay of ~20 years wrt. England ?!
i.e. in the decline and in the sexratio]

The initial increase in PUD between 1850 and 1950 was thought to be due to a shift in
the age of acquisition of H pylori. With the improvement in community hygiene, acqui-
sition of infection tended to be later in life during adolescence.
improving standards of hygiene

The increase in aspirin and/or NSAID consumption and the introduction
of potent antisecretory medications probably have not affected the long-term down-
ward trends of ulcer mortality

ulcerogenic drugs, however,

Genetic factors play a role in the development of PUD

my summary of their summary : unclear,unknown

==============================================
Methods: Mortality data from 6 countries between 1921 and 2004
were analyzed, including Denmark, France, Germany, The Netherlands,
Spain, and Switzerland. The age-specific death rates of gastric and
duodenal ulcers from each individual country were plotted as period-age
and cohort-age contours
striking similarities
The increase in nonsteroidal anti-inflammatory drug consumption
or introduction of potent antisecretory medications have not
affected the long-term downward trends of ulcer mortality
The surviving annual inpatient records of the last two to three
centuries from the Scottish
Royal Infirmaries of Aberdeen, Dundee, Edinburgh, and Glasgow w

the epidemiological analysis of gastric cancer, gastric and duodenal
peptic ulcer in the United States during the 18th and 19th century
came to rely on the hospital statistics from three cities, that is,
Boston, New York and Philadelphia. (i)

Hospitalization for gastric cancer, gastric ulcer, and duodenal ulcer were analysed

(UK, 1830-1970) the H.Pylori infection rate fell in the general population between 1800 and 2000
gastric ulcer was caused by H. pylori at age 5-10
and duodenal ulcer after age 15
declining infection rate and infection at older ages
birth cohort pattern
Conclusion
The birth-cohort phenomenon of ulcer disease can be explained by a receding
H. pylori infection accompanied by a simultaneous shift in its age of acquisition.


[I couldn't so well verify the birth-cohort pattern in the English data.
It could depend on the time-trend, the change in nutrition, lifestyle
rather than the time of birth, the experiences during childhood.
The birth cohort pattern is IMO less clear than with cancer deaths
or lung cancer deaths in England during that period (1900-2000) ]
------edit--------
after looking at the USA-data, I do doubt the Sonnenberg
birth-cohort pattern theory. I think it was rather the time
and the living circumstances at that time
- in USA especially the 1930s and 1940s -
that increased male peptic ulcer deaths. And not -or to a lower
degree - the conditions at the birth or childhood of the ulcer-deaths.

http://magictour.free.fr/USULC15.GIF
http://magictour.free.fr/usulc3.GIF



the biggest decline was in 1973-1978 , as with CHD
female rates increased in the 1950s, when male rates already went down
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Old 11-24-2015, 04:24 PM   #16
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An hypothesis: the dramatic decline in heart attacks in the United States is temporally
related to the decline in duodenal ulcer disease and Helicobacter pylori infection.
http://www.hubmed.org/display.cgi?uids=24689964
> the decline in heart attacks is temporally related to the decline in duodenal ulcer and by
> inference, Helicobacter pylori infection
-------------------------------------
possible role of H-pylori in several extragastric diseases
-------------------------------------
Helicobacter pylori—An Infectious Risk Factor for Atherosclerosis?
-------------------------------------
Recently (2014), the role of H. pylori infection in the development of ath-
erosclerosis and its clinical complications has received attention.
PCR studies have detected H. pylori DNA in atherosclerotic plaques,
although this finding remains controversial.
Atherosclerosis is now known to be a chronic
inflammatory disease of the arteries8, 9), although the
stimuli that trigger this inflammatory response remain
unclear.Chlamydia pneumoniae10, 11), cytomegalovirus12) and H.
pylori13, 14)
endotoxin
Platelets play a pivotal role in the pathogenesis of
atherosclerosis and its acute complications by adher-
ing to the dysfunctional endothelium or collagen and
releasing their granular contents upon activation8).
prothrombotic activity of H. pylori
http://scholar.google.de/scholar?cit... odt=0,5&hl=en
---------------------------------------------
Results: Overall, H. pylori infection was not associated with CVD (CHD and stroke)
mortality risk. (Japan,<2003)
---------------------------------------------------
The discovery that Bartonella henselae can infect and damage EPCs revitalizes the enduring
debate about the microbiological contribution to atherosclerosis,
--------------------------------------------------
Several studies have been published on this issue over the last year.[2014] Hughes et al. showed the
occurrence of a concomitant decline in the prevalence of both heart attacks and duodenal ulcers
in a military cohort of subjects born around 1930. The authors speculated that as duodenal ulcer
is strongly related to H. pylori infection, the concomitant decline of heart attacks may be due to
the interference with H. pylori eradication [5]. While inflammation has been shown to play a key
role in the destabilization of atherosclerotic plaques [6], Nakagawa et al. [6] demonstrated that
high serologic IL-6 levels are significantly associated with H. pylori infection, possibly playing a
role in ischemic heart disease (IHD). In a similar study, Figura et al. [7] reported high circulating
levels of IL-6 and B-type natriuretic peptide, a biomarker of heart failure, in patients with coronary
artery disease and infected by CagA-positive strains. To highlight the significant role of CagA-positive
strains in this argument, Ikeda et al. [8] recently showed that H. pylori infection in general is not
associated with a risk of myocardial infarction or stroke, in contrast to CagA positivity. In fact,
the association between myocardial infarction was only a trend (p = .10), and there was no
association with stroke. Concerning the possible role of H. pylori on the occurrence of some
atherosclerotic risk factors, Vahdat et al. [9] described a positive association between coinfection
with Chlamydia pneumoniae and H. pylori and essential hypertension. Taken together, these
results highlight the potential role of CagA-positive strains in the occurrence of cardiovascular
diseases.
Sealy-Jefferson et al. [10] demonstrated that antibody levels to H. pylori predicted the incidence
of strokes in a Mexican–American population (OR: 1.58; 95% CI: 1.09–2.28). On the other hand,
Laek et al. [11] studied a possible correlation between positivity to infectious agents, such as C.
pneumoniae, H. pylori, cytomegalovirus, herpes simplex virus, and hepatitis A virus, and
coronary artery calcium (CAC) but with negative findings.
-----------------------------------------------------------------------

The serum triglyceride and total cholesterol concentrations were significantly higher
in the males with positive IgG and IgA antibody titres for H. pylori [1999]
---------------------------------------------------------------------------------------
CagA-positive Helicobacter pylori strains enhanced coronary atherosclerosis by increasing
serum OxLDL and HsCRP in patients with coronary heart disease [2011]
------------------------------------------------------------------------------------
CagA-seropositive strains infection is significantly associated with susceptibility to
ischemic strokes and coronary heart diseases [review,2008]

---------------------------------
The serum triglyceride and total cholesterol concentrations were significantly higher
in the males with positive IgG and IgA antibody titres for H. pylori [1999]
---------------------------------------------------------------------------------------
CagA-positive Helicobacter pylori strains enhanced coronary atherosclerosis by increasing
serum OxLDL and HsCRP in patients with coronary heart disease [2011]
------------------------------------------------------------------------------------
CagA-seropositive strains infection is significantly associated with susceptibility to
ischemic strokes and coronary heart diseases [review,2008]
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Old 11-25-2015, 03:50 AM   #17
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https://en.wikipedia.org/wiki/Helicobacter_pylori
3 μm long with a diameter of about 0.5 μm.
highly motile owing to flagella
large diversity of strains and the genomes of three have been completely sequenced
The genome of the strain "26695" consists of about 1.7 million base pairs,
with some 1576 genes. The two sequenced strains show large genetic differences,
with up to 6% of the nucleotides differing.[23]
1907 transcriptional start sites
AAGGag motif
40-kb-long Cag pathogenicity island with 30 genes
ulcer-causing cagA gene coding a (1186-amino acid) protein
The low GC-content of the cag PAI relative to the rest of the Helicobacter genome
suggests the island was acquired by horizontal transfer from another bacterial species.[21]
[when ?]
http://www.nature.com/nature/journal.../388539a0.html
resemble their H. influenzae and E. coli homologues
similar to Arabidopsis thaliana
possible that H. pylori diverged early from the lineage that led to the gamma
Proteobacteria, and retained more ancient forms of enzymes that have been
subsequently replaced or have diverged extensively in H. influenzae and E.coli.

[rarely do I find analysis or speculation why it prefers males to kill]











http://www.ncbi.nlm.nih.gov/nuccore/?term=pylori

Found 175276 nucleotide sequences.

Helicobacter pylori J99, complete genome
1,643,831 bp circular DNA
Accession: AE001439.1

Helicobacter pylori B38 complete genome, strain B38
1,576,758 bp circular DNA
Accession: FM991728.1

Helicobacter pylori B8 complete genome
1,673,997 bp circular DNA
Accession: FN598874.1

Helicobacter pylori cag pathogenicity island, strain CC42C
36,207 bp linear DNA
Accession: FR666828.1

Helicobacter pylori cag pathogenicity island, strain L72
38,193 bp linear DNA
Accession: FR666841.1

...
http://jcm.asm.org/content/53/9/2877.full.pdf+html
FFPry and FFPaa phylogenetic trees were generated from 377
genome sequences and proteomes and annotated on the basis of
MLST classification and geographic origin (see Fig. S6 and S7 in
the supplemental material).

two major location subgroups (Africa and North America)
hpEurope or the hspAmerind
migration from East Asia via the Bering Strait and later, from
the 15th century onward, from Europe (18, 47)

presence of the cag PAI is strongly associated with the s1 subtype
of VacA

[so, was it maybe one -or just a few- recombination event that created the ulcer epidemic
starting in the 2nd half of the 19th century and gaining speed in the first
half of the 20th century with increased traveling ? And maybe also the
CHD epidemic ? was there cagPAI in the isolated Tokugawa Japan
before 1860 ?]

-------------------------------------------
--------------------------------------------------------------------------
http://www.old-herborn-university.de...ni_book_25.pdf

Helicobacter pylori is a highly versatile pathogen with a coevolution
of the stomach in mammals, birds and other animals.

Helicobacter pylori colonizes the human stomach shortly after weaning
until recently, when modern living habits and common antibiotic use in early
childhood prevent this colonization process. This fact was probably fa-
voured by an early rotavirus and other enteric and respiratory infections.
https://de.wikipedia.org/wiki/Meckel-Divertikel

H. pylori ppeared in the human stomach in our ancestors in Africa > 58,000 years ago
is present in all human populations worldwide today, and acquired early after weaning.

Probably all mammalian species including whales and dolphins seem to be
colonized in the stomach by Helicobacter or Helicobacter-like organisms

H. mustelae in ferrets and H. suis in piglets colonize the gastric mucosa
and cause mucosal ulcers much like H. pylori with the cagA pathogenicity is-
land (PAI) and vacuolating toxin.

an early H. suis infection may protect against a H. pylori nfection

H. pylori displays the highest level of genomic variability in bacteria with
a high frequency of recombination contributing to the great diversity

H. pylori is a unique human pathogen. The closest species to H. pylori may
be a gastric species reported in beluga whales and dolphins

--------------------------------------------------------------------------------
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4017034/
also ignores the special male-killing pattern of ulcer-disease that emerged and grew
in the early 20th century
-----------------------------------------------------------------------------

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3294863/
J-Western Forms of Helicobacter pylori cagA Constitute a Distinct Phylogenetic Group
with a Widespread Geographic Distribution

While much is known about the ancestry and molecular evolution of Western,East Asian,
and Amerindian cagA sequences, relatively little is understood about a fourth group,
known as “J-Western,” which has been detected mainly in strains from Okinawa, Japan.

ThecagPAIhasalowerG?Ccontentthan
the rest of the H. pylori chromosome and is flanked by direct
repeats, suggesting that it was acquired through a horizontal
transfer event (13).

the cag PAI (10, 21).

EPIYA-A and EPIYA-B motifs (in various numbers) are found in
nearly all CagA sequences.

Previousstudieshaveshownthatthereisahighlevelofgen etic
diversity among cagA genes from different H. pylori strains and
that cagA diversity has been driven by positive selection (18, 24,
25,44,59).

EPIYA-D motifs
have been identified almost exclusively in H. pylori strains from
East Asia, whereas EPIYA-C motifs have been found predomi-
nantly in non-Asian strains (Fig. 1) (27, 28, 30). Several studies
haveshownthatH.pyloristrainswithanEastAsianformofC agA
(EPIYA-D) are associated with an increased risk of gastric cancer
compared to strains with a Western form of CagA (EPIYA-C) (3,
6, 30, 32, 38, 40)

striking geographic
differences in cagA sequences (26, 36, 53, 60, 63).

blast for (26695)

Subsequently, insertions and dele-
tions(indels)andhypervariableregionswereremovedman uallyfromthe
sequence alignments, resulting in a final alignment length of 2,940 nucle-
otides (or 980 amino acids)

129 sequences , Sep.2010

------------------------------------------------------------------
If H. pylori prevalence did not change, did its viru-
lence change? This possibility is not supported by the
available data.
[Graham]
Although the risk of a clinical disease
outcome is approximately doubled when infected with a
more virulent strain (e.g., containing the cag pathogenicity
island or cag PAI), all known H. pylori are associated with
peptic ulcer and gastric cancer independent of whether
they possess one or more putative virulence factors (i.e.,
the differences are in degree of risk not in risk per se).

The ability of Europeans to export gastric cancer/atrophic gastritis to the
Americas[41] does not support the suggestion that there
was a sudden appearance of H. pylori or change in its
virulence in the West during the periods when it has been
speculated that peptic ulcers appeared as a new disease.

-----------------------------------------------------

helicobacter pylori doesn't spread as fast as influenza. It's mainly transmitted
from mother to baby, or at least at young age and then kept for the life.
The strains kept their evolution close to human evolution itself, over
10000s of years. Hard to imagine that a single recombination was
the cause of such an epidemic which only took some decades of
steep rise. And there is also the phenomenon of male preference
which suddenly appeared, in duodenal ulcer anyway, but also in
gastric ulcer which saw a balanced sexratio at 1900.

### so I step back from that idea (why did it take me so long ? )

============================================
here several comments about the original 1962- peptic ulcer birth cohort suggestion,
(before H.Pylori was known) as a review 40 years later in 2002.
http://www.med.mcgill.ca/epidemiolog...ns/Paper10.pdf

there seems to be consensus, that the birth cohort pattern does exist and was
subsequently confirmed, mainly by mortality data.
[which I do not yet quite see from my charts]

=============================================
http://journals.lww.com/coronary-art..._with.3 .aspx

Conclusion: These results support the association between CagA-positive H. pylori infection
and coronary atherosclerotic burden. Further studies are needed to better elucidate the
mechanism by which CagA-positive strains may promote atherosclerosis.

Patients with positive test result for H. pylori IgA were significantly more likely to have
higher total cholesterol and low-density lipoprotein (LDL) levels than IgA-negative patients.

In conclusion, the present data challenge the dogma on
the increasing prevalence of H. pylori colonization with age

H.Pylori patients had a 1.93 fold crude risk and 1.48 fold adjusted risk
of acute coronary syndrome in Taiwan 1998-2010
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Old 02-01-2016, 06:20 AM   #18
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I'd expected it to be higher in urban areas, but the converse is true for
North America and Western Europe.
In USA we have male/female deathratios from all causes
in the agegroup 45-54 :

year:urban,rural
-----------------
1921:1.23,1.19
1930:1.41,1.37
1939:1.64,1.70
1950:1.68,1.64
1959:1.68,1.95
1970:1.59,1.83
1980:1.71,1.76
1990:1.90,1.65
2000:1.68,1.67
2010:1.64,1.60

same numbers for CHD/isc :




that mid-age male surmortality from all causes is usually mostly due to CHD.
But it's also in infectious diseases,digestive organs, mental disorders, unnatural causes.
While it declines in Western countries already it's increasing in Eastern Europe, at least
until 1996 in most countries. And it's _more_ pronounced in rural areas.

==================================================
prevalence of CHD risk factors was 9.7%(3.2% clinical) in urban and 2.7%(0.6%) in rural Delhi/India , in 1985

1% in 1960 and 8% in 1995 in urban India , 2% in 1974 and 4% in 1995 in rural India
1.7%, 2.5% and 7.4% in males and 1.5%, 3.4% and 7.1% in females in villages,towns and cities
in N.-India, 1997
Moradabad, N.India,11.0%,3.9% (m,f urban) and 6.9%,2.6% (m,f rural) correlated with fat intake
prevalence of CHD rural=urban in Kashmir
Puerto Rico,1977,m45-64, urbans had higher CHD risk factors, and CHD was 1.5 times higher than rurals
Tianjin,China, 1998-2008 , CHD deaths 55380 male,49013 female, 67010 urban,37383 rural
Prospective Urban Rural Epidemiology (PURE) Study
Lower CHD and stroke mortality at higher altitudes in Switzerland
sex difference for HDL cholesterol was smallest 0.06 mmol/l in China and largest (0.40 mmol/l) in Canada.
100 countries,2004:BMI (Cholesterol) peaked at I$12500(8000) for females and I$17000(18000)
for males rel. food expenditure and ruralicty decreased CHD
+10% cholesterol => +30% CHD rates
Urban Chinese families reported more food variety and exercising
worse socio-economic situation, smoking,alcohol and rural residence => low fruit+vegetable.in ex Soviet
decreased 2001-->2010
Lodz,Poland 1999-2008, rural cir =418.7 urban cir =367.9
CHD unrelated to HDI (human development index) +developing,-developed
Netherlands,1995-2000, urban,non-married have lower cancer and heart mortality
Hypertension 23% (India) , 52% (Russia), 30% (Russia) and 83% (Ghana) undiagnosed
35% (Russia) and 87% (Ghana) untreated, "uncontrolled" in 3times more men
Fish consumption in the Russian Federation dropped dramatically during the
period of post Soviet reforms. At the same time CVD deaths increased.
High cardiovascular mortality in Russia cannot be explained by the classical risk factors.
The Arkhangelsk Study 2000
Metabolic syndrome in 25% of men and 32% of women in a city in S.Iran
attributes the decline in UK to improved treatment while incidence rate has
diminished little or hardly at all. known risk factors, explain only half
In most eastern countries, mortality rates remain relatively low, as in Russia and Japan.[2004]
prevalence of coronary artery disease (CAD) is low in South African blacks despite westernization
The mean INTERHEART Risk Score was highest in high-income countries, intermediate
in middle-income countries, and lowest in low-income countries (P<0.001). However, the
rates of major cardiovascular events (death from cardiovascular causes, myocardial
infarction, stroke, or heart failure) were lower in high-income countries than in middle-
and low-income countries (3.99 events per 1000 person-years vs. 5.38 and 6.43 events
per 1000 person-years, respectively; P<0.001). Case fatality rates were also lowest in
high-income countries (6.5%, 15.9%, and 17.3% in high-, middle-, and low-income
countries, respectively; P=0.01). Urban communities had a higher risk-factor burden
than rural communities but lower rates of cardiovascular events (4.83 vs. 6.25 events
per 1000 person-years, P<0.001) and case fatality rates (13.52% vs. 17.25%, P<0.001).
The use of preventive medications and revascularization procedures was significantly
more common in high-income countries than in middle- or low-income countries (P<0.001).
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Old 02-19-2016, 07:21 AM   #19
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http://ajcn.nutrition.org/content/ea...22317.abstract
conclusion: Egg or cholesterol intakes were not associated with
increased CAD [coronary artery disease] risk
[ in 1984–1989 in Finland? in males 42-60y ]


http://www.scienceworldreport.com/ar...rt-disease.htm
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Old 03-13-2016, 11:09 AM   #20
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smoking contribution to the gender gap in life expectancy 1955-2010 by country
http://eurpub.oxfordjournals.org/hig...aterial_S1.pdf
full article: http://europepmc.org/articles/pmc4512955

UNITED STATES OF AMERICA
Year GDLE SMOK BIO ONBF
1955 6.33 2.17 1.19 2.97
1960 6.68 2.56 1.22 2.90
1965 7.26 2.91 1.26 3.09
1970 7.72 3.07 1.29 3.35
1975 7.86 3.10 1.30 3.46
1980 7.42 2.85 1.27 3.30
1985 7.06 2.51 1.25 3.31
1990 6.95 2.21 1.24 3.51
1995 5.92 1.64 1.16 3.12
2000 5.27 1.23 1.10 2.94
2005 5.23 1.01 1.10 3.13

GDLE = gender difference in life expectancy at birth,
SMOK = contribution of smoking to GDLE,
BIO = contribution of biological factors to GDLE,
ONBF = contribution of other non‐biological factors to GDLE

-----------------------------------------------------------------------------

most of the gender "gap" in that period is due to coronary heart disease. But this suddenly
developed in 1920-1940 with the gender gap building up.
It declines since 1970 equally in middle-aged males and females
but the gender ratio remains at 2 while it was only at 1.1 in 1920

So, it doesn't seem that this was caused by smoking to a large part.
It doesn't quite fit the data for cigarette consumption either.
And there should be cohort effects as with lung cancer mortality.
There must be something else.

http://magictour.free.fr/uscirr3.GIF

[picture corrected 2016/03/13/2200 UTC, the first version
incorrectly used the population data for the death registration
States for 1900-1921 instead of "death registration area" (which
also included some big cities in non-registration-States]
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Old 03-19-2016, 02:17 AM   #21
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In 2010, nonoptimal intakes of ω‐6 (n‐6) polyunsaturated fat (PUFA), Saturated fat (SFA),
and trans fat (TFA) were estimated ... accounting for 10.3% and 7.7% of global
coronary heart disease (CHD), mortality.
http://jaha.ahajournals.org/content/...02891.abstract
Eastern Europe had the most absolute n-6 PUFA–attributable CHD deaths ~450/M/year
Oceania had the highest proportion of n-6 PUFA–attributable CHD deaths 18.6%
East Asia had both fewest absolute 60/M/y and lowest proportion 6.7%
PUFA–attributable CHD mortality.




---------------------------------------
While the naturally occurring TFAC16:1n-7t was associated with reduced risk, no increased
risk was found for industrially produced TFAs. [in Ludwigshafen, Germany,1998]
-------------------------------------------------------------------
I'd like to have their data, so to test how much CHD-mortality
depends/depended on these 3 fat-intakes.
So to plot mortality against each fat for the 148 countries,
compute the correlation coefficients, figure out the best delays
fat-intake <--> mortality.
Well, maybe they'll do that in a subsequent paper ?!
-----------now I found----
>We did not perform ecologic (correlative)
> analyses of dietary fats and CHD, which could be strongly
> biased by cross-national confounders and ecologic fallacy, but
> rather used comparative risk assessment based on external
> published evidence on etiologic effects on clinical CHD
> events

I don't understand this reasoning. It could be biased, yes, but let's
try it anyway and then discuss possible bias ?!
Or did they do it but didn't like the result ??

--------------------------------------------------------
================================================== =
Psychological language on Twitter predicts county-level
heart disease mortality
------------------------------

-----------------edit 2016/03/30-------------------------

some more snippets

In black Africans, CAD has, until recently[2009], been rather uncommon. (10)
10. Seftel, H.C. The rarity of coronary heart disease in South Africans. South African
Medical Journal 1978; 54: 99-105

Reliable ischaemic heart disease (IHD) mortality data are not available for the black
population of South Africa

In 1959 and 1960, an autopsy study at the Baragwanath Hospital (CHBH) in Soweto,
South Africa, reported only one case of CAD; in 1976, fourteen cases were reported. (12)

Historically, clinical coronary artery disease has also been remarkably rare in black
South Africans. Records from South Africa’s largest hospital, the CHBH showed that
in the early 1990s, on average, approximately 70 black patients with CAD were
admitted annually. (13)

The increase in the volume of
cases has been far less than expected, however, and CAD remains an unusual cause of
admission in black patients.

This low prevalence of CAD prevails in South Africa despite considerable
Westernization of lifestyle and the accompanying rise in risk factors for CAD, such as
obesity, atherogenic dyslipidaemia, hypertension and type 2 diabetes mellitus (DM).
(14)

On an adjusted basis,
the following five modifiable risk factors were found to be most predictive of this
event: smoking, raised apoB/apoA1 ratio, diabetes, hypertension and obesity. (20)


Ischaemic heart disease (IHD), previously considered rare in sub-Saharan Africa,
now [2009] ranks 8th among the leading causes of death in men and women in the region.

The major risk factors for IHD in sub-Saharan Africa include hypertension,
smoking, diabetes, abdominal obesity and dyslipidaemia. In the INTERHEART
Africa study, these risk factors contributed a population-attributable risk
of nearly 90% for acute myocardial infarction.

------------------------------------
High blood pressure results in 13% of CVD deaths, while tobacco results in 9%, diabetes 6%,
lack of exercise 6% and obesity 5%.
It is estimated that 90% of CVD is preventable
17.3M deaths (31.5%) in 2013 from CVD , 12.3M(25.8%) in 1990

1.7M deaths worldwide per year due to few fruits+vegs

----------------------------------------------------

global burden of disease study

http://magictour.free.fr/gbds2.PNG

seems to be declining everywhere since 2000
it never was high in Africa
-------------------------------------
there is an upward trend [2003] in all the regions of the sub-Saharan Africa. This trend is believed
to be related to the increasing frequencies of CAD risk factors in the subcontinent.
-------------------------------------
http://jech.bmj.com/content/early/20...06577.abstract
4 East Asian populations that vary in the timing of their modernisation,
Increases in sex ratios of CVD mortality began in earlier cohorts in Western
than in East Asian populations. Once begun, increases were more rapid in East Asia.
There is scant [=few] evidence that this increase is attributable to changing sex-specific rates of smoking.
----------------------------------------------------
---------------added 2017/02/13-------------------------------
http://article.sapub.org/10.5923.j.fph.20160602.04.html
Countries with low cardiovascular mortality showed higher levels of vegetable fat
consumption, while countries with high mortality rates showed higher levels of
animal fat consumption. No particular pattern was observed for dairy fat.
---------------------------------------------------------
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Old 03-22-2016, 03:17 PM   #22
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it seems that most researcher do not realize that the origin of CHD is still
mysterious, unresolved (IMO?!) - that none of the known "risk factors" explains
the emergence in USA,England in the 1920s with the excess
middle-age-male surmortality. They got it down meanwhile, but equally
in middle-age-male and female, so the male/female (50y) ratio is still
high and they found no risk factor which is male-specific.

Well, the whole emergence with (non-coronary) heart-deaths and cancer-deaths
since ~1850 is mysterious and unresolved...
Maybe those who survived all these epidemics which existed at
those times, were strong enough to withstand heart disease and cancer
(which more and more turn out to be inflammation induced processes,
although antibiotics don't help)
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Old 04-17-2016, 08:01 AM   #23
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ahh, dropsy.

When examining the deathrates from circulatory causes in the 19th century in USA or England,
I noticed the steep increase that started ~1850 , became slower since 1880, and increased
again since ~1920, [this times particularly in middle-aged-males due to coronary heart disease,]
and then peaked in ~1970 and declines since then.
But now, (after years!) I learned that this increase in the 19th century is mostly due to better
diagnosis of deaths that were previously coded as "dropsy". [ =edema , 1.) , 2.) ]
You will hardly find this with normal reading, keyword search - at least I didn't.
So I post this important fact here. Deaths from heart disease did probably not suddenly start
in ~1850 but were just not diagnosed and often attributed to "dropsy", which is not a disease,
but just a symptom.
However, the increase in CHD since ~1920 is not due to such a change in diagnosing,
although the coding changed from "angina pectoris" over "disease of coronary arteries"
to "ischemic heart disease.
It is clearly also seen in the middle-aged male/female ratio from deaths from all causes,
no matter how they are coded. (ratio increased a lot since 1920, but remains stable since 1960,
although the deaths are decreasing a lot in both sexes. So, the deathrates are again as low as
in 1920 but the middle-aged-sex-ratio is much higher now than in 1920, so what is different ?


1.) https://en.wikipedia.org/wiki/Dropsy
abnormal accumulation of fluid in the interstitium, located beneath the skin and in the cavities
of the body which can cause severe pain
When you add deaths from dropsy and heart disease from 1850-1880 then there is only a

2.) report of the mortality and vital statistics of the United States as returned at the tenth census
(June 1, 1880)
1880a_v12-02.pdf , page lxvii = page 45 into the .pdf
http://www2.census.gov/prod2/decenni...80a_v12-02.pdf
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Old 06-14-2016, 08:55 AM   #24
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urban vs. rural


http://www.cairn.info/revue-annales-...-1-page-33.htm
> In the United States in the xixth century, as in Europe in that era, there was a substantial
> mortality “penalty” to living in urban places
> (e.g., Williamson, 1982, 1990, ch. 9; Davis, 1973; Weber, 1899, ch 6; Brown, 1991; Vögele, 1994).
> By 1940, that urban penalty had been largely eliminated; and it was healthier, in many cases,
> to reside in a city than in the countryside. Part of the study of the great mortality transition
> in the United States is related to this phenomenon.

----------------------------------------------

I do observe a urban penalty in CO,GA,ID,KS,KY,LA,MS,MO,MT,NE,NC,SC,TN,WY,UT,(MN), (OR),(PA)
in 1922 [white population] , when that statistics ("table IV") ended in the public and was only
kept as manuscript since then.
There was a _rural_ penalty in New York and the North-East, although to smaller degree.
Most Southern States didn't report before ~1910, so that paper above probably discarded them.

It's a bit diffecult to compute the numbers for 1937,1938 (table 19,table II) but it doesn't seem that
much had changed between 1922 and 1937. E.g. New York vs. Missouri.
In 1939-1950 I can't find the data and urbanicity was missing in the 1950-census.
I may compute it for 1960 later ...

The urban penalty in the South [whites only] results from most causes -except infectious diseases- ,
especially cancer and heart disease, so it's not just the crowding argument or childhood mortality.

> lack of pure air, water and sunlight, together with uncleanly habits of life induced thereby.

this doesn't seem to explain it, IMO.

> The rural-urban gap was closing, but it had not been eradicated by 1940 as it had been
> for the white population.

> analysis of county level data from period 1930 to 1940 (Fishback, Haines, and Kantor, 2000).

> results were different for the South

deathrates by state , deaths per 1M population

Code:
1915,CA,13799,13581,0814,0810,2432,2279,1901,1689,0090,0104,0256,0340
1915,CO,12824,10429,0481,0431,1632,1156,1135,0829,0102,0051,0188,0156
1915,CT,14937,14858,0949,1347,2004,2355,1453,1725,0081,0110,0227,0333
1915,IN,13561,12205,0812,0954,1943,1923,1484,1475,0094,0121,0248,0234
1915,KS,12960,09371,0654,0649,1740,1314,1269,0994,0054,0055,0197,0181
1915,KY,13839,10541,0806,0379,1952,0938,1324,0732,0059,0046,0343,0098
1915,ME,17224,15138,0965,1318,2692,2622,1834,1860,0045,0163,0547,0412
1915,MD,15147,13029,0934,0849,2103,1681,1576,1314,0072,0090,0274,0184
1915,MA,14334,15048,0926,1310,2364,3172,1694,2215,0080,0152,0367,0619
1915,MI,14727,12533,0744,0912,1984,2157,1474,1699,0070,0106,0258,0233
1915,MN,11150,09641,0460,0599,1441,1244,1064,0989,0048,0043,0186,0118
1915,MO,14399,10622,0677,0574,1948,1157,1332,0861,0060,0058,0400,0157
1915,MT,14996,10166,0468,0430,1843,1042,1313,0780,0054,0036,0189,0108
1915,NH,16132,16098,0992,1571,2610,3378,1870,2335,0139,0228,0375,0630
1915,NJ,13602,14185,0742,1168,1774,2131,1353,1662,0072,0090,0140,0215
1915,NY,14312,15393,0648,1382,2139,3163,1681,2375,0060,0145,0189,0478
1915,NC,15228,12478,0766,0645,1489,1131,1132,0909,0052,0038,0174,0087
1915,OH,13818,12239,0892,1074,1920,2066,1419,1575,0077,0103,0252,0285
1915,PA,14876,12709,0745,0858,2046,1625,1582,1256,0062,0079,0183,0175
1915,RI,14942,14198,0968,0856,2245,2356,1577,1703,0080,0159,0358,0415
1915,UT,10393,09619,0493,0396,1451,1131,1132,0903,0049,0054,0125,0078
1915,VT,16315,14437,1063,1374,2730,2929,1834,2026,0167,0181,0521,0522
1915,VA,14225,10911,0921,0491,1748,1228,1392,1028,0074,0055,0164,0088
1915,WA,07848,08309,0414,0492,1189,1003,0870,0773,0059,0057,0107,0088
1915,WI,11679,10339,0615,0723,1459,1594,1022,1207,0059,0051,0210,0231

all,cer,cir,hea,ang,art (urban and rural) , 1915st.pdf, p156, table IV


1915,KY,all,13839,10541,gen,3792,3606,ner,1505,095 1,cir,1952,0938,res,1374,1014,dig,1296,1016,uro,15 53,0705,unn,1026,0619,ill,0059,0497


Code:
1922,CA,14173,13916,1020,0952,2750,2457,2224,1893,0156,0148,0197,0267
1922,CT,11972,12205,0924,1256,2016,2684,1610,2022,0116,0206,0162,0346    
1922,DE,12054,14287,0978,1339,1739,2306,1410,1774,0061,0231,0156,0142    
1922,FL,11816,10543,0660,0677,1883,1292,1251,0953,0271,0125,0186,0133 
1922,IL,11586,10886,0641,0844,2008,1847,1672,1442,0067,0101,0122,0220
1922,IN,11878,11978,0768,1108,1905,2164,1371,1600,0097,0162,0263,0311    
1922,ME,15868,14296,1334,1560,2560,2801,1738,2015,0216,0254,0476,0449    
1922,MD,12958,11729,0987,1114,2152,1833,1747,1403,0124,0132,0171,0206
1922,MA,12689,13480,0995,1446,2617,3444,1933,2454,0123,0165,0448,0702    
1922,MI,10611,12031,0638,1214,1728,2404,1296,1801,0069,0168,0213,0315    
1922,NH,14100,15070,1323,1693,2525,3268,1539,2129,0377,0299,0443,0747    
1922,NJ,11915,12681,0820,1263,1975,2410,1604,1915,0073,0120,0147,0241    
1922,NY,12437,14979,0677,1596,2424,3511,1996,2714,0106,0185,0187,0479    
1922,OH,11124,11569,0894,1279,1740,2188,1317,1688,0092,0130,0219,0291    
1922,RI,13201,12764,1205,1155,2281,2177,1800,1633,0099,0191,0266,0248
1922,VT,15810,14478,0948,1566,3133,3100,2082,2257,0392,0286,0515,0428    
1922,VA,11226,10021,0785,0678,1710,1395,1335,1117,0140,0084,0135,0135   -
1922,WA,10649,09591,0791,0744,1732,1500,1311,1118,0112,0108,0145,0186
1922,WI,10802,09721,0722,0795,1712,1593,1308,1268,0103,0084,0151,0159

1922,CO,16342,11802,0879,0640,2124,1312,1432,0923,0200,0080,0273,0196   -
1922,GA,12551,08339,0828,0487,1422,0766,1026,0622,0161,0049,0109,0048   -
1922,ID,14233,07538,0816,0440,1786,1005,1199,0759,0152,0069,0128,0093   -
1922,KS,13153,09738,0982,0859,1793,1518,1343,1134,0103,0094,0173,0182
1922,KY,13338,09234,0967,0466,2007,0896,1452,0680,0103,0051,0249,0115   -
1922,LA,14145,07152,0883,0275,2387,0802,1869,0617,0139,0052,0207,0047   -
1922,MS,15553,07946,1196,0375,1973,0847,1172,0677,0173,0070,0395,0056   -
1922,MO,13581,09636,0787,0726,2077,1250,1503,0926,0080,0063,0307,0197   -
1922,MT,13197,07368,0599,0386,1583,0980,1321,0774,0057,0057,0082,0059   -
1922,NE,13035,08317,0891,0695,2008,1275,1430,0952,0101,0074,0182,0135   -
1922,NC,13474,09836,0834,0647,1433,1061,1093,0916,0127,0054,0118,0045   -
1922,SC,16136,08808,1065,0499,2627,1085,1570,0889,0248,0067,0661,0060   -
1922,TN,13949,08625,0732,0370,1527,0754,1140,0622,0103,0048,0166,0045   -
1922,WY,14193,08538,0483,0393,1589,0899,0967,0691,0104,0039,0207,0067   -
1922,UT,12782,09088,0756,0357,1814,1118,1542,0971,0106,0057,0071,0040   -
1922,MN,11658,08392,0686,0660,1890,1375,1473,1087,0081,0059,0215,0150   -
1922,OR,13406,10352,1099,0984,2415,1627,1647,1279,0162,0137,0392,0120   -
1922,PA,13046,11533,0709,0921,2101,1821,1642,1372,0080,0107,0219,0237
1922,US,all,12682,10963,inf,1832,1934,can,1561,108 9,ner,1209,1277,
cir,2166,1685,ang,102,098,res,1415,1029,dig,1152,0 853,uro,1188,0884,
unn,981,818,ill,040,296




table IV , deathrates , both sexes, all ages

all,urban [all causes]
all,rural
cer,urban [cerebrovascular, stroke]
cer,rural
cir,urban [circulatory causes, except cerebrovascular]
cir,rural
hea,urban [heart disease]
hea,rural
ang,urban [angina pectoris]
ang,rural
art,urban [disease of arteries ]
art.rural



deathrates , all causes, urban and rural
1937,US,12954,09581
1937,AL,14908,07703
1937,KY,15625,09278
1937,MO,14020,09756
1937,NY,11643,13722
1937,TN,14476,08487

---------------edit-----------------------------

trying to get the population data by urbanicity ...
[rural-->urban seems to have changed especially in the 1940s
and 1950s , including the rural vs. urban mortality advantage
in the South

ipums , US historical population data https://usa.ipums.org

Steven Ruggles, Katie Genadek, Ronald Goeken, Josiah Grover,
and Matthew Sobek. Integrated Public Use Microdata Series:
Version 6.0 [Machine-readable database]. Minneapolis:
University of Minnesota, 2015.

-----------------------------------------
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Old 06-16-2016, 03:35 AM   #25
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here they suggest that electrification caused the CHD - "epidemic"
http://www.medical-hypotheses.com/ar...579-9/abstract
> Historical evidence that electrification caused the 20th century
> epidemic of “diseases of civilization

it it were so easy ... they would have already proved it.
As they did it with fat-diet,physical,activity,cholesterole,blood pressure etc.
Also in mice, in more direct data, electrificated communities, not just State-statistics.
Europe was electrificated earlier, but CHD started in USA
and then, why did it decline since 1970 so much ?
And why these mid-age males ?

Electrification correlates with remoteness, urbanicity, availability of certain new foods,
new living habits, so it could have contributed indirectly.

there are also books about this, a "movement" that electricity in general
is bad for health, all sorts of diseases. But in smaller dimensions,
not millions of deaths as with CHD

https://en.wikipedia.org/wiki/Electrification
> The electrification of households in Europe and North America began in the early 20th
> century in major cities and in areas served by electric railways and increased rapidly
> until about 1930 when 70% of households were electrified in the U.S.
> Rural areas were electrified first in Europe, and in the US the Rural Electric Administration,
> established in 1935 brought electrification to rural areas.[56]
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Last edited by gsgs; 06-16-2016 at 03:41 AM.
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